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Quizlet > Cardiology Review-Pearl > Flashcards

Cardiology Review-Pearl Flashcards

1
Q

Are aortic aneurysms more common in men or women?

A

Men (10:1) Other risk factors include HTN, atherosclerosis, DM, hyperlipidemia, smoking, syphilis, Marfan’s, and EDS

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2
Q

A pt presents with sudden-onset chest and back pain. Further work-up reveals an ischemic right leg. What is your diagnosis?

A

Suspect an acute aortic dissection when chest or back pain is associated with ischemic or neurologic defects

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3
Q

What CXR finding occurs with a thoracic aortic aneurysm?

A

Change in aortic appearance, mediastinal widening, hump in the aortic arch, pleural effusion (MC on the left), and extension of the aortic shadow

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4
Q

A 74-year old male presents with acute-onset testicular pain. Ecchymosis is present in the groin and scrotal sac. What is the diagnosis?

A

A ruptured aortic or iliac artery aneurysm

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5
Q

What physical findings suggest an acute aortic dissection?

A

BP differences between arms and legs, cardiac tamponade, and aortic insufficiency murmur

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6
Q

What x-ray study should be ordered for a pt with an abdominal mass and a suspected ruptured AAA?

A

None. The pt should go to the OR immediately. About 60% of AAA occur with calcification and appear on a lateral abdominal x-ray

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7
Q

What may an x-ray of a patient with an aortic dissection reveal?

A

Widening of the superior mediastinum, a hazy or enlarged aortic knob, an irregular aortic contour, separation of the intimal calcification from the outer aortic contour that is > than 5mm, a displaced trachea to the right, and cardiomegaly

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8
Q

What is the most common symptom of aortic dissection?

A

Interscapular back pain

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9
Q

Where do aortic dissections most often occur?

A

Proximal ascending aorta (60%). 20% of aortic dissections are found between the origin of the left subclavian and the ligamentum arteriosum in the descending aorta, and 10% are found in the aortic arch or the abdominal aorta. Dissection involves intimal tears propagated by hematoma formation.

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10
Q

What aortic aneurysm diameter is generally considered to be an indication of surgery: a.) in the thorax and b.) in the abdomen?

A

Those with non-dissecting thoracic aneurysms larger than 7cm in diameter are candidates for surgery. However, surgery should be considered with smaller aneurysms for those with Marfan’s, because of a higher incidence of rupture. Non-dissecting AAA larger than 4cm in diameter should be considered for repair.

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11
Q

Describe the Stanford classification of aortic dissections.

A

Standford Type A: Involve ascending aorta; Stanford Type B: Do not involve ascending aorta

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12
Q

What dissections can be treated medically?

A

Pts with Type B (and Debakey’s Type III) are eligible for medical, rather than, surgical treatment. Surgical treatment may be required for those with uncontrollable pain, aortic bleeding, hemodynamical instability, increasing hematoma size, or an impending rupture

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13
Q

What is the prognosis for an untreated aortic dissection?

A

20% of afflicted individuals die within 24 hours, 60% within 2 weeks, and 90% within 3 months. With surgical treatment, the 10 year survival rate is 40%. Redissection occurs in 25% of these pts within 10 years of the original episode

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14
Q

What murmur is expected in pts with substantial aortic stenosis?

A

A prolonged, harsh, loud (IV, V, or VI) systolic murmur

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15
Q

Where is the most common site of peripheral aneurysms that develop from arteriosclerosis?

A

The popliteal artery. Other sites include the femoral, carotid, and subclavian arteries

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16
Q

How long can ST and T changes persist after an episode of pain in unstable angina?

A

Several hours

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17
Q

Quincke’s pulse

A

Visible pulsations in the nail bed capillaries

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18
Q

Corrigan’s pulse

A

Collapsing pulse

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19
Q

deMusset’s sign

A

Head bobbing

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20
Q

Muller’s sign

A

Uvular pulsation during systole

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21
Q

Duroziez’s sign

A

Femoral artery murmurs during systole if the artery is compressed proximally and during diastole if the artery is compressed distally

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22
Q

Pulsus paradoxus

A

Drop in the systolic BP > 10mmHg with inspiration

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23
Q

What is the most common cause of aortic regurgitation in adults?

A

Mild aortic regurgitation frequently develops as a result of a bicuspid aortic valve. A severe aortic regurgitation is induced by rheumatic heart disease, syphilis, endocarditis, trauma, an idiopathic degeneration of the aortic valve, a spontaneous rupture of the valve leaflets, or aortic dissection

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24
Q

What are the signs and symptoms of acute aortic regurgitation?

