NUR 317 Cardiac Exam Study Guide 1 8

NUR 317 - Cardiac Exam Study Guide Define the following terms. Describe patient symptoms and conditions that could cause alterations in:
Cardiac Output
Volume of blood flowing through systemic or pulmonary circuit expressed in liters per min
Normal= 5 L/min (resting adult)
HRXSV= CO
Factors: preload, afterload, myocardial contractility, heart rate
As heart rate increases, this allows less time for diastole and the heart often cannot fill adequately. Therefore, a very rapid heart will often have a reduced cardiac output, especially in an elderly individual
Stroke Volume
Dependent on PRELOAD
Amount of blood ejected by the ventricle with each contraction
The volume of blood prior to the contraction (end diastolic vol) – the volume blood in the ventricle at the end of the contraction (end systolic vol) = SV
Applies equally to both left and right ventricles
Important determinant of cardiac output
Correlates with cardiac function
Frank-starling Law
SV is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting ). An increase in the volume or speed of venous return will increase preload, through the Frank-Starling law of the heart, will increase the stroke volume.
Decreased return will have opposite effect, causing a reduction in stroke volume
End Systolic Volume the volume blood in the ventricle at the end of the contraction
End Diastolic Volume
The volume of blood prior to the contraction
Ejection Fraction
Measures efficiency of left ventricular contractility
Percentage of blood ejected from the left ventricle with each contraction
Normal= 55-65%
Ventricular dysfunction results <or= 40%
The percentage of the volume in the left ventricle that is ejected through the aorta with each contraction.
Damage to the muscle fibers of the ventricles (through excessive stretching or from infarction) will decrease the ejection fraction and decrease the quality of a person’s life
Preload
Volume of blood in the ventricle at the end of diastole
Changes in ventricular preload dramatically affect ventricular stroke volume by the frank starling mechanism
The more the myocardial fibers are stretched, the great the force of contraction (rubber band)
When venous return is increased, the end-diastolic pressure and volume of the ventricle are increased (increases preload)
Hypovolemia resulting from a loss of blood leads to less ventricular filling (reduced preload)
Medications that cause vasodilation will decrease the preload
Nitroglycerin mainly dilates the venous system. This will cause increased pooling of blood in the veins, and will decrease the preload.
Increased intravascular volume and elevating the legs—increases preload
Increased preload, increases stroke volume
Decreased preload, decreases stroke volume
Results from alteration in the force of contraction of the cardiac muscle
When heart rate increase: diastolic filling time suffers
Decreased coronary artery filling
Heart has to overcome high pressures in aorta to eject blood (consumes more oxygen)
INCREASED PRELOAD:
Increased central venous pressure
Can result from decreased venous compliance (sympathetic vasoconstriction)
Vasoconstriction
Increased total blood volume, venour return augmented by increased respiratory activity, increased skeletal muscle pump activity
Gravity (head-down tilt)
Decreased heart rate which increases ventricular filling time
Increased aortic pressure which increases the afterload on the ventricle, reduces the stroke volume by decreasing ESV, and leads to secondary increase in preload increased ventricular compliance results in a greater expansion of the chamber during a given filling pressure
DECREASED PRELOAD
Decreased venous blood pressure, most commonly resulting from reduced blood volume (hemorrhage) or gravity causing blood to pool in lower limbs when standing upright.
