Tendon xanthomata: deposition of yellowish cholesterol rich material in the tendons, asociared with hyperlipidaemia. Eg on knuckles Xanthelasma: cholesterol deposits around the eyes. Corneal Arcus: deposition of cholesterol/lipid in the cornea. CRP : acute phase of protein produced predominantly by the liver in response to inflammatory cytokines
Chest Pain on Xray: evidence of another cause of chest pain such as air in the mediastinum (oesophageal rupture) or aortic dissection (widened mediastinum, pleural effusions).
Hypercoaguble state is part of normal physiological response to surgery which may promote coronary thrombosis.
What is cardiac tamponade?
Cardiac tamponade: acute failure due to collection of blood or fluid in the pericardial sack compressing the heart.
Sudden deterioration = may be bleeding into pericardial space.
Causes: pericarditis/malignant disease/trauma/rupture of free wall of myocardium following MI.
What are clinical features of cardiac tamponade?
Symptoms: tachycardia, hypotension, gross elevation of JVP, dyspnoea, collapse, soft heart sounds with early third heart sound, pulsus paradoxus, kussmaul’s sign
What is pulsus paradoxus?
Pulsus paradoxus: a large fall in BP during inspiration when the pulse may be impalpable.
What is Kussmaul’s Sign?
Kussmaul’sign: a paradoxical rise in the JVP during inspiration.
What is the first thing you should do if the patient is post op?
Open the chest! Use the sternotomy wires!
What would an ecg, xray and echo show to suggest someone has a cardiac tamponade?
ECG: (feautures of underlying disease eg MI/pericarditis)
ECG in large pericardial effusion: complexes are small and may see electrical alternans
Xray: enlarged globular heart/normal.
Echo: diagnose and locate where to aspirate.
What are electrical alternans?
Electrical alternans: a changing axis/amplitude with alternate beats caused by the heart swinging from side to side in the pericardial fluid.
How would you treat cardiac tamponade?
Percutaneous Pericardiocentesis = aspirate medial to cardiac apex / below xiphoid process.
Complications: arryhthmias, damage to coronary arteries, bleeding exacerbation of tamponade
Surgical drainage for viscous / loculated / recurrent effusion.
What sort of things should you check in HCU post-op after for example a valve replacement / CABG?
Watch out for bleeding! = if happening immediately give blood transfusion and if have high INR give FFP = Fresh Frozen Plasma.
Urine Output: acceptable = 0.5ml/kg/hour. Ideal = 1ml/kg/hour
JVP should be between 8-11. If men, familial, genetics. Marfan’s syndrome, thyrotoxicosis, rheumatic/ischaemic heart disease, atrial septal defect, hypertrophic cardiomyopathy.
What mitral valve leaflet, most commonly posterior prolapses into the left atrium abnormal ventricular contraction/papillary muscle strain/some mitral regurg.
What are the symptoms?
Atypical chest pain: submammary, stabbing or substernal, aching and severe or rarely similar to angina pectoris.
Palpitaions : abnormal ventricular contraction/ atrial/ventricular arryhtmias.
Sudden cardiac death rare but not unheard of : when valve prolapse is associated with severe mitral regurg surgery immediately.
What are the signs?
Mid systolic click (sudden tensing of valve and chordae snapping tight)
Late systolic/pan systolic murmur (from mitral regurg)
Echo: to look at the valve.
∫What is the treatment?
Beta blockers: for chest pain / palpitations.
Anticoagulation: to prevent thromboembolism.
Surgery: repair, replacement is rare, prophylaxis for endocarditis.
LUB DUB LUB DUB
Systolic murmurs : HOOT DUB
Diastolic murmurs : LUB HOOT
What is a bruit?
When a murmur occurs outside of the heart eg. Aortic aneurysm / narrowed carotied arteries.
What is a myxoma?
Myxoma: tumour of the heart tissue
Is aortic stenosis more common in men or women?
What is the commonest cause of AS? Describe its pathophysiology.
Calcific valve disease: mainly in the elderly.
Inflammatory process involving macrophages and T lymphocytes with initially thickening of subendothelium with adjascent fibrosis
Lesions contain lipoproteins which calcify increased stiffness decreased valve opening.
Why are there symptoms of angina in aortic stenosis?
Decreased left ventricular emptying left ventricular hypertrophy ischaemia.
Gets worse with excersise (as cannot increase CO)
What are some symptoms of left ventricular hypertrophy seen as a result aortic stenosis?
Syptoms: angina, arrythmias, left ventricular failure (although systolic function is normally preserved.)
What are the hallmark symptoms of Aortic stenosis?
Excersise induced syncope
No symptoms seen until it’s moderately severe after which poor prognosis – 2-3 years without surgery.
What are the signs of aortic stenosis?
Carotid Pulse: small volume and slow rising / plateau in nature.
Apex Beat: not normally displaced but is sustained + obvious.
Atrial kick: may feel a double impulse as the fourth heart sound (atrial contraction) may be felt.
Thrills: may feel systolic thrill in the aortic area.
Why isn’t the apex beat displaced in aortic stenosis even though technically the heart has gotten bigger?
Hypertrophy: (rather than dilatation) doesn’t produce noticeable cardiomegaly.
What sort of murmur does aortic stenosis produce?
Ejection systolic murmur = diamond shaped = crescendo decrscendo. =
Diamond shaped systolic murmur felt in the aortic area.
Longer if the disease is more severe.
May also hear : - systolic ejection click (unless valve immobile/calcified) – soft/inaudible second heart sound (when aortic valve becomes immobile) reversed splitting of second heart sound prominent fourth heart sound (atrial contraction. Happens unless mitral stenosis prevents it)
Does the intensity of an aortic stenosis murmur indicate the severity of the disease?
NO because it is lessened in reduced CO which occurs as the disease gets worse. – If really severe, may even become inaudible.
- Symptoms are a good indicator of severity.
What investigations would you do to look into aortic stenosis?
Chest Xray = small heart + prominent dilated ascending aorta.
Electrocardiogram = depressed ST segments + T wave inversion in ;eads 1,AVL,V5,V6 = the ones orientated towards the left ventricle)
Suggesting left ventricular hypertrophy + left atrial delay.
Normally sinus rhythm though ventricular arrythmias may develop.
Echo = thickened/calcified aortic valve cusps + left ventricular hypertrophy.
How would you measure the ejection gradient?
Gradient: CW Dopplar
Why would you carry out Cardiac Catheterisation?
Cardiac Catheterisation: documents gradient (systolic pressure difference) between aorta and left ventricle and left ventricular function.
Coronary Angiography: before recommending surgery.
How would you treat aortic stenosis?
Valvotomy: initially if the valve isn’t too severely deformed/heavily calcified = replacement afew years later.
Valvuloplasty: blowing up a balloon = bridge to surgery.
Valve Replacement: all patients end up needing it.
Percutaneous Valve Replacement: TAVI : when patients aren’t sutiable for open heart surgery.
Which valve are you listening for when you ask the patient to sit forwards and where do you put your stethoscope?
Mitral Regurg: left sternal edge in the fourth intercostals space with the patient leaning forwards, “and stop”. = high pitched early diastolic murmur
Maybe also listen to the femoral arteries.
What are the most common causes of aortic regurg?
Rheumatic fever/endocarditis complicating a previously damaged valve which is either congenital or damaged by rheumatic fever. Also syphilis.
Are men or women more effected?
75% patients = men (though rhematic fever cause is more so in women)
What changes occur to the heart in aortic regurg?
Left ventricular hypertrophy
Decreased coronary perfusion as diastolic pressure falls because of the aortic run-off during diastole (ie the heart relaxes, blood falls from the aorta back into the ventricle and thus less goes into the coronary arteries)
Increased ischaemia as the enlarged heart is beating less properly and so has greater O2 requirement.
What are the symptoms of aortic regurg?
Significant symptoms occur when left ventricular failure occurs.
Pounding of the heart : from left vent dilatation
What’s the pulse like in aortic regurg?
Bounding or collapsing
Displaced and forceful apex beat
High pitched early diastolic murmur
Commonly an ejection systolic murmur as well from volume overload.
Quincke’s Sign = capillary pulsation in the nail beds
De Musset’s Sign = head nodding with each heart beat.
Duroziez’s Sign = to and from murmer in the femoral artery
Pistol shot femorals = sharp bang heard on auscultation of femoral arteries in time with heart beat
What would investigations show?
Chest Xray: left ventricular enlargement and dilatation of ascending aorta, valve may be calcified (syphilis/valvular disease)
ECG: sinus rhythm, tall R waves, left leads: inverted T waves, right leads : deep S waves as signs of left vent hypertrophy.
Echo: vigourous contraction and dilated left ventricle, enlarged aortic root.
How do you treat aoritic regurg?
Treat underlying cause of valve damage (endocarditis/syphilis)
Surgery: before symptoms get too bad: prosthetic (degeneration and calcification) or mechanical (warfarin) valve replacements.
Antibiotic prophylaxis against endocarditis after surgery.
Rumbling mid-diastolic murmur with sometimes an opening snap– left lower sternal edge on inspiration (may be mistaken for mitral stenosis)
Is tricuspid stenosis very common?
No, it’s rare, women > men
Rheumatic valve disease, accompanying mitral and or aortic valve disease.
Reduced CO which is restored to normal when the right atrial pressure increases but as a result there is (as blood not able to dispere pressure by traveling through the lungs)
Systemic Venous conjestion hepatomegaly, ascites, dependent odema.
What are the symptoms of tricupsid stenosis?
Abdominal pain : hepatomegaly
What are the signs of tricuspid stenosis?
Prominent jugular venous a wave (although unusual to remain in sinus rhythm)
Describe the investigation you’d see:
Chest xray: prominent right atrial bulge
ECG: peak P wave in lead 2 (enlarged right atrium)
Echo: abnormal valve is not easily seen
Cardiac catheterization = gradient between right ventricle and atrium + dilated right atrium
How would you treat tricuspid stenosis?
Blowing pansystolic murmur est heard on inspiration on lower left sternal edge.
When does this occur?
May occur whenever the right ventricle dilates =
Cor Pulmonale, myocardial infarction, pulmonary hypertension
Rheumatic heart disease, infective endocarditis, carcinoid syndrome, Ebstein’s anomaly, congenital abnormalities
High right atrial and systemic vneous pressure Symptoms of right heart failure.
Large jugular venus cv wave
Palpable liver pulsates in sytole
How would you treat tricuspid regurg?
Functional = normally disappears with medical management
Surgery: eg in drug users with infective endocarditis
Harsh mid systolic ejection murmur, inspiration, left of sternum, 2nd intercostal space
Pulmonary closure = delayed and soft
Right ventricular heave
Right ventricular fourth sound
Prominent jugular a wave
Right ventricular hypertrophy right atrial hypertrophy
Pulmonary obstruction death/ fatigue / syncope / symptoms of right heart failure.
What would you see on the Xray of someone with Pulmonary Stenosis?
Xray: prominent pulmonary artery (post stenotic dilatation)
ECG” left and right ventricular hypertrophy
How would you treat it?
Decrescendo diastolic murmur, sounds like aortic regurg
Is pulmonary stenosis or regurge more common?
Due to pulmonary hypertension which causes the pulmonary valve ring to dilate
Is pulmonary regurg a serious problem?
No usually causes no symptoms and treatment is rarely needed
Prosthetic: degrade (after ten years), vegetations, thrombosis, calcifications
Mechanical: durable, thrombogenic (give anticoagulation like warfarin), lifetime
Anitbiotic prophylaxis is necessary post op to prevent prosthetic valve endocarditis
What is cardiac catheterisation?
Specially esogned catherer inserted into vein/artery guided into heart under radiographic fluroscopic guidance measure intracardiax pressures/taje saples from chambers/obtain angiograms.
A brief guide to Cardiac Pain:
Site: centre of the chest
Radiation: neck/jaw/upper/lower arms/back
Character: may be discomfort rather than pain/ dull/constricting/chokin/heavy, described as “squeezing/crushing/burning/aching”. Hand gestures used for ischaemic pain.
Ischamic Pain: use of hand gestures, onset after exertion/emotion/large meal/cold wind + breathlessness
Is NOT : sharp/stabbing/pricking/knifelike
Pleuritic Pain: described as “sharp/catching” sensation exacerbated by breathing/coughing/movement.
Musculoskeletal Pain: asociated with a specific movement (eg bending/strerching/turning) and is after rather than during exertion. May be local tenderness. Some causes: arthritis,costochondritis,intercostal muscle injury, coxsachie viral infections, trauma.
Onset: cardiac pain gradually builds up. (Angina/MI)
If Sudden onset = aortic dissection/massive pulmonary embolism/pneumothorax + autonomic disturbance (also happens with MI which takes afew minutes to come on and comes with breathlessness) sweating/nausea/vomitting/
What would be your differential diagnoses of chest pain?
Pyschological aspects of chest pain: look for features of anxiety/neurosis + lacks predictable link with excersise. Consider that they might know someone who’s died of heart disease.
Myocarditis/pericarditis: retrosternally to the left / in the left/right shoulder – varies in intensity with phase of movement and respiration. “Sharp/catch” pain, history of prodromal viral illness.