A

Dyspnea, tachycardia, tachypnea, and chest pain

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25
Q

What is the most common cause of aortic stenosis in pts under age 50? Over age 50?

A

Under 50: Calcification of congenital bicuspid aortic valves (1% of the population has congenital bicuspid valves); Over 50: Calcification of degenerating leaflets

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26
Q

What triad of symptoms characterizes aortic stenosis?

A

Syncope, angina, and left heart failure. As the disease progresses, systolic BP decreases and pulse pressure narrows

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27
Q

What are the clinical findings in a patient with aortic stenosis?

A

Angina, dyspnea on exertion, syncope, sustained apical impulse, narrow pulse pressure, parvus et tardus, systolic ejection crescendo-decrescendo murmur that radiates to the neck, systolic ejection click (not heard in severe cases when the valve is so stenosed that it is immobile), paradoxically split S1 and soft S2, and audible s4

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28
Q

What rhythm is produced by Wolf-Parkinson-White syndrome?

A

AV reciprocating tachycardia

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29
Q

What are the common causes of multifocal atrial tachycardia?

A

COPD, CHF, sepsis, and methylxanthine toxicity. Treat the arrhythmia with magnesium, verapamil, or B-blocking agents

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30
Q

How is atrial flutter treated?

A

Initiate AV nodal blockade with B-blockers, CCBs, or digoxin. If necessary, treat a stable patient with chemical cardioversion by using class IA agents, such as procainamide or quinidine, after digitalization. If this tx fails or if the pt is unstable, electrocardiovert at 25 to 50 J

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31
Q

What are some cases of atrial fibrillation?

A

HTN, rheumatic heart disease, pneumonia, thyrotoxicosis, ischemic heart, pericarditis, ethanol intoxication, PE, CHF and COPD

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32
Q

How is atrial fibrillation treated?

A

Control rate with B-blockade or CCB (such as verapamil or diltiazem) then convert with procainamide, quinidine, or verapamil. Digoxin may be considered, although its effect will be delayed. Syncronized cardioversion at 100 to 200J should be performed on an unstable pt. In a stable pt with a-fib of unclear duration, anticoaglation should be considered for 2 to 3 weeks prior to chemical or electrical cardioversion. Watch for hypotension with the administration of negative inotropes

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33
Q

What are some causes of SVT?

A

Digitalis toxicity, pericarditis, MI, COPD, pre-excitation syndromes, mitral valve prolapse, rheumatic heart disease, pneumonia, and ethanol

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34
Q

What mechanism most commonly produces SVTs?

A

Reentry. Another common cause is abnormal automaticity (i.e., ectopic foci)

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35
Q

What is the tx for SVT caused by digitalis toxicity?

A

Stop the digitalis, treat the hypokalemia, and administer magnesium or phenytoin. Provide digoxin specific antibodies to the unstable patient. Avoid cardioversion

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36
Q

What is the tx for stable SVT not caused by digitalis toxicity or WPW syndrome?

A

Vagal maneuvers, adenosine, verapamil, or B-blockers

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37
Q

Describe the key feature of Mobitz I (Wenckebach) second degree AV block.

A

A progressive prolongation of the PR interval until the atrial impulse is no longer conducted. If symptomatic, atropine and transcutaneous/transvenous pacing is required

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38
Q

Describe the key feature of Mobitz II second degree AV block.

A

A constant PR interval in which one or more beats fail to conduct

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39
Q

What is the tx for Mobitz II second degree AV block?

A

Atropine and transcutaneous/transvenous pacing, if symptomatic

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40
Q

Carotid massage or Valsalva maneuver is useful for slowing supraventricular rhythms. When is carotid massage contraindicated?

A

With ventricular arrhythmias, dig toxicity, stroke, syncope, seizures, or in those with a carotid bruit

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41
Q

What are some common vagal maneuvers?

A

Breath holding, valsalva (bearing down as if having a bowel movement), stimulating of the gag reflex, squatting, pressure on the eyeballs, and immersing the face in cold water

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42
Q

Which is more common: premature atrial beats or ventricular beats?

A

Premature atrial beats. Palpitations that occur because of premature atrial beats are generally benign and asymptomatic. Reassurance is the only treatment. Less frequent but more serious causes of atrial premature beats include pheochromocytoma and thyrotoxicosis. Random PVCs are also benign but common in the general population. Runs of PVCs or associated symptoms of dyspnes, angina, or syncope require investigation and are most likely related to an underlying heart disease.

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43
Q

What are the diagnostic criteria for a Q wave?