Impaired atrial contraction that can result from atrial arrhythmias such as atrial fibrillation
Increased heart rate (atrial tachycardia) which reduces ventricular filling time
Ventricular diastolic failure (decreased ventricular compliance) caused, for example, by ventricular hypertrophy or impaired relaxation (lusitropy)
Inflow (mitral and tricupsid) valve stenosis, which reduces ventricular filling
Nitroglycerin (vasodilation)

Afterload
Resistance to ejection of blood from the left ventricle
Represents the resistance against which the ventricle must pump
Indicates how much effort the ventricles must put forth to force blood into the systemic circulation
Important determinant of myocardial energy consumption
INCREASED AFTERLOAD
High total peripheral resistance (AEB high systolic blood pressure)
Systemic and Pulmonary (right ventricle) Hypertension
Aortic and pulmonary stenosis
Vasopressors-----drugs that cause arterial constriction
HIGH BLOOD PRESSURE
DECREASE AFTERLOAD
Vasodilators, other drugs that reduce either the systemic or pulmonic blood pressure or both
LOW BLOOD PRESSURE
Systemic Vascular Resistance
Refers to the resistance to blood flow offered by all of the systemic vasculature, excluding the pulm vasculature. Aka= total peripheral resistance (TPR
Determined by factors that influence vascular resistance in individual vascular beds. Mechanisms that cause vasoconstriction increase SVR. Primarily determined by changes in blood vessel diameters but can also be from blood viscosity
SVR= (MAP-CVP) / CO
Differentiate between how Alpha and Beta receptors act on the cardiovascular system
Alpha 1
Vascular smooth muscle—VASOCONSTRICTION
Heart--- increased contractility
Alpha 2
Presynaptic membrane--- INHIBITION of norepinephrine
Vascular smooth muscle--- VASCONSTRICTION
Beta 1
Heart--- increased contractility, increased HR, increased conduction
Juxtaglomerular cells--- increased renin secretion
Beta 2
Smooth muscle-- VASODILATION
When performing a physical exam, what symptoms do you look for in the patient with cardiovascular disease?
CVD most common cause of hospitilization <85, leading death cause >85
Orthostatic vital signs – pulse increases a blood pressure drops with sitting upright or standing. Sign the body does not have enough cardiac output to compensate for the position change
Jugular venous distention – sign of right-sided heart failure – the right ventricle is not pumping well so the pressure backs up into the venous system.
Pulse deficit – you hear more beats with an apical pulse than you feel at the radius
Heart sounds may be muffled or you may hear a S3, S4 or a new murmur
What are the primary diagnostic studies used to diagnose cardiovascular diseases and conditions?
•Detailed health history and physical
•12-lead ECG
•Chest X-Ray
•Exercise stress testing
•Echocardiogram
•Serum cardiac markers
•Coronary angiography
___ Baseline Blood Studies:
Na+ : water retention common in CHF
K+ : arrhthmias or death
Ca+ and Mg+ : arrhythmias
WBC: infection
Hgb : anemia and O2 carrying capacity
Hct: anemia/hydration status
Platelet count: bleed tendencies
What Blood tests are used to diagnose cardiovascular conditions?
Creatine kinase
Found in skeletal muscle, brain and heart
When tissue damage—it is released into blood
Isoenzymes: organ specific
CK-MM= skeletal muscle
Normally 100%, will decrease in MI, and increase over 4-5 days
CK-BB= brain
Normally 0%-not present
No increase in MI
CK- MB= myocardial
Normally 0% in blood stream, present only in heart
Will increase > 5% in MI or level of 10 in MI
Rise: 4-6 hours post MI
Peaks: 12- 24 hrs post MI
WNL: 48-72hrs
If negative <48hrs following chest pain, NOT due to MI
Other factor that can elevate CK= IM injections, trauma, surgery, muscular dystrophy, marathon runners
Cardiac- Specific Troponins
Myocardial muscle protein
Released in response to injury
Troponin T and Troponin I
Rise 4-5 hrs, peaks 12-18 hr
Not detected in unaffected person
WNL several weeks post acute MI
Cardiac profile/ cardiac enzymes
Enzymes= proteins within all living cells which act as catalysts to initiate or accelerate biochemical reactions
Some enzymes are organ specific—all relative to onset of chest pain
Myoglobin
Found in skeletal and cardiac muscle
Earliest serum marker--- good for early presenters
1st enzyme to increase when damage occurs increase in 30-60 mins post MI, peaks 6-9hrs later, WNL-24hrs may be used for exclusion—if serum levels do not elevate in 3-6hrs after onset of pain, can rule out MI however, since it is first to elevate, if pt delays coming in, you may not even see this elevate, will rise, peak and return to normal within 24hours most diagnostic if obtained within 12 hrs of onset of chest pain rapid increase in MI 1-3 hrs may reach 85% to 95% (nearly peak) within 4-6 hrs of chest pain doubling of its normal value strongly suggests MI neuromuscular disorders, strenuous exercise, IM injections, CABG