Mitral Valve prolapse: left sided chest apins that could be muscoloskeletal might be MVP.
Oesophageal Pain: mimics angina but get a history of eating/drinking/oesophageal reflux.
What is Stable Angina?
Stable Angina: effort-related chest discomfort = COMES ON WITH EXCERSISE = fixed stenoisis + demand led ischaemia + predictable + relation to effort excersise tolerance test.
Normal physical exam but look out for hyperlipidaemia/diabetes, left ventricular dysfunction (dyskinetic apezx beat, gallop rhythm) + arterial disease (carotid bruit/peripheral vascular disease) + heart murmur (otherwise is probably CAD)
Investigations: FBC/ fasting glucose test/lipids/thyroid function test/12-lead ECG/excersise test
What does the term “Acute Coronary Syndrome” mean?
ACS = prolonged + severe cardiac chest pain at rest = could be unstable angina/MI.
Require urgent attention to avoid serious events signs of hypotension/heart failure/ecg changes (ST elevation/depression)/biochemical markers like troponin 1+2 do ecg and look at biochemical markers + keep in hospital until >12 hours without pain/signs(troponin, creatinine kinase, myoglobin)
Unstable angina: = dynamic stenoisis (clots forming) + supply led ischaemia + unpredictable ecg/biochemical markers like troponin.
Dyspnoea:Cardiac causes = Acute Pumonary Odema/ Chronic Heart Failure/Angina
What are causes of Acute Pulmonary Odema?
Major event eg MI in a previously healthy heart/ atrial fibrillation in a diseased heart.
Increase in left ventricular diastolic pressure increase in pressure in left atrium, pulmonary veins +capillaires.
What are the symptoms of Acute Pulmonary Odema?
Rapid shallow respiration + recruitment of accessory muscles, coughing, wheezing = cardiac asthma, sputum = profuse/frothy/blood streaked/pink, crepitations + ronchi on auscultation, fighting for breath (so stand up/sit up), unable to speak, distressed, cyanosed, agitated, sweaty, pale, (may also be signs of right heart failure)
Describe dyspnoea in Chronic Heart Failure:
First presents on moderate exertion (walking uphill) and gets worse and worse till patient struggles getting from room-room.
Symptoms: Orthopneoa, Paroxysmal Nocturnal Dyspnoea, Cheyne Stokes Respiration
What is the mechanism behind orthopnoea?
Lying down increases venous return to the heart heart has to suddenly work harder, requiring more oxygen breathlessness.
What is the mechanism behind PND?
Sleeping, fluid shifts from interstitial tissues in the peruperies into the circulation within 1-2 hours of lying down (as the heart is not beating strongly enough to maintain adequate pressure) causes pulmonary odema to develop they sit up fighting for breath.
What is Cheyne Stokes Respiration?
Cheyne Stokes Respiration: cyclic pattern (slowly diminshing respiration leading to aponoea progressivbely increasing respiration and hyperventilation accompanied by panic) of respiration due to reduced sensitivity of respiratory centre to CO2.
Occurs in: left ventricular failure, diffuse cerebral athersclerosis, stroke/heady injury, exagerated by sleep/barbituates/narcotics.
Heart disease like CAD and stroke correlates with blood pressure at any age anti hypertensive therapy reduces this risk. Degree of risk depends on the combination of risk factors.
There exists malignant/accelerated phase hypertension where everything happens very quickly and death occurs within months controlled reduction over 24-36 hours. Headaches may be a sign of malignant hypertension.
Bad = high salt/alcohol/obesity/lack of excersise/impaired interuterine growth. Little evidence that stress causes it.
What causes hypertension?
95% = idiopathic.
Mostly asymptomatic, sometimes headache, normally found randomly so have BP checked every five years.
Secondary Causes: alcohol, pregnancy, renal disease, endocrine disease (Phacromocytoma = paroxysmal headache, palpitation, sweating), drugs, coarction of the aorta.
What is Coarction of the Aorta? How might it be picked up?
Coarctation of the aorta, or aortic coarctation, is a congenital condition whereby the aorta narrows in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.
Can you find anything on examination of someone with hypertension?
May be some findings : left ventricular hypertrophy (apical heave), accentuation of second heart sound, a fourth heart sound, abnormal optic fundi, evidence of peripheral vascular disease.
How do you diagnose hypertension?
BP Check. If first reading is high wait five minutes to take the second one.
Ambulatory BP checks: generally 12/7 mmhg lower than normal BP check.
What are the aims of treating hypertension?
Just want to reduce the risk of adverse cardiovascular events like CAD, stroke, heart failure. Treatment is more effective in those at higher risk, eg the elderly. Can use a chart to work out the relative risk looking at BP, smoking, diabetes, cholesterol, ecg.
Follow up every 3 months.
What is the non-drug therapy for treating hypertension?
Obesity, reduced alcohol and salt, excersise, fruit and veg, no smoking, yes oily fish and diet low in sat fat.
What sort of drugs can be used to treat hypertension?
CONSIDER: cost/convenience/responsiveness to treatment/freedom from side effects
Combination therapy may be more effective and fewer side effects.
Thiazide Type Dieuretics: blocks the NaCl Symporter in the DCT. (Increase the absorption of Ca2+ aswell)
Daily : 2.5mg bendroflumethiazide / 0.5mg cyclopenthiazide
Loop Dieuretics: block the NaK2Cl Cotransporter in the ascending Loop f Henle. (May be used in conjunction with ACE Inhibitors)
40mg/day Furosemide/Frusemide or 1mg/day Bumetanide
BETA BLOCKERS (Beta-adrenoreceptor antagonists : cardioselective, preferentially block beta1-adrenoreceptor in the heart. Beta 2 adrenoreceptors control vasodilation and bronchodilation so watch out for giving beta blockers to people with asthma/COPD.
100-200mg/day Meotprolol or 50-100mg Atenolol daily or Bisprolol 5-10mg daily
Labetalol : combined Beta and a-adrenorecptor antagonist, may be more effective than pure beta blockers.
ACE INHIBITORS : inhibit conversion of angiotensin 1 to angiotensin 2. Watch out for giving to people with renal failure. Check electrolytes and creatinine before and 1-2 weeks after starting. If creatinine increases, stop treatment and image the renal arteries with MRA
Catopril 25-75mg/day or Enalapirl 20mg/day (causes excessive growth of hair) or Ramipril 5-10mg/day or Lisinopril 10-20mg/day
Side Effects: first dose hypotension, cough, rash, hyperkaleamia, renal dysfunction, dusgeusia
ANGIOTENSIN 2 RECEPTOR ANTAGONISTS = same as ACEI but don’t influence bradykinin metabolism so no cough
Losartan 50-100mg daily, Valsartan 40-160 mg daily
CALCIUM ANTAGONISTS: calcium chanel blockers, act by relaxing smooth muscle in the arterial walls. Particularily useful in elderly.
Amlodipine 5-10 mg/day or Nefidipine 30-90mg/day (causes gum hyperplasia)
Side Effects : flushing, palpitations, fluid retention
Rate limiting calcium antagonists: when hypertension exists with angina, may cause bradycardia.
Dilitazem 200-300mg/day or Verapamil 240mg daily (causes constipation)
VASODILATORS (A BLOCKERS)
A-adrenoreceptor antagonists eg
Prazosin 0.5-20mg/day. Indoramin 25-100 mg twice daily, Doxazosin 1-4mg/day
Act directly on smooth muscle:
Hydralazine 25-100mg 12 hourly (causes SLE like syndrome) or Minoxidil 10-50mg daily (increased facial hair so not for female patients)
Side Effects : first dose and postural hypotension, headache, tachycardia, fluid retention.
CENTRALLY ACTING: effective but cause fatigue and are normally poorly tolerated.
Methyldopa 250mg 8 hourly or Clonidine 0.05-0.1mg 8-hourly
ADJUVANT DRUG THERAPY
Asprin : antiplatelet drug, reduces cardiovascular risk.
Side Effects : may cause bleeding particularly intracerebral haemorrhage.
Benefits outweight risks in patients: >50years with hypertension or with target organ damage / diabetes / 10 yr CHD risk >15%
Statins: reduce hyperlipidaemia and cardiovascular risk.
Cost in the main constraint. Use : total serum cholesterol > 5mmol/L and established vascular disease / hypertension with >30% risk developing CHD.
Which ethnic groups is hypertension more common in?
American black, Japanese
-40-60% explained by genetics.
Breifly describe the target organ damage that occurs with hypertension:
Vessels: dilate and become torturous, walls become less compliant, widespread atheroma (CAD/cerebrovascular disease)
Larger arteries (>1mm) = thickend internal elastic lamina, smooth muscle hypertrophied, fibrous tissue deposited.
Smaller arteries: hyaline ateriosclerosis occurs in th wall, lumen narrows, aneurysms may develop
These changes increase aggrevate hypertension by increasing vascular resistance and reducing renal function.
CNS: stroke (infarction/haemmorhage) = more common with hypertension, hypertensive encephalopathy
What is hypertensive encephalopathy?
Rare condition of hypertension and neuroligcal symptoms, like transient disturbances in sppech/vision, paraesthesiae, disorientation, fits and loss of consciousness, papilloedema
What is papillodema?
Optic disc swelling caused by increased intracranial pressure
Retina get retinopathy with varying degrees of severity.
Heart: mainly higher incidence of CAD, left ventricular hypertrophy even failure, atrial fibrillation.
Kidneys: proteinuria and progressive renal failure.
What is fundoscopy?
Fundoscopy = opthalmoscopy = looking into the eyes.
What are signs of left ventricular hypertrophy?
Forceful apex beat, and fourth heart sound (which occurs presystole) do an ecg/echocardiogram.
- Tall R wave in lead V5 or V6.
Is Nocturia a significant finding?
Nocturia : common in stress/alcohol excess/early sign of heart failure due to loss of renal concentrating ability/ feature of prostatism (do a rectal exam).
What non-cardiovascular cause may trigger atrial fibrillation?
What is Gamma-glutamyl transpeptidase a marker for?
Liver function? might be raised when there is alcohol excess.
What is the resting CO?
Resting CO: 5L
ECG and Heart Block
How fast does paper move through the ecg machine?Ecg = 25mm.secHow long is one large square?One large square: 0.2 secondsHow long is one small square? One small square: 0.04 secondsHow many squares make up one second?5What are “leads” when talking about the ecg?Leads: different viewpoints of the heart’s electrical activity. What is an electrode?Electrode: the physical wire connecting the heart to the machine. What is a 12-lead ecg?6 Chest leads : V1,V2,V3,V4,V5,V6 = look in a coronal plane6 limb leads: 1,11,111, aVR, aVL,aVF - Current running towards the leads causes positive deflection- Current running aways from leads causes negative deflection- Changes in leads’ normal pattern may suggest damage/abnormality in that part of the heart eg MI on inferior surface of the heart à abnormality in 11,111,aVF- Activation of the nodes doesn’t produce obvious waves in the ecg, it’s the conduction through the atria/ventricles that produces the waves- The AV node acts as a monitor to regulate how many depolarisations/beats get through to the ventricles from the SA node. Which leads look at the inferior surface of the heart?Inferior surface: 11,111,aVF à ST elevation = acute MIWhich leads look at the anterior surface of the heart?Leads V1-V4What does an anterior surface MI look like on the ecg?Anterior MI: elevated ST segment in those leads with Q waves in V1-V3What does the p wave indicate?P Waves: atrial depolarization from SA node across the atria. - little muscle so the voltage generated is relatively small. - Postive deflection in all but the aVR leadWhat is the PR interval?PR Interval: time taken for the depolarization wave to pass from origin in the SA node, across the atria, and through the AV node into the ventricles- Measure from beginning of P wave to beginning of R wave- Normally 3-5 small squares = 0.12-0.2 s What is the next step after an impulse has left the AV node?AV node à Bundle of His divdes into à- left and right bundle branches in the interventricular septum à Purkinje Fibres.Describe what the QRS complex is:
How does the left bundle branch divide?
Has anterior and posterior fascicles.
What direction does the Q wave go?
The first upwards one is called the R wave whether or not there is a q wave.
The QRS complex is positive or negative depending on whether the R or the S wave is bigger depends on the view the lead has of the heart. Eg leads looking from the right will be dominated by the S wave and be negatively deflected. Leads looking from the left will be positive because they will have a large voltage coming towards them.
How do you record an ecg?
Ask patient to lie down and relax
Clean the skin with spirit wipe and remove excess hair.
Attach 6 chest leads and 4 limb leads (one to each limb)
Paper speed: 25mm/s Calibration mark: 10mm=1mV
What is the p wave?
What is the pr interval?
Start of atrial depolarisation to start of ventricular depolarisation
What is the QRS complex?
What is the ST segment?
Pause in electrical activity (no more electrical current can be passed through the myocardium) before repolarisation
What is the T wave?
What is the QT interval?
Total time taken by ventricular depolarisation and repolarisation
What is the U wave?
Uncertain : possibly interventricular septal repolarisation / slow ventricular repolarisation
Depressed ST = ischaemia
Elevated ST = MI
What is the first heart sound?