A

More than 0.04 seconds and at least one-quarter the size of the R wave in the same lead. Beware, ECGs can be normal in up to 10% of acute MIs.

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44
Q

What is the most common side effect of esmolol, labetalol, and bretylium?

A

Hypotension

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45
Q

What side effect can occur with a rapid infusion of procainamide?

A

Hypotension. Other side effects include QRS/QT prolongation, ventricular fibrillation, and Torsade de pointe.

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46
Q

What are some ADRs of lidocaine?

A

Drowsiness, nausea, vertigo, confusion, ataxia, tinnitus, muscle twitching, respiratory depression, and psychosis

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47
Q

What artery is usually affected by arterial occlusive disease in diabetics?

A

The popliteal artery. Because of diabetic neuropathy and the potential for the development of a necrotizing infection in a leg with compromised circulation, it is very important that patients with diabetes are knowledgeable about pedal hygiene

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48
Q

What is Budd-Chiari syndrome?

A

Thrombosis in the hepatic vein resulting in abdominal pain, jaundice, and ascites

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49
Q

What is the cause of Prinzmetal’s angina?

A

Coronary artery vasospasm with or without fixed stenotic lesions. Prinzmetal’s angina is more often associated with ST segment elevation than with depression. CCBs are the drugs of choice to treat this condition. B-blockers are contraindicated in pts who have vasospasm without fixed stenotic lesions

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50
Q

80-90% of pts who experience sudden non-traumatic cardiac arrest are in what rhythm?

A

Ventricular fibrillation. Early defibrillation is the key. In an acute MI, the infarction zone becomes electrically unstable. Ventricular fibrillation is most common during original coronary occlusion or when the coronaries begin to reperfuse

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51
Q

In CPR, what is the ventilation to compression ratio for one rescuer? For 2 rescuers?

A

1 rescuer: 2 breaths to 15 compressions; 2 rescuers: 1 breath to 5 compressions

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52
Q

Which is the most common type of cardiomyopathy?

A

Dilated cardiomyopathy (all 4 chambers). This condition is induced by progression of myocarditis, alcohol, adriamycin, diabetes, pheochromocytoma, thiamine deficiency, thyroid disease, and valve replacement. The other types of cardiomyopathies are hypertrophic and restrictive/obliterative pregnancy

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53
Q

Which is the most common type of cardiac faILURE: high or low output?

A

Low output failure. Reduced stroke volume, lowered pulse pressure, and peripheral vasoconstriction are all signs of low output failure

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54
Q

What is the most common cause of low output heart failure in the US?

A

CAD. Other causes include congenital heart disease, cor pulmonale, dilated cardiomyopathy, HTN, hypertrophic cardiomyopathy, infection, toxins, and valvular heart disease

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55
Q

Compare the mortality rate from CHF between the sexes

A

Women fare slightly better. The 5-year mortality rate for a female with CHF is 45%, as compared to 60% for males. The majority of deaths from CHF result from ventricular arrhythmias

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56
Q

Describe the 3 stages of CXR findings in CHF:

A

Stage I: Pulmonary arterial wedge pressure (PAWP) of 12-18mmHg. Blood flow increases in the upper lung fields (cephalization of pulmonary vessels); Stage II: PAWP of 18-25mmHg. Interstitial edema is evident with blurred edges of blood vessels and Kerly B lines; Stage III: PAWP >25mmHg. fluid exudes into alveoli with the generation of the classic butterfly pattern of perihilar infiltrates

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57
Q

Which do nitrates affect: preload or afterloaD?

A

Predominantly preload

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58
Q

Which does hydralazine affect: preload or afterload?

A

Afterload

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59
Q

True or False: Prazosin, captopril, and nifedipine affect afterload

A

TRUE

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60
Q

When is dobutamine used in CHF?

A

When heart failure is not associated with severe hypotension. Dobutamine is a potent inotrope with some vasodilation activity

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61
Q

When is dopamine selected in CHF?

A

When a patient is in shock. Dopamine is a vasoconstrictor and a positive inotrope

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62
Q

What is the most common cause of right ventricular heart failure?

A

Left ventricular heart failure

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63
Q

Hypotension is a symptom of left or right heart failure?

A

Left

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64
Q

Hepatomegaly is a symptom of left or right heart failure?

A

Right

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65
Q

Orthopnea is a symptom of left or right heart failure?

A

Left

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66
Q

Cough is a symptom of left or right heart failure?

A

Left

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67
Q

Dyspnea on exertion is a symptom of left or right heart failure?

A

Left

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68
Q

Abdominal distention is a symptom of left or right heart failure?