C- Reactive Protein (CRP)
Non-specific marker of inflammation
Lowest risk: <1mg/L
Moderate risk: 1-3 mg/L
High risk: >3mg/L
Predictor of cardiac disease in patients with normal lipid values (esp women)
Statin drugs (lipid lowering drugs) may be prescribed to decrease inflammation
Inflammation may trigger MI---people with abdominal fat deposits typically have high levels of inflammation in their bodies
Shows high sensitivity for developing MI in acute coronary syndrome
Sensitive acute phase reactants---may increase 100 fold in :
Trauma—MI, post x4 days, bacterial/viral infections, rheumatic fever, RA, and malignancy
Historically used to assess inflammatory activity in pts with acute infection, determine infections post op and to detect transplant rejection
Homocystine
Amino acid produced during protein catabolism
Contributes to atherosclerosis by:
Damaging inner lining of vessels
Promoting plaque build up
Altering clotting mechanism
Treated with B6, B12, folic acid to decrease levels
B- Type Natriuretic Peptide- BNP
Hormone produced by the ventricles of the heart
Increases in response to ventricular volume expansion and pressure overload
Best diagnostic tool for heart failure (HF)
Distinguishes between shortness of breath from cardiac vs resp etiology
Comes in synthetic form of IV infusion in severe heart failure--- Natrecor (neseritide)
This is a balancing act to administer because people with severe heart failure have poor cardiac outputs. It is important to keep the blood pressure low so that the heart doesn’t have to work so hard but the blood pressure needs to be high enough for perfusion of the body tissues. Often with neseritide, it is hard to get that balance. Often the BP drops too low and the IV rate needs to be adjusted
Serum Lipid Profile
Risk for cardiac disease is assessed by dividing the total cholesterol by the HDL level
Target values: <5 men, <4.4 women
HDL (healthy) ---transporter of cholesterol
Recommended >40 (Men) >50 (women)
Low risk for CAD >60mg/dL
High risk for CAD <40mg/dL
LDL (lousy) ----recommended < 100 mg/dL if any risk factors
Triglycerides---main storage form of lipids
Therefore more elevated with obesity
Desirable: <150 mg/dL
The higher the HDL, the better. It is OK to have a total cholesterol above 200 as long as most of it is HDL. If the person has no risk factors at all, the recommended level for LDL is bellow 130. But the more risk factors a person has, the lower the recommended LDL level. With one risk factor (heart disease) the recommended level is below 100. If the person also has diabetes, the recommended level is below 70. This is very difficult to do in someone who most likely has a genetic predisposition for an elevated cholesterol. The person may need more than one medication (statin and a fibrate for example) but the more meds that are added the greater the potential for side effects
What are the primary cardiac markers? What do alterations in these markers mean?

What do you expect to see on the chest x-ray in cardiac disease?
Chest X-ray shows:
Contours
Heart size
Heart enlargement may indicate a congenital defect of heart failure.
Configuration
Displacement
Enlargement
Pulmonary congestion
May indicate a lung problem but can also be due to left-sided HF
Fluid in the pericardial space
Differentiate between noninvasive and invasive cardiac testing electrocardiogram EKG/ECG
12 lead rate, rhythm, electrical conduction
1 point in time changes in ST segment, T wave and Q wave indicate ischemia telemetry monitoring portable continuous in 1 lead (sometimes 2, depending) arryhtmias holter monitor
24hr EKG recoring in 1-2 leads patient keeps written diary of activities and chest pain arrythmias things that affect EKG: atrial and ventricular hypertrophy, conduction delays, pericarditis, pulm infarct, K Ca Mg levels, signal averaged EKG- SAE, malignant ventricular dysrrhythmias, prior to EP studies

exercise or stress testing cardiac symptoms may often occur only with activity due to the increased myocardial demand of oxygen treadmill or stationary bike with EKG monitoring non-exercise: pharmacological stress test
IV persantine or dobutamine
Testing for:
Efficiency of the heart during stress, EKG changes r/t activity, arrythmias, perfusion with IV isotope to see areas of the myocardium not being perfused.