Atrioventricular valves closing
What is the second heart sound?
The semi-lunar valves closing.
Current flowing towards the lead in the heart has a positive inflection.
The right atrium conducts before the left atrium (as the SAN node is in the right atrium) causing there actually to be two mini humps which merge together to make the p wave.
P Mitrale = when there is a delayed left atrium.
How long is a normal QRS complex?
>120ms = bundle branch block
Is the endo or epicardial action potential longer?
Endocardial AP is longer.
Where do you put all of the limb leads?
V1 and V2 : either side of the sternum in the fourth intercostals space
V4 : midaxillary line 5th intercostals space
V3 = the septum = diagonal line in between V2 and V4
V5 : anterior axiallary line 5th intercostals space
V6 : midaxillary line 5th intercostals space
What is a heart block?
Conduction disturbance happening at some point in the path of conduction from the SA node to the ventricles = Sinoatrial block, Atrioventricular block, Right Bundle Branch block, Left Bundle Branch Block, Left posterior fasicicular hemiblock, Left anterior fascicular hemiblock
What is a Sinoatrial Node block?
SAN BlocK = when the SA node conducts as normal but the impulse fails to reach the atria, hence there is no P wave.
What is atrioventricular block?
1ST Degree: longer PR interval as the message just takes longer to pass from the atria to the ventricles.
2ND Degree: some atrial impulses fail to be conducted to the ventricles.
3rd Degree: there is no conduction between the atria and the ventricles.
What is Bundle Branch block?
When there is a block in the brances if there is a block in both branches it is effectively like third degree heart block.
Can be rate dependant = compromised areas of heart conduction can’t keep up with rate of the conduction of impulses. (eg development of bundle branch block in SVT might look like VT)
What are escape rythms?
Escape rythyms: (appear later than expected) when there is a failure of either of the nodes to generate an impulse or there is a complete failure of conduction the heart has a number of subsidery pacemakers =
AV Junction = can take over as pacemaker if there’s nothing coming from the SAN node = 40-60bpm
Ventricular Myocardium = if SAN and AV fail = 15-40bpm with broad QRS complexes
Don’t suppress them, rather determine why they’ve happened and treat the underlying problem.
What are ectopic beats?
Ectopics (appear earlier than expected, also called “extrasystoles”/”premature beats”) = can occur anywhere in the heart but classified into
Atrial = p waves that occur earlier than expected and have an abnormal shape = may/may not get conducted through the AV node.
AV junctional = give rise to QRS complex earlier than expected (won’t have a p wave directly before). May also retrogradely activate the atria and may cause an inverted p wave.
Ventricular ectopics = (can be harmless or associated with more harmful arryhtmias especially with heart disease) broad earlier than expected QRS complexes, and there may be retyrograde conduction inverted p waves.
Giving antiarrythmics doesn’t necessarily decrease mortality, so only give if person is symptomatic.
Cardiac ablation/ICD = for malignant/dangerous arrhythmias.
Right Ventricular Outflow tract ectopics: left bundle branch block morphology with interior exis on the ECG = apparently have a good prognosis?!
What happens when a ventricular ectopic occurs at the same time as a T wave?
R on T ectopics: can trigger ventricular arrhythmias.
What does the term bigeminy describe?
Bigeminy: when one ectopic follows every normal beat.
What is an inverted p wave?
The atria being depolarised retrogradly eg in ectopic beats.
How do you work out the cardiac rate?
300 divided by the number of big squares between QRS complexes
Questions you should ask:
Where does the impulse arise from? = SA node, atria, AV junction, ventricles
How is the impulse conducted? = Normal/accelerated (eg WPW syndrome)/blocked
How is the patient?
Know the clinical details, why it was recorded, make a note of it for people interpreting it later.
Is ventricular activity present?
= Are there QRS complexes? If there is no electrical activity present : does the patient have a pulse (if not then they’re in asystole = you will still see a bit of baseline artefact, completely flat suggests the leads aren’t connected), are the electrodes connected, is the setting on the moniter too low?
What is the rate?
Is the ryhtm regular/irregular?
Is the spacing between the QRS complexes the same throughout?
Eg Atrial fibrillation/sinus arrhythmia/supraventricular rythym with intermittent AV blocke/Ectopic beats
Is the QRS width normal/broad?
Normal = less than 0.12s / 120ms = 3 small squares
Ventricular rhythms : are generated in ventricular myocardium
Supraventricular rythms = anywhere up to and including the AV junction
Bundle branch blocks = wide QRS bcause problems with His-Purkinje system within the ventricles relies on conduction through myocytes which takes longer
Wid/Broad QRS = either
Ventricular Rythm (from ventricles rather than AV node)
Supraventricular Rhythm (normal) but aberrant conduction
Narrow QRS = less than 120ms/ three small squares = impulse must have started in AV node = supraventricular rhythm.
What is a supraventricular rythm?
Supraventricular rythms = anywhere up to and including the AV junction
Is atrial activity present?
Can be : P waves (orientation indicates where the depolarisation initiated = postivite in Lead 2 = near/in SAN node, inverted = retrograde = close to or in AV node
/flutter waves (atrial flutter = 300/min = saw tooth baseline)
/fibrillation waves (AF = random chaotic atrial impulses = 400-600bpm = chaotic low amplitude baseline activity)
/ unclear activity (eg p waves hidden in QRS complexes,
/absent (sinus arrest/SA block)
How are atial and ventricular activity related?
Every QRS associated with P wave = being activated by common source
More P waves than QRS : blocked conduction between atria and ventricles
More QRS than P waves: AV dissociation with ventricles operating independently of atria at a higher rate/
When would you see a broad QRS complex?
Broad complex tachycardia is always assumed to be VT unless proven otherwise.
When impulses are not travelling in the His-Purkinje system but rather being conducted through myocytes = eg Bundle branch block, ventricular ectopics , in VT (impulses can’t travel through His-Purkinje system unless the impulse starts in the AV node.
VT more likely in old people. Probably won’t see signs of bundle branch block (V1 V6) rather independent atrial activity (independent P wave activity/fusion beats/capture beats), QRS>0.14s/3.5 small squares, concordance in leads V1-V6, a shift in QRS axis of 40degress or more, left or right.
SVT : more likely in young people with conduction problems (V1 V6) with no previous cardiac history.
What is a Supraventricular tachycardia?
Supraventricular tachycardia: HR >100bpm that originates above the ventricles. Eg sinus tachycardia, AF, atrial tachycardia, AV-reentry tachycardias
What is a fusion beat?
When ventricles are activated by an atrial impulse and ventricular impulse arriving simultaneously.
What is a Capture beat?
Capture Beat: atiral impulse “captures” ventricles for a beat normal QRS which may be preceded by normal p wave.
What is “concordance”?
When something is the same direction in lots of different leads.
Heart Sounds and Murmurs
What does the S1 heart sound represent?
LUB : S1: tricuspid and mitral valves closing (a minimally split first heart sound may be normal)
What does S2 heart sound represent?
DUB : S2: pulmonary and aortic valves closing (this will sound split at peak inspiration)
When does systole descibe in the heart beat?
Systole = ventricular contraction = the time between heart sound 1 and 2
When does diastole describe?
Diastole = the heart relaxing = in between S2 and S1
What does pan systolic mean?
Pan Systolic: throughout systole eg mitral regurg
What do the S3 and s4 sounds represent?
Sound of blood moving through the atria
S3: the natural filling
S4: the atria contracting to squeeze the rest of the blood out.
When is the third heart sound heard?
Early in diastole (remember it’s the sound of the atria filling)
Very low, listen with the bell at the apex, heard better with patient lying on their left side
When you hear something that sounds like tennese, what are you hearing?
The third heart sound
When might you hear S3 and S4 heart sounds?
S3 and S4 = in conjestive heart failure / increased flow
In a normal heart beat is the aortic or the pulmonary valve louder?
It is abnormal for heart sounds to be louder on the left than the right as generally the aortic valve (heard on the right) is louder than the pulmonary (heard on the right) eg in pulmonary hypertension / aortic stenosis
What is a murmur?
Audible flow eg caused by turbulance = affected by diameter, narrowing, roughness, and flow rate.
Name two Systolic Murmurs:
Systolic murmurs aren’t necessarily pathological = may hear them in pregnancy, hyperthyroidism, exercise and anemia treat them and the murmur goes away
Heard in early systole, is short frequency, and midrange frequency.
Heard best in the pulmonary area, loudest on inspiration
With increased heart rate (eh 120 bpm) systole and diastole are of about equal length
How fast does paper move through the ecg machine?
Ecg = 25mm.sec
How long is one large square?
One large square: 0.2 seconds
How long is one small square?
One small square: 0.04 seconds
How many squares make up one second?
What are “leads” when talking about the ecg?
Leads: different viewpoints of the heart’s electrical activity.
What is an electrode?
Electrode: the physical wire connecting the heart to the machine.
What is a 12-lead ecg?
6 Chest leads : V1,V2,V3,V4,V5,V6 = look in a coronal plane
6 limb leads: 1,11,111, aVR, aVL,aVF
Current running towards the leads causes positive deflection
Current running aways from leads causes negative deflection
Changes in leads’ normal pattern may suggest damage/abnormality in that part of the heart eg MI on inferior surface of the heart abnormality in 11,111,aVF
Activation of the nodes doesn’t produce obvious waves in the ecg, it’s the conduction through the atria/ventricles that produces the waves
The AV node acts as a monitor to regulate how many depolarisations/beats get through to the ventricles from the SA node.
Which leads look at the inferior surface of the heart?
Inferior surface: 11,111,aVF ST elevation = acute MI
Which leads look at the anterior surface of the heart?
What does an anterior surface MI look like on the ecg?
Anterior MI: elevated ST segment in those leads with Q waves in V1-V3
What does the p wave indicate?
P Waves: atrial depolarization from SA node across the atria. little muscle so the voltage generated is relatively small.
Postive deflection in all but the aVR lead
What is the PR interval?
PR Interval: time taken for the depolarization wave to pass from origin in the SA node, across the atria, and through the AV node into the ventricles
Measure from beginning of P wave to beginning of R wave
Normally 3-5 small squares = 0.12-0.2 s
What is the next step after an impulse has left the AV node?
AV node Bundle of His divdes into left and right bundle branches in the interventricular septum Purkinje Fibres.
Describe what the QRS complex is:
Heart Failure causes increased venous pressure because the ventricles fail so there is a back up of blood in the systemic circulation.
What is Starling’s Law of the Heart?
Starling’s Law of the heart, which states that the force of contraction is proportional to the end-diastolic stretch of the myocardium (although only up to a certain point).
As cardiac output is reduced compensatory RAA (increased blood volume) and sympathetic stimulation (tachycardia) occur.
Why may there be pulmonary effusion in heart failure?
There is increased left atrial back pressure, increased blood volume, and pulmonary capillary pressure also rises.
The RAA means there is increased blood volume with decreased oncotic pressure of plasma proteins meaning that more fluid is pushed into the interstitium of the lung causing them: to become stiffer and make breathing more difficult. fluid accumulates in the alveoli of the lung leading to reduced gas exchange and severe shortness of breath.
Why might a patient experience orthopnoea in heart failure?
Breathlessness lying down: lying down there becomes more blood in the pulmonary circulation due to decreased effects of gravity there is increased capillary pressure fluid moves into lung interstitium and alveoli reduced area for gas exchange and shortness of breath.
What is Paroxysmal Nocturnal Dyspnoea?
PND: is orthopnoea when you’re asleep, causing you to wake up and sit up gasping for breath. (So that the fluid moves to the bottom of the lungs and they can breathe again.)
How is the fluid in pulmonary effusion removed from in the alveoli?
Active transport of sodium and chloride across the alveolar epithelial barrier.
When does non-cardiac pulmonary odema occur?
Noncardiogenic pulmonary odema: permeability is increased from direct/indirect lung tissue injury (incl acute pulmonary distress syndrome)
The exudate has a high protein content.
What are the most important risk factors in heart disease?
High BP, diabetes, smoking, cholesterol level, positive family history, previous heart problems
What is heart failure:
Heart Failure= a syndrome = any structural/functional disorder that impairs pumping.
50% Mortality at five years.
Initially there are compensatory mechanisms which eventually become pathophysiological eg peripheral vasoconstriction and sodium retention.
- Mild decreased heart function causes venous pressure which increases diastolic volume (due to less blood being ejected during systole because of poor heart function and higher pressure in the venous system – Stahling’s Law compensates).
There is decreased ejection fraction
- In more severe heart failure : there is large increase in venous pressure causing dyspnoea (odema in the interstitial and alveolar fluid and hepatic enlargement/ascites caused by increased systemic pressure) and CO is maintained by tachycardia to make up for the decreased stroke volume.
Cannot increase CO to faciliatate excersise = hence breathlessness on exertion (Angina)
Outflow resistance ie Afterload
Pulmonary/systemic resistance. Physical characteristcs of vessel walls. Volume of blood that is ejected.
- As afterload increases, CO decreases increased end diastolic volume increased ventricle dilatation.
