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Cardiology Flashcards

1
Q

What is the clinical management of coronary artery disease? (clinic setting) What is the primary benefit of each element?

A
  • Aspirin, metoprolol, statins for mortality benefit
  • Nitrates for angina pain (no mortality benefit)
  • ACE-I’s/ARB’s in further management for stable cases if pt has CHF, systolic dysfunction, or low EF
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2
Q

What is a common side effect/adverse effect shared by both ACEs and ARBs?

A

Hyperkalemia

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3
Q

What is the role of angiography in the diagnosis and management of CAD?

A

To determine who is a candidate for CABG. Angiography is NOT needed for Dx. You can initiate the following tx’s w/o angiography.

  • aspirin + metoprolol + statins (mortality benefit)
  • nitrates (angina pain)
  • ACE/ARB (for low EF)
  • clopidogrel, prasugrel, or ticagrelor (acute MI or cannot tolerate ASA)
  • ranolazine (if pain persists)
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4
Q

What are the indications for CABG?

A
  • 3 coronary vessels w/ >70% stenosis
  • L main coronary artery stenosis >50-70%
  • two vessels occluded in diabetic pt
  • two or three vessels occluded w/ low EF
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5
Q

Systolic dysfunction is AKA

A

HFrEF

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6
Q

What’s the main difference between saphenous vein graft and internal mammary artery graft?

A

Internal mammary artery graft remains open for 10yrs; vein grafts begin to occlude after 5yrs
- no difference in needs for medications

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7
Q

What is ranolazine and when do you add it to a pt’s CAD meds?

A

Anti-angina med; add if pain is not controlled with nitro

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8
Q

Patients with which conditions MUST be on a statin?

A

atherosclerotic dz –> CAD, PAD, stroke, aortic disease
Diabetics w/ LDL >100

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9
Q

At what 10-year cardiovascular risk should a statin be initiated?

A

> 7.5%

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10
Q

What class of lipid-lowering drug shows dramatic reduction in LDL but unclear mortality benefit?

A

Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors

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11
Q

What is the goal (lab value) of lipid management tx in patients w/ CAD?

A

LDL <70; all pts w/ ACS should be on a statin

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12
Q

All patients with ACS should be on…

A

A statin

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13
Q

If a statin alone doesn’t lower LDL to <70 for pts w/ CAD (or equivalent atherosclerotic dz) and/or diabetes, what medication do you add?

A

Ezetimibe

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14
Q

What are risk factors in lipid management?

A
  • tobacco use
  • HTN
  • low HDL <40
  • FmHx of early heart disease (female relatives <65, male relatives <55)
  • Age (males >45, females >55)
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15
Q

What is the most common side effect of statins?

A

Liver toxicity; 2% of pts will stop statins due to transaminase elevation
- routinely check LFTs and lower dose/change statin if intolerance occurs

  • rhabdomyolysis is less common; routine monitoring of CPK is not indicated
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16
Q

What is the most important reason for using statins over other meds that lower LDL, triglycerides, total cholesterol and increase HDL?

A

Statins have the greatest mortality benefit when compared to cholestyramine, gemfibrozil, ezetimibe, and niacin

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17
Q

When/why might icosapent be added to statins?

A

When triglycerides are elevated

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18
Q

When is it appropriate to consider PCSK9 inhibitors for a patient?

A

When you’ve added ezetimibe to their statin and LDL is still extremely high

statin –> ezetimibe –> PCSK9 inhibitor

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19
Q

How do PCSK9 inhibitors work? In what heritable disease might they be chosen?

A

Injectable drug that blocks clearance of LDL the blood by the liver
- may bring down extremely high LDL in familial hypercholesterolemia
- evolocumab and alirocumab massively increase helpatic clearance of LDL but do not clearly lower mortality

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20
Q

When can a patient resume sexual activity following MI?

A

Within several days if there is no continued chest pain/dyspnea (should coincide w/ discharge); the bigger the MI, the longer the delay in sexual activity should be

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21
Q

What is the most common cause of erectile dysfunction after MI?

