Step-Up To Medicine: Cardiovascular

Front 1

Stable angina pectoris

Back 1

Due to FIXED atherosclerotic lesions that narrow the major coronary arteries. Coronary ischemia is due to an imbalance between blood supply and oxygen demand, leading to inadequate perfusion. Stable angina occurs when oxygen demand exceeds available blood supply

Front 2

Risk factors for Ischemic Heart Disease

Back 2

(1) DM; (2) HLD (elevated LDL); (3) HTN; (4) Smoking; (5) Age (men >45, women >55); (6) Family history of premature CAD or MI in first degree relative: men <45, women <55 ears); (7) Low HDL; (8) Elevated homocysteine

Front 3

Prognostic Indicators of CAD

Back 3

(1) Left ventricular function (EF%) - normal is >50%, if <50%, associated with increased mortality; (2) Vessels involved (severity/extent of ischemia) - Left main coronary artery-poor prognosis because it covers approximately 2/3 of the heart; two or three-vessel CAD associated with worse prognosis

Front 4

Clinical Features of Stable Angina

Back 4

(1) Chest pain or substernal pressure, lasts <10-15 minutes (usually 1-5) and described as heaviness, pressure, squeezing; (2) Brought on by exertion or emotion; (3) Relieved with rest or NTG

Front 5

Diagnosis of CAD

Back 5

(1) Resting EKG - usually normal in patients with stable angina; (2) Q waves are consistent with prior MI; (3) If ST segment or T wave abnormalities are present during an episode of chest pain, then treat as for unstable angina

Front 6

Stress EKG

Back 6

(1) Test involves recording ECG before, during, and after exercise on a treadmill; (2) Test is 75% sensitive IF patients are able to exercise sufficiently to increase HR to 85% of maximum predicted value for age; (3) Exercise-induced ischemia results in subendocardial ischemia, producing ST segment depression; (4) Other positive findings include onset of heart failure or ventricular arrhythmia during exercise or hypotension; (4) PATIENTS WITH A POSITIVE STRESS EKG SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 7

When is a stress EKG generally considered positive?

Back 7

If the patient develops any (1) ST-depression; (2) Chest Pain; (3) Hypotension; (4) Significant arrhythmias

Front 8

Stress Echocardiography

Back 8

(1) Performed before and immediately after exercise. Exercise-induced ischemia is evidenced by wall motion abnormalities (e.g., akinesis or dyskinesis) not present at rest; (2) Favored by many cardiologists over stress EKG. It is more sensitive in detecting ischemia, can assess LV size and function, and can diagnose valvular disease; (3) Again, patients with a POSITIVE TEST SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 9

Stress myocardial perfusion imaging

Back 9

Stress-test' aka P-Thal (Persantine-Thallium); (1) Viable myocytes extract thallium 201 from blood during exercise. No radioisotope uptake means no blood flow to an area of the myocardium; (2) It is IMPORTANT to determine wther the ischemia is reversible, i.e., whether the areas of hypoperfusion are perfused over time as blood flow eventually equalized. Areas of REVERSIBLE ischemic may be rescued with PTCA or CABG. Irreversible ischemia, however, indicates infarcted tissue that cannot be salvaged

Front 10

Pharmacologic Stress Test

Back 10

Performed if the patient cannot exercise. IV adenosine, dipyramidole, or dobutamine can be used. The cardiac stress induced by these agents takes the place of exercise. This can be combined with an EKG, an echocardiogram, or nuclear perfusion imaging. (2) These agents cause generalized coronary vasodilation; because diseases coronary arterires are already maximally dilated at rest to increase blood flow, they receive relatively less blood flow when the entire coronary system is pharmacologically vasodilated; (3) Dobutamine increases myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility

Front 11

Cardiac Catheterization with Coronary Angiography

Back 11

(1) Coronary angiography - definitive test for CAD. Indicated in patients being considered for revascularization (PTCA or CABG); (2) Contrast is injected into coronary vessels to visualize any stenotic lesions. This defines the location and extent of coronary disease; (3) If coronary artery disease is severe (e.g., left main or three-vesel disease), refer patient for surgical revascularization

Front 12

Risk Factor Modification in Ischemic Heart Disease

Back 12

(1) Smoking cessation cuts CAD risk in half by 1 year after quitting; (2) HTN - vigorous BP control reduces risk of CHD, especially in diabetic patients; (3) Hyperlipidemia - reduction in serum cholesterol with lifestyle modification and HMG-CoA reductase inhibitors reduces CAD risk; (4) DM - strict glycemia control is thought to have less effect on macrovascular disease risk than microvascular disease but should still be emphasized; (5) Obesity - weight loss modifies other risk facotrs DM, HTN, and HLD) and provides other health benefits; (6) Exercise is critical; minimizes emotional stress, promotes weight loss, and helps reduce other risk factors; (7) Diet: Reduce intake of saturated fat and cholesterol; (8) Hyperhomocystinemia - value of treating yet to be established

Front 13

Medical Therapy in Ischemic Heart Disease

Back 13

(1) Aspirin; (2) Beta-blockers; (3) Nitrates; (4) Calcium Channel Blockers; (5) If CHF is present, treatment with ACE-I and diuretics may also be indicated

Front 14

Aspirin

Back 14

Indicated in ALL patients with CAD; DECREASES MORBIDITY - reduces risk of MI!

Front 15

Beta Blockers

Back 15

Block sympathetic stimulation of heart, reduce HR, BP, and contractility, thereby decreasing cardiac work (i.e., Beta-blockers lower myocardial oxygen consumption); Have been shown to REDUCE FREQUENCY OF CORONARY EVENTS

Front 16

Nitrates

Back 16

Cause generalized vasodilation. (1) Relieve angina; rduce preload, therefore the load and oxygen demand; (2) May prevent angina when taken before exertion; (3) Effect on prognosis is unknown; main benefit is symptomatic relief; (4) Can be administered orally, sublingually, transdermally, or intravenously

Front 17

Calcium Channel Blockers

Back 17

Cause coronary vasodilation and afterload reduction. Now considered a SECONDARY TREATMENT when beta-blockers and/or nitrates are not fully effective

Front 18

Revascularization

Back 18

(1) May be preferred for high risk patients, although some controversy exists as to whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%; (2) Two methods for revascularization: PTCA and CABG; (3) Revascularization does NOT reduce incidence of MI, but does result in significant improvement in symptoms

Front 19

Percutaneous Transluminal Coronary Angioplasty (PTCA)

Back 19

Should be considered in patients with one or two vessel disease. Best if used for proximal lesions. RESTENOSIS is a significant problem (up to 40% within first 6 months); however, if there is no evidence of restenosis at 6 months, it usually does not occur. STENTS SIGNIFICANTLY REDUCE the rate of restenosis

Front 20

Coronary Artery Bypass Grafting (CABG)

Back 20

Treatment of choice in patients with high-risk disease. Indicated in patients with left main disease, 3-vessel disease with reduced left ventricular function, two-vessel disease with proximal LAD stenosis, or severe ischemia for palliation of symptoms

Front 21

Unstable Angina: Pathophysiology

Back 21

Oxygen demand is UNCHANGED. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand. USA is significant because it indicates STENOSIS that has enlarged via thrombosis, hemorrhage, or plaque rupture. It may lead to total occlusion of a coronary vessel.

Front 22

What characterizes Unstable Angina pain?

Back 22

(1) Patients with angina at rest; (2) Patients with new-onset angina that is severe and worsening; (3) Patients with chronic angina with increasing frequency, duration, or intensity of chest pain

Front 23

Diagnosis of USA

Back 23

(1) Exclude MI; (2) Patients with USA have a higher risk of adverse events during stress testing. These patients should be stabilized with medical management before stress testing or should undergo cardiac catheterization initially.

Front 24

Acute Coronary Syndrome - what is it?

Back 24

The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion; The term generally refers to unstable angina or acute MI

Front 25

How do you differentiate USA from NSTEMI?

Back 25

Both are considered together because it is difficult to distinguish the two based on patient presentation. If cardiac enzymes are elevated, then the patient has NSTEMI

Front 26

Treatment of Unstable Angina

Back 26

(1) Aspirin; (2) Beta-blockers; (3) LMWH or UFH for at least 2 days (keep PTT 2-2.5x normal); (4) Nitrates are first-line therapy; (5) Glycoprotein Iib/IIIa inhibitors (abciximab, tirofiban) can be helpful adjuncts in USA, especially if patient is undergoing PTCA or stenting.

Front 27

Treatment of USA after acute treatment

Back 27

(1) ASA, Beta-blockers, nitrates; (2) Treat DM, HTN; (3) Treat with statin; (4) Consider folic acid for hyperhomocystinemia

Front 28

Prinzmetal's Angina

Back 28

Involves transient coronary vasospasm that usually is accompanied by a fixed atherosclerotic lesion (75% of cases) but can also occur in normal coronary arteries. (1) Episodes of angina occur at rest, associated with ventricular dysrhythmias; (2) Hallmark is transient ST segment elevation (not depression!) on EKG during chest pain, which represents transmural ischemia; (3) Coronary angiography is definitive test - displays coronary vasospasm when the patient is given IV ergonovine to provoke chest pain; (4) Vasodilators - CCBs and nitrates have been proven to help

Front 29

What is an MI?

Back 29

Necrosis of the myocardium 2/2 interruption of blood supply (after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis). Most cases are due to acute coronary thrombosis: atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel. Most patients with MI have history of angina, risk factors for CAD, or history of arrhythmias

Front 30

Clinical Features of AMI

Back 30

(1) Chest pain: intense substernal pressure, often described as 'crushing' and 'elephant on top of chest'; (2) Radiation to neck, jaws, arms, or back, commonly to the left side; (3) Similar to angina pectoris in character and distribution but much more severe and lasts longer; (4) Some patients may have epigastric discomfort

Front 31

Can an MI be asymptomatic?

Back 31

YES! (1) In up to 1/3 of patients, painless infarcts or atypical presentations occur; this is most likely in postoperative patients, the elderly, diabetic patients, and women; (2) Other symptoms: dyspnea, diaphoresis, weakness, fatigue, N/V, sense of impending doom, syncope

Front 32

What is the MCC of sudden cardiac death?

Back 32

Ventricular fibrillation

Front 33

What are the signs and symptoms of a right ventricular infarct?

Back 33

Inferior EKG changes, hypotension, elevated jugular venous pressure, hepatomegaly, and CLEAR LUNGS

Front 34

Diagnosis of AMI - markers of ischemia/infarction include:

Back 34

(1) Peaked T waves: occur very early, may be missed; (2) ST segment elevation indicates transmural injury and can be diagnostic of an acute infarct; (3) Q waves: evidence for necrosis (specific) - Q waves are usually seen late; typically not seen acutely; (4) T wave inversion is sensitive but NOT specific; (5) ST segment depression: subendocardial injury

Front 35

ST segment elevation infarct

Back 35

Transmural, involving entire thickness of the wall; tends to be larger

Front 36

Non-ST segment elevation infarct

Back 36

Subendocardial (involves inner one third to one half of the wall); tends to be smaller, and presentation is similar to USA - cardiac enzymes will differentiate the two

Front 37

Cardiac Enzymes

Back 37

Currently the gold standard for MI; (1) CK-MB: increases within 4-8 hours and returns to normal in 48-72 hours; reaches a peak in 24 hours. When measured within 24-36 hours of onset of chest pain, has greater than 95% sensitivity and specificity; Levels of total CK and CK-MB should be measured on admission and every 8 hours thereafter for 24 hours; (2) Troponins I and T - most IMPORTANT test to order; increases within 3-5 hours and returns to normal in 5-14 days; reach a peak in 24-48 hours. Greater sensitivity and specificity than CK-MB. NOTE: troponin I can be falsely elevated in patients with renal failure

Front 38

What is meant by 'serial enzymes'?

Back 38

Cardiac enzymes are drawn serially - once on admission and every 8 hours until 3 samples are obtained. The higher the peak and the longer enzyme levels remain elevated, the more severe the myocardial injury and the worse the prognosis

Front 39

Treatment of MI

Back 39

(1) ASA; (2) Beta-blockers; (3) ACE-I; (4) Statins; (5) Oxygen; (6) Nitrates; (7) Morphine sulfate; (8) Heparin; [remember: MONA has Hep A,B]

Front 40

What therapies have been shown to reduce mortality in MI?

Back 40

(1) ASA, (2) Beta-blockers; (3) ACE-I

Front 41

Anterior Infarct EKG changes

Back 41

ST elevation in V1-V4 early, Q waves in leads V1-V4 late

Front 42

Posterior Infarct EKG changes

Back 42

Large R wave in V1 and V2, ST segment depression in V1 and V2, Upright and prominent T waves in V1 and V2

Front 43

Lateral Infarct EKG changes

Back 43

Q waves in leads I and aVL (late change)

Front 44

Inferior Infarct EKG changes

Back 44

Q waves in II, III, aVF (late change)

Front 45

Pump Failure (CHF)

Back 45

Most common cause of in-hospital mortality after MI; if mild, treat with ACE-I, diuretic. If severe, may lead to cardiogenic shock; invasive hemodynamic monitoring may be indicated

Front 46

Risk of stroke after acute-MI

Back 46

Patients who suffer an acute MI have a high risk of stroke during the next 5 years. The lower the EF and the older the patient, the higher the risk of stroke

Front 47

Ventricular tachycardia

Back 47

Sustained VT requires treatment: if patient is hemodynamically unstable, electrical cardioversion is indicated. If patient is hemodynamically stable, start antiarrhythmic therapy with IV amiodarone

Front 48

Ventricular fibrillation

Back 48

Immediate unsynchronized defibrillation and CPR are indicated

Front 49

AV block

Back 49

(1) Associated with ischemic involving conduction tracts; (2) 1st and 2nd degree (type I) blocks do not require treatment; (3) Second-degree (type II) and third-degree block: prognosis is dire in setting of anterior MI - emergent placement of a temporary pacemaker is indicated (with later placement of a permanent pacemaker). If inferior MI, prognosis is better, and IV atropine may be used initially. If conduction is not restored, a temporary pacemaker is appropriate

Front 50

Free wall rupture

Back 50

(1) Catastrophic, usually fatal event that occurs during the first two weeks after MI (90% within 2 weeks, most commonly 1-4 days after MI). 90% mortality rate, usually leads to hemopericardium and cardiac tamponade; (3) Treatment: hemodynamic stabiliation, immedaite pericardiocentesis, and surgical repair

Front 51

Rupture of interventricular septum

Back 51

(1) Greater potential for successful therapy than with a free wall rupture, although this is also a critical event; emergent surgery is indicated; (2) Occurs within 10 days after MI; (3) Likelihood of survival correlates with size of defect

Front 52

Papillary muscle rupture

Back 52

(1) Produces MITRAL REGURGITATION; (2) If suspected, obtain Echo immediately; (3) Emergent surgery is needed (mitral valve replacement is usually necessary)as well as afterload reduction with sodium nitroprusside or intra-aortic balloon pump (IABP)

Front 53

Ventricular pseudoaneurysm

Back 53

Incomplete free wall rupture (myocardial rupture is contained by pericardium); (2) Bedside echo may show the pseudoaneurysm, surgical emergency because these tend to become a free-wall rupture

Front 54

Ventricle aneursym

Back 54

Rarely rupture (in contrast to pseudoaneurysm); associated with a high incidence of ventricular tachyarrhythmias; Medical mangement may be protective, surgery to remove aneursym may be appropriate in some patients

Front 55

Acute pericarditis

Back 55

Treatment consists of ASPIRIN ONLY! NSAIDs and corticosteroids are contraindicated and may hinder myocardial scar formation

Front 56

Dressler's Syndrome ('post-myocardial infarction syndrome')

Back 56

Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occuring weeks to months after an MI. ASPIRIN is the most effective therapy

Front 57

Congestive Heart Failure

Back 57

Clinical syndrome resulting from the heart's inability to meet the body's circulatory demands under normal physiological conditions

Front 58

Pathophysiology of CHF

Back 58

(1) Decreased cardiac output = (2) Activation of RAAS and Sympathetic NS = (3) Systemic vasoconstriction and volume retention = (4) Increased venous return, resulting in increased preload. This maintains CO. However, in severe CHF, increased preload does not result in increased CO. Increased LVEDV causes increased LVEDP, which is transmitted back to pulmonary veins and leads to symptoms of pulmonary congestion

Front 59

Frank-Starling relationship

Back 59

(1) In a normal heart, increasing preload results in greater contractility; (2) When preload is low (at rest), there is little difference in performance between a normal and a failing heart. However, with exertion a failing heart produces less contractility and symptoms occur.