Contractility of myocardium
There is over activation of the sympathetic nervous system having damaging effects on the heart.
Hypoxia reduces myocardial contractility.
Salt and water retention
Increased venous pressure salt and water retention.
Decreased renal perfusion activation of rennin-angiotensin system further increased venous pressure.
Increased ventricular wall stress promotes ventricular dilatation (bad!) and RAA system may be toxic to myocardial cells.
Alteration of ventricular size shape and function due to pathological compensation and MI, cardiomyopathy, hypertension, valvular disease.
Ventricular dilatation =Hypertrophy, loss of myocytes, increased interstitial fibrosis,
- There is prolongation of the calcium current elongation of contraction and relaxation.
- There may be changes in myocardial protein expression for the worse (reversion to fetal protein).
- There may be apoptosis of myocytes.
- Atrial stretch release of ANP, NMPA, C-type peptide (induces diuresis, natriuresism vasodilatation, suppression of RAA) = may be markers of heart disease?
- Endothelium dependent vasodilatation of peripheral vessels may be impaired due to abnormal release of NO and endothelin (which causes vasocontriction, sympathetic stimulation, RAA activation, left ventricular hypertrophy) Endothelin antagonists are being developed.
Left ventricular systolic dysfunction
Right Ventricular systolic dysfunction = either secondary to LVSD or pulmonary hypertension, right ventricular infarction, right arrythmias, congenital heart disease.
Diastolic Heart Failure: = more common in eldery hypertensive patients. Symptoms and signs of heart failure with preserved left ventricular ejection fraction >45-50% + abnormal ventricular relaxtion.
= Exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue.
= Cardiomegaly, third and fourth heart sounds, elevated JVP, tachycardia, hypotension, bi-basal crackles (pulmonary odema), pleural effusion, ankle odema, ascites, tender hepatomegaly.
Blood Tests: FBC, luver biochemistry, urea and electrolytes, cardiac enymes (acute heart failure), BNP/terminal end of proBNF, thyroid function
Chest Xray: cardiomegaly, pulmonary conjestion with upper lobe diversion, fluid in fissures, Kerley B lines, pulmonary odema
Ecg: ischaemia, hypertension, arrythmia
Echocardiography: cardiac chamber dimension, systolic and diastolic function, region wall motion abnormalities, valvular heart diseases, heart myopathies
Stress echocardiography: assessment of viability in dysfunctional myocardium
Nuclear Cardiology: eg. Radionucleotide angiography RNA = ventricular ejection fraction, SPECT/PET scan =myocardial ischaemia and assessment of viability in dysfunctional myocardium
CMR = cardiac MRI
Cardiac catheterisation = diagnose ischameic heart failure, measurement of pulmonary artery pressure, left atrial pressure, left ventricular end-diastolic pressure
Cardiac biopsy: diagnoses cardiac myopthaties eg amyloid
Cardiopulmonary Excersise Testing VO2 (peak oxygen consumption) predictive of hospital admission/death / 6minute excersise walk.
Ambulatory 24-hour ECG monitering – suspected arrythmia. Determine if defib is appropriate.
Identify aggrevating factors and illiminate.
Education, obesity control, diet (low salt, fluid restriction if severe, moderate alchol, lots of omega-3 polyunsaturated fatty acids, stop smoking, bed rest with daily leg excersises to avoid DVT, low-level endurance excersise in compensated heart failure (20-30 mins walking 2-3 times/week), vaccination against pneumococcal disease/influenza, air travel IS possible, people on Viagra (pde5 inhibitors) may induce profound hypotension, no driving large lorries
Functional capacity: VO2 max, exceresise tolerance test, echocardiography
Fluid status: body weight, U&Es, clinical
Cardiac Rhythm: ECG 24 hour tape
- Troponins and CRP = prognostic value]
What does ADH/vasopressin do?
ADH/vasopressin: increases water retention by causing uptake of aquaporins in collecting ducts.
What does the hormone endothelin cause in the body?
What does adeno mean?
Adeno: coming from a gland / from the glands. Eg adenocarcinoma / adenopathy.
What is mesothelium?
Mesothelium: cells of mesoderm origin that give rise to the simple squamous epithelium covering true serous membranes: pericardium, perit
Give examples of tissues with squamous cell epithelium:
Lining of upper respiratory tract/gut
Second most common form of cancer after basal cell carcinoma. Mainly in areas exposed to light, x3 more common in men than women, may metastisise.
What is rheumatology?
Rheumatology: internal medicine dealing with joints, soft tissues, autoimmune diseases, vasculitis, and heritable connective tissue disorders.
What is a PET scan?
PET scan: uses radiation, or nuclear medicine imaging, to produce 3-dimensional, color images of the functional processes within the human body. PET stands for positron emission tomography. The machine detects pairs of gamma rays which are emitted indirectly by a tracer (positron-emit ting radionuclide) which is placed in the body on a biologically active molecule.
What is meant by a “resection” in medicine?
Resection: the excision of a part of bone or an organ eg. Large bowel resection = removing part of the large bowel.
What does the JVP measure?
What is the insulating layer called between the atrium and the ventricles in the heart?
What is Starling’s Law of the heart?
Starling’s Law: increased preload increased stroke volume.
What is preload?
Preload: diastolic volume – the blood coming to the heart from the rest of the body.
Which cholinergic nerves supply the heart and what is their effect?
Vagus nerve: supplies SA and AV node via M2 muscarinic receptors, and under basal conditions has an inhibitory effect on sympathetic nerves supplying the heart.
Which lung has three lobes?
Right lung: has three lobes.
Which coronary artery does the circumflex artery come off?
Left stem of coronary artery left coronary (left anterior descending) and the circumflex ( left circumflex marginal artery).
Describe how the left main coronary artery divides:
Left main coronary circumflex and left anterior descending artery.
What is meant by “normal sinus rhythm”?
Normal sinus rhythm: a normal heart beat.
Normally 60-100 bpm.
What is the normal sinus rhythm?
Sinus rhythm: 60-100 bpm.
How do veins drain the heart?
Venous drainage: into the right atrium vias the coronary sinus.
What is the coronary sinus?
Coronary Sinus: dilatation of veins draining the myocardium which empty into the right atrium
What does the right coronary artery mainly supply?
Right coronary: SA node and AV node (60% and 90% of people) so disease here may cause sinus bradycardia/ AV nodal block.
What does the left coronary artery mainly supply and thus what happens when it’s diseased?
Left coronary: majority of left ventricle – stenosis is dangerous and complete blockage = rarely compatible with life.
What is the Bayliss myogenic response?
Part of autoregulation - The ability of blood vessels to contract when distended.
What is the “vasodilator washout effect”?
Part of autoregulation : Vasodilator washout effect: vasoconstriction triggered by decrease in the concentration of tissue metabolites.
What is the effect of NO on smooth muscle and how is it used to treat the heart?
NO: causes contraction of smooth muscle (via guanylate cyclase and cGMP) = protects against atherosclerosis, high BP, heart failure, and thrombosis.
What does ACE enzyme do?
ACE enzymw: angio 1 angio 2 = vasconstrictor effects and aldosterone release increased sodium absorption.
Which enzyme stops platelets from clotting and how?
PGI2 (prostaglandin I2) prevents platelet aggregation.
Produced in endothelial cells by COX enzyme.
- NO also aids.
How does aspirin work?
Aspirin: inhibits the COX pathway inplatelets but doesn’t effect PGI2 synthesis.
What is clopidogrel?
Clopidogrel: antithrombotic agent = ADP receptor antagonist.
Which cell signalling molecule facilitates the growth of new blood vessels?
What is the Ductus Arteriosus?
Ductus arteriosus: diverts blood coming from the right ventricle from the pulmonary artery to the aorta in the fetus.
What sort of blood does the Pulmonary Artery carry and to where?
PA: leaves the right ventricle to take deoxygenated blood to the lungs.
What are the main symptoms of heart disease?
Heart disease: chest pain, dyspnoea, palpitations, syncope, fatigue, peripheral odema.
What is the NYHA “cardiac status” grading? Know the different grades.
Grade 1: uncompromised = no breathlessness.
Grade 2: slightly compromised = on severe exertion.
Grade 3: moderately compromised = on mild exertion.
Grade 4: severely compromised = breathless at rest.
What does statin pleiotopy mean?
Statin pleiotropy: the fact that statins not only lower your cholestereal they also have some effect in making the plaques regress.
What should you remember to consider in heart disease? ABC…
Fags, fat, and family
Genes and gender
What is the main characteristic of angina?
Rheumatic Fever and Endocarditis
NB Infective Endocarditis and Rheumatic Fever are different as Rheumatic Fver is specifically group strepp A antibody cross reactivity which may cause generalised carditis whereas Infective Endocarditis is when there is a microbial infection of the actual heart valve or lining the the chamber.
What is rheumatic fever?
Affects: children/young adults 5-15
Where: Asia, Africa, South America, up to 100/100,000
What is the mechanism of Rheumatic Fever?
An inflammatory disease involving antibody cross reactivity involving heart,joints,skin and brain.
2-3 weeks following streptococcal pyogenes infection like streptococcal pharyngitis or scarlet fever.
Abnormal response to infection with specific strains of group A streptococci
Antigens cross-react with cardiac myosin and sarcolemmal membrane protein
Antibodies produced mediate inflammation in endo,myo,and pericardium and joints and skin.
How do people present?
High fever following a sore throat.
Classic : Fever, anaorexia, lethargy and joint pains (normally about two-three weeks after) following streptococcal pharyngitis (may not present with sore throat).
Other : Arthritis (75% = early on when antibodies are high = acute, painful, asymmetric and migratory inflammation of large joints which are red,swollen and tender lasting day-week, should respond to aspirin), skin rashes (Erythema marginatum in less than 10%), carditis, neurological changes (see explained below), Nodules (3 weeks after onset of oher manifestation so confirm rather than make the diagnosis) How can you tell if someone’s had it?
Combination of symptoms plus : Serological evidence of strep infection eg antistreptloysin O antibody ASO
Leucocytosis, raised ESR, raised CRP, throat swab culture (group A B-haemolytic streptococci)
Xray: cardiomegaly, pulmonary conjestion
ECG: first and second degree heart block, T wave inversion, reduction in QRS voltages
Echo: cardiac dilataion and valve abnormalities.
What is carditis?
Carditis: = pan = endo, myo and peri = more likely if the patient is younger. (Most people at 3, only a third in adolescence) – look for cardiomegaly / pulmonary conjestion
Symptoms: breathlessness (from heart failure/pericardial effusions), palpitations/chest pain (from pericarditis/pancarditis), tachycardia, cardiac enlargement, new/changed murmurs, syncope
Which is a common murmur to hear in carditis?
Soft systolic murmur of mitral regurg
Tricupsid and pulmonary valves are rarely involved
Why might cardiac failure occur?
Cardiac failure: from myocardial dysfunction and or mitral or aortic regurg.
Will see changes on the ecg
Conduction defects may occur and cause syncope
What is Sydenham’s Chorea/St Vitus Dance?
Sydenmham’s Chorea/St Vitus Dance: neurological manifestation of Rheumatic Fever = in 1/3 of cases, more common in females
3 months after episode of acute rheumatic fever. There is usually spontaneous recovery within a few months. ¼ will go on to develop chronic rheumatic valve disease.
Symptoms: emotional lability, followed by involuntary choriform movements of hands, feet or face, speech may be explosive or halting, http://www.youtube.com/watch?v=RnxqqW_nH0k How do you treat an acute attack of Rheumatic Fever?
Limit cardiac damage and relieve symptoms = bed rest (no strain on the heart : 2-6 weeks),
Benzathine penicillin 1.2 million units i.m or
Oral phenoxymethlpenicillin 250mg 6-hourly for 10 days = eliminates any residual streptococcal infection. Erythromycin if they’re allergic to penicillin.
Asprin for the arthritis – if it responds quickly, confirms the diagnosis.
Corticosteroids – for rapid relief of symptoms.
Antibiotic prophylaxis = if they’re at risk of getting it again.
What is Chronic Rheumatic Heart Disease?
Not like acute, rather get progressive fibrosis mainly of heart valves (eg mitral may get fusion of valve commissures and shortening of chordate tendinae) but perio and myocardium as well heart failure and conduction disorders.
At least half of people with RF with carditis, mainly in women, may be asymptomatic for years, may be hard to find RF or chorea in the history.
Mitral valve: 90% cases
Then aortic then tricuspid then pulmonary.
What is Infective Endocarditis?
Infective Endocarditis = microbial infection of the heart valve (native or prosthetic) / lining of cardiac chamber / blood vessel / congenital anomaly eg septal defect
What is the usual causative organism?
Causative organism:mainly bacteria
Also: rickettsia (Coxiella burnetti – Q fever endocarditis) / Chlamydia / fungus
Symptoms: asymptomatic, intermittent claudication (from arterial insufficiency), night/rest pain, tissue loss (ulceration and or ganagrene = in chronic or acute cases)
When is limb ischaemia classified as significant?
Ankle Brachial Index pressure index of less than 0.8 at rest.
If asymptomatic may be because they don’t want to or cant walk very far.