A

Anxiety; B-blockers may be most common med associated w/ ED, but anxiety is a more common cause.

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22
Q

What medication must be discontinued in a post-MI patient before initiating treatment for erectile dysfunction w/ sildenafil?

A

Nitrates

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23
Q

Can you distinguish HFrEF (systolic dysfunction) from HFpEF (diastolic dysfunction) based on symptoms alone?

A

No; clues may be HTN, valvular heart dz, and MI, but an echo is required to make the final diagnosis.

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24
Q

How does CHF typically present?

A

SOB (especially exertional dyspnea) in a person w/ any of the following
- edema
- rales
- ascites
- JVD
- S3 gallop
- orthopnea
- paroxysmal nocturnal dyspnea
- fatigue

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25
Q

What is the underlying mechanism which causes rales?

A

Increased hydrostatic pressure develops in the pulmonary capillaries from L heart pressure overload. This causes transudation of liquid into the alveoli. During inhalation, alveoli open with a popping sound referred to as rales.

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26
Q

What is the worst manifestation of CHF?

A

Pulmonary edema, a clinical diagnosis; it is more important to remove volume from the vascular system than it is to perform any diagnostic testing

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27
Q

What is most important in diagnosing pulmonary edema?

A

SOB, rales, S3, and orthopnea are more important in making a dx than any single diagnostic test.

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28
Q

How does carvedilol work?

A

Beta-1 and Beta-2 antagonist + alpha-1 antagonist –> anti-arrhythmic, anti-ischemic, and antihypertensive

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29
Q

What initial tests should be ordered in the case of suspected CHF? What can they show you?

A

CXR –> pulmonary vascular congestion, cephalization of flow, effusion, cardiomegaly
EKG –> sinus tachy, atrial and ventricular arrhythmia
Oximetry (possibly blood gas) –> hypoxia, respiratory alkalosis
Echo –> distinguish HFrEF vs HFpEF

(order these tests simultaneously w/ initial treatments –> O2, furosemide, nitrates, morphine)

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30
Q

What is the mechanism of cephalization of flow seen in pulmonary edema?

A

The lung bases are generally more full of blood because of gravity. As fluid builds up, it fills vessels from the bases up, which moves the fluid toward the head.

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31
Q

What is the mechanism of dobutamine, inamrinone, and milrinone?

A

Inamrinone and milrinone are phosphodiesterase inhibitors –> increase contractility, decrease afterload through vasodilation –> similar effect to dobutamine

Dopamine increases contractility, increases afterload through vasoconstriction

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32
Q

Dobutamine is less effective for patients on what cardiology med?

A

Beta-blocker

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33
Q

What is the mechanism of respiratory alkalosis in CHF?

A

Fluid overload causes hypoxia –> causes hyperventilation –> decreases pCO2 –> causes alkalosis

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34
Q

What is the treatment of acute CHF?

A
  • preload reduction to control acute symptoms
  • if no response, positive inotrope

*digoxin is never used for acute treatment but can be used to slow the rate of A-fib

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35
Q

What are three positive inotropes used IV in the ICU?

A

Dobutamine, inamrinone, milrinone

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36
Q

What is the best treatment for a patient with V-tach and pulmonary edema?

A

Synchronized cardioversion
- also for pulmonary edema + new a-fib, a-flutter, SVT

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37
Q

When is unsynchronized cardioversion used?

A

V-fib or V-tach without a pulse

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38
Q

When do you use nesiritide in the treatment of pulmonary edema?

A

As part of preload reduction only if dobutamine, inamrinone, and milrinone fail

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39
Q

What is nesiritide and what does it do for a patient with pulmonary edema?

A

Synthetic atrial natriuretic peptide; decreases symptoms of SOB

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40
Q

When do you obtain a brain natriuretic peptide (BNP) level in the management of pulmonary edema?