Front 60

Systolic dysfunction

Back 60

Caused by impaired contractility - abnormality is decreased ejection fraction. Causes include recent MI (MCC), cardiomyopathy, myocarditis

Front 61

Diastolic dysfunction

Back 61

Caused by impaired ventricular filling during diastole (either impaired relaxation of increased stiffness or both); Echo shows impaired relaxation of LV. Causes include (1) HTN leading to myocardial hypertrophy (MCC), (2) Valvular disease such as Aortic stenosis, mitral stenosis, and aortic regurgitation, (3) Restrictive cardiomyopathy (amyloid, sarcoid, hemochromatosis)

Front 62

Symptoms of left-sided heart failure

Back 62

(1) Dyspnea; (2) Orthopnea; (3) Paroxysmal Nocturnal Dyspnea; (4) Nocturnal cough; (5) Confusion and memory impairment 2/2 impaired brain perfusion; (6) Diaphoresis and cool extremities at rest in desperately ill patients

Front 63

Signs of left-sided heart failure

Back 63

(1) Displaced PMI (to the left) due to cardiomegaly; (2) Pathologic S3 (ventricular gallop) with rapid filling phase into a concompliant LV chamber; (3) Heard best at apex with bell of stethoscope

Front 64

NYHA class I

Back 64

Symptoms occur with vigorous activities such as playing a sport. Patients are nearly asymptomatic

Front 65

NYHA class II

Back 65

Symptoms occur with prolonged or moderate exertion, such as climbing a flight of stairs or carrying heavy packages. Slight limitation of activities

Front 66

NYHA class III

Back 66

Symptoms occur with usual activities of daily living, such as walking across the room or getting dressed. Markedly limiting

Front 67

NYHA class IV

Back 67

Symptoms occur at rest. Incapacitating

Front 68

S4 gallop

Back 68

Atrial systole 'into' a noncompliant left ventricular chamber, heard best at left sternal border with bell.

Front 69

Pleural effusion

Back 69

Crackles and rales at lung bases; dullness to percussion and decreased tactile fremitus of lower lung fields

Front 70

What does an increased intensity of the pulmonic component A2/P2 of second heart sound indicated?

Back 70

Pulmonary Hypertension

Front 71

Signs and Symptoms of RSHF

Back 71

(1) Peripheral pitting edema; (2) Nocturia - 2/2 increased venous return with elevation of legs; (3) JVD; (4) Hepatomegaly, hepato-jugular reflux; (5) Ascites; (6) Right ventricular heave

Front 72

Diagnosis of CHF

Back 72

(1) Cardiomegaly on CXR; (2) Kerley B lines are short horizontal lines near periphery of the lung near the costophrenic angles, and indicate pulmonary congestion secondary to dilatation of pulmonary lymphatic vessels; (3) Prominent interstitial markings; (4) Pleural effusion

Front 73

Echocardiogram

Back 73

(1) Initial test of choice whenever CHF is suspected based on history, examination, CXR; (2) Useful in determining whether systolic or diastolic dysfunction predominantes, and determines whether the cause of CHF is due to a pericardial, myocardial, or valvular process; (3) Estimates EF (very important!): patients with systolic EF <40% should be those with preserved LV EF >40%

Front 74

Treatment of Systolic dysfunction CHF: Diuretics

Back 74

Most effective means of providing SYMPTOMATIC relief to patients with moderate to severe CHF; Have NOT been shown to reduce mortality or improve prognosis! (3) Lasix > HCTZ > Spironolactone

Front 75

Treatment of Systolic dysfunction CHF: ACE-I

Back 75

Cause venous and arterial vasodilation, decreasing preload and afterload. The combination of a diuretic and an ACE inhibitor should be the initial treatment in most symptomatic patients. ACE-INHIBITORS REDUCE MORTALITY, PROLONG SURVIVAL, and ALLEVIATE SYPTOMS in mild, moderate and severe CHF

Front 76

Treatment of Systolic dysfunction CHF: ARBs

Back 76

Used in patients unable to take ACE-I due to side effect of cough, but should NOT replace ACI-I if patient tolerates an ACE-I

Front 77

Treatment of Systolic dysfunction CHF: Beta-blocker

Back 77

Proven to DECREASE MORTALITY in patients with post-MI heart failure; reported to improve symptoms of CHF; may slow progression of heart fialure by slowign down tissue remodeling. Should be given to STABLE patients with mild to moderate CHF (class I, II, and III) unless CI

Front 78

Treatment of Systolic dysfunction CHF: Hydralazine and Isosorbide dinitrates

Back 78

Can be used in patients who cannot tolerate ACE-inhibitors. Combination of hydralazine and isosorbide dinitrate has been shown to improve mortality in CHF, but not as effective as ACE inhibitors and require inconvenient dosing schedules

Front 79

Treatment of Systolic dysfunction CHF: Digitalis

Back 79

Positive inotropic agent, useful in patients with EF <30%, severe CHF, or severe atrial fibrillation. Provides short-term symptomatic relief, but has NOT been shown to improve mortality! Can be added to diuretics and ACE-I in severe CHF; check serum digoxin level periodically

Front 80

Signs of digoxin toxicity

Back 80

(1) GI: nausea/vomiting, anorexia; (2) Cardiac: ectopic (ventricular) beats; AV block causing a regular junctional escape rhythm to start, Afib; (3) CNS: visual disturbances, disorientation

Front 81

Premature Atrial Complexes (PACs)

Back 81

Early beat arising from the atria, firing on its own 2/2 adrenergic excess, drugs, EtOH, tobacco, electrolyte imbalance, ischemia, and infection. On EKG, look for early P waves that differ in morphology from the normal sinus P wave (because these P waves originate within the atria and NOT the sinus node). QRS complex is normal because conduction below the atria is normal.

Front 82

Premature Ventricular Complexes (PVCs)

Back 82

Early beat that fires on its own from a focus in the ventricle and then spreads to the other ventricle. Causes include hypoxia, electrolyte abnormalities, stimulants, caffiene, and medications. Because conduction is NOT through normal conduction pathways, but rather through ventricular muscle, it is SLOWER than normal, causing a wide QRS. Wide, bizarre QRS complexes followed by a compensatory pause are seen. A P wave is not usually seen because it is buried within the QRS complex

Front 83

Atrial fibrillation (Afib)

Back 83

(1) Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally IRREGULAR, RAPID VENTRICULAR RATE. Instead of intermittently contracting, the atria quiver continuously; (2) Atrial rate is over 400bpm, but most impulses are blocked at the AV node, so ventricular rate ranges between 75 and 175. (3) Patients with AFib and underlying heart disease are at a markedly increased risk for adverse events, such as thromboembolism and hemodynamic compromise

Front 84

Causes of Afib

Back 84

(1) Heart disease: CAD, MI, HTN, MVP; (2) Pericarditis and pericardial trauma [surgery]; (3) Pulmonary disease, including PE; (4) Hyper/hypothyroidism; (5) Systemic illness [sepsis, malignancy, DM]; (6) Stress; (7) Excessive EtOH [holidary heart syndrome]; (8) Sick sinus syndrome; (9) Pheochromocytoma

Front 85

Clinical features of Afib

Back 85

(1) Fatigue and exertional dyspnea; (2) Palpitations, dizziness, angina, or syncope; (3) Irregularly irregular pulse; (4) Blood stasis (secondary to ineffective contraction) leads to formation of intramural thrombi, which can embolize to the brain

Front 86

EKG findings of Afib

Back 86

Irregularly irregular rhythm, with irregular RR intervals and excessively rapid series of tiny, erratic spikes on EKG with a wavy baseline and no identifiable P waves

Front 87

Treatment of Afib in hemodynamically unstable patient

Back 87

Immediate electrical cardioversion to sinus rhythm

Front 88

Treatment of Afib in hemodynamically stable patient

Back 88

(1) Rate control: target is 60-100bpm. CCBs are preferred, beta-blockers are an alternative. If LV systolic dysfunction is present, consider digoxin or amiodarone; (2) Cardioversion to sinus rhythm (after rate control established). Electrical cardioversion preferred, but can use IV ibutilide, procainamide, flecainide, sotalol, or amiodarone for pharmacologic conversion; (3) Anticoagulation to prevent embolic CVA. If Afib present >48 hours, risk of embolization during cardioversion is 2-5%!, therefore anticoagulate patients for 3 weeks before and 4 weeks after cardioversion. An INR of 2-3 is is the anticoagulation goal range. To avoid waiting 3 weeks for OAT, obtain a TEE to image the LA. If no thrombus is present, start IV heparin and perform cardioversion within 24 hours. Patients still require anticoagulation after cardioversion

Front 89

Three main goals of Afib/Aflutter treatment

Back 89

(1) Control ventricular rate; (2) Restore NSR; (3) Assess need for anticoagulation. The AFFIRM trial should that rate control is superior to rhythm control in Afib treatment

Front 90

Chronic Afib treatment

Back 90

(1) Rate control with BB or CCB; (2) Anticoagulation in patients with lone Afib (no underlying heart disease or other CV risk factors) under age 60 is not required because they are at low risk for embolization (ASA may be appropriate). Treat all other patients with chronic anticoagulation

Front 91

Atrial Flutter: Pathophysiology

Back 91

One irritable automaticity focus in the atria fires at 250-350bpm, giving rise to regular atrial contractions. Atrial rate between 250-350 bpm. Ventricular rate is one-half to one-third the atrial rate. The long refractory period in the AV node allows one one of every two or three flutter waves to conduct to the ventricles

Front 92

Causes of Atrial Flutter

Back 92

(1) COPD - most common association; (2) Heart disease - rheumatic heart disease, CAD, CHF; (3) ASD

Front 93

Treament of Atrial Flutter

Back 93

Same as for Atrial Fibrillation - (1) Control rate; (2) Restore NSR; (3) Anticoagulation

Front 94

Multifocal Atrial Tachycardia

Back 94

Usually occurs in patients with severe pulmonary disease (COPD). EKG findings = variable P wave morphology, variable PR and RR intervals. At least 3 different P wave morphologies are required to make an accurate diagnosis! Can also be diagnosed by use of vagal maneuvers or adenosine to show AV block without disrupting the atrial tachycardia

Front 95

Treatment of MAT

Back 95

Improving oxygenation and ventilation. If LV function is preserved, acceptable treatments include CCBs, BB, digoxin, amiodarone, IV flecainide, and IV propafenone. If LV function is not preserved, use digoxin, diltiazem, or amiodarone. Electrical cardioversion is ineffective and should not be used

Front 96

Paroxysmal Supraventricular Tachycardia: Pathophysiology

Back 96

Most often due to reentry. Two types: AV nodal reentrant tachycardia and Orthodromic AV reentrant tachycardia

Front 97

AVNRT

Back 97

Two pathways (one fast and one slow) within the AV node, so the reentrant circuit is within the AV node. MCC of SVT! Initiated or teminated by PACs. EKG findings = narrow QRS complexes with no discernible P waves (P waves are buried within the QRS complex). This is because the circuit is short and conduction is rapid, so impulses exit to activate atria and ventricles simultaneously

Front 98

Orthodromic AVRT

Back 98

Accessory pathway between atria and ventricles that conducts retrogradely. Called a 'concealed bypass tract' and is a common cause of SVTs. Initiated or terminated by PACs of PVCs. EKG: narrow QRS complexes with P waves which may or may not be discernible, depending on the rate. This is because the accessory pathway is some distance from the AV node (reentrant circuit is longer), and there is a difference in the timing of activation of the atria and ventricles

Front 99

Treatment of SVT

Back 99

(1) Maneuvers that stimulate the vagus delay AV conduction and thus block the re-entry mechanism: the Valsalva maneuver, carotid sinus massage, breath holding, and head immersion in cold water (or placing an ice bag to the face); (2) Acute treatment: Pharmacologic therapy with IV adenosine [agent of choice] due to its short duration of action and effectiveness in terminating SVTs; works by decreasing sinoatrial and AV nodal activity (3) IV verapamil and IV ismolol or digoxin are alternatives in patients with preserved LV function; (4) DC cardioversion if drugs are not effective or if unstable; almost always successful. (5) RF caheter ablation of either the AV node or the accessory tract (depending on which is the accessory pathway) is preferred if episodes are recurrent and symptomatic

Front 100

Wolff-Parkinson-White Syndrome

Back 100

(1) An accessory conduction pathway from atria to ventricles causes premature ventricular excitation because it lacks the delay seen in the AV node; (2) May lead to paroxysmal tachycardia. Diagnosis on EKG: narrow complex tachycardia, short P-R interval, and a delta wave; (3) Rx: RF ablation of one arm of reentrant loop of accessory pathway is an effective treatment. Avoid drugs active on AV node like digoxin because they may accelerate conducntion through the accessory pathway