Critical limb ischaemia: ABPI index less than 55mmHg : trivial injuries do not heal, allows bacteria to enter gangrene/ulceration.
Without vascularisation amputation and or death.
Where is there pain in intermittent claudication?
Pain: calf, thigh and or buttock.
Tightness or cramp like pain, relieved with rest.
Other causes: is normally arterial cause, but can be due to venous or neurogenic.
What is night/rest pain and why does it happen?
Night pain pain 1-2 hours after falling asleep usually in the instep.
Why: beneficial effects of gravity are lost on lying down + in sleep reduction in HR, CO and BP makes it worse.
May end up sleeping in a chair which gives them odema and makes the pain worse.
Rest Pain: indicates severe multi-level arterial disease, gets worse at night.
How do you differentiate between neuropathic pain (in diabetes) and rest pain?
Neuropathic: not confined to foot, has burning/tingling/numbness, not relieved by dependency, is worse at night though.
What are signs and causes of acute limb ischaemia?
6 Ps : Pulseless, pallor, perishing cold, paraesthesia, paralysis, pain on squeezing muscle
Causes: Embolic (eg in AF), thrombotic (probs in atherosclerosis), compartment syndrome (when there is increased pressure in fascial compartment)
What is white leg syndrome?
Acute artieral occlusion intense spasm of the arterial tree distal to blockage marble white few hours fills with deoxygenated blood = mottling blue/light purple which blanches on pressure if ischaemia progresses goes dark blue/black and doesn’t blanch large patches of fixed staining and blistering and liqufaction.
What are symptoms of chronic limb ischaemia?
Absence of body hair, arterial claudication, absent or diminished pedal pulses, pain, positive Buergers Test
What might be the causes of intermittent leg pain which makes it hard to walk?
Intermittent claudication from peripheral artertial disease
Neurological : spinal canal stenosis
Why are the legs more affected than the arms?
Less good blood supply and they are more affected by atherosclerosis.
What would you want to know about pain in the legs?
Site: is it in both at the same time?
Calf = intermittent claudication
Buttock/thigh pain = maby be compromised arterial supplu in aorta/iliacs
Does it make them stop/can you walk through the pain?
What happens when you stop? (Claudication stops within 5 mins)
Does anything affect the pain? Eg cold weather/slowing down
Describe the arterial blood supply in the legs:
What is Peripheral Vacualr Disease in lay terms?
Narrowing of the arteries mainly in the legs (both) from atheroma = Like scale that develops in pipes tissues downstream have reduced blood supply which can cause symptoms and problems.
What sort of examinations should you consider doing?
BP, Cardio exam, resp exam with lung function, peripheral circulation and pulses (dorsalis pedis, posterior tibial, popliteal, femoral, dopplar scan to look at pulses, abdominal exam for aortic aneurysm, capillary refill (time and compare on both sides), fundoscopy to look at vessels, skin for xanthoma/xanthalamsma, corneal arcus
What is dopplar scaning used to look at?
Using ultrasound to examine vascular structures in real time
When would you test for d dimers?
They’re a marker of fibrin products which may be released in DVT.
What is the Ankle-Brachial Index? ankle-brachial index (ABI) (can be measured at bedside). Using the Doppler the pressure at the brachial artery and at the posterior tibial artery are measured, using a blood pressure cuff on the arm and the calf to determine the systolic pressure at both sites . The ankle systolic pressure is divided by the brachial pressure, both measured in the supine position.
Normally, the ratio is more than 1.
Less than 0.95, significant narrowing of one or more blood vessels in the legs is indicated.
Less than 0.8, pain in the foot, leg, or buttock may occur during exercise
Less than 0.4, symptoms may occur when at rest.
0.25 or below, severe limb-threatening PAD is probably present. There is no abnormality in the respiratory system despite the symptoms
What other investigations might you want to do?
ECG, Electrolytes/urea/creatinine, glucose, liver function test, ESR, FBC, Chest-xray (smokers), ultrasound, respiratory function tests, lipid profile
Why would you do ESR?
Rules out arteritis rather than atheroscleorosis.
What are normal glucose values in the blood?
What is Leriche’s Syndrome?
Leriche Syndrome : chronic lower limb ischaemia characterised by: intermittent claudication in the buttocks, pale, cold legs, sexual impotence, absent femoral pulses
Caused by aorto-iliac obstruction (e.g. saddle embolism at bifurcation of the aorta). The vessels above and below may be relatively normal.
How would you manage peripheral vascular disease?
Smoking cessation, check for hypertension, weight loss, increase excersise, lower cholesterol, angioplasty, bypass graft
What do you want to know when someone has a blackout?
Determine whether it could be epilepsy, did the person change colour
What are signs of ventricular tachycardia?
Wide QRS >140ms, AV dissociation, independent P waves, capture/fusion beats, beat to beat variability of QRS, looks like ventricular ectopics, history of ischaemic heart disease, concordance (chest leads all positive or all negative), absence of any rS, RS, or Rs complexes in chest leads 2
Name two side effects of Amiodarone – what is it used to treat?
Amiodarone used to treat arrhythmias = UV sensitivity and lung fibrosis (restrictive pattern)
What are some causes of Restrictive lung patterns in lung function tests?
Restrictive lung defects = caused by stiffness in the lungs/reduced lung compliance from infiltration in the lung, abnormalities in chest wall limiting expansion or something else occupying space within the thorax. Examples: pulmonary fibrosis, sarcoidosis idiopathic pulmonary fibrosis, associated with connective tissue disease like rheumatoid, drug induced (cytoxicosis, amiodarone), dust diseases (asbestoces, pneumoconiosis), chest wall abnormalities, kyphoscoliosis, muscle weakness, external restriction of lung expansion, pneumothorax, pleural effusion
NB : ectopic beats are not unusual or necessarily pathological
What is chronic leg ulceration? What are the differences between arterial and venous ulceration?
Caused by variety of things – can be artieral or venous.
Don’t bandage unless you know there is adequate arterial circulation (feel for pulses/check ABPI)
Muscles push blood from superfisical veins to deep veins, valves prevent retrograde flow.
Great Saphenous – anterior to MEDIAL malleolus behind the knee medial thigh common femoral vein @ saphofemoral junction.
Short Saphenous: behind LATERAL malleolus posterior aspect of calf --? Popliteal vein @ saphenopopliteal junction
What are the four main venous diseases? (Most common in the legs)
Varicose veins, superfiscial thrombosis (red painful area over affected vein), DVT (deep seated pain with swelling), chronic venous insufficiency and ulceration (may be painless or pain is relieved by elevating leg
What are the four cardinal signs?
Discolouration (pigmentation due to deposition of haemosidrein from breakdown of extra-vasated blood = deep blue/black/purple or bright red)
Ulceration = wounds from malfunctioning valves= usually above medial malleolus, in severe venous disease, patients may not ask for medical attention for years.
Always accompanied by lipodermatosclerosis
What is lipodermatosclerosis?
Lipodermatosclerosis: inflammation of fat layer beneath the skin. (Without varicose veins may suggest malignancy.)
Severity of symptoms doesn’t necessarily correlate with severity of disease.
What happens in chronic venous insufficiency and what changes would you see?
Skin changes in lower leg: varicose eczesma, lipodermatosclerosis, ulceration due to sustained venous hypertension which is due to reflux (90%) or obstruction 10% in the superfisical and or deep veins.
What are varicous veins?
Varicous veins: dilated tortuous veins from incompetend valves in the vein
Symptoms: aching discomfort, itching, feeling of swelling, worse prolonged standing/at end of the day What is Superficial Venous Thrombophlebitis?
Inflammation of superfiisical veins associated with itranluminal, usually sterile, thrombosis ie a clot in the superfisicial vein.
In 10% patients with varicose veins, more if preggers – may be from injury to vein/recurrent insertion of IV line.
Types of venous thrombosis:
Most common is DVT in the leg with PE to the lung (asymptomatic PE is thought to be present in 30% of patients with DVT)
Jugular vein thrombosis, upper limb DVT, cerebral sinus thrombosis, intra-abdominal venous thrombosis.
Arms: eg from recurrent trauma such as with body builders, arm swelling, discomfort, swollen, cyanosed/mottled skin, superfisicial distended veins
1/1000, mortality 1-3%.
What are the risk factors for getting a DVT?
Patient factors: increasing age, obesity, varicose veins, previous DVT, family history, pregnancy, puerperium, oestrogen containing pill, immobility, travel, IV drug use into femoral vein, surgery, MI, IBS, malignancy, nephritic syndrome, pneumonia,
Haematological disorders: Polycythaemia rubra vera, essential thrombocythaemia, deficiency of anti-coagulants: antithrombin, protein C, protein S, Paroxysmal nocturnal haemoglobinuria, Gain-of-function prothrombotic mutations (factor V Leiden, prothrombin gene G20210A, myelogibrosis), Antiphospholipid syndrome (lupus anticoagulant, anticardiolipin antibody)
What is puerperium? puerperium covers the 6-week period following birth
What does a DVT look like?
Lower limb:starts distally = pain, swelling, increase in temperature and dilatation of superfiscial veins, normally unilateral,
What are causes of unilateral leg swelling?
DVT, traumatic calf muscle tear (ask about physical activity), Baker’s cyst (often with rheumatoid arthritis)
How can you tell the difference between DVT and cellulitis?
Infective cellulits: marked skin erythema + heat localised in well-demarcated area of the leg, look for wound/ulcer for entry of infection.
How can you rank the likelihood of patients having a DVT?
Well’s Scoring system see end of page
Which investigations do you do to look in to DVT?
Well’s Score = 1 point per : cancer, paralysis/immobilisation, bedridden, tendernous, entire leg swollen calf swelling, pitting oedema, collateral superfiscial veins
D Dimer (if normal don’t suspect DVT, but if increased doesn’t necessarily mean they have a DVT)
Compression ultrasound = really good sensitivity for clots involving popliteal or above but lower for diagnosing calf vein thrombosis
How do you manage DVT?
Thrombolysis (if threatening limb)
Anticoagulation with low molecular weight Heparin followed by coumarin anticoagulant like Warfarin to get INR 2-3
What is the target INR for treatment of DVT?
What is the optimum anti-coagulation period?
6 weeks – 6 months
What do you do if patient can’t handle anticoagulation or they keep on getting PEs?
Insert a inferior vena cava filter
Recurrance of DVTs: 2-3% if have risk factors, 10% if it was spontaneous
What is Post-thrombotic syndrome?
Post thrombotic syndrome: persistant leg swelling, heaviness, discolouration,
Caused by: damage of venous valves by thrombus
Complications: ulceration around the medial malleolous.
How does Heparin work? What sort of drug is it?
Heparin = ANTI-COAGULANT inactivates thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism = causing the prevention of the formation of clots.
Low molecular weight Heparin : eg Enoxiparin
Name two anticoagulants:
Heparin and Warfarin
Name a thrombolytic:
Streptokinase and all the “ases”
What is Enoxiparin?
Acute cough: less than three weeks
Chronic cough: more than 8 weeks
Is the alveolar or the pleural pressure greater?
Alveolar, due to elastic recoil of the lungs.
NSAIDs have a role in development/precipitation of asthma in 5% patients.
Pneumothorax = spontaneous/secondary to emphysema/pulmonary fibrosis
What are the symptoms of a spontaneous pneumothorax?
Chest pain (acute onset, ipsilateral), dyspnoea, tachypnoea, hypoxia
Risk factors for developing spont. Pneumothorax?
Height/ smoking (menx20, womenx10)/ COPD/ diffuse parenchymal lung disease/ bronchiectasis/some forms of pneumonia
Why does being tall make you more likely to have pneumothorax?
Alveoli are subjected to a greater mean distending pressure over time, leading to subpleural bleb formation these blebs can burst (especially at apex o f lung) form a pneumothorax.
What are the symptoms of a medium Pulmonary embolism? small or medium PE: dyspnoea, pleuritic chest pain, if pulmonary infarction, haemoptysis. On examination there may be a pleural rub and tachypnoea
What are the symptoms of a massive PE?
Severe central chest pain and rapidly become shocked, pale and sweaty, marked tachypnoea and tachycardia. (Emergency as syncope and death can follow.)
On examination the patient is shocked, centrally cyanosed, with elevation of JVP, right ventricular heave and accentuation of the pulmonary component of the second heart sound.
What is pneumonia?
Pneumonia is consolidation of areas of the lung with an inflammatory infiltrate, caused by infection with bacteria, viruses, or other organisms. (inflammation of the lungs that can be caused by a variety of different things – aha!)
What are some symptoms of bacterial pneumonia?
Develops abruptly, may include chest pain, fever, shaking (rigors), chills, shortness of breath, and tachycardia, tachyopnoea.
What signs suggest an emergency pneumonia?
Medical emergency: high fever, tachycardia, low blood pressure, cyanosis, and mental confusion.
Watch out for severe abdominal pain which might accompany = don’t let is confuse you, as it may be irritation of the diaphragm pleura.
Why shouldn’t you give someone with asthma beta blockers?
Bronchioles normally have parasympathetic innervation which produces bronchoconstriction so by inhibiting the sympathetic nervous system you get default parasymp action. Hence they are best avoided in asthmatics/asthma attacks.