A

To establish diagnosis of CHF in a patient w/ SOB; may help distinguish between PE, PNA, asthma, and CHF
- BNP elevates in CHF but is nonspecific; normal BNP makes CHF diagnosis unlikely

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41
Q

What are the readings of a right heart cath in pulmonary edema?

A
  • decreased cardiac output
  • increased systemic vascular resistance
  • increased wedge pressure
  • increased right atrial pressure

(dec. CO due to pump failure –> backup of blood into L atrium –> inc. wedge pressure)
Inc. R atrial pressure = JVD
sympathetic outflow increases to attempt to maintain intravascular filling pressure

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42
Q

Wedge pressure (on R heart cath) is the same as what intracardiac pressure?

A

Left atrial pressure
(left ventricle failure = increased left atrial pressure = increased wedge pressure)

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43
Q

Long-term management of HFrEF is centered around which medications?

A

ACEs (or ARBs), beta-blockers, mineralocorticoid receptor antagonists (spironolactone or eplerenone)

*an ARB (ex: valsartan) combined w/ angiotensin neprilysin inhibitor (ARNI) like sacubitril is effectively equal to an ACE in HFrEF

These meds are indicated for CHF pts w/ systolic dysfunction at ANY stage of disease

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44
Q

Which beta-blockers are proven to lower mortality in CHF?

A

Metoprolol, carvedilol, bisoprolol

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45
Q

What are some common side effects of spironolactone which may cause male CHF patients to switch? What’s the alternative med?

A

Antiandrogenic! May cause gynecomastia and erectile dysfunction. Eplerenone has no antiandrogenic effects but also lowers mortality in CHF.

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46
Q

What is the most common side effect of MRAs like spironolactone or eplerenone? What medication can you give to curb this effect if you need to continue the MRA?

A

Hyperkalemia; patiromer (oral Ca/K exchange drug) or zirconium will lower the potassium and allow you to continue needed meds

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47
Q

How does hydralazine help treat CHF?

A

Reduces afterload in combination w/ nitrates; can be added to
- enhance mortality benefit (only some patients)
- substitute for ACE/ARB/ARNI
- decrease symptoms in patients already on ACE, ARB, beta-blockers, ARNI, digoxin, and diuretics whose symptoms are not controlled

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48
Q

What is the benefit of SGLT2 inhibitors in HFrEF?

A

Lower mortality; decrease progression of renal insufficiency

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49
Q

What is the role/utility of digoxin in HFrEF?

A
  • Decreases symptoms and frequency of hospitalizations
  • Does NOT lower mortality
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50
Q

Do diuretics lower mortality in CHF?

A

Nope, sorry

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51
Q

What medication is primarily used to manage HFpEF?

A

MRA (spironolactone or eplerenone); ACEs have unclear benefit and digoxin is of no benefit

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52
Q

What CHF med causes transient excess brightness of vision?

A

Ibavradine

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53
Q

What is the next step in managing a patient with CHF who is still dyspneic after using ACEs, beta-blockers, diuretics, digoxin, and mineralocorticoid inhibitors?

A
  • Sacubatril/valsartan: use in place of ACE
  • Canagliflozin, dapagliflozin, empagliflozin
  • Ivabradine: SA nodal inhibitor that slows heart rate; add to HFrEF if pulse >70 or beta-blockers can’t be used
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54
Q

What agents offer mortality benefit for CHF?

A

ACE/ARB, beta-blocker, ARNI, SGLT2, MRA

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55
Q

What is the most common cause of death in CHF?

A

Arrhythmia

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56
Q

What is the EF threshold for ICD placement in CHF patients?

A

<35%

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57
Q

When is biventricular pacemaker the answer for CHF?

A

When EF <35% and QRS>120

(the wider the QRS, the better!!)*

*when QRS >150, there is a greater decrease in mortality and symptom reduction

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58
Q

When do patients with CHF need warfarin?

A

Only with A-fib in the presence of a metal valve or mitral stenosis

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59
Q

Symptomatic bradycardia is an absolute contraindication to what class of mortality-lowering CHF med?