A

Right

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69
Q

Paroxysmal nocturnal dyspnea is a symptom of left or right heart failure?

A

Left

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70
Q

Hemoptysis is a symptom of left or right heart failure?

A

Left

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71
Q

S3 gallop is a symptom of left or right heart failure?

A

Left

72
Q

Early satiety is a symptom of left or right heart failure?

A

Right

73
Q

Jugular venous distention is a symptom of left or right heart failure?

A

Right

74
Q

Ascites is a symptom of left or right heart failure?

A

Right

75
Q

Rales are a symptom of left or right heart failure?

A

Left

76
Q

What is the rate of restenosis after percutaneous transluminal coronary angioplasty?

A

20-30% restenose within 6 months, 40% restenose within a year. Successful dilation occurs in 90% of the cases but because of the high rate of restenosis, this option is less attractive than CABG

77
Q

What is the restenosis rate of coronary vessels following a coronary artery bypass graFT (CABG)?

A

When using veinous grafts, there is a 50% restenosis rate within 5-10 years. When the internal mammary artery is used, there is only a 5% restenosis rate at 10 years. Occlusion of the grafts are caused by anastomy, trauma of the vessel, postoperative adhesions, or atherosclerosis

78
Q

How are acute MI, angina pectoralis, and Prinzmetal’s angina differentiated?

A

The pain is similar but typically differs in radiation, duration, provocation, and palliation. Obtaining an accurate history is the most important tool in the dx of chest pain. Angina pectoralis: aggravated by exercise, cold, and excitement, but is relieved by rest and nitro; Prinzmetal’s angina: occurs at rest, during normal activity, and generally at night or early morning-lasts longer than angina pectoralis; Acute MI: produces pain with a greater radius of radiation that may last for hours

79
Q

A pt presents to the hospital one month after placement of a mechanical prosthetic valve with fever, chills, and a leukocytosis. Endocarditis is suspected. Which bacterium is most commoN?

A

Staphylococcus aureus or Staphylococcus epidermidis

80
Q

Which arteries are most commonly involved in giant cell arteritis?

A

The carotid artery and its branches. Tx includes high doses of corticosteroids

81
Q

What HTN meds should be avoided in diabetics?

A

Diuretics and B-blockers. These drugs increase insulin resistance. ACE inhibitors are the drugs of choice for the tx of HTN in diabetics

82
Q

While taking your boards, why might you become severely annoyed if seated next to a person on ACE inhibitors?

A

ACE inhibitors produce a cough in 15% of patients

83
Q

What percentage of HTN is secondary?

A

Five percent. Seecondary HTN should be sespected in pts under age 35, pts with sudden-onset HTN, and those without a family history for HTN

84
Q

What is the most common cause of secondary HTN?

A

Renal perenchymal disease. In women, the most common cause is oral contraceptives. In pts over 50, secondary HTN can usually be attributed to renal artery stenosis. Other causes include pheochromocytoma, coarctation of the aorta, drugs (cocaine), hyperthyroidism, aldosteronism, and Cushing’s syndrome

85
Q

What % of pts with aortic dissection are hypertensive?

A

70-90%

86
Q

What % of hypertensive patients are afflicted with left ventricular hypertrophy?

A

50%. This is the reason that HTN is a major risk factor for MI, CHF, and sudden death

87
Q

What are the side effects of thiazide diuretics?

A

Hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia, hypomagnesemia, and hyponatremia

88
Q

Which drugs should be administered to lower the BP in a pt with thoracic aortic dissection?

A

Sodium nitroprusside. A B-blocker should also be used to reduce the dp/dt (Propagation speed)

89
Q

A pt has a history of episodic blood pressure elevations. She complains of headache, diarrhea, and skin pallor. Probably diagnosis?

A

Pheochromocytoma

90
Q

What is the most common complication of nitroprusside?

A

Hypotension. Thiocyanate toxicity accompanied by blurred vision, tinnitus, change in mental status, muscle weakness, and seizures is more prevalent in pts with renal railure or prolonged infusions. Cyanide toxicity is uncommon. However, this type of toxicity may occur with hepatic dysfunction, after prolonged infusions, and in rates greater than 10mg/kg/min.

91
Q

Define hypertensive emergency:

A

Elevated diastolic blood pressure >115mmHg with associated end organ dysfunction or damage

92
Q

How quickly should a pts BP be lowered in a hypertensive emergency?

A

Gradually over 2-3 hours to 140-160mmHg systolic and 90-110mmHg distolic. To prevent cerebral hypoperfusion, the BP should not be decreased by more than 25% of the mean arterial pressure.