What may be the cause of breathlessness that has been lasting for minutes?
PE, pneumothorax, asthma, acute left ventricular failure, inhaled foreign body.
How can you differentiate asthma from pneumonia or PE?
On examination : the abscence of clinical markers of infection make pneumonia unlikely The abscence of Rt Heart strain makes a large PE unlikely
What should you ask about the breathlessness?
Any accompanying pain/ onset/ have you experienced this before (asthma), have you done any recent travel/moved house (sitting down = PE, new house = allergens)
How is pericardial pain characterised?
It’s relieved by sitting up and forward.
Describe hyperresponsiveness of the airways in asthma:
Their airways react to irritant or allergic stimuli by narrowing through muscle contraction and an inflammatory response in the airway wall.
What are the main symptoms of asthma?
Wheezing, coughing, shortness of breath, chest tightness.
How can you diagnose that the cause is asthma?
Lack of focal signs in chest or on CXR, the quiet chest and reduced PEFR
What is theophylline?
Theophylline: bronchodilator drug used to treat asthma.
Which immediate investigations would you carry out to diagnose an asthma attack?
ABG, ABG on 40% O2, D-dimers, Electrolytes urea creatinine, FBC (may have increased eosinophils in asthma), Chest Xray, respiratory function tests.
Which two later investigations would you carry out?
C Reactive protein, liver function test.
What might show up on a blood test when someone has pneumonia?
Increased CRP, Neutrophilia + decreased haemoglobin due to blood lost in to a consolidated lung.
Have a look at electrolytes, urea, creatinine, as pneumonia may develop hyponatraemia, dehydration and impaired renal function, which have implications for fluid management.
Liver function tests: may be disturbed in acute pneumonia
Air Bronchogram: to look for consolidation of the lung but the airways remaining patent
What is the normal range of arterial blood gases?
What might exacerbate asthma?
Viral infections, mould, pollen, air pollution.
Most attacks gradually worsen over hours/days but may also be sudden.
What do you need to order immediately if you think someone’s having an asthma attack?
PEF: always do immediately = compared to previous values/percentage of predicted.
ABG: to assess the PaCO2 to decide what sort of oxygen therapy.
Chest Xray: only if pneumothorax is suspected.
What are signs of acute severe asthma?
PEF 33-50% predicted, RR >25/min, Heart Rate >100bpm, inability to complete sentances in one breath.
What are life threatening signs?
PEF 7kPa, antibiotics, diuretics
What is Doxapram?
Doxapram: respiratory stimulant ONLY used when patient is lacking respiratory drive
What are other measures?
Home ventilation at night can keep CO2 down during the day.
Lung transplantation: not when there is chronic bilateral pulmonary infection such as in cystic fibrosis/ chronic bronchiectasis.
Pulmonary Hypertension and Cor Pulmonale
What is pulmonary hypertension?
Pulmonary Hypertension = mean arterial pressure >25mmHg at rest or >30mmHg in excersise + pulmonary capillary wedge pressure 240 dynes/s/cm5.
Also look at degree of functional disturbance based on NYHA grades 1-V1.
What are the causes pulmonary hypertension?
Pulmonary Arterial: connective tissue disease, congenital systemic to pulmonary shunts, portal hypertension, HIV infection, exposure to drugs/toxins, persistant pulmonary HT of the newborn
Pulmonary Venous: left sided atrial or vent heart disease, left sided valvular heart disease, pulmonary veno-occlusive disease, pulmonary capillary haemangiomatosis
Disorders of resp system/hypoxaemia: COPD, DPLD, sleep-disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude, neonatal lung disease, alveolar capillary dysplasia, severe kyphoscoliosis
Chronic thromboembolic disease: thromboembolic destruction of proximal pulmonary arteries, in situ thrombosis, sickle cell disease
Miscellaneious: inflammatory conditions, extrinsic compression of central pulmonary veins, Primary Pulmonary Hypertension (20-30 year old women)
What are the clinical features of Pulmonary Hypertension?
Presents insidiously, diagnosed late.
Symptoms: breathlessness, chest pain, fatigue, palpitation, syncope.
Signs: elevated JVP (prominent a wave if in sinus rythm), parasternal heave (right ventricular hypertrophy), accentuation of pulmonary component of second heart sound, right ventricular third heart sound.
What should you look for in the ecg and Xray?
ECG: right ventricular heave/hypertrophy
Xray: enlarged pulmonary arteries, peripheral pruning, right ventricle enlargement
Transthoracic echocardiography: dopplar assessment of triscuspid regurg jet estimate pulmonary arterial pressure
Right heart catheterisation: assess pulmonary haemodynamics + measure vasodilator responsiveness.
How do you manage Pulmonary Hypertension?
Prescribed as appropriate : Oxygen, dieuretics, digoxin , smoking cessation
Selected therapy : High dose calcium blockers, prostaglandins (eoi-prostenol/prostacyclin/iloprost therapy), PDE5 inhibitor (sildenafil), oral endothelin antagonist (bosentan)
Extreme: heart-lung transplantation, pulmonary thromboendartectomy, atrial septostomy (creation of left-right shunt to decompress right ventricle + improve haemodynamic performance at expense of shunting and hypoxaemia)
What is Cor Pulmonale?
Cor Pulmonale: Cor pulmonale is failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart. Ie Pulmonary Hypertension caused by respiratory disease. eg COP (50%), DPLD, sleep-disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude, neonatal lung disease, alveolar capillary dysplasia, severe kyphoscoliosis
Describe the pathophysiology of Cor Pulmonale :
Thought that chronic hypoxia leads to pulmonary arteriolar constriction through excessive action of the physiological mechanism that acts to maintain the balance of ventilation and perfusion in the lungs. (As oxygen is a vasodilator!)
Chronic hypercapnoea and respiratory acidosis causing pulmonary vasoconstriction.
Anatomic disruption of the pulmonary vascular bed due to primary lung disease (for example in emphysema, pulmonary thromboembolic disease and pulmonary fibrosis).
Increased blood viscosity due to lung disease and its effects (for example in secondary polycythaemia).
What are the symptoms of Cor Pulmonale?
Worsening tachypnoea (particularly at rest)
Fatigue and lassitude
Worsening exertional dyspnoea (with deterioration in exercise tolerance)
Worsening cough (particularly if non-productive)
Angina-type chest discomfort – often non-responsive to nitrates (thought to be due to right ventricular ischaemia or stretching of pulmonary artery during exertion)
Haemoptysis (due to pulmonary arteriolar rupture or leakage)
Hoarseness – occurs occasionally (due to compression of the left recurrent laryngeal nerve by dilated pulmonary artery)
Exertional syncope – a late symptom (indicating severe disease)
Late-stage hepatic congestion can cause symptoms (anorexia, jaundice and right-upper-quadrant abdominal discomfort)
What are signs of Cor Pulmonalae?
Peripheral odema, raised JVP, hepatomegaly, ascites, intercostal indrawing
Cyanosis and plethora
Chest markedly hyper-expanded
Laboured respiratory effort
Decreased air entry, crackles and wheeze in chest due to underlying pulmonary pathology
Systolic bruits over lung fields – due to turbulent hyperdynamic pulmonary artery flow
Left parasternal or subxiphoid heave (sign of right ventricular hypertrophy)
Distended neck veins with raised and/or prominent JVP and visible a or v waves
3rd/4th heart sounds and pan-systolic murmur of tricuspid regurgitation over right heart
Split second heart sound with loud pulmonary component
Systolic ejection murmur with sharp ejection click over pulmonary artery (advanced sign)
Diastolic pulmonary regurgitation murmur over pulmonary artery (advanced sign)
Marked hepatojugular reflux due to hepatic congestion
Hepatomegaly ± liver pulsatility if significant associated tricuspid regurgitation
Jaundice in advanced cases
Ascites in advanced cases
Peripheral pitting oedema
What is cardiac asthma?
Cardiac asthma is a medical symptom, of wheezing, coughing or shortness of breath which may be pulmonary odema due to congestive heart failure = back up of fluid into the lungs due to left-sided heart failure. (Same symptoms of asthma but different mechanism so bronchodilators won’t work but might actually make it worse treat the heart failure.)
What is conjestive heart failure?
Same as “heart failure” = means heart can’t sufficiently pump blood around the body SOB, odema, excersise intolerance.
What is a pneumothorax?
Air in pleural space
Primary: smoking, tall, blebs
Secondary: pre-existing lung disease, higher mortality rates
What are the symptoms of pneumothorax?
Sudden onset unilateral pleuritic chest pain and breathlessness.
>15% of hemithorax = may get decreased/absent chest sounds + resonant percussion.
What might you find on examination of someone with a pneumothorax?
Cool peripheries, tachycardic, increased resp rate (the increased resp rate and tachycardia might be to avoid pain (breathing too deeply) / because of the pain.
Unilaterally : reduced expansion, resonant percussion, reduced tactile fremitus, reduced breath sounds
Which investigations would you do now and later?
Now: FFBC, ABG, Chest Xray, ECG (do ecgs whenever there is chest pain)
Later: coagulation studies (if drain needs inserting need to know if clotting is normal), ESR, CRP, Electrolytes urea creatine, lung function tests
What is a tension pneumothorax?
Tension pneumothorax: (has a valve) when communication between airway and pleural space acts as one way valve air enters pleural space during inspiration but can’t exit during expiration large amounts of air accumulates increase in pressure.
Signs: shifted mediastinum to the opposite side (may not shift if malignant disease/scarring has splinted the mediastinum), compression of the opposite lung, impairement of venous return cardiovascular compromise = reduced CO = requires urgent attention.
Symptoms: rapidly progressive breathlessness + marked tachycardia, hypotension, cyanosis, tracheal displacement away from the silent hemithorax.
Closed type: when the communication between the airway and pleural space seals off as the lung deflates + does not re-open = negative mean pleural pressure = spontaneous reabsorption of air and reexpansion of lung occurs over a few days.
Don’t fly as the trapped air expands at high altitude.
Open type: communication fails to seal and air continues to pass freely between bronchial tree and pleural space eg bronchopleural fistula (can transmit infection) = positive mean pleural pressure.
Seen following rupture of emphsymatous bulla, tuberculous cavity, lung abscess into the pleural space. Tension pneumothorax
What sort of investigations would you perform in a pneumothorax?
X-ray: lack of lung markings, mediastinal shift
CT Scan: can differentiate between air being a bulla, and air in the pleural space (avoid misguided aspiration)
How do you manage a pneumothorax?
Use for 15 hours/day, 20 is better.
Also give it after exacerbations = give controlled 24% / 28% to avoid respiratory depression/worsening acidosis.
Bullaectomy : young patients where the bulla is compressing normal lung functioning.
Upper lobe emphysema lung volume reduction surgery.
Others: influenza vaccine, pneumococcal vaccination, holistic care,
Palliative care: morphine for breathlessness, benzodiazepines for anxiety.
How do you assess the prognosis of someone with COPD?
Inverse to age, proportional to post-bronchodilator FEV1.
What is an acute exacerbation of COPD?
Acute exacerbation: increase in symptoms + decrease in lung function and health status.
Caussed by: bacteria/virus/change in air quality
Management: home emergency pack containing oral corticosteroids and if appropriate antibiotics.
Hospitalisation = collapse (my patient), cyanosis, peripheral odema, alteration in consciousness.
How do you manage someone with an acute exacerbation?
Oyxgen therapy: give controlled 24% / 28% to avoid respiratory depression/worsening acidosis.
Bronchodilators = nebulised short acting B2 antagonist + anticholinergic
Corticosteroids: oral prednisolone, 30mg for 10 days. (Provision for osteoporosis)
Antibiotic therapy: when there is an increase in sputum purulence, sputum volume or breathlessness.
Aminopenicillin / Macrolide / Co-amoxiclav where there are known B-lactamase organisms
Non-invasive ventilation: is patient remains tachypnoeic/acidotic.
Additional therapy: In odema give dieuretics,
IV aminophylline but may induce arrhythmias/drug interactions.
How do you decide whether to discharge a patient or not?
If clinically stable and on maintenance medication.
Nurse led hospital at home team = provides short term nebuliser loan improves discharge rates and additional support for patient.
Upper Resp Tract Infections
Are bacteria or viruses the common cause of URTIs?
Acute coryza = common cold = most common = Rhinoviruses : coronoavirus, enterovirus, adenovirus, respiratory synctital virus
Bacteria = acute tonsillitis, otitis media, epiglottitis
Which bacteria causes whooping cough?
Lower Resp Tract Infections
What is pneumonia?
Acute respiratory illness with recently developed radiological shadowing (segmental/lobar/multilobar)
Lobar Pneumonia: radiological and pathological term referring to homogenous consolidation in one/more lung lobe often with associated pleural inflammation.
Bronchopneumonia: patchy alveolar consolidation with bronchial and bronchiolar inflammation often affecting both lower lobes.
Who gets community acquired pneumonia?
Very old and very young, with higher mortality rates in both groups.
Kills more children than any other illness.