A

beta-blockers

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60
Q

What valvular dz is more common in young females and the general population?

A

Mitral valve prolapse

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61
Q

What valvular dz is more common in healthy young athletes?

A

HOCM (hypertrophic obstructive cardiomyopathy)

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62
Q

What valvular dz is more common in pregnant patients and immigrants?

A

Mitral stenosis

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63
Q

What valvular dz is more common in patients w/ Turner syndrome or coarctation of the aorta?

A

Bicuspid aortic valve

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64
Q

What valvular dz is more common in patients with palpitations and atypical chest pain not associated w/ exertion?

A

Mitral valve prolapse

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65
Q

Which murmurs are systolic?

A

Aortic stenosis, mitral regurgitation, mitral valve prolapse, and hypertrophic obstructive cardiomyopathy

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66
Q

Which murmurs are diastolic?

A

Aortic regurgitation, mitral stenosis

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67
Q

What is the most common cause of death in the US?

A

Coronary artery disease

*CAD kills more women than breast cancer

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68
Q

What are the risk factors for CAD?

A
  • DM (most dangerous risk factor)
  • HTN
  • tobacco use
  • HLD
  • PAD
  • obesity
  • inactivity
  • FmHx (females <65, males <55)
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69
Q

What is the most common cause for non-cardiac chest pain?

A

GERD

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70
Q

What signs/symptoms are clues to ischemic dz as the cause of chest pain?

A
  • chest pain that doesn’t change w/ body position or respiration
  • dull quality
  • 15-30 minutes in duration
  • occurs on exertion
  • substernal w/ radiation to jaw or L arm
  • not associated w/ chest wall tenderness
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71
Q

What symptoms indicate a patient with chest pain has something that is NOT CAD? What DDxs are suggested by each of these symptoms?

A
  • pleuritic pain (PE, pna, pleuritis, pericarditis, pneumothorax)
  • positional pain (pericarditis)
  • tenderness (costochondritis)
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72
Q

Which valve problem causes holosystolic blowing murmur?

A

Mitral regurgitation

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73
Q

What is an S3 gallop? What causes it?

A

Rapid ventricular filing during diastole causes a splash sound known as S3

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74
Q

What is an S4 gallop? What causes it?

A

Atrial systole in a stiff or noncompliant left ventricle; “bang”
- heard just before S1 in left ventricle hypertrophy

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75
Q

What is the most accurate test for ischemic chest pain patients? Is it also the best initial test?

A

Most accurate –> CKMB
Best initial –> EKG (always always always)

*if a question makes you choose between initial therapies and EKG, choose treatment first

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76
Q

What is the best test to detect a reinfarction a few days after initial MI?

A

CK-MB

Both CKMB and troponin rise 3-6 hours after onset of chest pain and have nearly the same specificity, but CKMB stays high for only 1-2 days while troponin stays high for 1-2 weeks

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77
Q

Which cardiac enzyme rises first in ischemia?

A

Myoglobin; rises as early as 1-4 hours after onset of chest pain

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78
Q

When do you get a stress test on a patient w/ suspected cardiac ischemia?

A
  • case is NOT acute
  • initial EKG/enzyme test do not yield clear diagnosis
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79
Q

When is exercise thallium test or stress echo the answer in a suspected CAD case?

A

When EKG is unreadable for ischemia, LBBB is present, digoxin is in use, pacemaker is in place, L ventricular hypertrophy is present or there is baseline abnormality of ST segment

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80
Q

When is dipyridimole or adenosine thallium stress test or dobutamine echo the answer in a suspected CAD case?

A

When patients cannot exercise to target heartrate (>85% of max)
- COPD
- amputation
- deconditioning
- weakness/prior stroke
- lower extremity ulcer/injury
- dementia
- prohibitive obesity

81
Q

What is the next test that should be ordered after an abnormal cardiac stress test?