Front 101

Ventricular tachycardia

Back 101

(1) Rapid and repetitive firing of 3 or more PVCs in a row, at a rate of between 100 and 250bpm; (2) AV dissociation is present, i.e., sinus P waves continue with their cycle, unaffected by the tachycardia; (3) Originates below Bundle of His; (4) Sustained VT lasts longer than 30 seconds and is almost always symptomatic - associated with hypotension and/or myocardial ischemia; can progress to VFib without treatment

Front 102

Torsades de pointes

Back 102

(1) Rapid polymorphic VT. Dangerous arrhythmia that often can lead to Vfib. (2) Associated with many factors that prolong the QT interval (e.g., congenital QT syndromes, tricyclic antidepressants, anticholinergics, electrolyte abnormalities, ischemia. (3) IV Magnesium provides cardiac stabilization

Front 103

Ventricular Fibrillation

Back 103

Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output. Most episodes of Vfib begin with VT. Ischemic heart disease is the most common cause

Front 104

Recurrence of Vfib

Back 104

If Vfib is not associated with acute MI, recurrence rate is high (up to 30% within first year!). These patients require chronic therapy: either prophylactic antiarrhythmic therapy (amiodarone) or AIDC. If Vfib develops within 48h of AMI, long-term prognosis is favorable, and recurrence rate is low (2% at 1 year). Chronic therapy is not needed in these patients

Front 105

Dilated Cardiomyopathy

Back 105

(1) MC type of Cardiomyopathy; an insult (ischemia, infection, alcohol, etc) causes dysfunction of the left ventricular contractility. Associated with poor prognosis; many die within 5 years of onset of symptoms; (2) CAD (with prior MI) is the most common cause

Front 106

Clinical features of dilated cardiomyopathy

Back 106

(1) Symptoms and signs of left and right-sided heart CHF develop; (2) S3 and S4, as well as murmurs of mitral or tricuspid insufficiency may be present

Front 107

Treatment of dilated cardiomyopathy

Back 107

(1) Similar to treatment of CHF: digoxin, diuretics, vasodilators, and cardiac transplantation; (2) Remove offending agent if possible; (3) Anticoagulation should be considered because patients are at increased risk of embolization

Front 108

Hypertrophic Cardiomyopathy

Back 108

Most cases are inherited as an autosomal dominant trait. (1) Main problem is diastolic dysfunction 2/2 stiff, hypertrophied ventricle with elevated diastolic filling pressures. These pressures increase further with factors that increase HR and contractility (such as exercise) or decrease left ventricular filling (e.g., the Valsalva maneuver). (2) Patients may also have a dynamic outflow obstruction 2/2 asymmetric hypertrophy of the interventricular septum

Front 109

What effect do standing, Valsalva, and leg raise maneuvers have on the intensity of murmurs?

Back 109

These maneuvers decrease LV volume and thus diminish the intensity of all murmurs except MVP and HCM.

Front 110

How does squatting effect the intensity of murmurs?

Back 110

Squatting increases the intensity of all murmurs except MVP and HCM

Front 111

How does a sustained handgrip effect the intensity of murmurs?

Back 111

A sustained handgrip increases the intensity of MVP murmur, but diminishes the intensity of HCM murmur. Sustained handgrip increases systemic resistance

Front 112

Restrictive Cardiomyopathy

Back 112

Infiltration of the myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance. Systolic dysfunction is variable and usually occurs in advanced disease

Front 113

Stable angina pectoris

Back 113

Due to FIXED atherosclerotic lesions that narrow the major coronary arteries. Coronary ischemia is due to an imbalance between blood supply and oxygen demand, leading to inadequate perfusion. Stable angina occurs when oxygen demand exceeds available blood supply

Front 114

Risk factors for Ischemic Heart Disease

Back 114

(1) DM; (2) HLD (elevated LDL); (3) HTN; (4) Smoking; (5) Age (men >45, women >55); (6) Family history of premature CAD or MI in first degree relative: men <45, women <55 ears); (7) Low HDL; (8) Elevated homocysteine

Front 115

Prognostic Indicators of CAD

Back 115

(1) Left ventricular function (EF%) - normal is >50%, if <50%, associated with increased mortality; (2) Vessels involved (severity/extent of ischemia) - Left main coronary artery-poor prognosis because it covers approximately 2/3 of the heart; two or three-vessel CAD associated with worse prognosis

Front 116

Clinical Features of Stable Angina

Back 116

(1) Chest pain or substernal pressure, lasts <10-15 minutes (usually 1-5) and described as heaviness, pressure, squeezing; (2) Brought on by exertion or emotion; (3) Relieved with rest or NTG

Front 117

Diagnosis of CAD

Back 117

(1) Resting EKG - usually normal in patients with stable angina; (2) Q waves are consistent with prior MI; (3) If ST segment or T wave abnormalities are present during an episode of chest pain, then treat as for unstable angina

Front 118

Stress EKG

Back 118

(1) Test involves recording ECG before, during, and after exercise on a treadmill; (2) Test is 75% sensitive IF patients are able to exercise sufficiently to increase HR to 85% of maximum predicted value for age; (3) Exercise-induced ischemia results in subendocardial ischemia, producing ST segment depression; (4) Other positive findings include onset of heart failure or ventricular arrhythmia during exercise or hypotension; (4) PATIENTS WITH A POSITIVE STRESS EKG SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 119

When is a stress EKG generally considered positive?

Back 119

If the patient develops any (1) ST-depression; (2) Chest Pain; (3) Hypotension; (4) Significant arrhythmias

Front 120

Stress Echocardiography

Back 120

(1) Performed before and immediately after exercise. Exercise-induced ischemia is evidenced by wall motion abnormalities (e.g., akinesis or dyskinesis) not present at rest; (2) Favored by many cardiologists over stress EKG. It is more sensitive in detecting ischemia, can assess LV size and function, and can diagnose valvular disease; (3) Again, patients with a POSITIVE TEST SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 121

Stress myocardial perfusion imaging

Back 121

Stress-test' aka P-Thal (Persantine-Thallium); (1) Viable myocytes extract thallium 201 from blood during exercise. No radioisotope uptake means no blood flow to an area of the myocardium; (2) It is IMPORTANT to determine wther the ischemia is reversible, i.e., whether the areas of hypoperfusion are perfused over time as blood flow eventually equalized. Areas of REVERSIBLE ischemic may be rescued with PTCA or CABG. Irreversible ischemia, however, indicates infarcted tissue that cannot be salvaged

Front 122

Pharmacologic Stress Test

Back 122

Performed if the patient cannot exercise. IV adenosine, dipyramidole, or dobutamine can be used. The cardiac stress induced by these agents takes the place of exercise. This can be combined with an EKG, an echocardiogram, or nuclear perfusion imaging. (2) These agents cause generalized coronary vasodilation; because diseases coronary arterires are already maximally dilated at rest to increase blood flow, they receive relatively less blood flow when the entire coronary system is pharmacologically vasodilated; (3) Dobutamine increases myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility

Front 123

Cardiac Catheterization with Coronary Angiography

Back 123

(1) Coronary angiography - definitive test for CAD. Indicated in patients being considered for revascularization (PTCA or CABG); (2) Contrast is injected into coronary vessels to visualize any stenotic lesions. This defines the location and extent of coronary disease; (3) If coronary artery disease is severe (e.g., left main or three-vesel disease), refer patient for surgical revascularization

Front 124

Risk Factor Modification in Ischemic Heart Disease

Back 124

(1) Smoking cessation cuts CAD risk in half by 1 year after quitting; (2) HTN - vigorous BP control reduces risk of CHD, especially in diabetic patients; (3) Hyperlipidemia - reduction in serum cholesterol with lifestyle modification and HMG-CoA reductase inhibitors reduces CAD risk; (4) DM - strict glycemia control is thought to have less effect on macrovascular disease risk than microvascular disease but should still be emphasized; (5) Obesity - weight loss modifies other risk facotrs DM, HTN, and HLD) and provides other health benefits; (6) Exercise is critical; minimizes emotional stress, promotes weight loss, and helps reduce other risk factors; (7) Diet: Reduce intake of saturated fat and cholesterol; (8) Hyperhomocystinemia - value of treating yet to be established

Front 125

Medical Therapy in Ischemic Heart Disease

Back 125

(1) Aspirin; (2) Beta-blockers; (3) Nitrates; (4) Calcium Channel Blockers; (5) If CHF is present, treatment with ACE-I and diuretics may also be indicated

Front 126

Aspirin

Back 126

Indicated in ALL patients with CAD; DECREASES MORBIDITY - reduces risk of MI!

Front 127

Beta Blockers

Back 127

Block sympathetic stimulation of heart, reduce HR, BP, and contractility, thereby decreasing cardiac work (i.e., Beta-blockers lower myocardial oxygen consumption); Have been shown to REDUCE FREQUENCY OF CORONARY EVENTS

Front 128

Nitrates

Back 128

Cause generalized vasodilation. (1) Relieve angina; rduce preload, therefore the load and oxygen demand; (2) May prevent angina when taken before exertion; (3) Effect on prognosis is unknown; main benefit is symptomatic relief; (4) Can be administered orally, sublingually, transdermally, or intravenously

Front 129

Calcium Channel Blockers

Back 129

Cause coronary vasodilation and afterload reduction. Now considered a SECONDARY TREATMENT when beta-blockers and/or nitrates are not fully effective

Front 130

Revascularization

Back 130

(1) May be preferred for high risk patients, although some controversy exists as to whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%; (2) Two methods for revascularization: PTCA and CABG; (3) Revascularization does NOT reduce incidence of MI, but does result in significant improvement in symptoms

Front 131

Percutaneous Transluminal Coronary Angioplasty (PTCA)

Back 131

Should be considered in patients with one or two vessel disease. Best if used for proximal lesions. RESTENOSIS is a significant problem (up to 40% within first 6 months); however, if there is no evidence of restenosis at 6 months, it usually does not occur. STENTS SIGNIFICANTLY REDUCE the rate of restenosis

Front 132

Coronary Artery Bypass Grafting (CABG)

Back 132

Treatment of choice in patients with high-risk disease. Indicated in patients with left main disease, 3-vessel disease with reduced left ventricular function, two-vessel disease with proximal LAD stenosis, or severe ischemia for palliation of symptoms

Front 133

Unstable Angina: Pathophysiology

Back 133

Oxygen demand is UNCHANGED. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand. USA is significant because it indicates STENOSIS that has enlarged via thrombosis, hemorrhage, or plaque rupture. It may lead to total occlusion of a coronary vessel.

Front 134

What characterizes Unstable Angina pain?

Back 134

(1) Patients with angina at rest; (2) Patients with new-onset angina that is severe and worsening; (3) Patients with chronic angina with increasing frequency, duration, or intensity of chest pain

Front 135

Diagnosis of USA

Back 135

(1) Exclude MI; (2) Patients with USA have a higher risk of adverse events during stress testing. These patients should be stabilized with medical management before stress testing or should undergo cardiac catheterization initially.

Front 136

Acute Coronary Syndrome - what is it?

Back 136

The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion; The term generally refers to unstable angina or acute MI

Front 137

How do you differentiate USA from NSTEMI?

Back 137

Both are considered together because it is difficult to distinguish the two based on patient presentation. If cardiac enzymes are elevated, then the patient has NSTEMI

Front 138

Treatment of Unstable Angina

Back 138

(1) Aspirin; (2) Beta-blockers; (3) LMWH or UFH for at least 2 days (keep PTT 2-2.5x normal); (4) Nitrates are first-line therapy; (5) Glycoprotein Iib/IIIa inhibitors (abciximab, tirofiban) can be helpful adjuncts in USA, especially if patient is undergoing PTCA or stenting.

Front 139

Treatment of USA after acute treatment

Back 139

(1) ASA, Beta-blockers, nitrates; (2) Treat DM, HTN; (3) Treat with statin; (4) Consider folic acid for hyperhomocystinemia

Front 140

Prinzmetal's Angina

Back 140

Involves transient coronary vasospasm that usually is accompanied by a fixed atherosclerotic lesion (75% of cases) but can also occur in normal coronary arteries. (1) Episodes of angina occur at rest, associated with ventricular dysrhythmias; (2) Hallmark is transient ST segment elevation (not depression!) on EKG during chest pain, which represents transmural ischemia; (3) Coronary angiography is definitive test - displays coronary vasospasm when the patient is given IV ergonovine to provoke chest pain; (4) Vasodilators - CCBs and nitrates have been proven to help

Front 141

What is an MI?

Back 141

Necrosis of the myocardium 2/2 interruption of blood supply (after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis). Most cases are due to acute coronary thrombosis: atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel. Most patients with MI have history of angina, risk factors for CAD, or history of arrhythmias

Front 142

Clinical Features of AMI

Back 142

(1) Chest pain: intense substernal pressure, often described as 'crushing' and 'elephant on top of chest'; (2) Radiation to neck, jaws, arms, or back, commonly to the left side; (3) Similar to angina pectoris in character and distribution but much more severe and lasts longer; (4) Some patients may have epigastric discomfort

Front 143

Can an MI be asymptomatic?

Back 143

YES! (1) In up to 1/3 of patients, painless infarcts or atypical presentations occur; this is most likely in postoperative patients, the elderly, diabetic patients, and women; (2) Other symptoms: dyspnea, diaphoresis, weakness, fatigue, N/V, sense of impending doom, syncope

Front 144

What is the MCC of sudden cardiac death?

Back 144

Ventricular fibrillation

Front 145

What are the signs and symptoms of a right ventricular infarct?

Back 145

Inferior EKG changes, hypotension, elevated jugular venous pressure, hepatomegaly, and CLEAR LUNGS

Front 146

Diagnosis of AMI - markers of ischemia/infarction include:

Back 146

(1) Peaked T waves: occur very early, may be missed; (2) ST segment elevation indicates transmural injury and can be diagnostic of an acute infarct; (3) Q waves: evidence for necrosis (specific) - Q waves are usually seen late; typically not seen acutely; (4) T wave inversion is sensitive but NOT specific; (5) ST segment depression: subendocardial injury

Front 147

ST segment elevation infarct

Back 147

Transmural, involving entire thickness of the wall; tends to be larger

Front 148

Non-ST segment elevation infarct

Back 148

Subendocardial (involves inner one third to one half of the wall); tends to be smaller, and presentation is similar to USA - cardiac enzymes will differentiate the two

Front 149

Cardiac Enzymes

Back 149

Currently the gold standard for MI; (1) CK-MB: increases within 4-8 hours and returns to normal in 48-72 hours; reaches a peak in 24 hours. When measured within 24-36 hours of onset of chest pain, has greater than 95% sensitivity and specificity; Levels of total CK and CK-MB should be measured on admission and every 8 hours thereafter for 24 hours; (2) Troponins I and T - most IMPORTANT test to order; increases within 3-5 hours and returns to normal in 5-14 days; reach a peak in 24-48 hours. Greater sensitivity and specificity than CK-MB. NOTE: troponin I can be falsely elevated in patients with renal failure

Front 150

What is meant by 'serial enzymes'?