93
Q

What drig can be used for almost all hypertensive emergencies?

A

Sodium nitroprusside. It assists in relaxing smooth muscle tissue through the production of cGMP. As a result, there is decreased preload and afterload, decreased oxygen demand, and a slightly increased heart rate with no change in myocardial blood flow, cardiac output, or renal blood flow. The duration of action is 1-2 minutes. Sometimes B-blockade is required to treat rebound tachycardia

94
Q

Define hypertensive urgency:

A

Dangerously elevated diastolic BP >115mmHg without signs of end organ damage. BP should gradually be reduced over 24-48 hours.

95
Q

Define uncomplicated hypertension:

A

Diastolic blood pressure <115mmHg without symptoms of end organ damage. Uncomplicated HTN does not require acute treatment.

96
Q

What lab findings confirm a hypertensive emergENCY?

A

UA: RBCs, red cell casts, proteinuria; BUN & CR: elevated; X-ray: aortic dissection, pulmonary edema, or coarctation of the aorta; ECG: LVH and cardiac ischemia

97
Q

What are the signs and symptoms of hypertensive encephalopathy?

A

N/V, headache, lethargy, coma, blindness, nerve palsies, hemiparesis, aphasia, retinal hemorrhage, cotton wool spots, exudates, sausage linking, and papilledema. Treat with lebatolol or sodium nitroprusside and lower the mean arterial pressure to approximately 120mmHg

98
Q

What is the most common source of acute mesenteric ischemia?

A

Arterial embolism (40-50%). The source is usually the heart, generally from a mural thrombus. The most common point of obstruction is the superior mesenteric artery

99
Q

What lab results strongly suggest that a pt has mesenteric ischemia?

A

Leukocytosis > 15,000, metabolic acidosis (sometimes with anion gap), hemoconcentration, and elevated phosphate and amylase

100
Q

Which type of myocardial infarction is more often associated with thrombosis: transmural or subendocardial?

A

Transmural. Thrombolytic therapy increases left ventricle ejection fraction post MI, reduces the development of post infarction CHF, and can reduce early MI mortality by 25%

101
Q

How much aspirin should a post MI pt ingest daily to reduce the incidence of reinfarction?

A

160 to 325 mg/day

102
Q

What is the most common cause of death during the first few hours of a MI?

A

Cardiac dysrhythmias, generally ventricular fibrillation

103
Q

When treating early MIs, B-blockers decrease the risk of reinfarction. Which pts should not receive B-blockers?

A

Pts with hypotension, diabetes, CHF, severe left ventricular dysfunction, AV block, bradycardia, asthma, or another bronchospastic disease

104
Q

How common are PVCs in post MI pts?

A

90% will have PVCs within the first few weeks. Concern arises if the PVCs are complex, which is the case in 20-40% of MI pts. Risk of sudden death in post MI pts with complex PVCs increases 2-5 times

105
Q

What percentage of the LV myocardium must be damaged to induce cardiogenic shock?

A

40%. 25% or more results in heart failure

106
Q

What % of MIs are clinically unrecognized?

A

5-10%

107
Q

A non-Q wave infarction is usually associated with what?

A

Subsequent angina or recurrent infarction. Non-Q wave infarctions also have lower in-hospital mortality rate compared to Q wave MIs

108
Q

Why do T waves invert in an AMI?

A

Infarction or ischemia causes a reversal of the sequence of repolarization, i.e., endocardial-to-epicardial as opposed to normal epicardial-to-endocardial

109
Q

What ECG changes arise is a true posterior infarction?

A

Large R wave and ST depression in V1 and V2

110
Q

What conduction defects commonly occur in an anterior wall MI?

A

The dangerous kind. Damage to the conducting system results in a Mobitz II or third degree AV block

111
Q

How should PSVT be treated during an AMI?

A

Vagal maneuvers, adenosine, or cardioversion. Stable pts may be able to tolerate negative inotropes, such as verapamil or even B-blockers

112
Q

A pt presents one day after discharge for an AMI with a new, harsh systolic murmur along the left sternal border and pulmonary edema. What is the diagnosis?

A

Ventricular septal rupture. Dx is confirmed with Swan-Ganz catheterization or echo. The tx regime includes nitroprusside, for afterload reduction, and possibly an intra-aortic balloon pump followed by surgical repair

113
Q

When does cardiac rupture usually occur in pts who have suffered acute MIs?

A

50% arise within the first 5 days, and 90% occur within the first 14 days post MI

114
Q

Which type of infarct commonly leads to papillary muscle dysfunction?