A

Angiography (do NOT order angiography if stress test is normal)

82
Q

Which is more dangerous if found on a cardiac stress test, reversible or irreversible ischemia?

A

Reversible ischemia; fixed defects (equivalent when at rest or under stress) are scars from previous infarction and do not need angiography

83
Q

What’s the best initial test to evaluate valve function or ventricular wall motion?

A

Echo

84
Q

What’s the most accurate method of evaluating ejection fraction?

A

MUGA scan

85
Q

What is the best initial treatment for ACS?

A

Aspirin (PO, chewed, or sublingual) due to its immediate effect inhibiting platelets
- reduces mortality by 25% in acute MI
- reduces mortality by 50% for unstable angina

86
Q

What five medications make up the treatment for ACS?

A
  • Aspirin
  • Beta-Blockers
  • ACE/ARB
  • Statin
  • Nitrates (pain reduction only; no mortality benefit)
  • O2 if patient is hypoxic

*Dual antiplatelet therapy (DAPT) in acute MI; aspirin combined w/ clopidogrel/ticagrelor/prasugrel

87
Q

What are the components of DAPT (dual anti-platelet therapy) and which category of ACS warrants it?

A

ASA + clopidogrel, ticagrelor, or pasugrel

In acute MI only

88
Q

What’s the time window for angioplasty (PCI) for a STEMI?

A

Within 90 minutes of arrival to ED (“door to balloon in 90 minutes”)

89
Q

What do you do for a STEMI if angioplasty cannot be performed w/in 90 minutes of arrival to the ED?

A

Give thrombolytics, so long as it hasn’t been >30 minutes since arrival

90
Q

In which cases is thrombolytic therapy indicated for ACS patients?

A
  • unable to do angioplasty within 90 minutes, but able to administer thrombolytics within 30 minutes for STEMI
  • chest pain lasting <12 hours with ST elevation in 2 leads
  • new LBBB
91
Q

Do beta blockers affect mortality in ACS? Within what time window should they be administered?

A

Yes, but timing is not important like w/ ASA, PCI, or thrombolytics

92
Q

What medications should be given to all patients w/ ACS but will only reduce mortality if systolic/LV dysfunction is present?

A

ACE/ARB

93
Q

What single treatment has the greatest efficacy in lowering mortality in STEMI?

A

Urgent angioplasty (PCI)

94
Q

What is the most common cause of death in both CHF and MI? How do beta-blockers counteract this?

A

Ventricular arrhythmia caused by ischemia

B-blockers are both anti-ischemic and anti-arrhythmic. Slower heart rate –> more time for coronary artery perfusion; increased LV filling time –> increased stroke volume and cardiac output

95
Q

Which medications always lower mortality in ACS?

A

ASA, clopidogrel/prasugrel/ticagrelor, thrombolytics, metoprolol, statins

96
Q

When should verapamil or diltiazem be used in the treatment of ACS?

A

If a pt is intolerant of beta-blockers (severe asthma, prinzmetal angina)

97
Q

What are the diagnostic tests and treatments for valve rupture after MI?

A

Tests: echo
Tx: ACE, nitroprusside, intra-aortic balloon pump as bridge to surgery

98
Q

When is pacemaker the answer for acute MI?

A
  • 3rd degree heart block
  • Mobitz II, 2nd degree heart block
  • bifascicular block
  • new LBBB
  • symptomatic bradycardia
99
Q

What are the diagnostic tests and treatments for cardiogenic shock after MI?

A

Tests: echo, R heart cath
Tx: ACE, urgent revascularization

100
Q

What are the diagnostic tests and treatments for septal rupture after MI?

A

Tests: echo, R heart cath w/ increase in saturation from RA to RV
Tx: ACE, nitroprusside, surgery

101
Q

What are the diagnostic tests and treatments for myocardial wall rupture after MI?

A

Tests: echo
Tx: pericardiocentesis, surgery

102
Q

What are the diagnostic tests and treatments for sinus bradycardia after MI?