The goal is to get the person’s heart rate us so that the heart is stressed. If you have a patient on beta-blockers going to a stress test, check with the cardiologist before giving those meds that day
Thallium scan
Perfusion study—myocardial uptake of radioactive isotope
With or without stress test
Isotope---thallium, cardiolyte
Isotope injected IV
Heart scan 5-10 min after injection
Heart scan 2-4 hrs after injection
Allows observation of coronary artery blood flow. Can reveal intracardiac shunts, motion of ventricle, size of heart chambers
An IV injection of thallium is given and then a motion picture to show the flow of blood (with the thallium) through the heart
Transthoracic echocardiogram
Ultrasonic visualization of structure and function of heart
Size of chambers
Motion of walls of the chambers and valves
Blood flow through heart
Pericardial effusion
Intracardiac tumors or clots
Magnetic resonance imaging
Computed tomography
Less invasive. Very useful for most things. However, prior to cardioversion, the cardiologist is likely to order a trans-esophageal echo
Transesophageal Echocardiography (TEE)
Ultrasonic visualization of the posterior heart
INVASIVE---performed by MD
Offers better view of atria
Scope inserted into esophagus—posterior views of heart
Consent needed, NPO prior, IV access, IV conscious sedation, anesthetize the throat, monitor ECG, VS, SPO2 before, during and after, have O2 available
Indications:
Assess fx of prosthetic valves, dx endocarditis, evaluate valvular regurgitation and congenital abnormalities, examine aorta for dissecting aneurysms, may be done if a pt has a fib and cardioversion is being considered. This would be to check for the presence of any clots in the atria
Monitor LV wall during OR, measure EJ Fraction, when regular echo insufficient---obesity, COPD, chest wall trauma, inconclusive
Nuclear Cardiology
Multigated acquisition (MUGA) scan
Also called cardiac blood pool scan
Pts blood is mixed with radioisotope
Provides information on :
Heart wall motion during systole and diastole
Cardiac valves
Ejection fraction
Recordings are made of radioactivity over a specific area of the body
Electrophysiology (EP) study
Invasive, EP lab
Records intracardiac electrical activity
Reproduce an arrhythmia, origin of arrhythmia, path of arrhythmia, evaluates effectivens of drug therapy
Determines need for pacemaker, automatic implanted cardioverter defibrillator (AICD) or ablation
Usually ventricular or supraventricual arrythmias, conduction disorders, workup fro syncope—sick sinus syndrome or tachyarrhythmias
Similar to angiography only veins used vs. arterial system—spasm or occlusion
Bundle of his studies
Conduction intervals, refractory periods and recovery times
Cardiac Catheterization/Angiography
INVASIVE
Inpatient or outpatient procedure
Performed under fluoroscopy with a radiopaque catheter
Purpose:
Visualization of coronary artery and great vessels
Blood flow, function of chambers and valves
Measurement of ejection fraction
Evaluating abnormal stress test
Indicated in chest pain, syncope ischemic heart disease, cholesteremia, family heart disease
To dx CAD, valve problems, or complications from MI
Can measure hemodynamic pressures, cardiac output, abg’s
Also used to visualize perfusion after revascularization
How is the kidney protected from oxidative damage caused by contrast dye used in diagnostic procedures such as cardiac catherization? Which patients are most at risk from contrast dye administration side effects?
Patients at risk: allergic to dye—anaphylaxis, acute renal failure (kidney disease pts)
Monitor BUN and creatitnine. Do not take metformin (diabetic pts) prior to dye use
Premedicate: IV Benadryl (antihistamine) IV solumederol (steroid, antiinflamm)
Prevent kidney damage from the IV contrast dye use…
Acetylcysteine (Mucamyst)
Antioxidant—prevents oxidative tissue damage
IV administration: 1 mg/kg IV per hr 10-12 hrs pre and post procedure
PO administration: 600 mg PO BID on day before and day of procedure
Mix in approx 30 ml juice or diet coke
Tastes TERRIBLE and smells like sulfer
Comes in pills in some institutions
Define Hypertension.
----worldwide epidemic (affects 28% of Americans) direct relationship b/w HTN and CVD idiopathic HTN—affects 90-95% of individuals with HTN. Asymptomatic. Sustained increase in systolic and diastolic pressures.
Used to be called “essential hypertension” because it was so common in the elderly that doctors thought the higher BP must be “essential” (required for adequate perfusion) in older people. Some people do have symptoms, typically an occipital headache that increases with stress and exercise
Patho:
Multicausal increase in total peripheral resistance
Hereditary: sclerotic changes in resistance vessels
Sodium sensitivity: possible defect in sodium excretion. Increases in total body fluids
Altered RAA mechanism: high plasma renin levels results in increased conversion of angioII. Results in direct arterial constriction
Increased SNS activity
Possible “resetting of autonomic BP control mechanisms
Increased vasconstriction, increased HR, increased renin release
Increased resistance (often due to overweight)
High metabolic demands of increased body mass
Requires increased cardiovascular workload
Increased insulin levels stimulates SNS activity
Inhibits vasodilation
Endothelium dysfunction
Smooth muscle hypertrophy, sodium accumulation in smooth muscle, normally secretes nitric oxide and prostacyclin which keeps BP down, secretes endothelin which is a vasoconstrictor and causes adhesion and aggregation of neutrophils and platelets
Renal system
RAAS system---vasoconstriction and sodium and water retention.