A

Inferior wall MI. Signs and symptoms include a mild transient systolic murmur and pulmonary edema

115
Q

A pt presents 2 weeks post AMI with chest pain, fever, and pleuropericarditis. A pleural effusion is detected on CXR. What is the diagnosis?

A

Dressler’s (post myocardial infarction) syndrome. This syndrome is caused by an immunologic reaction to myocardial antigens.

116
Q

What percentage of pts over age 80 experience chest pain with an AMI?

A

Only 50%. 20% experience diaphoresis, stroke, syncope, and/or acute confusion

117
Q

What are the most common causes of myocarditis in the US?

A

Viruses. Other causes include post viral myocarditis, an autoimmune response to recent viral infection, bacteria (diphtheria and TB), fungi, protozoa (Chagas’ disease), and spirochetes (Lyme disease).

118
Q

What percentage of non-anticoagulated pts with mitral stenosis experience systemic emboli?

A

25%. Pts with chronic atrial fibrillation or mitral stenosis should be chronically anticoagulated to prevent atrial mural thrombi

119
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease. The most common initial symptom is dyspnea

120
Q

What physical findings may be associated with mitral stenosis?

A

Prominent a-wave, early-systolic left parasternal lift, loud and snapping first heart sound, and early-diastolic opening snap with a low-pitched mid-diastolic rumble that crescendos into S1

121
Q

A mid-systolic click with a late systolic crescendo murmur is indicative of what cardiac disease?

A

Mitral valve prolapse

122
Q

Is mitral valve prolapse more common among men or women?

A

Women have a stronger genetic link to the disease. However, only 2-5% of the entire population has symptomatic MVP

123
Q

What age group typically develops MVP syndrome?

A

Pts in their 20s and 30s. Most pts with MVP are asymptomatic. MVP syndrome is symptomatic with chest pain, fatigue, palpitations, postural syncope, and dizziness

124
Q

What is the hallmark sign of mitral valve prolapse?

A

A midsystolic click, sometimes accompanied by a late systolic murmur. MVP is largely a clinical diagnosis. An ECG is performed to assess the degree of prolapse. Other clinical findings include a laterally-displaced, diffuse apical pulse; decreased S1; split S2; and a holosystolic murmur radiating to the axilla

125
Q

How do fixed-rate and demand modes of pacemakers differ?

A

Fixed-rate mode produces an impulse at a continuous specific rate, regardless of the patient’s own cardiac activity. Demand mode detects the patient’s electrical activity and triggers only if the heart is not depolarizing

126
Q

What is the tx for ventricular fibrillation in a pt with a pacemaker?

A

Defibrillation, but be sure to keep the paddles away from the pacer

127
Q

What is the average life span of a pacemaker?

A

4-6 years

128
Q

A 25-year old pt presents with splinted breathing and sharp, precordial chest pain that radiates to the back. The pain increases with inspiration and is mildly relieved by placing the pt forward in a sitting position. What might the ECG show?

A

The ECG may reveal intermittent supraventricular tachycardias, ST-segment depression in aVR and VI, ST-segment elevation in all other leads, PR depression, and T-wave inversion may arise. The pt probably has pericarditis

129
Q

What is the most common cause of pericarditis?

A

Idiopathic. Other causes are MI, post viral syndrome, aortic dissection that has ruptured into the pericardium, malignancy, radiation, chest trauma, connective tissue disease, uremia, and drugs, i.e., procainamide or hydralazine

130
Q

What physical finding indicates acute pericarditis?

A

Pericardial friction rub. The rub is best heard at the left sternal border or apex with the pt in a forward sitting position. Other findings include fever and tachycardia

131
Q

What will be the appearance of a pericardial effusion on an x-ray?

A

A water bottle silhouette

132
Q

What is the tx for pericarditis without effusion?

A

A 2 week tx of 650mg aspirin every 4 hours, if no contraindications exist. Ibuprofen, indomethacin, or colchicine are other alternatives. The use of corticosteroids is contraversial, because recurrent pericarditis is common when doses are tapered

133
Q

Rheumatic heart disease is the most common cause of stenosis of what 3 heart valves?

A

Mitral, aortic (along with congenital bicuspid valve), and tricuspid

134
Q

What is the 1-year recurrence rate for patients who have been resuscitated from sudden cardiac death?

A

30%

135
Q

Describe the Trendelenburg test for varicose veins.

A

Raise the leg above the heart and then quickly lower it. If the leg veins become distended immediately after this test is performed, valvular incompetency is evident

136
Q

Splinter hemorrhages, Osler’s nodes, Janeway lesions, petechiae, and Roth’s spots can be indications of what process?