A

Test: EKG
Tx: atropine –> pacemaker if still symptomatic

103
Q

What are the tests/treatments for 3rd degree (complete) heart block after MI?

A

EKG; atropine and pacemaker

104
Q

What are the tests/treatments for right ventricular infarction after MI?

A

EKG; fluid loading

105
Q

What medications should all patients post-MI go home on?

A
  • DAPT
  • beta-blocker
  • statin
  • ACE/ARB
106
Q

How does management of NSTEMI differ from that of STEMI?

A
  • no thrombolytics
  • heparin is used routinely (LMW&raquo_space;> unfractionated)
  • glycoprotein IIb/IIIa inhibitors lower mortality (esp if undergoing PCI)
107
Q

Which are the only murmurs that decrease with leg raising and squatting?

A

Mitral valve prolapse + HOCM

108
Q

Which murmurs become louder with leg raising and squatting?

A

Aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation, ventricular septal defect and all right-sided lesions

109
Q

How does squatting/raising the legs impact venous return to the heart?

A

Increases venous return (squatting squeezes the leg veins, pushing blood toward the heart; leg raising uses gravity to increase flow from legs toward chest)

110
Q

How does valsalva/studden standing affect venous return to the heart?

A

Decreases venous return (Valsalva increases intrathoracic pressure)

111
Q

Which heart murmurs increase with valsalva/moving from sitting to standing?

A

HOCM + mitral valve prolapse

112
Q

How does handgrip maneuver affect the heart/blood flow?

A

Increases afterload by compressing arteries of the arm

  • works in the opposite way of an ACE (which decreases afterload) so it worsens murmurs which would improve with an ACE
113
Q

Which murmurs are worsened by handgrip maneuver?

A

Aortic regurgitation, mitral regurgitation, ventricular septal defect

  • essentially pushes blood backward in AR/MR or from LV to RV in the case of VSD
114
Q

Which murmurs improve w/ handgrip maneuver?

A

Mitral valve prolapse and HOCM, aortic stenosis

115
Q

How does an ACE treat aortic regurgitation/mitral regurgitation?

A

Afterload reduction increases forward flow of blood into the aorta

116
Q

Why is the murmur heart in HOCM improved by handgrip maneuver?

A

Left ventricle will not empty completely –> LV remains larger in volume –> larger LV relieves the obstruction

117
Q

How does amyl nitrate affect afterload?

A

Increases afterload through vasodilation

118
Q

Which murmur is not affected by handgrip or amyl nitrate?

A

Mitral stenosis

119
Q

Which murmurs increase with handgrip (increased afterload)?

A

Aortic regurg, mitral regurg, ventral septal defect

120
Q

Which murmurs increase with amyl nitrate (reduced afterload)?

A

Aortic stenosis, HOCM, mitral valve prolapse

121
Q

Which heart murmurs can be treated with an ACE?

A

Mitral regurg and aortic regurg

122
Q

What is the best initial test for valvular lesions? What is the most accurate test?

A

Initial: echo
Most accurate: L heart cath

123
Q

What tests should be ordered for valvular lesion assessment (at least on Step 3 CCS)?

A

Echo, EKG, CXR

124
Q

Can pharmacological therapy delay the progression of regurgitant valvular lesions?

A

No, but vasodilators should be used if HTN is present (ACE, ARB, nifedipine);

125
Q

When should surgical valve repair/replacement be performed in patients with regurgitant lesions?

A

If echo shows low EF or increased LV end-systolic diameter

126
Q

Which valvular disease can be treated by valve replacement via catheter?

A

Aortic stenosis

127
Q

When should transesophageal echo (TEE) be ordered?

A

When TTE (transthoracic echo) isn’t completely diagnostic

128
Q

How should mitral stenosis be treated?

A

Balloon valvuloplasty, even in pregnant patients

129
Q

How should severe aortic stenosis be treated?

A

Valve replacement, even in very old patients as it is well-tolerated; catheter –> open surgery

  • transcatheter aortic valve replacement (TAVR) has better efficacy and fewer adverse effects than surgical replacement
130
Q

What role do diuretics play in treatment of stenotic valvular lesions?