Renal medulla secretes prostaglandins that can promote vasodilation (remember inflamm)
Natriuretic peptides are secreted by the heart cells with increased pressure in the atria and ventricles
Antagonize the effects of ADH and aldosterone and result in excretion of Na and H2O
How is blood pressure regulated?
Exercise, medications
Differentiate between primary and secondary hypertension.
Primary
Genetics and envirionment lead to either….
Insulin resistance
Vasoconstriction
Increased periph resistance
Sustained HTN
Dysfunction of SNS, RAA, adducing, and natriuretic hormones
Vasoconstriction or
Increased periph resistance
Renal and salt water retention
Increased blood voume
Inflammation
Renal and salt water retention
Increased blood volume
Sustained HTN
Secondary
Less than 10% of all HTN is secondary to another disorder
Reflects pathological or compensatory mechanism of the primary problem
Systemic disease process that raises the peripheral vascular resistance or cardiac output
Renal disease
Vascular diseases
Endocrine disorers (pheochromocytoma)
Brain lesions trauma What are the most common complications of hypertension?
Complicated HTN
Chronic hypertensive damage to the walls of systemic blood vessels
Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media
Malignant HTN
Rapidly progressive htn
Diastolic pressure is usually >140
Must be reduced bust must be brought down gradually to maintain cerebral perfusion
How is hypertension diagnosed?
Monitoring BP value
Normal BP= 120/80. Pre HTN= sbp 120-140 dbp 80-90. Class I HTN sbp 140-160 dbp 90-100. Class II HTN= sbp >160 or dbp >100
How is hypertension treated?—see meds in pp (too many to list)
Lifestyle medications (continuous treatment of meds!)
Describe the causes, symptoms and treatment of hypertensive crisis
Severe, abrupt increase in DBP (defined as >140)
Develops over hours or days
Rate of increase in BP is more important than the absolute value
Severe headache, nausea, vomiting, seizures, cerebral edema, confusion, coma, death
Often occurs in pts with a hx of htn who have “failed to comply” with meds or who have been under-medicated ----can occur with use of cocaine, amphetamines, PCP, LSD
May use nitroprusside (Nipride)
Potent IV vasodiltor
Only used in ICU and ER
Must monitor BP at least every 15 mins, more often with initiation
Will deteriorate into cyanide---must be protected from light
---*the body can more readily compensate for slow gradual changes rather than sudden changes
What is the etiology of Coronary Heart Disease?
Describe modifiable vs. nonmodifiable risk factors (TABE 34-1 in book!)
Health promotion:
Identify people at risk
Health hx---- use of prescription/nonprescription meds
Presence of cardiovascular symptoms
Environmental patterns: diet, activity
Values and beliefs about health and illness
Cultural and ethinic differences:
Middle-aged white men have the highest incidence of CAD
African Americans have increased incidence of early-age onset of CAD
Native Americans have lower rates of CAD and lower death rates from CAD than non-hispanic whites
What is angiogenesis? What role does collateral circulation play?
Collateral circulation
Normally some arterial anastomoses (connections) exist within the coronary circulation
When occlusion slowly over a long period, there is a greater chance of adequate collateral circulation developing
Collateral growth
Growth and extent of collateral circulation is attributed to :
Inherited predisposition to develop new vessels (angiogenesis)
Presence of chronic ischemia
Slow, progressive blockage of an artery results in greater chance of adequate collateral formation
Rapid-onset CAD or coronary spasm results in inadequate blood flow r/t poor collateral formation
How is CAD treated? What are the primary types of medications used?
Strategies to reduce risk factors are effective but often underprescribed:
Treatment of HTN and hyperlipidemia. Increased exercise. Dietary changes
What is the Pathophysiology of Angina?