A

They are physical signs associated with infective endocarditis

137
Q

True or False: Osler’s nodes are usually nodular and painful

A

True. In contrast, the macular Janeway lesions are painless

138
Q

What % of pts with infective endocarditis display peripheral manifestations of the disease?

A

50%

139
Q

What is bacterial endocardiTIS?

A

Blood-borne bacteria that attach onto damaged or abnormal heart valves or on the endocardium near anatomic defects

140
Q

How is bacterial endocarditis diagnosed?

A

By evidence of valvular vegitations on echo combined with a positive blood culture

141
Q

Who is at high risk for developing endocarditis?

A

People with prosthetic heart valves, previous incidents of endocarditis, complex congenital heart disease, IV drug use, and surgically devised systemic pulmonary shunts

142
Q

What are the risk-factors for endocarditis?

A

IV drug use, prosthetic valves, acquired valvular heart disease, hypertrophic cardiomyopathy, hemodialysis, peritoneal dialysis, indwelling venous catheters, post cardiac surgery, rheumatic heart disease, and incorrected congenital conditions.

143
Q

What are the most common organisms associated with endocarditis?

A

Streptococcus viridans, S. aureus, Enterococcus, and fungal organisms. S. aureus is responsible for 75% of left-sided (aortic and mitral involvement)

144
Q

What is more common in the general population: left-sided or right-sided endocarditis?

A

Left-sided (aortic and mitral involvement)

145
Q

What is more common in drug abusers: left-sided or right-sided disease?

A

Right-sided (60%)

146
Q

How is infective endocarditis treated?

A

IV antibiotics for 4-6 weeks. Close f/u is necessary and the pt should have a series of 2 separate negative blood cultures to demonstrate resolution. If resolution of the infection does not occur promptly, embolization occurs, or fulminant CHF ensues, then surgical valve replacement is indicated

147
Q

What are THE ECG changes associated with pericarditis?

A

Concave upward ST elevation in at least 7 leads except V1 and aVR. PR segment depression may also be present

148
Q

What is the most frequently reported bacterial isolate in pts with myocardial abscesses?

A

Staphylococcus aureus

149
Q

What is the clinical picture of myocardial abscesses?

A

Low-grade fevers, chills, leukocytosis, conduction system abnormalities, nonspecific ECG changes and signs and symptoms of acute MI

150
Q

What is mural endocarditis?

A

Inflammation and disruption of the nonvalvular endocardial surface of the cardiac chambers

151
Q

What is the presentation of mural endocarditis?

A

The presentation is similar to infective valvular endocarditis

152
Q

What are the risk factors for mural endocarditis?

A

Usually, mural endocarditis is from seeding of an abnormal area of endocardium during bacteremia or fungemia. Infectious thrombi from pulmonary veins, ventricular aneurysms, mural thrombi, chordal friction lesions, pacemaker lead insertion sites, idiopathic hypertropic subaortic stenosis, jet lesions from ventriculoseptal defects, and other congential defects are other factors. Immunocompromised pts are also at increased risk

153
Q

What is the clinical presentation of prosthetic vascular graft infection?

A

Erythema, skin breakdown, or purulent drainage. Other symptoms may be thrombosis of the graft, fluid around the graft, or pseudoaneurysm formation

154
Q

What are complications for arterial catheterization?

A

Thrombosis (19-38%), infection (4-23%), pseudoaneurysm, and rupture

155
Q

What is the most frequent cause of mitral stenosis?

A

Rheumatic fever.

156
Q

What % of pts with rheumatic mitral stenosis are female?

A

66% or two-thirds

157
Q

What % of patients with rheumatic heart disease have pure mitral stenosis?

A

25%. An additional 40% have combined mitral stenosis and mitral regurgitation

158
Q

What are the principle symptoms in mitral stenosis?

A

Dyspnea is most common. Pts with severe mitral stenosis can experience orthopnea, hemoptysis, chest pain, and frank pulmonary edema, often precipitated by exertion, fever, URI, sexual intercourse, pregnancy or onset of rapid atrial fibrillation

159
Q

What are the 2 most serious complications of mitral stenosis?

A

Thromboembolism, most often occurring in the setting of atrial fibrillation, and pulmonary edema

160
Q

What maneuvers can one do to differentialte the opening snap of mitral stenosis from a split S2 sound?

A

Sudden standing widens the A2-opening snap interval whereas a split S2 narrows on standing. Progressive narrowing of the A2-OS interval on serial examinations suggests an increase in the severity of mitral stenosis

161
Q

What is the most accurate noninvasive technique for quantifying the severity of mitral stenosis?