Back 150

Cardiac enzymes are drawn serially - once on admission and every 8 hours until 3 samples are obtained. The higher the peak and the longer enzyme levels remain elevated, the more severe the myocardial injury and the worse the prognosis

Front 151

Treatment of MI

Back 151

(1) ASA; (2) Beta-blockers; (3) ACE-I; (4) Statins; (5) Oxygen; (6) Nitrates; (7) Morphine sulfate; (8) Heparin; [remember: MONA has Hep A,B]

Front 152

What therapies have been shown to reduce mortality in MI?

Back 152

(1) ASA, (2) Beta-blockers; (3) ACE-I

Front 153

Anterior Infarct EKG changes

Back 153

ST elevation in V1-V4 early, Q waves in leads V1-V4 late

Front 154

Posterior Infarct EKG changes

Back 154

Large R wave in V1 and V2, ST segment depression in V1 and V2, Upright and prominent T waves in V1 and V2

Front 155

Lateral Infarct EKG changes

Back 155

Q waves in leads I and aVL (late change)

Front 156

Inferior Infarct EKG changes

Back 156

Q waves in II, III, aVF (late change)

Front 157

Pump Failure (CHF)

Back 157

Most common cause of in-hospital mortality after MI; if mild, treat with ACE-I, diuretic. If severe, may lead to cardiogenic shock; invasive hemodynamic monitoring may be indicated

Front 158

Risk of stroke after acute-MI

Back 158

Patients who suffer an acute MI have a high risk of stroke during the next 5 years. The lower the EF and the older the patient, the higher the risk of stroke

Front 159

Ventricular tachycardia

Back 159

Sustained VT requires treatment: if patient is hemodynamically unstable, electrical cardioversion is indicated. If patient is hemodynamically stable, start antiarrhythmic therapy with IV amiodarone

Front 160

Ventricular fibrillation

Back 160

Immediate unsynchronized defibrillation and CPR are indicated

Front 161

AV block

Back 161

(1) Associated with ischemic involving conduction tracts; (2) 1st and 2nd degree (type I) blocks do not require treatment; (3) Second-degree (type II) and third-degree block: prognosis is dire in setting of anterior MI - emergent placement of a temporary pacemaker is indicated (with later placement of a permanent pacemaker). If inferior MI, prognosis is better, and IV atropine may be used initially. If conduction is not restored, a temporary pacemaker is appropriate

Front 162

Free wall rupture

Back 162

(1) Catastrophic, usually fatal event that occurs during the first two weeks after MI (90% within 2 weeks, most commonly 1-4 days after MI). 90% mortality rate, usually leads to hemopericardium and cardiac tamponade; (3) Treatment: hemodynamic stabiliation, immedaite pericardiocentesis, and surgical repair

Front 163

Rupture of interventricular septum

Back 163

(1) Greater potential for successful therapy than with a free wall rupture, although this is also a critical event; emergent surgery is indicated; (2) Occurs within 10 days after MI; (3) Likelihood of survival correlates with size of defect

Front 164

Papillary muscle rupture

Back 164

(1) Produces MITRAL REGURGITATION; (2) If suspected, obtain Echo immediately; (3) Emergent surgery is needed (mitral valve replacement is usually necessary)as well as afterload reduction with sodium nitroprusside or intra-aortic balloon pump (IABP)

Front 165

Ventricular pseudoaneurysm

Back 165

Incomplete free wall rupture (myocardial rupture is contained by pericardium); (2) Bedside echo may show the pseudoaneurysm, surgical emergency because these tend to become a free-wall rupture

Front 166

Ventricle aneursym

Back 166

Rarely rupture (in contrast to pseudoaneurysm); associated with a high incidence of ventricular tachyarrhythmias; Medical mangement may be protective, surgery to remove aneursym may be appropriate in some patients

Front 167

Acute pericarditis

Back 167

Treatment consists of ASPIRIN ONLY! NSAIDs and corticosteroids are contraindicated and may hinder myocardial scar formation

Front 168

Dressler's Syndrome ('post-myocardial infarction syndrome')

Back 168

Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occuring weeks to months after an MI. ASPIRIN is the most effective therapy

Front 169

Congestive Heart Failure

Back 169

Clinical syndrome resulting from the heart's inability to meet the body's circulatory demands under normal physiological conditions

Front 170

Pathophysiology of CHF

Back 170

(1) Decreased cardiac output = (2) Activation of RAAS and Sympathetic NS = (3) Systemic vasoconstriction and volume retention = (4) Increased venous return, resulting in increased preload. This maintains CO. However, in severe CHF, increased preload does not result in increased CO. Increased LVEDV causes increased LVEDP, which is transmitted back to pulmonary veins and leads to symptoms of pulmonary congestion

Front 171

Frank-Starling relationship

Back 171

(1) In a normal heart, increasing preload results in greater contractility; (2) When preload is low (at rest), there is little difference in performance between a normal and a failing heart. However, with exertion a failing heart produces less contractility and symptoms occur.

Front 172

Systolic dysfunction

Back 172

Caused by impaired contractility - abnormality is decreased ejection fraction. Causes include recent MI (MCC), cardiomyopathy, myocarditis

Front 173

Diastolic dysfunction

Back 173

Caused by impaired ventricular filling during diastole (either impaired relaxation of increased stiffness or both); Echo shows impaired relaxation of LV. Causes include (1) HTN leading to myocardial hypertrophy (MCC), (2) Valvular disease such as Aortic stenosis, mitral stenosis, and aortic regurgitation, (3) Restrictive cardiomyopathy (amyloid, sarcoid, hemochromatosis)

Front 174

Stable angina pectoris

Back 174

Due to FIXED atherosclerotic lesions that narrow the major coronary arteries. Coronary ischemia is due to an imbalance between blood supply and oxygen demand, leading to inadequate perfusion. Stable angina occurs when oxygen demand exceeds available blood supply

Front 175

Risk factors for Ischemic Heart Disease

Back 175

(1) DM; (2) HLD (elevated LDL); (3) HTN; (4) Smoking; (5) Age (men >45, women >55); (6) Family history of premature CAD or MI in first degree relative: men <45, women <55 ears); (7) Low HDL; (8) Elevated homocysteine

Front 176

Prognostic Indicators of CAD

Back 176

(1) Left ventricular function (EF%) - normal is >50%, if <50%, associated with increased mortality; (2) Vessels involved (severity/extent of ischemia) - Left main coronary artery-poor prognosis because it covers approximately 2/3 of the heart; two or three-vessel CAD associated with worse prognosis

Front 177

Clinical Features of Stable Angina

Back 177

(1) Chest pain or substernal pressure, lasts <10-15 minutes (usually 1-5) and described as heaviness, pressure, squeezing; (2) Brought on by exertion or emotion; (3) Relieved with rest or NTG

Front 178

Diagnosis of CAD

Back 178

(1) Resting EKG - usually normal in patients with stable angina; (2) Q waves are consistent with prior MI; (3) If ST segment or T wave abnormalities are present during an episode of chest pain, then treat as for unstable angina

Front 179

Stress EKG

Back 179

(1) Test involves recording ECG before, during, and after exercise on a treadmill; (2) Test is 75% sensitive IF patients are able to exercise sufficiently to increase HR to 85% of maximum predicted value for age; (3) Exercise-induced ischemia results in subendocardial ischemia, producing ST segment depression; (4) Other positive findings include onset of heart failure or ventricular arrhythmia during exercise or hypotension; (4) PATIENTS WITH A POSITIVE STRESS EKG SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 180

When is a stress EKG generally considered positive?

Back 180

If the patient develops any (1) ST-depression; (2) Chest Pain; (3) Hypotension; (4) Significant arrhythmias

Front 181

Stress Echocardiography

Back 181

(1) Performed before and immediately after exercise. Exercise-induced ischemia is evidenced by wall motion abnormalities (e.g., akinesis or dyskinesis) not present at rest; (2) Favored by many cardiologists over stress EKG. It is more sensitive in detecting ischemia, can assess LV size and function, and can diagnose valvular disease; (3) Again, patients with a POSITIVE TEST SHOULD UNDERGO CARDIAC CATHETERIZATION

Front 182

Stress myocardial perfusion imaging

Back 182

Stress-test' aka P-Thal (Persantine-Thallium); (1) Viable myocytes extract thallium 201 from blood during exercise. No radioisotope uptake means no blood flow to an area of the myocardium; (2) It is IMPORTANT to determine wther the ischemia is reversible, i.e., whether the areas of hypoperfusion are perfused over time as blood flow eventually equalized. Areas of REVERSIBLE ischemic may be rescued with PTCA or CABG. Irreversible ischemia, however, indicates infarcted tissue that cannot be salvaged

Front 183

Pharmacologic Stress Test

Back 183

Performed if the patient cannot exercise. IV adenosine, dipyramidole, or dobutamine can be used. The cardiac stress induced by these agents takes the place of exercise. This can be combined with an EKG, an echocardiogram, or nuclear perfusion imaging. (2) These agents cause generalized coronary vasodilation; because diseases coronary arterires are already maximally dilated at rest to increase blood flow, they receive relatively less blood flow when the entire coronary system is pharmacologically vasodilated; (3) Dobutamine increases myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility

Front 184

Cardiac Catheterization with Coronary Angiography

Back 184

(1) Coronary angiography - definitive test for CAD. Indicated in patients being considered for revascularization (PTCA or CABG); (2) Contrast is injected into coronary vessels to visualize any stenotic lesions. This defines the location and extent of coronary disease; (3) If coronary artery disease is severe (e.g., left main or three-vesel disease), refer patient for surgical revascularization

Front 185

Risk Factor Modification in Ischemic Heart Disease

Back 185

(1) Smoking cessation cuts CAD risk in half by 1 year after quitting; (2) HTN - vigorous BP control reduces risk of CHD, especially in diabetic patients; (3) Hyperlipidemia - reduction in serum cholesterol with lifestyle modification and HMG-CoA reductase inhibitors reduces CAD risk; (4) DM - strict glycemia control is thought to have less effect on macrovascular disease risk than microvascular disease but should still be emphasized; (5) Obesity - weight loss modifies other risk facotrs DM, HTN, and HLD) and provides other health benefits; (6) Exercise is critical; minimizes emotional stress, promotes weight loss, and helps reduce other risk factors; (7) Diet: Reduce intake of saturated fat and cholesterol; (8) Hyperhomocystinemia - value of treating yet to be established

Front 186

Medical Therapy in Ischemic Heart Disease

Back 186

(1) Aspirin; (2) Beta-blockers; (3) Nitrates; (4) Calcium Channel Blockers; (5) If CHF is present, treatment with ACE-I and diuretics may also be indicated

Front 187

Aspirin

Back 187

Indicated in ALL patients with CAD; DECREASES MORBIDITY - reduces risk of MI!

Front 188

Beta Blockers

Back 188

Block sympathetic stimulation of heart, reduce HR, BP, and contractility, thereby decreasing cardiac work (i.e., Beta-blockers lower myocardial oxygen consumption); Have been shown to REDUCE FREQUENCY OF CORONARY EVENTS

Front 189

Nitrates

Back 189

Cause generalized vasodilation. (1) Relieve angina; rduce preload, therefore the load and oxygen demand; (2) May prevent angina when taken before exertion; (3) Effect on prognosis is unknown; main benefit is symptomatic relief; (4) Can be administered orally, sublingually, transdermally, or intravenously

Front 190

Calcium Channel Blockers

Back 190

Cause coronary vasodilation and afterload reduction. Now considered a SECONDARY TREATMENT when beta-blockers and/or nitrates are not fully effective

Front 191

Revascularization

Back 191

(1) May be preferred for high risk patients, although some controversy exists as to whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%; (2) Two methods for revascularization: PTCA and CABG; (3) Revascularization does NOT reduce incidence of MI, but does result in significant improvement in symptoms

Front 192

Percutaneous Transluminal Coronary Angioplasty (PTCA)

Back 192

Should be considered in patients with one or two vessel disease. Best if used for proximal lesions. RESTENOSIS is a significant problem (up to 40% within first 6 months); however, if there is no evidence of restenosis at 6 months, it usually does not occur. STENTS SIGNIFICANTLY REDUCE the rate of restenosis

Front 193

Coronary Artery Bypass Grafting (CABG)

Back 193

Treatment of choice in patients with high-risk disease. Indicated in patients with left main disease, 3-vessel disease with reduced left ventricular function, two-vessel disease with proximal LAD stenosis, or severe ischemia for palliation of symptoms

Front 194

Unstable Angina: Pathophysiology

Back 194

Oxygen demand is UNCHANGED. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand. USA is significant because it indicates STENOSIS that has enlarged via thrombosis, hemorrhage, or plaque rupture. It may lead to total occlusion of a coronary vessel.

Front 195

What characterizes Unstable Angina pain?

Back 195

(1) Patients with angina at rest; (2) Patients with new-onset angina that is severe and worsening; (3) Patients with chronic angina with increasing frequency, duration, or intensity of chest pain

Front 196

Diagnosis of USA

Back 196

(1) Exclude MI; (2) Patients with USA have a higher risk of adverse events during stress testing. These patients should be stabilized with medical management before stress testing or should undergo cardiac catheterization initially.

Front 197

Acute Coronary Syndrome - what is it?

Back 197

The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion; The term generally refers to unstable angina or acute MI

Front 198

How do you differentiate USA from NSTEMI?

Back 198

Both are considered together because it is difficult to distinguish the two based on patient presentation. If cardiac enzymes are elevated, then the patient has NSTEMI

Front 199

Treatment of Unstable Angina

Back 199

(1) Aspirin; (2) Beta-blockers; (3) LMWH or UFH for at least 2 days (keep PTT 2-2.5x normal); (4) Nitrates are first-line therapy; (5) Glycoprotein Iib/IIIa inhibitors (abciximab, tirofiban) can be helpful adjuncts in USA, especially if patient is undergoing PTCA or stenting.