----angina is the clinical manifestation of reversible cardiac ischemia characteristics: 1. Chest pain that occurs intermittently over long period of time
2. Same pattern of onset, duration and intensity. 3. Pain at rest is unusual
Patho/etiology:
Temporary, reversible myocardial ischemia
O2 demand > O2 supply
Insufficient blood flow r/t narrowing of coronary arteries by athersclerosis
For ischemia to occur, the artery is usually 75% or more stenosed
Differentiate between the various types of Angina
Silent ischemia
Nocturnal angina
Angina decubitus
Prinsmetal’s (variant) angina
Microvascular angina
Differentiate between ACS, SCD, and Acute MI
How is each condition diagnosed and treated?
What are the primary complications of each?
ACUTE CORONARY SYNDROME (ACS)
Prolonged ischemia that is not immediately reversible
Deterioration of once a stable plaque
Stable plaque ruptures
Stimulates platelet aggregation
Localized vasoconstriction
Thrombus formation
Systemic inflammation may be the etiology
Unstable angina (UA)
ST-segment elevation (STEMI)
Non-ST segment elevation myocardial infarction (NSTEMI)
Clinical manifestations:
Cardiovascular
Initially, increased HR and BP, then decreased BP (secondary to decrease CO)
Crackles, jugular venous distention, abnormal heart sounds (S3 or S4, new murmur)
SUDDEN CARDIAC DEATH (SCD)
Unexpected death from cardiac causes
Most deaths occur outside of hospital CAD accounts for about 80% of all SCDs abrupt disruption in cardiab fx, resulting in loss of CO and cerebral blood flow death usually within 1 hour of onset of acute symptoms (angina, palpitations) most SCDs caused by ventricular dysrhythmias (ventricular tachycardia)
ACUTE MYOCARDIAL INFARCTION (MI)
Sustained ischemia (>20 mins)
Irreversible myocardial cell death (necrosis)
Necrosis of entire thickness of myocardium takes 4-6 hrs
Degree of altered fx depends on the area of the heart involved and the size of the infarct
Complications:
Dysrythmias, heart failure, cardiogenic shock, papillary muscle dysfunction, ventricular aneurysm, acute pericarditis, dressler syndrome
What is heart failure and why is HF a significant problem in the US?
Describe the primary risk factors, etiology and compensatory mechanisms
What roles do the sympathetic nervous system and neurohormonal response play?
Describe the Frank Starling Principle and the role it plays in heart function
Differentiate between the etiology and symptoms seen in Right-Sided vs. Left-Sided HF
How is heart failure managed? What are the goals of therapy

What are the primary properties of cardiac tissue that affect the generation and transmission of impulses?
Why are cardiac cells called a syncytium?
What electrolytes are essential to depolarization-repolarization? Describe their movement across the cardiac cell wall.
Describe each of the major components in the electrical conduction pathway. What wave forms do these components represent on the EKG tracing?
What is a cardiac lead? What is the primary difference between a 12-lead tracing and a rhythm strip tracing? What are the uses of each?
What do the PR interval and the QRS duration measure? What is the normal width of each? If the width is prolonged, what does that mean? How do medications affect the width of these components?
How is the cardiac rate determined on the rhythm strip? What must be present for a rhythm to be called sinus?
Define ectopy. What risk do ectopic beats pose to the cardiac output?
Identify the primary characteristics of the following rhythms. What risk do they pose to the patient’s cardiac output? Which are potentially lethal? How are these rhythms treated?
Sinus Bradycardia
Sinus Tachycardia
Junctional Rhythm
Atrial Fibrillation
Atrial Flutter
First Degree AV Block
Second Degree Mobitz Type I
Second Degree Mobitz Type II
Third Degree AV Block
Ventricular Tachycardia
Ventricular Fibrillation
Asystole
How are pacemakers used to improve cardiac output?
What is a demand pacemaker?
If the patient has an implanted pacemaker, what do you expect to see on the EKG tracing?
How is pacemaker failure diagnosed? What risk does pacemaker failure pose to the patient?
Differentiate between the etiology, pathophysiology, clinical manifestations and treatment of
Infective Endocarditis
Acute Pericarditis
Valvular Heart Disease
What is an aortic aneurysm? How is it diagnosed? What is the risk if the aneurysm ruptures? How can aneurysm be repaired?
What is peripheral arterial disease?
How is it diagnosed? Who is most at risk?
What is the treatment for PAD?
Differentiate between arterial and venous insufficiency.
How is a DVT diagnosed and treated? How can a DVT be prevented?