A

Doppler echocardiography

162
Q

What is the medical management strategy of rheumatic mitral stenosis?

A

1.) PCN prophylaxis for B-hemolytic streptococcal infections and prophylaxis for infective endocarditis; 2.) Aggressive and prompt tx of anemia and infections; 3.) Avoidance of strenuous exertion; 4.) Oral diuretics and Na restriction if symptomatic; 5.) B-blockers to reduce HR; 6.) Cardioversion of atrial fibrillation, if possible; 7.) Aggressive slowing of refractory atrial fibrillation; and 8.) Anticoagulant therapy in pts who have experienced 1 or more thromboembolic episodes, or who have mechanical prosthetic valves

163
Q

What is the indication for mitral valve surgery or balloon valvuloplasty in pts with mitral stenosis?

A

Moderate symptoms (Class II) or greater in a pt with moderate to severe mitral stenosis (mitral valve orifice size less than 1.0cm2 per square meter BSA-less than 1.5 to 1.7cm2 mitral valve area in normal-sized adults)

164
Q

What are the most common causes of acute mitral regurgitation?

A

Acute myocardial infarction with papillary muscle dysfunction (1%% of acute MI results in acute mitral regurg) or papillary muscle rupture (0.3% of acute MI), infective endocarditis, chordae tendinae rupture secondary to chest trauma, rheumatic fever, mitral valve prolapse, and hypertrophic cardiomyopathy with rupture of chordae tendinae

165
Q

What are the physical findings of patients with chronic mitral regurgitation?

A

Harsh, pansystolic murmur heard best at the apex, radiating to the axilla or the base. The murmur is diminished by maneuvers that decrease preload or afterload, such as amyl nitrate inhalation, Valsalva, or standing and increases with maneuvers that increase preload or afterload, such as squatting, handgrip, or phenylephrine administration

166
Q

Which is the best test to assess the detailed anatomy of rheumatic mitral valve disease and determine whether mitral valve replacement is necessary or whether reconstruction is feasible?

A

Transesophageal echocardiography

167
Q

What is the appropriate medicalmanagement of mitral regurgitation?

A

Vasodilator therapy with ACE inhibitors is the hallmark of therapy, even in pts who are asymptomatic. Diuretics are used in pts with severe MR. Cardiac glycosides, such as digoxin, are indicated in pts with severe MR and clinical evidence of heart failure. Endocarditis prophylaxis is indicated in all pts with MR. Anticoagulation should be given to all pts in atrial fibrillation

168
Q

What is the classic triad of symptoms of aortic stenosis?

A

Syncope (often exertional), angina, and heart failure

169
Q

What is the most common cause of aortic stenosis in pts: 1.) Over age 65; 2.) Under age 65?

A

1.) Over age 65: Calcific degeneration of the aortic leaflets; 2.) Under age 65: Calcification of congenitally bicuspid aortic valves (50%) followed by rheumatic heart disease (25%)

170
Q

Once pts with aortic stenosis become symptomatic, what is their average survival without valve replacement?

A

From the onset of syncope or angina, the mean survival is 2-3 years. From the onset of CHF, the mean survival is 1.5 years.

171
Q

How does a heart murmur reflect the severity of aortic stenosis?

A

The longer the duration of the murmur and the greater the increase in intensity of the murmur, the more severe the aortic stenosis. The degree of loudness of the murmur is not as important in assessing severity.

172
Q

What is the best pharmacologic therapy for patients with asymptomatic aortic stenosis?

A

Without contraindications, B-blockers are the best agents as they are the most useful in treating the left ventricular hypertrophy and its sequelae that develop as a result of aortic stenosis

173
Q

A 68-year old female with severe asymptomatic aortic stenosis suddenly complains of dyspnea and palpitations. On ECG, she is found to be in atrial fibrillation with a ventricular rate of 130 bpm. What is the most appropriate action to be taken?

A

Immediate DC cardioversion, followed by a search for previously unrecognized mitral valve disease. Once stabilized, the pt should be referred for cardiac catheterization and aortic valve replacement

174
Q

What is mitral valve prolapse syndrome?

A

A symptom complex consisting of palpitations, chest pain, easy fatigability, exercise intolerance, dyspnea, orthostatic phenomena, and syncope or pre-syncope in pts with mitral valve prolapse, predominantly related to autonomic dysfunction

175
Q

What disorders are seen with increased frequency in pts with mitral valve prolapse syndromE?

A

Graves’ disease, asthma, migraine headaches, sleep disorders, fibromyosis, and functional gastrointestinal syndromes

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