Front 200

Treatment of USA after acute treatment

Back 200

(1) ASA, Beta-blockers, nitrates; (2) Treat DM, HTN; (3) Treat with statin; (4) Consider folic acid for hyperhomocystinemia

Front 201

Prinzmetal's Angina

Back 201

Involves transient coronary vasospasm that usually is accompanied by a fixed atherosclerotic lesion (75% of cases) but can also occur in normal coronary arteries. (1) Episodes of angina occur at rest, associated with ventricular dysrhythmias; (2) Hallmark is transient ST segment elevation (not depression!) on EKG during chest pain, which represents transmural ischemia; (3) Coronary angiography is definitive test - displays coronary vasospasm when the patient is given IV ergonovine to provoke chest pain; (4) Vasodilators - CCBs and nitrates have been proven to help

Front 202

What is an MI?

Back 202

Necrosis of the myocardium 2/2 interruption of blood supply (after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis). Most cases are due to acute coronary thrombosis: atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel. Most patients with MI have history of angina, risk factors for CAD, or history of arrhythmias

Front 203

Clinical Features of AMI

Back 203

(1) Chest pain: intense substernal pressure, often described as 'crushing' and 'elephant on top of chest'; (2) Radiation to neck, jaws, arms, or back, commonly to the left side; (3) Similar to angina pectoris in character and distribution but much more severe and lasts longer; (4) Some patients may have epigastric discomfort

Front 204

Can an MI be asymptomatic?

Back 204

YES! (1) In up to 1/3 of patients, painless infarcts or atypical presentations occur; this is most likely in postoperative patients, the elderly, diabetic patients, and women; (2) Other symptoms: dyspnea, diaphoresis, weakness, fatigue, N/V, sense of impending doom, syncope

Front 205

What is the MCC of sudden cardiac death?

Back 205

Ventricular fibrillation

Front 206

What are the signs and symptoms of a right ventricular infarct?

Back 206

Inferior EKG changes, hypotension, elevated jugular venous pressure, hepatomegaly, and CLEAR LUNGS

Front 207

Diagnosis of AMI - markers of ischemia/infarction include:

Back 207

(1) Peaked T waves: occur very early, may be missed; (2) ST segment elevation indicates transmural injury and can be diagnostic of an acute infarct; (3) Q waves: evidence for necrosis (specific) - Q waves are usually seen late; typically not seen acutely; (4) T wave inversion is sensitive but NOT specific; (5) ST segment depression: subendocardial injury

Front 208

ST segment elevation infarct

Back 208

Transmural, involving entire thickness of the wall; tends to be larger

Front 209

Non-ST segment elevation infarct

Back 209

Subendocardial (involves inner one third to one half of the wall); tends to be smaller, and presentation is similar to USA - cardiac enzymes will differentiate the two

Front 210

Cardiac Enzymes

Back 210

Currently the gold standard for MI; (1) CK-MB: increases within 4-8 hours and returns to normal in 48-72 hours; reaches a peak in 24 hours. When measured within 24-36 hours of onset of chest pain, has greater than 95% sensitivity and specificity; Levels of total CK and CK-MB should be measured on admission and every 8 hours thereafter for 24 hours; (2) Troponins I and T - most IMPORTANT test to order; increases within 3-5 hours and returns to normal in 5-14 days; reach a peak in 24-48 hours. Greater sensitivity and specificity than CK-MB. NOTE: troponin I can be falsely elevated in patients with renal failure

Front 211

What is meant by 'serial enzymes'?

Back 211

Cardiac enzymes are drawn serially - once on admission and every 8 hours until 3 samples are obtained. The higher the peak and the longer enzyme levels remain elevated, the more severe the myocardial injury and the worse the prognosis

Front 212

Treatment of MI

Back 212

(1) ASA; (2) Beta-blockers; (3) ACE-I; (4) Statins; (5) Oxygen; (6) Nitrates; (7) Morphine sulfate; (8) Heparin; [remember: MONA has Hep A,B]

Front 213

What therapies have been shown to reduce mortality in MI?

Back 213

(1) ASA, (2) Beta-blockers; (3) ACE-I

Front 214

Anterior Infarct EKG changes

Back 214

ST elevation in V1-V4 early, Q waves in leads V1-V4 late

Front 215

Posterior Infarct EKG changes

Back 215

Large R wave in V1 and V2, ST segment depression in V1 and V2, Upright and prominent T waves in V1 and V2

Front 216

Lateral Infarct EKG changes

Back 216

Q waves in leads I and aVL (late change)

Front 217

Inferior Infarct EKG changes

Back 217

Q waves in II, III, aVF (late change)

Front 218

Pump Failure (CHF)

Back 218

Most common cause of in-hospital mortality after MI; if mild, treat with ACE-I, diuretic. If severe, may lead to cardiogenic shock; invasive hemodynamic monitoring may be indicated

Front 219

Risk of stroke after acute-MI

Back 219

Patients who suffer an acute MI have a high risk of stroke during the next 5 years. The lower the EF and the older the patient, the higher the risk of stroke

Front 220

Ventricular tachycardia

Back 220

Sustained VT requires treatment: if patient is hemodynamically unstable, electrical cardioversion is indicated. If patient is hemodynamically stable, start antiarrhythmic therapy with IV amiodarone

Front 221

Ventricular fibrillation

Back 221

Immediate unsynchronized defibrillation and CPR are indicated

Front 222

AV block

Back 222

(1) Associated with ischemic involving conduction tracts; (2) 1st and 2nd degree (type I) blocks do not require treatment; (3) Second-degree (type II) and third-degree block: prognosis is dire in setting of anterior MI - emergent placement of a temporary pacemaker is indicated (with later placement of a permanent pacemaker). If inferior MI, prognosis is better, and IV atropine may be used initially. If conduction is not restored, a temporary pacemaker is appropriate

Front 223

Free wall rupture

Back 223

(1) Catastrophic, usually fatal event that occurs during the first two weeks after MI (90% within 2 weeks, most commonly 1-4 days after MI). 90% mortality rate, usually leads to hemopericardium and cardiac tamponade; (3) Treatment: hemodynamic stabiliation, immedaite pericardiocentesis, and surgical repair

Front 224

Rupture of interventricular septum

Back 224

(1) Greater potential for successful therapy than with a free wall rupture, although this is also a critical event; emergent surgery is indicated; (2) Occurs within 10 days after MI; (3) Likelihood of survival correlates with size of defect

Front 225

Papillary muscle rupture

Back 225

(1) Produces MITRAL REGURGITATION; (2) If suspected, obtain Echo immediately; (3) Emergent surgery is needed (mitral valve replacement is usually necessary)as well as afterload reduction with sodium nitroprusside or intra-aortic balloon pump (IABP)

Front 226

Ventricular pseudoaneurysm

Back 226

Incomplete free wall rupture (myocardial rupture is contained by pericardium); (2) Bedside echo may show the pseudoaneurysm, surgical emergency because these tend to become a free-wall rupture

Front 227

Ventricle aneursym

Back 227

Rarely rupture (in contrast to pseudoaneurysm); associated with a high incidence of ventricular tachyarrhythmias; Medical mangement may be protective, surgery to remove aneursym may be appropriate in some patients

Front 228

Acute pericarditis

Back 228

Treatment consists of ASPIRIN ONLY! NSAIDs and corticosteroids are contraindicated and may hinder myocardial scar formation

Front 229

Dressler's Syndrome ('post-myocardial infarction syndrome')

Back 229

Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occuring weeks to months after an MI. ASPIRIN is the most effective therapy

Front 230

Congestive Heart Failure

Back 230

Clinical syndrome resulting from the heart's inability to meet the body's circulatory demands under normal physiological conditions

Front 231

Pathophysiology of CHF

Back 231

(1) Decreased cardiac output = (2) Activation of RAAS and Sympathetic NS = (3) Systemic vasoconstriction and volume retention = (4) Increased venous return, resulting in increased preload. This maintains CO. However, in severe CHF, increased preload does not result in increased CO. Increased LVEDV causes increased LVEDP, which is transmitted back to pulmonary veins and leads to symptoms of pulmonary congestion

Front 232

Frank-Starling relationship

Back 232

(1) In a normal heart, increasing preload results in greater contractility; (2) When preload is low (at rest), there is little difference in performance between a normal and a failing heart. However, with exertion a failing heart produces less contractility and symptoms occur.

Front 233

Systolic dysfunction

Back 233

Caused by impaired contractility - abnormality is decreased ejection fraction. Causes include recent MI (MCC), cardiomyopathy, myocarditis

Front 234

Diastolic dysfunction

Back 234

Caused by impaired ventricular filling during diastole (either impaired relaxation of increased stiffness or both); Echo shows impaired relaxation of LV. Causes include (1) HTN leading to myocardial hypertrophy (MCC), (2) Valvular disease such as Aortic stenosis, mitral stenosis, and aortic regurgitation, (3) Restrictive cardiomyopathy (amyloid, sarcoid, hemochromatosis)

Front 235

Symptoms of left-sided heart failure

Back 235

(1) Dyspnea; (2) Orthopnea; (3) Paroxysmal Nocturnal Dyspnea; (4) Nocturnal cough; (5) Confusion and memory impairment 2/2 impaired brain perfusion; (6) Diaphoresis and cool extremities at rest in desperately ill patients

Front 236

Signs of left-sided heart failure

Back 236

(1) Displaced PMI (to the left) due to cardiomegaly; (2) Pathologic S3 (ventricular gallop) with rapid filling phase into a concompliant LV chamber; (3) Heard best at apex with bell of stethoscope

Front 237

NYHA class I

Back 237

Symptoms occur with vigorous activities such as playing a sport. Patients are nearly asymptomatic

Front 238

NYHA class II

Back 238

Symptoms occur with prolonged or moderate exertion, such as climbing a flight of stairs or carrying heavy packages. Slight limitation of activities

Front 239

NYHA class III

Back 239

Symptoms occur with usual activities of daily living, such as walking across the room or getting dressed. Markedly limiting

Front 240

NYHA class IV

Back 240

Symptoms occur at rest. Incapacitating

Front 241

S4 gallop

Back 241

Atrial systole 'into' a noncompliant left ventricular chamber, heard best at left sternal border with bell.

Front 242

Pleural effusion

Back 242

Crackles and rales at lung bases; dullness to percussion and decreased tactile fremitus of lower lung fields

Front 243

What does an increased intensity of the pulmonic component A2/P2 of second heart sound indicated?

Back 243

Pulmonary Hypertension

Front 244

Signs and Symptoms of RSHF

Back 244

(1) Peripheral pitting edema; (2) Nocturia - 2/2 increased venous return with elevation of legs; (3) JVD; (4) Hepatomegaly, hepato-jugular reflux; (5) Ascites; (6) Right ventricular heave

Front 245

Diagnosis of CHF

Back 245

(1) Cardiomegaly on CXR; (2) Kerley B lines are short horizontal lines near periphery of the lung near the costophrenic angles, and indicate pulmonary congestion secondary to dilatation of pulmonary lymphatic vessels; (3) Prominent interstitial markings; (4) Pleural effusion

Front 246

Echocardiogram

Back 246

(1) Initial test of choice whenever CHF is suspected based on history, examination, CXR; (2) Useful in determining whether systolic or diastolic dysfunction predominantes, and determines whether the cause of CHF is due to a pericardial, myocardial, or valvular process; (3) Estimates EF (very important!): patients with systolic EF <40% should be those with preserved LV EF >40%

Front 247

Treatment of Systolic dysfunction CHF: Diuretics

Back 247

Most effective means of providing SYMPTOMATIC relief to patients with moderate to severe CHF; Have NOT been shown to reduce mortality or improve prognosis! (3) Lasix > HCTZ > Spironolactone

Front 248

Treatment of Systolic dysfunction CHF: ACE-I

Back 248

Cause venous and arterial vasodilation, decreasing preload and afterload. The combination of a diuretic and an ACE inhibitor should be the initial treatment in most symptomatic patients. ACE-INHIBITORS REDUCE MORTALITY, PROLONG SURVIVAL, and ALLEVIATE SYPTOMS in mild, moderate and severe CHF

Front 249

Treatment of Systolic dysfunction CHF: ARBs

Back 249

Used in patients unable to take ACE-I due to side effect of cough, but should NOT replace ACI-I if patient tolerates an ACE-I

Front 250

Treatment of Systolic dysfunction CHF: Beta-blocker

Back 250

Proven to DECREASE MORTALITY in patients with post-MI heart failure; reported to improve symptoms of CHF; may slow progression of heart fialure by slowign down tissue remodeling. Should be given to STABLE patients with mild to moderate CHF (class I, II, and III) unless CI

Front 251

Treatment of Systolic dysfunction CHF: Hydralazine and Isosorbide dinitrates

Back 251

Can be used in patients who cannot tolerate ACE-inhibitors. Combination of hydralazine and isosorbide dinitrate has been shown to improve mortality in CHF, but not as effective as ACE inhibitors and require inconvenient dosing schedules

Front 252

Treatment of Systolic dysfunction CHF: Digitalis

Back 252

Positive inotropic agent, useful in patients with EF <30%, severe CHF, or severe atrial fibrillation. Provides short-term symptomatic relief, but has NOT been shown to improve mortality! Can be added to diuretics and ACE-I in severe CHF; check serum digoxin level periodically

Front 253

Signs of digoxin toxicity

Back 253

(1) GI: nausea/vomiting, anorexia; (2) Cardiac: ectopic (ventricular) beats; AV block causing a regular junctional escape rhythm to start, Afib; (3) CNS: visual disturbances, disorientation

Front 254

Premature Atrial Complexes (PACs)

Back 254

Early beat arising from the atria, firing on its own 2/2 adrenergic excess, drugs, EtOH, tobacco, electrolyte imbalance, ischemia, and infection. On EKG, look for early P waves that differ in morphology from the normal sinus P wave (because these P waves originate within the atria and NOT the sinus node). QRS complex is normal because conduction below the atria is normal.