Step pneumonaie most common cause (produce rust coloured sputum)
Viral = esp in children
Ask occupation / living conditions / travel (water sources) / pets
What are the clinical features of pneumonia?
Acute illness : fever / rigors / shivering / vomiting / loss of appetite / headache / breathlessness / cough (short painful and dry turns to expectoration of mucopuruluant sputum) / occasional haemoptysis / pleurtic chest pain (may be referred to shoulder or anterior abdominal wall) / upper abdominal tenderness (in lower lobe pneumonia associated with hepatitis)
Describe the pathophysiology:
Consolidation: from proteinaceous fluid and inflammatory cells congest airspaces
Looks like a liver on cut surface with phases of red and then grey hepatisation
Increased conductivity hear bronchial breathing, whispering pectoriloquy, crackles
What would you hear on the chest of someone with pneumonia?
May hear : Bronchial breathing, whispering pectoriloquy, crackles
Name some complications of pneumonia which you might see on xray:
Parapneumonic effusion, suppurative pneumonia/lung abcess, intrapulmonary abcess formation, empyema, retension of sputum causing lobar collapse, DVT and PE, pneumothorax, ARDS, renal failure, multi-organ failure, ectopic absess formation, hepatitis, pericarditis, myocarditis, meningoencephalitlis, pyrexia due to drug hypersensitivity.
What investigations would you do to determine if what they have in pneumonia?
Lobar pneumonia: “homogenous localised opacity suggestive of consolidation”
Microbiological results though it may be managed without these.
ABG: when sats are less than 93% to determine ventilator failure/acidosis.
When would you send someone to ITU?
CURB score 4-5, persisting hypoxia despite O2, progressive hypercapnia, severe acidosis, circulatory shock, reduced conscious level.
What might the bloods of someone with CAP look like?
White cell count:
Neutrophil leucocytosis : >15x10^9 = bacterial eitiology.
Atypical organism : normal / marginally raised
Very high (>20x10^9/l) or very low (8kPa, Saturation>92% High conc 35%
Fluid balance IV/oral/inotropic support if needed
Antibiotic therapy 7-10 day course of oral antibiotics, which one depends on what hospital you’re in (takes longer for legionella,klebsiella,staphylococcal pneumonias)
IV : impaired consciousness/can’t swallow/malabsorption
Eg Amoxycillin 500mg 8 hourly
Allergic to penicillin Clarithromycin 500mg 12 hourly / Erythromycin 500mg 6 hourly orally
Pain Relief: relieve pain to allow patients to breath normally and cough efficiently.
Paracetamol/ Co-codamol/NSAIDs/opiates (though seriously watch out if they have breathing difficulties)
Physiotherapy: assist exporation when people aren’t coughing because of the pain/ mucus plugging bronchial collapse/
Nutritional support (prolonged illness)
What are the aims of O2 therapy?
PaO2 >8kPa, Saturation>92%
High conc 35% (humidified as long as no hypercapnia in COPD)
How long does it take to get over pneumonia?
Normally prompt but fever may last days and Xray may stay funny for months.
Hospital Aquired Pneumonia
What is HAP?
Pneumonia that occurs at least 2 days after admission into hospital.
What are the bugs behind HAP?
Early onset = 4-5 days = like CAP
Late onset = generally Gram-negative bacteria (Escherichia, pseudomonas,klebsiella), Staph Aureus (including MRSA), and anaerobes
Who is likely to get pneumonia in hospital?
Reduced host defence against bacteria: immunodeficiencies (steroids,diabetes,malignancy), reduced cough reflex (post op), disordered mucocilliary clearance (anaesthetic agents), bulbar/vocal cord palsy
Aspiration of nasopharyngeal/gastric secretions: immobility, reduced consciousness, vomiting, dysphagia, achalasia, severe reflux
Bacteria introduced into lower resp tract: intubation/tracheostomy, infected ventilators/nebulisers/bronchoscopes, dental/sinus infection
Bacteraemia:abdominal sepsis, IV cannula infection, infected emboli
Who would you suspect of having HAP?
Purulant sputum/endotracheal secretions, new radiological infiltrates, increased O2 requirements, temperature > 38.3, leucocytosis, leucopenia,
Do normal tests and may also do Bronchoalveolar lavage.
How would you treat HAP?
Third generation cephalosporin (eg cefotaxime) with an aminoglycoside (eg gentamicin)
Monocyclic B-lactam (eg aztreonam) and flucloxacillin
How do you treat MRSA?
IV Vancomycin or oral doxycycline, rifampicin, or linezolid
What is the average mortality of HAP?
How may you prevent HAP?
Good hygiene, minimise aspiration, lim,it the use of stress ulcer prophylaxis with proton pump inhibitors, oral antiseptic to disinfect the upper airway (chlorhexidine 2%), in ITU sometimes selective decontamination of dijestive tract if patients need ventilation for over 48 hours
What is bronchoalveolar lavage?
Bronchoalveolar lavage (BAL) is a medical procedure in which a bronchoscope is passed through the mouth or nose into the lungs and fluid is squirted into a small part of the lung and then recollected for examination.
Achalasia ( /eɪkəˈleɪziə/), also known as esophageal achalasia, achalasia cardiae, cardiospasm, and esophageal aperistalsis, is an esophageal motility disorder involving the smooth muscle layer of the esophagus and the lower esophageal sphincter
What is suppurative pneumonia?
Destruction of the lung parenchyma by the inflammation process, there are microabcesses on histological level + pulmonary abcess on xray.
What do pulmonary absesses look like on xray?
Lesion with large localised collection of pus/
Cavity lined by chronic inflammatory tissue from which pus has escaped by rupture into bronchus
On Xray: abscess with cavitation and fluid level.
Send sputum and blood for culture.
What would a halo sign on an xray suggest?
Halo sign = aspergillis
What causes pulmonary abscesses / suppruative pneumonia?
- Inhalation of septic material : eg in operation, aspiration (watch out for throat palsey/achalasia/alcholism)
- Complicate local obstruction from neoplasm/foreign body.
- Bacterial infection of pulmonary infarct/collapsed lobe
- Community aquired MRSA
- Lemierre’s Syndrome: anaerobe Fusobacterium necrophorum
- Injecting drug users: haematogenous lung abscess often in association with endocarditis
- Aspiration pneumonia: exogenous lipid pneumonia from aspiration of animal/vegetable/mineral oils.
What are the most likely causative organisms in a lung that was previously healthy?
Staph Aureus / Klebsiella Pneumoniae
Mostly caused by common aerobes and anaerobes found in the mouth and URT
How do you treat it?
Anaerobic organism metronidazole
Fibrosis / bronchiectasis are common after infection has passed
Pneumonia in the Immunocompramised patient:
Durgs/disease mean that normal pathogens in the body become “opportunistic”
Fever, cough, breathlessness but really varies depending on how ill/what patient has to start with
Induced sputum, HRCT – often too ill to do any invasive investigations
What are the advantage of devliering NIV via a hood? (Like a submarine)
Patient can expectorate, communicate and feed.
What is bronchoalveolar lavage?
Bronchoalveolar lavage (BAL) is a medical procedure in which a bronchoscope is passed through the mouth or nose into the lungs and fluid is squirted into a small part of the lung and then recollected for examination.
Achalasia ( /eɪkəˈleɪziə/), also known as esophageal achalasia, achalasia cardiae, cardiospasm, and esophageal aperistalsis, is an esophageal motility disorder involving the smooth muscle layer of the esophagus and the lower esophageal sphincter
What is a Pulmonary Embolism?
When there is migration of a venous emboli from the systematic veins into the pulmonary arterial system resuting in varying degrees of obstruction of pulmonary arterial blood flow.
What are the causes of PE?
DVT (79%), septic emboli (endocarditis), tumour, fat, air, amniotic fluid, placenta.
Risk increases with number of risk factors.
Describe a classical presenatation:
Shortness of breath and chest pain
Consider: MI, Pulmonary embolism, Pneumonia with inflammation of overlying pleura, Pneumothorax
What are the three main risk factors for developing a thrombus?
Which investigations would you do to investigate someone with a suspected PE?
Chest Xray: excluding other key differentials like pneumothorax and pneumonia.
- Might see normal / infiltrates / atelectasis / effusions / combination / decreased pulmonary markings
ECG: rule out other differentials like acute MI and pericarditis.
May get sinus tachycardia and t wave inversion
Large PE might cause right heart strain or appearance of right bundle branch block
ABG: reduced PaO2 with normal/reduced PaCO2.
Metabolic acidosis : in acute massive PE with cardiovascular collapse.
D-Dimer: when cross linked fibrin undergoes endogenous fibrinolysis.
CT Pulmonary Angiography: visulaise extent and distribution of PE.
Ventilation-perfusion scanning: for patients without significant cardiopulmonary disease and a normal chest X-ray.
Colour dopplar ultrasound: to look at the leg for DVT.
Echo: for differential and to assessment of acute circulatory collapse.
What is circulatory collapse?
When the circulation fails to maintain the delivery of oxygen and nutrients to tissues and the excretion of CO2 and metabolites.
What is acute circulatory collapse?
When the blood supply to the heart fails.
What are signs of circulatory collapse?
Confusion, Pulse - rapid, weak, thready, Respiration - shallow, irregular, labored
Blood Pressure - low, falling, Mental State - confused, sluggish, anxious, Eyes - pupils may be dilated, Skin - cold, clammy, sweating
Name some conditions in which you might see elevated D-Dimer: PE, MI, pneumonia, sepsis.
What is pleuritic chest pain?
Pain that gets worse when you breath in.
Sharp, localized, worse when you breathe in
Directly involving the pleura: pneumothorax, trauma
Spread from underlying lung pathology: pneumonia, PE from pulmonary embolus
(Major heart stuff)
Acute right heart failure
Occlusion of segmental pulmonary artery infarction +- effusion
Chronic occlusion of pulmonary vasculature
Right heart failure
Faintness or collapse
Crushing central chest pain
Pleuritic chest pain
Late symtoms of pulmonary hypertension/right heart failure
Major circulatory collapse
Right ventricular gallop ryhtm
Decreased urinary output
Effusion (often blood stained)
Low –grade fever
Minimal early on
Signs of right heart failure
Enlarged pulmonary artery trunk
Anterior T wave inversion
Right bundle branch block
RV Hypetrophy and strain
Very abnormal :
Decreased Pa02 or
Exertional decrease in O2 / desaturation on fomal excersise testing
Musculoskeletal Chest Pain
Other causes of pulmonary hypertension
Acutely breathless + hypoxaemic + normal chest xray
Bilateral changes with unilateral chest pain
How do you manage PE?
Prompt recognition and treatment may be life saving
IV Fluids/plasma expander: for circulatory shock.
Opiates: for pain and distress (watch out in the hypotensive patient)
External cardiac massage: if desperate : may dislodge and break up and large central embolus.
Heparin : reduces further propagation of clots, risk of further emboli, reduces mortality (at least 5 days, start oral warfarin in that time, don’t stop until INR > 2)
Long term low intensity warfarin
Thrombolysis: in acute massive PE with cardiogenic shock.
- If no shock look for right ventricular dilatation and hypokinesis or severe hypoxaemia.
- Screen carefully for haemorrhagic risk as high risk of intracranial haemorrhage.
Surgical pulmonary embolectomy: high mortality risk.
Inferior vena caval filter: for people for which anticoagulation is contraindicated.
What sort of prognosis can people with PE expect?
Increased risk of recurrance highest in the first 6-12 months afterwards.
10 years : less than 1/3 have recurrant event
Bad outcome : if lasting right ventricular dysfunction/ persisting pulmonary hypertension.
Why aren’t ionotropic agents helpful?
The hypoxic right ventricle is near maximally stimulated by endogenous catecholamines.
Don’t give dieuretics / vasodilators which will reduce CO.
What sort of questions might you ask about breathlessness?
How far can you walk before becoming breathless?
How did the breathlessness start?
(Acute = PE/pneumothorax, Slow onset = pneumonia/asthma)
Does it change or is it the same all the time?
Site and radiation Pain in the chest could come from any of the structures within the thorax. Central chest pain could be: cardiac chest pain due to infarction (often radiating to left arm and jaw) or pericarditis oesophageal pain (spasm, rupture or oesophagitis) pain from an aortic dissection (progression from anterior to posterior).
Localised chest pain could be: pleuritic (pneumonia or pleurisy or any other cause of inflammation of the pleura-pleurisy) musculoskeletal (e.g. rib fracture, ankylosing spondylitis or costochondritis or muscle strain) referred pain from the vertebrae
Dermatological (for example a dermatomal pain in Varicella zoster infection (shingles))
Thoracic pain can also come from abdominal structures such as the gall bladder and pancreas. The commonest cause of chest pain is the so called atypical chest pain for which there is no clear structureal explanation. 10
Onset and character
Sudden-onset chest pain is suggestive of cardiac chest pain or pleuritic pain. The character of the pain is important: crushing or dull pain is likely to be myocardial infarction constricting pain is likely to be angina, oesophagitis or anxiety sharp pain is likely to come from the pleura or pericardium tearing pain is likely to come from an aortic dissection.
How much does the pain limit the patient?