Front 255

Premature Ventricular Complexes (PVCs)

Back 255

Early beat that fires on its own from a focus in the ventricle and then spreads to the other ventricle. Causes include hypoxia, electrolyte abnormalities, stimulants, caffiene, and medications. Because conduction is NOT through normal conduction pathways, but rather through ventricular muscle, it is SLOWER than normal, causing a wide QRS. Wide, bizarre QRS complexes followed by a compensatory pause are seen. A P wave is not usually seen because it is buried within the QRS complex

Front 256

Atrial fibrillation (Afib)

Back 256

(1) Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally IRREGULAR, RAPID VENTRICULAR RATE. Instead of intermittently contracting, the atria quiver continuously; (2) Atrial rate is over 400bpm, but most impulses are blocked at the AV node, so ventricular rate ranges between 75 and 175. (3) Patients with AFib and underlying heart disease are at a markedly increased risk for adverse events, such as thromboembolism and hemodynamic compromise

Front 257

Causes of Afib

Back 257

(1) Heart disease: CAD, MI, HTN, MVP; (2) Pericarditis and pericardial trauma [surgery]; (3) Pulmonary disease, including PE; (4) Hyper/hypothyroidism; (5) Systemic illness [sepsis, malignancy, DM]; (6) Stress; (7) Excessive EtOH [holidary heart syndrome]; (8) Sick sinus syndrome; (9) Pheochromocytoma

Front 258

Clinical features of Afib

Back 258

(1) Fatigue and exertional dyspnea; (2) Palpitations, dizziness, angina, or syncope; (3) Irregularly irregular pulse; (4) Blood stasis (secondary to ineffective contraction) leads to formation of intramural thrombi, which can embolize to the brain

Front 259

EKG findings of Afib

Back 259

Irregularly irregular rhythm, with irregular RR intervals and excessively rapid series of tiny, erratic spikes on EKG with a wavy baseline and no identifiable P waves

Front 260

Treatment of Afib in hemodynamically unstable patient

Back 260

Immediate electrical cardioversion to sinus rhythm

Front 261

Treatment of Afib in hemodynamically stable patient

Back 261

(1) Rate control: target is 60-100bpm. CCBs are preferred, beta-blockers are an alternative. If LV systolic dysfunction is present, consider digoxin or amiodarone; (2) Cardioversion to sinus rhythm (after rate control established). Electrical cardioversion preferred, but can use IV ibutilide, procainamide, flecainide, sotalol, or amiodarone for pharmacologic conversion; (3) Anticoagulation to prevent embolic CVA. If Afib present >48 hours, risk of embolization during cardioversion is 2-5%!, therefore anticoagulate patients for 3 weeks before and 4 weeks after cardioversion. An INR of 2-3 is is the anticoagulation goal range. To avoid waiting 3 weeks for OAT, obtain a TEE to image the LA. If no thrombus is present, start IV heparin and perform cardioversion within 24 hours. Patients still require anticoagulation after cardioversion

Front 262

Three main goals of Afib/Aflutter treatment

Back 262

(1) Control ventricular rate; (2) Restore NSR; (3) Assess need for anticoagulation. The AFFIRM trial should that rate control is superior to rhythm control in Afib treatment

Front 263

Chronic Afib treatment

Back 263

(1) Rate control with BB or CCB; (2) Anticoagulation in patients with lone Afib (no underlying heart disease or other CV risk factors) under age 60 is not required because they are at low risk for embolization (ASA may be appropriate). Treat all other patients with chronic anticoagulation

Front 264

Atrial Flutter: Pathophysiology

Back 264

One irritable automaticity focus in the atria fires at 250-350bpm, giving rise to regular atrial contractions. Atrial rate between 250-350 bpm. Ventricular rate is one-half to one-third the atrial rate. The long refractory period in the AV node allows one one of every two or three flutter waves to conduct to the ventricles

Front 265

Causes of Atrial Flutter

Back 265

(1) COPD - most common association; (2) Heart disease - rheumatic heart disease, CAD, CHF; (3) ASD

Front 266

Treament of Atrial Flutter

Back 266

Same as for Atrial Fibrillation - (1) Control rate; (2) Restore NSR; (3) Anticoagulation

Front 267

Multifocal Atrial Tachycardia

Back 267

Usually occurs in patients with severe pulmonary disease (COPD). EKG findings = variable P wave morphology, variable PR and RR intervals. At least 3 different P wave morphologies are required to make an accurate diagnosis! Can also be diagnosed by use of vagal maneuvers or adenosine to show AV block without disrupting the atrial tachycardia

Front 268

Treatment of MAT

Back 268

Improving oxygenation and ventilation. If LV function is preserved, acceptable treatments include CCBs, BB, digoxin, amiodarone, IV flecainide, and IV propafenone. If LV function is not preserved, use digoxin, diltiazem, or amiodarone. Electrical cardioversion is ineffective and should not be used

Front 269

Paroxysmal Supraventricular Tachycardia: Pathophysiology

Back 269

Most often due to reentry. Two types: AV nodal reentrant tachycardia and Orthodromic AV reentrant tachycardia

Front 270

AVNRT

Back 270

Two pathways (one fast and one slow) within the AV node, so the reentrant circuit is within the AV node. MCC of SVT! Initiated or teminated by PACs. EKG findings = narrow QRS complexes with no discernible P waves (P waves are buried within the QRS complex). This is because the circuit is short and conduction is rapid, so impulses exit to activate atria and ventricles simultaneously

Front 271

Orthodromic AVRT

Back 271

Accessory pathway between atria and ventricles that conducts retrogradely. Called a 'concealed bypass tract' and is a common cause of SVTs. Initiated or terminated by PACs of PVCs. EKG: narrow QRS complexes with P waves which may or may not be discernible, depending on the rate. This is because the accessory pathway is some distance from the AV node (reentrant circuit is longer), and there is a difference in the timing of activation of the atria and ventricles

Front 272

Treatment of SVT

Back 272

(1) Maneuvers that stimulate the vagus delay AV conduction and thus block the re-entry mechanism: the Valsalva maneuver, carotid sinus massage, breath holding, and head immersion in cold water (or placing an ice bag to the face); (2) Acute treatment: Pharmacologic therapy with IV adenosine [agent of choice] due to its short duration of action and effectiveness in terminating SVTs; works by decreasing sinoatrial and AV nodal activity (3) IV verapamil and IV ismolol or digoxin are alternatives in patients with preserved LV function; (4) DC cardioversion if drugs are not effective or if unstable; almost always successful. (5) RF caheter ablation of either the AV node or the accessory tract (depending on which is the accessory pathway) is preferred if episodes are recurrent and symptomatic

Front 273

Wolff-Parkinson-White Syndrome

Back 273

(1) An accessory conduction pathway from atria to ventricles causes premature ventricular excitation because it lacks the delay seen in the AV node; (2) May lead to paroxysmal tachycardia. Diagnosis on EKG: narrow complex tachycardia, short P-R interval, and a delta wave; (3) Rx: RF ablation of one arm of reentrant loop of accessory pathway is an effective treatment. Avoid drugs active on AV node like digoxin because they may accelerate conducntion through the accessory pathway

Front 274

Ventricular tachycardia

Back 274

(1) Rapid and repetitive firing of 3 or more PVCs in a row, at a rate of between 100 and 250bpm; (2) AV dissociation is present, i.e., sinus P waves continue with their cycle, unaffected by the tachycardia; (3) Originates below Bundle of His; (4) Sustained VT lasts longer than 30 seconds and is almost always symptomatic - associated with hypotension and/or myocardial ischemia; can progress to VFib without treatment

Front 275

Torsades de pointes

Back 275

(1) Rapid polymorphic VT. Dangerous arrhythmia that often can lead to Vfib. (2) Associated with many factors that prolong the QT interval (e.g., congenital QT syndromes, tricyclic antidepressants, anticholinergics, electrolyte abnormalities, ischemia. (3) IV Magnesium provides cardiac stabilization

Front 276

Ventricular Fibrillation

Back 276

Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output. Most episodes of Vfib begin with VT. Ischemic heart disease is the most common cause

Front 277

Recurrence of Vfib

Back 277

If Vfib is not associated with acute MI, recurrence rate is high (up to 30% within first year!). These patients require chronic therapy: either prophylactic antiarrhythmic therapy (amiodarone) or AIDC. If Vfib develops within 48h of AMI, long-term prognosis is favorable, and recurrence rate is low (2% at 1 year). Chronic therapy is not needed in these patients

Front 278

Dilated Cardiomyopathy

Back 278

(1) MC type of Cardiomyopathy; an insult (ischemia, infection, alcohol, etc) causes dysfunction of the left ventricular contractility. Associated with poor prognosis; many die within 5 years of onset of symptoms; (2) CAD (with prior MI) is the most common cause

Front 279

Clinical features of dilated cardiomyopathy

Back 279

(1) Symptoms and signs of left and right-sided heart CHF develop; (2) S3 and S4, as well as murmurs of mitral or tricuspid insufficiency may be present

Front 280

Treatment of dilated cardiomyopathy

Back 280

(1) Similar to treatment of CHF: digoxin, diuretics, vasodilators, and cardiac transplantation; (2) Remove offending agent if possible; (3) Anticoagulation should be considered because patients are at increased risk of embolization

Front 281

Hypertrophic Cardiomyopathy

Back 281

Most cases are inherited as an autosomal dominant trait. (1) Main problem is diastolic dysfunction 2/2 stiff, hypertrophied ventricle with elevated diastolic filling pressures. These pressures increase further with factors that increase HR and contractility (such as exercise) or decrease left ventricular filling (e.g., the Valsalva maneuver). (2) Patients may also have a dynamic outflow obstruction 2/2 asymmetric hypertrophy of the interventricular septum

Front 282

What effect do standing, Valsalva, and leg raise maneuvers have on the intensity of murmurs?

Back 282

These maneuvers decrease LV volume and thus diminish the intensity of all murmurs except MVP and HCM.

Front 283

How does squatting effect the intensity of murmurs?

Back 283

Squatting increases the intensity of all murmurs except MVP and HCM

Front 284

How does a sustained handgrip effect the intensity of murmurs?

Back 284

A sustained handgrip increases the intensity of MVP murmur, but diminishes the intensity of HCM murmur. Sustained handgrip increases systemic resistance

Front 285

Restrictive Cardiomyopathy

Back 285

Infiltration of the myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance. Systolic dysfunction is variable and usually occurs in advanced disease

Front 286

Causes of Restrictive Cardiomyopathy

Back 286

(1) Amyloidosis; (2) Sarcoidosis; (3) Hemochromatosis; (4) Scleroderma; (5) Carcinoid syndrome; (6) Idiopathic

Front 287

Clinical features of restrictive cardiomyopathy

Back 287

(1) Elevated filling pressures cause dyspnea and exercise intolerance; (2) Right-sided signs and symptoms are present for the same reason

Front 288

Myocarditis

Back 288

(1) Inflammation of the myocardium with many possible causes (e.g., Coxsackie B), bacteria (group A strep in Rheumatic fever, Lyme disease, mycoplasma, and so on), SLE, medications (e.g. sulfonamides); can also be idiopathic. Look for elevations in cardiac enzymes and ESR; Rx: supportive

Front 289

Acute pericarditis: complications

Back 289

(1) Pericardial effusion; (2) Cardiac tamponade - can occur in up to 15% of patients; close observation is important

Front 290

Clinical features of acute pericarditis

Back 290

(1) Chest pain - not always present, but often severe and PLEURITIC (can differentiate from pain of MI because of association with breathing); can be localized to retrosternal and left precordial regions and radiates to the trapezius ridge and neck; (3) Pain is positional; it is aggravated by lying supine, coughing, swallowing, and deep inspiration. Pain is relieved by sitting up and leaning forward. Pain is not always present, depending on the cause (often absent in rheumatoid pericarditis)

Front 291

Cardinal manifestations of acute pericarditis

Back 291

(1) Chest pain; (2) Pericardial friction rub; (3) EKG changes - diffuse ST elevations; (4) Pericardial effusion (with or without tamponade)

Front 292

Pericardial friction rub

Back 292

Caused by friction between visceral and parietal pericardial surfaces; A scratching, high-pitched sound heard best during expiration with patient sitting up and with stethoscope placed firmly against the chest

Front 293

Diagnosis of acute pericarditis

Back 293

(1) Diffuse ST elevation and PR depression; (2) ST segment returns to normal; (3) T wave inverts; (4) T wave returns to normal. An echo is often normal, but will show an effusion if suspected

Front 294

Treatment of acute pericarditis

Back 294

(1) Most cases are self-limited, resolve in 2-6 weeks; (2) Treat underlying cause if known; (3) NSAIDs are the mainstay of therapy; (4) Glucocorticoids may be tried if pain does not respond to NSAIDs, but should be avoided if at all possible

Front 295

Constrictive pericarditis

Back 295

(1) Fibrous scarring of the pericardium leads to rigidity and thickening of the pericardium, with obliteration of the pericardial cavity; (2) The fibrotic, rigid pericardium restricts the diastolic filling of the heart. (3) The most prominent physical finding: elevated central venous pressure with massive JVD; (4) Kussmaul's sign = JVD fails to decrease during inspiration; (5) Pericardial knowck - corresponding to the abrupt cessation fo ventricular filling

Front 296

Pericardial effusion

Back 296

Defined as any cause of acute pericarditis that can lead to exudation of fluid into the pericardial space; (1) Can occur in association with ascites and pleural effusion in salt and water retention states such as CHF, cirrhosis, and nephrotic syndrome; (3) Important clinically because it MAY LEAD TO CARDIAC TAMPONADE!

Front 297

Cardiac tamponade

Back 297

Pericardial effusion that impairs diastolic filling of the heart. Characterized by the elevation and equalization of intracardiac and intrapericardial pressures; (2) It is the RATE of fluid accumulation that is important, not the amount; REMEMBE: Ventricular filling is impaired during diastole!! Decreased filling = decreased stroke volume and decreased cardiac output

Front 298

Causes of cardiac tamponade

Back 298

(1) Penetrating (less commonly blunt) trauma to the thorax, such as gunshot and stab wounds; (2) Iatrogenic: central line placement, pacemaker insertion, pericardiocentesis, etc; (3) Pericarditis: idiopathic, neoplastic, uremic; (4) Post-MI with free-wall rupture

Front 299

Clinical findings in cardiac tamponade

Back 299

(1) Elevated JVP is the most common finding; prominent x descent with absent y descent is seen on venous waveforms; (2) Narrowed pulse pressure 2/2 decreased stroke volume; (3) Pulsus paradoxus = exaggerated decrease in the amplitude of the femoral or carotid pulse during inspiration. Pulse gets strong during expirationand weak during inspiration

Front 300

Beck's Triad (Cardiac Tamponade)

Back 300

(1) Hypotension; (2) Muffled heart sounds; (3) JVD

Front 301

Aortic Stenosis: Signs of poor prognosis

Back 301

Development of angina, syncope or heart failure is a sign of poor prognosis. Survival is similar to that of the normal population before the development of these three classical symptoms: (1) Angina (35%) - average survival = 3 years. (2) Syncope (15%) - average survival = 2 years; (3) Heart failure (50%) - average survival = 1.5 years

Front 302

Key Signs of Mitral Valve Prolapse

Back 302

(1) Systolic clicks; (2) Midsystolic rumbling murmur that increases with standing and the Valsalva maneuver and decreases with squatting; (3) Sustained HANDGRIP INCREASES the murmur of MVP; in contrast, it decreases the murmur of hypertrophic cardiomyopathy

Front 303

Course of Aoritc Stenosis

Back 303

Patients are usually asymptomatic for years until middle or old age despite severe obstruction. Clinical features include exertional syncope and heart failure symptoms such as dyspnea on exertion, orthopnea, or PND. Signs of AS include a harsh, crescendo-descrescendo systolic murmur in the 2nd RUSB that radiates to the carotids, an S4, parvus et tardus [diminished and delayed carotid upstrokes] and sometimes a precordial thrill

Front 304

Pathophysiology of Aortic Regurgitation

Back 304

Regurgitant flow increases LV and diastolic volume. LV dilatation and hypertrophy occur in response in order to maintain stroke volume and prevent diastolic pressure from increasing excessively. Over time, these compensatory mechanisms fail, leading to increased left-sided and pulmonary pressures. The resting LV EF% is usually normal until advanced disease. MC Exam FINDING = Widened pulse pressure 2/2 increased systolic BP, decreased systolic BP

Front 305

Treatment of acute aortic regurgitation

Back 305

This is a medical emergency and needs an emergent aortic valve replacement!

Front 306

Acute Mitral regurgitation

Back 306

Abrupt elevation of left atrial pressure in setting of normal LA size and compliance, causing backflow into pulmonary circulation with resultant pulmonary edema. Cardiac output decreases because of decreased forward flow, so hypotension and shock can occur

Front 307

Murmur of Mitral Regurgitation

Back 307

Holysystolic murmur (starts with S1, continues through S2) at the apex, radiates to back or clavicular area; Afib is the MC finding

Front 308

What is Epstein's anomaly?

Back 308

A congenital malformation of the tricuspid valve in which there is downward displacement of the valve into the RV

Front 309

Cause of tricuspid regurgitation

Back 309

Usually secondary to RV dilatation [LV failure is most common cause, but also right ventricular infarction, inferior wall MI, or cor pulmonale 2/2 pulmonary HTN]

Front 310

Clinical features or tricuspid regurgitation

Back 310

(1) Signs and symptoms of RVF (ascites, hepatomegaly, edema, JVD; (2) Pulsatile liver; (3) Blowing holosystolic murmur at LLSB

Front 311

Rheumatic Heart Disease

Back 311

Complication of streptococcal pharyngitis; immunologically mediated systemic process that may cause valvular abnormalities secondary to acute rheumatic fever. MC valvular abnormality is mitral stenosis, but patients may have aortic or tricuspid involvement as well

Front 312

Diagnosis of acute rheumatic fever (requires 2 MAJOR or 1 MAJOR + TWO MINOR)

Back 312

MAJOR = (1) Migratory polyarthritis, (2) Erythema marginatum, (3) Cardiac involvement [pericarditis, CHF, valve disease], (4) Chorea, (5) Subcutaneous nodules. MINOR = (1) Fever, (2) Elevated ESR, (3) Polyarthralgias, (4) Prior history of rheumatic fever, (5) Prolonged PR interval, (6) Evidence of preceding streptococcal infection

Front 313

Treatment of rheumatic heart disease

Back 313

(1) Treat streptococcal pharyngitis with PCN or erythromycin to prevent rheumatic fever; (2) Acute rheumatic fever is treated with NSAIDs. CRP is used to monitor treatment; (3) Patients with history of rheumatic fever should receive antibiotic prophylaxis with erythromycin or amoxicillin for dental/GI/GU proecdures; (4) Treat the valvular pathology of rheumatic heart disease

Front 314

Infective endocarditis

Back 314

Acute = 2/2 Staph aureus (virulent), occurs on a normal heart valve, and if untreated, fatal within 6 weeks. Subacute = 2/2 Strep viridans and enterococcus; occurs on damaged heart valves and takes >6 weeks to cause death if untreated

Front 315

Native valve endocarditis

Back 315

S. viridans is the MC organism in native valve endocarditis; other organisms include S. aureus and enterococcus, as well as HACEK group (Hemophilus, Actinobaccilus, Cardiobacterium, Eikenella, and Kingella

Front 316

Prosthetic valve endocarditis

Back 316

Staphylococci are the MC cause of early-onset endocarditis; symptoms appear within 60 days of surgery (S. epidermidis > S. aureus). Streptococci are the most common cause of late-onset endocarditis; symptoms appear 60 days after surgery

Front 317

Endocarditis in IV drug users

Back 317

Frequently presents with right-sided endocarditis; S. aureus is the most common cause; other organisms include enterococci and streptococci. Fungi (mostly Candida) and gram-negative rods (mostly Pseudomonas) are less common causes

Front 318

What should you suspect in a patient with a new heart murmur and unexplained fever?

Back 318

Endocarditis. Get a TEE to diagnose (Better than TTE). Infective endocarditis is almost always fatal if left untreated

Front 319

When is endocarditis prophylaxis indicated?

Back 319

When patients with known valvular heart disease or prosthetic valves are bout to undergo oral surgery or GI/GU surgery

Front 320

Nonbacterial Thrombotic Endocarditis (Marantic Endocarditis)

Back 320

(1) Associated with debilitating illnesses such as metastatic cancer [found in up to 20% of cancer patients]; (2) Sterile deposits of fibrin and platelets form along the closure line of cardiac valve leaflets; (3) Vegetations can embolize to the brain and periphery; (4) Although the use of heparin may be appropriate, no studies have confirmed its efficacy

Front 321

Nonbacterial Verrucous Endocarditis (Libman-Sacks Endocarditis)

Back 321

(1) Typically involves the aortic valves in patients with SLE; (2) Characterized by the formation of small, warty vegetations on BOTH SIDES OF VALVE LEAFLETS and may present with regurgitant murmurs; (3) Rarely gives rise to infective endocarditis, but can be a source of systematic embolization; (4) Treat underlying SLE and anticoagulate

Front 322

Types of Atrial Septal Defects

Back 322

(1) Ostium secundum (MC, 80% of cases) occurs in central portion of interatrial septum; (2) Ostium primum - occurs low in the septum; (3) Sinus venosus defects - occur high in the septum

Front 323

Pathophysiology of ASDs

Back 323

(1) Oxygenated blood from LA passes into RA, increasing right heart output and thus pulmonary blood flow; (2) Leads to increased work of the right side of the heart: As shunt size increases, RA and RV dilatation occurs with pulmonary-to-systemic flow ratios greater than 1.5:1.0; (3) Pulmonary Hypertension is a serious sequelae, but is rare in ASD

Front 324

Clinical Course of ASDs

Back 324

(1) Patients usually asymptomatic until middle age (around 40), thereafter, symptoms may begin and include exercise intolerance, dyspnea on exertion, and fatigue.

Front 325

Clinical Features of ADSs

Back 325

Wide, fixed splitting of S2; diastolic flow 'rumble' across tricuspid valve area secondary to increased blood flow; TEE is diagnostic for ASD. RBBB and Right Axis deviation may be seen; atrial abnormalities can also be seen

Front 326

Complications of ASD

Back 326

(1) Pulmonary HTN - does not occur before 20 years of age, but is a common finding in patients over age 40; (2) EISENMENGER'S DISEASE is a late complication seen in a minority of patients, in which irreversible pulmonary HTN leads to a reversal of the shunt, heart failure, and cyanosis; (3) Right heart failure; (4) Atrial arrhythmias, especially Afib; (5) Stroke can result from paradoxical emboli or Afib

Front 327

Treatment of ASD

Back 327

Surgical repair when pulmonary-to-systemic blood flow ratio is greater than 1.5:1 or 2:1 if patient is asymptomatic

Front 328

Ventricular Septal Defects

Back 328

MOST COMMON CONGENITAL CARDIAC MALFORMATION; Blood flows from high pressure LV to RV resulting in increased pulmonary blood flow. Large defects eventually lead to pulmonary HTN, whereas small defects do not change pulmonary vascular hemodynamics

Front 329

Clinical features of VSD

Back 329

Symptoms: (1) Elevated pulmonic vascular resistance gives rise to CHF, growth failure, and recurrent lower respiratory infections. A large shunt with a very high PVR (Eisenmenger's reaction) gives rise to SOB, DOE, chest pain, and cyanosis; Signs: (1) Harsh, blowing holosystolic murmur with thrill. Smaller defect = louder murmur.

Front 330

Complications of VSD

Back 330

(1) Endocarditis; (2) Progressive aortic regurgitation; (3) Heart failure; (4) Pulmonary HTN and shunt reversal (Eisenmenger's)

Front 331

Coarctation of the Aorta

Back 331

(1) Narrowing/constriction of the aorta, usually at the origin of the left subclavian artery near the ligamentum arteriosum, which leads to obstruction between the proximal and distal aorta, and thus increased LV afterload.

Front 332

Clinical features of Coarctation of the aorta

Back 332

(1) HTN in upper extremities with hypotension in lower extremities; (2) Well-developed upper body with underdeveloped lower half; (3) Midsystolic murmur best heart over the back; (4) Symptoms include HA, cold extremities, claudication with exercise, and leg fatigue

Front 333

Patent Ductus Arteriosus

Back 333

(1) Communication between the aorta and pulmonary artery that persists after birth; (2) During fetal life, prostaglandins and lower oxygen tension maintain the ductus arteriosus. Blood is shunted away from nonfunctional lungs; normally closes within days after birth; (3) Becomes a left-to-right shunt in life outside the womb if it remains patent (blood flows from aorta into pulmonary artery); (4) Associated with vongenital rubella syndrome, high altitude, and premature births; (5) Pathophysiology: Large L->R shunt results in volume overload, pulmonary HTN, and right sided heart failure

Front 334

What does a loud P2 indicate?

Back 334

Signs of Pulmonary HTN

Front 335

What is the murmur of a PDA?

Back 335

A loud, continuous 'machinery-like' murmur at the left second intercostal space

Front 336

Treatment of PDA

Back 336

(1) If pulmonary vascular disease is absent: surgical ligation; (2) If severe pulmonary HTN or right-to-left shunt is present, do NOT correct PDA. Surgery is contraindicated!

Front 337

Hypertensive Emergency

Back 337

Systolic BP >220 and/or diastolic BP >120 IN ADDITION TO END-ORGAN DAMAGE. Immediate treatment is indicated!

Front 338

Hypertensive Urgency

Back 338

Elevated BP levels alone without end-organ damage. Rarely require emergency threapy and can be managed with attempts to lower BP over a period of 24h

Front 339

Signs of End-organ damage in hypertensive emergency

Back 339

(1) Eyes: papilledema; (2) CNS: AMS or intracranial hemorrhage, Hypertensive encephalopathy; (3) Kidneys: renal failure or hematuria; (4) Heart: unstable angina, MI, CHF with pulmonary edema, aortic dissection; (5) Lungs: pulmonary edema;

Front 340

Causes of Hypertensive Emergency

Back 340

(1) Noncompliance with antihypertensive medications; (2) Cushing's syndrome; (3) Drugs such as cocaine, LSD, methamphetamines; (4) Hyperaldosteronism; (5) Eclampsia; (6) Vasculitis; (7) Alcohol withdrawal; (8) Pheochromocytoma; (9) Noncompliance with dialysis

Front 341

Hypertensive Emergency Treatment

Back 341

(1) Reduce MAP by 25% in 1-2hrs. Goal is NOT to immediately achieve normal BP, but to get patient out of danger, then reduce BP gradually; (2) If severe (diastoli pressure >130) or if hypertensive encephalopathy is present, IV agents such as nitroprusside, labetalol, or nitroglycerin are appropriate; (3) In patients who are in less immediate danger, oral agents are appropriate: captopril, clonidine, labetalol, and diazoxide

Front 342

Aortic Dissection: predisposing factors

Back 342

(1) Longstanding systemic HTN (present in 70% of cases); (2) Trauma; (3) Connective tissue diseases such as Marfan's and Ehlers-Danlos syndrome; (3) Bicuspid aortic valve; (5) Coarctation of the aorta; (6) Third trimester of pregnancy

Front 343

Stanford classification of Aortic Dissection

Back 343

(1) Type A (Proximal) involves the ascending aorta (includes retrograde extension from descending aorta); (2) Type B (Distal) is limited to the descending aorta

Front 344

Diagnosis of Aortic Dissection

Back 344

(1) CXR shows WIDENED MEDIASTINUM (>8mm on AP view); (2) TEE has good sensitivity and specificity and can be performed at bedside

Front 345

Treatment of Aortic Dissection

Back 345

(1) Initiate medical therapy IMMEDIATELY - IV beta blockers to lower heart rate and diminish force of left ventricular ejection; IV sodium nitroprusside to lower systolic BP < 120mmHg. For type A dissections - surgical management, For type B dissections, medical management

Front 346

Abdominal Aortic Aneurysm

Back 346

Abnormal localized dilation of the aorta. Most occur between the renal arteries and the iliac bifurcation. Incidence increases with age; more common in men

Front 347

Causes of AAA

Back 347

(1) Most cases, there is atherosclerotic weakening of the aortic wall. Other predisposing factors include trauma, HTN, vasculitis, smoking, and positive family history; (2) Syphilis and connective tissue abnormalities (Marfan's and Ehlers-Danlos) are associated with thoracic aneurysms, but they may involve the lower aorta as well

Front 348

Clinical Features of AAA

Back 348

(1) Usually asymptomatic, discovered on either abdominal examination or a radiological study done for another reason; (2) Sense of 'fullness'; (3) Pain may or may not be present - if present, located in the hypogastrium and lower back and usually throbbing in character; (4) Pulsatile MASS on abdominal examination

Front 349

Symptoms suggestion sudden rupture of AAA

Back 349

(1) Sudden onset of severe pain in the back or lower abdomen, radiating to the groin, buttocks, or legs; (2) Grey Turney's sign (ecchymoses on back and flanks) and Cullen's sign (ecchymoses around umbilicus)

Front 350

Rupture of an AAA

Back 350

(1) Triad of ABDOMINAL PAIN, HYPOTENSION, and PALPABLE PULSATILE ABDOMINAL MASS indicates a ruptured AAA and emergent laparotomy is indicated.