Chest pain due to a myocardial infarction is often accompanied by nausea and sweating. Chest pain associated with dyspnoea could be cardiac, pleuritic or due to anxiety or pulmonary embolism.
Precipitating and relieving factors
Precipitating factors: worse on exercise, emotions or palpitations is suggestive of cardiac pain worse on inspiration and coughing is suggestive of pleuritic pain worse on pressure on the sternum is suggestive of a fractured rib.
Relieving factors: better on stopping exercise suggests cardiac pain better on taking antacids suggests oesophagitis better on leaning forward suggests pericarditis.
Risk factors for cardiovascular disease
It would be important to elicit Mrs Baker’s risk factors. The six main ones you should consider are:
1. history of cigarette smoking
3. high LDL cholesterol concentration
5. family history of cardiovascular disease exercise Loss of recoil pressure and airway collapse further upstream,
CO2 dissolves more readily in the blood whereas there is a non-linear between Pa02 and HB saturation
There is pulmonary vasulature remodeling and impaired cardiac performance
Muscle layer : hypertrophic atrophic replaced by fibrotic tissue
Treatment with prednisolone to prevent the inflammatory process
chronic bronchitis emphysema (defined in pathological terms as destruction of alveolar walls, resulting in enlargement of airspaces) inflammatory bronchiolitis involving the small airways (10Kpa,
Possible Resp exam picture in COPD:
Respiratory rate 18/min
Expansion equal but reduced
Tactile vocal fremitus normal
Early inspiratory crackles at the lung bases
Skin/oral mucosa = no abnormalities
What are signs of hyperinflation/increased lung volumes seen in COPD? absence of the apex beat palpable liver the reduced but equal expansion
What is Cor Pulmonale?
Cor pulmonale: (in patients with advanced COPD) heart disease defined as secondary to disease of the lung.
What is gaseous partial pressure?
Partial pressure: pressure a gas from a gas mixture would exert if it occupied the same volume alone.
How much oxygen can one Hb bind?
4x O2 molecules
Is oxygen saturation a good reflection of oxygen partial pressure in the body?
No, there is little effect on saturation in increased Pa02 between 8-13kPa in the body. Therefore giving oxygen only helps if the PA02 is very low in the body : between 4-6KPa.
When will you be able to see cyanosis?
Greater than 5g of desaturated Hb in the body.
What causes a rightward shift on an oxygen dissociation curve?
Right: drops off more 02 = increased C02, acidic pH, increased temp, increased 2,3 DPG
What causes a leftward shift on an o2 curve:
Left: fetal Hb, decreased PCO2, increased pH, decreased DPG.
When is there a downward shift?
CO poisoning is downwards and slightly left.
How much 02 do mitchondria need?
How long can the brain withstand hypoxia?
What are causes of hypoventilation?
Hypoventilation: opiates, barbituates, alcohol, muscular dystrophy, polio, kyphosis, midbrain pathology,
What are causes of hypercapnia?
Hypercapnia: hypoventilation, head injury, anaethetic drugs, chronic lung disease
What are the symptoms of hypercapnia?
Flushed skin, full pulse, increased BP, CO2 retention hand flap, muscle twitching, confusion, convulsions, coma, decreased ventilation, death.
Whar are causes of hyperventilation?
Hyperventilation: myocarditis, emphysema, acute respiratory distress syndrome, renal failure, stroke, aspirin overdose, anxiety, pain
What are causes of hypocapnia?
Hypocapnia: hyperventilation, low PaO2, acidosis, excessive mechanic ventilation
What are the symptoms of hypocapnia?
Dizziness, visual disturbances = as low PCO2 causes vasconstriction and thus cerebral hypoxia. pins and needles, stiff muscles, tetanus = low PC02 alkalosis decreased plasma Ca2+ increased muscle excitability.
What percentage of pulmonary embolisms are fatal?
Where do most pulmonary embolisms come from?
Pelvic/abdominal veins. May also come from femoral DVT / axillary thrombosis.
What is haemoptysis?
Haemoptysis: the coughing up of blood originating from the respiratory tract below the level of the larynx.
What are causes of odema?
Too much pressure in the blood vessels
Not enough protein in the bloodstream to hold fluid in the plasma.
What are the causes of pulmonary odema?
Cardiogenic = high pressure in the blood vessels due to poor heart function.
Non cardiogenic = ARDS
What is ARDS?
Acute respiratory distress syndrome (ARDS) : integrity of the alveoli become compromised as a result of underlying inflammatory response, and this leads to leaky alveoli that can fill up with fluid from the blood vessels.
What are some causes of ARDS?
Caused by: severe infections, trauma, lung injury, inhalation of toxins, lung infections, cocaine smoking, or radiation to the lungs. In ARDS, the integrity of the alveoli become compromised as a result of underlying inflammatory response, and this leads to leaky alveoli that can fill up with fluid from the blood vessels.
– Clincical Features
– Procedures Basic Science Pathology
–Differential Diagnosis – Management
– Social and Psychological Impact
– Implications for Public Health – Ethical aspects
What is the prognosis for people with lung cancer?
1 Year: 30%
5 years: 6-8%
90% lung carcinomas = from smoking (risk proportionate to number of cigarettes you smoke)
Now more women die of lung cancer than breast cancer.
Primary bronchial carcinomas: arise from bronchial epithelium or mucous glands.
Squamous cell : 35% = may undergo central necrosis and cavitation/resemble lung abcess on xray
Adenocarcinoma : 30%
Small-cell: 20% (metastisise more?)
May involve the pleura (directly or through lymphatics), may extend/invade into chest wall = pain,
Lympathic spread: to mediastinal and supraclavicular lymph nodes.
Blood borne metastises: liver, bone, brain, adrenals, skin.
Which is the most aggressive form of cancer?
Small cell .(Dont do resection surgery for fear of it spreading)
Where might Secondary tumours of the lung come from?
Secondary lung tumours: from breast/kidney/uterus/ovary/testes/thyroid/
What might be some of the clinical presentations of lung cancer?
Cough: often dry. (May be purulent if there’s secondary infection)
If smoker’s cough changes character suspect cancer. #
Haemoptysis (also consider TB)
What are symptoms of complete bronchial obstruction? (They vary with size)
Complete obstruction: breathlessness, mediastinal displacement (towards the obstructed side with emphysema (overfilling with air) to compensate on the other side), dullness to percussion with reduced breath sounds.
Partial obstruction: monophonic, unilateral wheeze that fails to clear with coughing,
If you see pneumonia that recurs in the same place and is slow to respond to treatment think cancer .
When might you hear stridor?
Stridor: when lower trachea/carina/main bronchi are narrowed by primary tumour/compression from lymph nodes.
Breathlessness (collapse/pneumonia/pleural effusion/tumour compressing phrenic nerve causing diaphragmatic paralysis.
Pain and nerve entrapment
Intercostals nerve pain in thoracic dermatome.
Cancer in apex of the lung Horner’s Syndrome
Maliganant destruction of T1 and C8 Pancoast’s syndrome
What is Horner’s Syndrome and when might you see it?
Horner’s Syndrome: ipsilateral partial ptosis, enophthalmos, miosis and hypohidrosis of the face)
Cancer in the lung apex due to involvement of sympathetic chain at or above stellate ganglion.
What is Pancoast’s Syndrome and when might you see it?
Pancoast’s: pain in shoulder and inner aspect of the arm, sometimes with small muscle wasting in the hand
In malignant destruction of T8/C1 in lower part of brachial plexus in apical lung tumour
Oesophagus = dysphagia. Percardium = arrhythmia/pericardial effusion.
Superior vena cava obstruction by malignant nodes (most commonly caused by bronchial carcinoma) = swelling/suffusion of neck and face, conjunctival odema, headache, dilated veins on chest wall
Left recurrent laryngeal nerve (tumours in left hilum) vocal cord paralysis, voice alteration, bovine cough
What is a bovine cough?
Cough lacking normal explosive character
What is enophthalmos?
Enophthalmos = posterior displacement of the eyes/sunken eyes.
Palpable lymph nodes
Metastatic spread: neurological defects/epileptic seizures/personality change/jaundice/bone pain/skin nodules
Digital clubbing (may be with HPOA)
What is HPOA?
HPOA = Hypertrophic Pulmonary Osteoarthropathy = periostitis of long bones, most commonly distal tibia, fibula, radius, ulna, = pain/tenderness/pitting odema on the shins.
Non-metastatic extra pulmonary effects:
Eg Small cell carcinoma syndrome of inappropriate ADH and ACTH
Squamous cell carcinoma hypercalcaemia.
Which investigations would you perform to look into lung cancer?
Histological Characterisation = Biopsy : do biopsy and brushing using flexible bronchoscope (ie bronchoscopy)
Do percutaneous needle biopsy under CT/ultrasound for tumours too far away = small risk of pneumothorax.
Do three sputum samples if they can’t handle invasive procedure.
Imaging = Chest Xray, Bone Scan (detects cellular activity in bone = metastases), CT (extent of the disease)
Bronchoscopy: to look at what’s there and send samples.
Lung Function Tests: to see if surgery is viable to ascertain whether remaining lung function will be sufficient.
Bloods: FBC (look for anaemia), coagulation studies,
Clinical biochemistry: ABG (worry about anything less than 93%), CRP, Calcium/phosphate/alkaline phosphatise (may see hypercalcaemia in LC), D-dimers, Electrolytes,urea,creatine (measurements of kidney function), Liver Function Testd (in case it’s metastisised into liver),
Microbiology: Sputum culture (look for antibiotic resistance), Acid fast bacilli (for TB)
Histopathology: Cytology (to look at content), Histology (to identify tumour type)
What do you do in patients with pleural effusions?
Pleural effusions pleural aspiration and biopsy.
How do you treat lung cancer?
Can surgery be used in lung cancer?
Surgery: complete resection can be curative but only possible for about 25%. Otherwise give palliative care.
Radiotherapy: ok but more effective in palliation of distressing complications (super vena cava obstruction, recurrent haemoptysis, pain from chest wall invasion, obstruction of trachea/bronchi, metastases to brain)
Chemotherapy: (may extend life up tp months)
Combination chemo therapy is better than single
Nausea and vomiting give 5-HT3 receptor antagonists
Neoadjuvant and Adjuvant therapy: eg in combination with surgery
Laser therapy and stenting: for symptoms of major airway obstruction
What is Palliative care?
WHO: The active total care of a person and their carers, where the disease is no longer amenable to curative therapy’
What are the three main symptoms after diagnosis of lung cancer that patients experience?
Fatigue, Pain, SOB,
Name, hospital number, address and contact details of patients;
55 year old male accountant;
Presentation to A&E complaining of 2 day history of haemoptysis on the background of a 5 week history of pleuritic chest pain and long history of shortness of breath, the latter having recently become more severe;
Weight loss of 10-12kg over the past six months despite a healthy appetite;
On examination – tachypnoeic (respiratory rate of 28), tachycardic (109 bpm), hypoxia and evidence of cyanosis breathing air and finger clubbing present. Examination of the chest revealed signs of left upper lobe collapse;
Blood tests revealed a normochromic, normocytic anaemia, neutrophilia, hypercalcaemia, raised alkaline phosphatase, hypoxia and significantly raised liver enzymes;
Chest x-ray confirmed collapse of the left upper lobe and a possible peri-hilar mass, confirmed as an obstructing endobronchial lesion on bronchoscopy;
Histology confirmed squamous cell carcinoma of the lung;
Staged as T 3N 2M 1 disease – 4.5 cm tumour, >2cm from the carina with involvement of chest wall structures, ipsilateral peri-hilar lymph nodes and distant metastases to the liver. Deemed inoperable;
Hypercalcaemia paraneoplastic in origin due to tumour production of PTHrP, started on bisphosphonate therapy to reduce serum calcium level;
Bronchoscopy performed to debulk tumour and stent airway in order to relieve obstruction. Patient started on radiotherapy and chemotherapy (cisplatin) to help control symptoms;
Started on codeine for analgesia as pain appears refractory to NSAIDs;
Patient informed of diagnosis and prognosis and made aware of palliative care team referral;
Appointment will be made for patient to return to chest clinic for a follow-up appointment two weeks after his discharge.
What is haematemisis?
Haematemisis: vomiting up blood.
Questions to ask about breathlessness:
When/how did it start? Is there something you thought brought it on? Is it getting better/worse/staying the same? How has it progressed over the last few weeks? Is it worse in any particular position? Any history of asthma/allergy/ resp or cardiac disorders? Is there an associated wheeze?
Where is the blood in haemoptysis coming from?
From the lesion which is vascular eg tumour
From the lung vasculature: which has been damaged in the process eg TB, pulmonary odema
Pulmonary odema: pink, frothy sputum
TB/malignancy: streaks of blood (from erosion of blood vessel)
Inflamm condition: eg Bronchiectasis, chronic bronchitis, TB = haemoptysis with purulent sputum
PE: sudden onset cough with haemoptysis
What are signs of left upper lobe collapse?
Left upper lobe collapse : tracheal deviation towards the left hand side, reduced chest wall movement on the left combined with absent breath sounds, vocal fremitus and dullness to percussion
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