Front 351

Treatment of AAA

Back 351

(1) Management depends on size of aneurysm; If >5cm in diameter and symptomatic, surgical resection with synthetic graft placement is recommended. The infrarenal aorta is replaced with a Dacron facric tube; (2) The management of asymptomatic aneurysms <5cm is controversial. Periodic imaging is recommended to follow up growth. No 'safe' size exists, however, and small AAAs can rupture

Front 352

Peripheral Vascular Disease (Chronic Arterial Insufficiency)

Back 352

Occlusive atherosclerotic disease of lower extremities; patients usually have coexisting CAD (with CHF, history of MI, and so on) and other chronic medical problems like diabetes, lung disease

Front 353

Leriche's Syndrome

Back 353

Atheromatous occlusion of distal aorta just above the bifurcation causing bilateral claudication, impotence, and absent/diminished femoral pulses

Front 354

What is the MC site of occlusion/stenosis in PVD?

Back 354

The superficial femoral artery (in Hunter's canal). Other sites include popliteal artery, and aortoiliac occlusive disease

Front 355

Symptoms of PVD

Back 355

(1) Intermittent claudication [cramping leg pain reliably reproduced by same walking distance and relieved by rest]; (2) Rest pain [continuous] usually felt over the distal metatarsals. Often PROMINENT AT NIGHT - awakens patient from sleep. Hanging feet over side of bed or standing relieves the pain - extra perfusion to ischemic areas due to gravity. Rest pain is always worrisome - suggests severe ischemia such that frank gangrene of involved limb may occur without intervention

Front 356

Signs of PVD

Back 356

(1) Diminished or absent pulses, muscular atrophy, decreased hair growth, thick toenails, and decreased skin temperature; (2) Ischemic ulceration (usually on toes) with localized skin necrosis that may be 2/2 local trauma that does not heal; (3) Pallor on elevation and rubor on dependency in advanced disease

Front 357

Diagnosis of PVD

Back 357

(1) Ankle-to-brachial index (ABI) is the ratio of the systolic BP at the ankle to the systolic BP at the arm. Normal ABI is >1.0; Claudication ABI <0.7, Rest pain ABI <0.4; (2) Pulse volume recordings - pulse wave forms represent volume of blood/heart beat at sequential sites down the leg. Large wave form indicates good collateral blood flow; (3) Arteriography (contrast in vessels and radiographs) is the GOLD STANDARD for diagnosing and locating PVD, but it is only needed if surgery is being considered

Front 358

Treatment of PVD

Back 358

(1) Conservative management for intermittent claudication - [a] stop SMOKING. It is linked to progression of atherosclerosis and causes vasoconstriction. [b] graduated exercise program: walk to claudication, rest, then continue walking; [c] foot care, especially in diabetics; [d] atherosclerotic risk factor reduction (control of HLD, HTN, wt, DM, etc); [e] avoid extremes of temperature; [f] ASA may be helpful; [g] Trental (pentoxifylline) lowers blood viscosity, improving flow, and may be helpful. (2) Surgical treatment: Indications: rest pain, ischemic ulcerations (tissue necrosis), severe symptoms refractory to conservative treatment that affects quality of life or work. Options include surgical bypass grafting (5yr patency rate of 70%) or angioplasty-balloon dilatation

Front 359

What causes calf claudication?

Back 359

Femoral or popliteal peripheral vascular disease; aortoiliac occlusive disease causes buttock and hip claudication (in addition to the calves)

Front 360

Acute Arterial Occlusion: general characteristics

Back 360

Acute occlusion of an artery, usually caused by embolization. The common femoral artery is the most common site of occlusion. Less commonly, in situ thrombosis is the cause; (2) Sources of emboli = [a] heart (85%) 2/2 AFib, post-MI, endocarditis, or myxoma; [b] Aneurysms; [c] Atheromatous plaque

Front 361

Acute Arterial Occlusion: clinical features

Back 361

Remember the six P's! (1) PAIN - acute onset, patient can tell you precisely when and where it happened. The pain is VERY severe, and the patient may have to sit down or may fall to the ground. (2) PALLOR; (3) POLAR (cold); (4) PARALYSIS; (5) PARESTHESIAS; (6) PULSELESSNESS (use Doppler to assess)

Front 362

Acute Arterial Occlusion: treatment

Back 362

(1) Main goal: assess viability of tissues to salvage the limb! Skeletal muscle can tolerate 6 hours of ischemia; perfusion should be reestablished within this time frame. (2) If paralysis or paresthesias are present, amputation is probably necessary; (3) Immediately anticoagulate with IV heparin; (4) Surgical embolectomy is indicated via cutdown and Fogarty baloon; bypass is reserved for embolectomy failure; (5) Treat any complications such as compartment syndrome that may occur

Front 363

Cholesterol Embolization Syndrome

Back 363

Cholesterol crystals originating from a proximal source (e.g., atherosclerotic plaque) most commonly the abdominal aorta, iliacs, and femoral arteries. It is often triggered by a surgical or radiographic intervention or by thrombolytic therapy. It presents with small, discrete areas of tissue ischemia, resulting in blue/black toes, renal insufficiency, and/or abdominal pain or bleeding (latter due to intestinal hypoperfusion). Treatment is supportive. DO NOT ANTICOAGULATE!. Control BP. Think livedo reticularis, eosinophilia!

Front 364

Mycotic aneurysm

Back 364

An aneurysm resulting from damage to the aortic wall secondary to INFECTION. Blood cultures positive in most cases. Rx: IV antibiotics, surgical excision

Front 365

Leuetic Heart

Back 365

Complication of SYPHILITIC AORTITIS, usually affecting men in their 40s-50s. Aneurysm of the aortic arch with retrograde extension backward to cause aortic regurgitation and stenosis of the aortic branches, most commonly the coronary arteries. Treatment: IV PCN, surgical repair

Front 366

Deep Vein Thrombosis: risk factors

Back 366

(1) Age >60; (2) Malignancy; (3) Prior history of DVT, PE, or varicose veins; (4) Hereditary hypercoagulable states; (5) Prolonged immobilization or bed rest; (6) Cardiac disease, especially CHF; (7) Obesity; (8) Major surgery, esp of pelvis (orthopedic procedures); (9) Major trauma; (10) Pregnancy, estrogen use

Front 367

Virchow's Triad

Back 367

(1) Endothelial injury; (2) Venous stasis; (3) Hypercoagulability

Front 368

Clinical Features of DVT

Back 368

Classic findings (all have low sensitivity and specificity): (!) Lower-extremity pain and swelling, worse with dependency/walking, better with elevation/rest; (2) Homan's sign [calf pain on ankle dorsiflexion]; (3) Palpable cord; (4) Fever. NOTE: Only 50% of Pts with classic DVT findings have a DVT, and only 50% of patients with documented DVT have the classic findings!

Front 369

Why do only 50% of patients with DVT have the classic findings?

Back 369

Because there is often a superficial venous system that is patent, so the classic findings of DVT (erythema, pain, cords) will not occur because blood drains from these patent veins. This is why only half of all patients with DVT have the classic findings

Front 370

Diagnosis of DVT

Back 370

(1) Doppler analysis and Duplex U/S - initial test for DVT; noninvasive, but highly operator-dependent; High sensitivity and specificity for detecting proximal thrombi (popliteal and femoral), not so for distal (calf vein) thrombi; (2) Venography - most accurate test for DVT of calf veins; Invasive and frequently used, but allows visualization of the deep and superficial venous systems, and allows assessment of patency and valvular competence

Front 371

D-dimer testing in DVT

Back 371

Has a very high sensitivity (95%) but low specificity (50%); can be used to rule out DVT when combined with Doppler and clinical suspicion. D-dimer is a cross-linked fibrin degradation product formed by plasmin and found with a high sensitivity in patients with clotting activity. It is therefore most useful as a means to rule out thrombosis

Front 372

Postthrombotic syndrome (chronic venous insufficiency)

Back 372

(1) Occurs in approximately half of patients with acute DVT; (2) Residual venous obstruction and valvular incompetence lead to ambulatory HTN

Front 373

Phlegmasia cerulea dolens

Back 373

(1) Occurs in extreme cases of DVT - indicates that major venous obstruction has occurred; (2) Severe leg edema compromises arterial supply to the limb, resulting in impaired sensory and motor function; (3) Venous thrombectomy is indicated

Front 374

Treatment of DVT

Back 374

(1) Anticoagulation! Helps prevent propagation of the thrombus; Heparin bolus followed by constant infusion, titrated to maintain the PTT at 1.5-2x aPTT; (2) Start warfarin once aPTT is therapeutic and continue for 3-6 months. Anticoagulate to INR at 2.0-3.0. (3) Continue heparin until INR has been therapeutic for 48 hours.

Front 375

Other treatment options for DVT

Back 375

(1) Thrombolytic therapy - speeds up clot resolution; indicated in patients with massive PE, hemodynamically unstable, those with right sided heart failure, and those with no CI for thrombolytics; (2) Prophylactic IVC filter - for patients at high risk who have an absolute contraindication to other forms of prophylaxis; effective only in preventing PE, not DVT

Front 376

Chronic Venous Insufficiency (Venous Stasis Disease)

Back 376

(1) aka postphlebitic syndrome; (2) CVI may involve the superficial, deep, or both venous systems; (3) History of DVT is the underlying cause in most cases: [a] DVT causes destruction of venous valves in the deep venous system. Valvular incompetence results in gravitational pressure of the blood column to be transmitted to the ankles; [b] valves in perforator veins are also damaged 2/2 chronically elevated deep venous pressure, inhibiting transmission of blood from superficial to deep, as normally occurs. This leads to ambulatory VENOUS HYPERTENSION

Front 377

Ambulatory venous hypertension

Back 377

(1) Interstitial fluid accumulation, resulting in edema; (2) Extravasation of plasma proteins and RBCs into subcutaneous tissues, resulting in brawny induration and pigmentation (a brown-black color) of skin

Front 378

Pathophysiology of Chronic Venous Insufficiency (Venous Stasis Disease)

Back 378

(1) Local capillary blood flow and hypoxia of tissues; (2) Even mild trauma trauma may precipitate tissue death and ulcer formation; (3) Venous ulcers usually develop medially from the instep to above the ankle, overlying an incompetent perforator vein

Front 379

Clinical features of Chronic Venous Insufficiency (Venous Stasis Disease)

Back 379

(1) Swelling of the leg - aching/tightness of involved leg; often worse at end of day; (2) Symptoms worsened by period of sitting or inactive standing; (3) Leg elevation provides relief of symptoms [opposite is true in arterial insufficiency]; (4) Chronic changes include thin, atrophic, shiny, cyanotic skin; (5) Brawny induration develops with chronicity

Front 380

Venous ulcers

Back 380

(1) Less painful than ulcers associated with arterial insufficiency; (2) Usually located just above the medial malleolus; (3) Often rapidly recur

Front 381

Treatment of CVI

Back 381

(1) Leg elevation above heart; (2) Avoiding long periods of sitting and standing. If ulcers develop: (1) Wet-to-dry saline dressing (3x/day); (2) Unna venous boot (external compression stocking). If do not heal, apply split-thickness skin grafts with or without ligation of adjacent perforator veins

Front 382

Superficial Thrombophlebitis

Back 382

(1) Virchow's triad implicated; (2) In upper extremities, usually occurs at the site of an IV infusion; (3) In lower extremities, usually associated with varicose veins secondary to static blood flow in these veins

Front 383

What is superficial thrombophlebitis that occurs in different locations over a short period of time?

Back 383

This is migratory superficial thrombophlebitis, and usually occurs 2/2 occult malignancy, usually of the pancreas

Front 384

Clinical features of superficial thrombophlebitis

Back 384

(1) Pain, tenderness, induration, and erythema along the course of the vein; (2) A tender cord may be palpated

Front 385

Treatment of superficial thrombophlebitis

Back 385

(1) No anticoagulants are required - rarely causes PE! (2) Localized thrombophlebitis - mild analgesic (ASA) is all that is required in most cases; continue activity; (3) SEVERE thrombophlebitis (with pain and cellulitis) - once symptoms resolve, ambulation with elastic stockings is recommended. Antibiotics usually are not necessary unless the process is suppurative, in which case drainage is indicated

Front 386

Shock: symptoms

Back 386

(1) Lactic acidosis; (2) Renal (anuria/oliguria); (3) CNS dysfunction (altered mentation). Shock is characterized by its effect on cardiac output, systemic vascular resistance, and volume status.

Front 387

Cardiogenic shock

Back 387

Occurs when heart is unable to generate a cardiac output sufficient to maintain tissue perfusion. Can be defined as SBP < 90mmHg with urine output <20ml/hr and adequate LV filling pressure. MCC = s/p acute MI. May also see with cardiac tamponade or tension pneumothorax. NOTE: JVP/PCWP is only elevated in cardiogenic shock

Front 388

Vasopressors in cardiogenic shock

Back 388

(1) Dopamine is the initial drug utilized most often; (2) Dobutamine may be used in combination with dopamine to further increase cardiac output; (3) Norepinephrine or phenylephrine may be used in severe or resistant cases

Front 389

Intra-aortic balloon pump

Back 389

Device that gives 'mechanical support' to a failing heart. Works opposite to the normal pumping action of the heart; 'pumps' during diastole, 'relaxes' during systole. Facilitates ventricular emptying by deflating just before onset of systole reducing afterload and increases coronary perfusion by inflating at the onset of diastole (increasing diastolic pressure). The net effect is enhanced myocardial oxygenation and increased cardiac output. Often utilized in cardiogenic shock, mechanical complications of MI, and bridge to surgery in aortic stenosis

Front 390

Should IV fluids be used if left ventricular pressures are elevated in cardiogenic shock?

Back 390

HELL NO! IV fluids are likely to be harmful if LV pressures are elevated.

Front 391

Septic Shock

Back 391

Associated with severe peripheral vasodilation (flushing, warm skin). There is a SEVERE decrease in SVR as a result

Front 392

Neurogenic shock

Back 392

Results from failure of sympathetic nervous system to maintain adequate vascular tone (sympathetic denervation). Causes include spinal cord injury, severe head injury, severe head injury, spinal anesthesia, pharmacologic sympathetic blockade. Characterized by peripheal vasodilation with decreased SVR. WARM, WELL-PERFUSED SKIN, Hypotension.

Front 393

Cardiac Neoplasms

Back 393

Primary tumors of heart are rare; mets from other primary tumors are more common (75% of cardiac neoplasms).

Front 394

Atrial myxomas

Back 394

Benign gelatinous growth, usually pedunculated and usually arising from the interatrial septum of the heart in the region of the fossa ovalis. It is the most common primary cardiac neoplasm. Although benign, can embolize, leading to metastatic disease or can cause relative valvular dysfunction. Hear a diastolic PLOP that changes characteris with changing body positions. Rx: Surgical excision