A

Can decrease pulmonary vascular congestion but are less effective than anatomic repair

valsalva improves murmur = indication for diuretics

131
Q

If amyl nitrate improves a murmur, what medication is indicated?

A

ACE (AR, MR, VSD)

132
Q

Which murmurs can be treated with diuretics?

A

Those which improve (decrease) w/ standing/valsalva
- AS
- AR
- MS
- MR
- VSD

133
Q

How does aortic stenosis usually present?

A

chest pain in older patients w/ hx of HTN
- CAD may be present in 50% of cases

(syncope + CHF are less common presentations)

134
Q

What is the prognosis for aortic stenosis in patients with coronary dz, syncope, and CHF?

A

coronary dz: 3-5yrs
Syncope: 2-3yrs
CHF: 1.5-2yrs

135
Q

What is the character of the aortic stenosis murmur?

A

crescendo-decrescendo systolic murmur best heard at the second R intercostal space w/ radiation to the carotid arteries
- may have delayed carotid upstroke

136
Q

What is the difference in the medical management/prognosis of a porcine/bovine valve vs mechanical?

A

Porcine/bovine requires no anticoagulation but only lasts 10 years

Mechanical valve lasts longer but requires warfarin therapy w/ goal INR 2-3

137
Q

What causes aortic regurgitation?

A

HTN, rheumatic heart disease, endocarditis, cystic medial necrosis
- more rarely: Marfan syndrome, ankylosing spondylitis, syphilis, reactive arthritis

138
Q

What are the most common symptoms of aortic regurg?

A

SOB and fatigue

139
Q

What is the murmur associated w/ aortic regurg?

A

Diastolic decrescendo at the L sternal border
- increases in intensity w/ leg raising, squatting, handgrip

140
Q

What are some key exam findings indicative of aortic regurg?

A

Quincke pulse: arterial/capillary pulsations in fingernails
Corrigan pulse: high bounding pulses
Musset sign: head bobbing up and down w/ each pulse
Duroziez sign: murmur over femoral artery
Hill sign: blood pressure gradient much higher in lower extremities

141
Q

What are the best diagnostic tests for valvular disease?

A

TTE < TEE (more accurate) < L heart cath (most accurate)

142
Q

What is the treatment for aortic regurg?

A
  • ACEs, ARBs, and nifedipine if there is hypertension
  • Loop diuretic (furosemide) if fluid overloaded
  • Surgery if EF<55% or LV end systolic diameter >55, regardless of symptoms
143
Q

What is the most common cause of mitral stenosis?

A

Rheumatic fever (more frequent in immigrant populations; relatively low rates in US)
- may also occur in pregnancy due to increased plasma volume

144
Q

What are some special features of mitral stenosis?

A
  • Dysphagia (large LA compresses esophagus)
  • Hoarseness (pressure on recurrent laryngeal nerve)
  • A-fib (may lead to stroke)
145
Q

What is the murmur associated w/ mitral stenosis?

A

Diastolic rumble after opening snap (extra sound in diastole)
- the worse the MS, the closer the snap to S2

146
Q

What is the best initial treatment of mitral stenosis? What’s the most effective?

A

First: diuretics (do not alter progression)
Most effective: balloon valvuloplasty (can and should be provided for pregnant women)

147
Q

What are the causes of mitral regurg?

A

HTN, ischemic heart dz, and any condition that causes dilation of the heart

148
Q

What’s the most common symptom of mitral regurg?

A

Dyspnea on exertion

149
Q

What is the murmur associated w/ mitral regurg?

A

Holosystolic murmur that obscures S1/S2 at apex, radiating to axilla
- increased w/ leg raising, squatting, handgrip

150
Q

What is the treatment of mitral regurg? When is surgery indicated?

A

ACEs, ARBs, nifedipine + furosemide if fluid overloaded

Valve replacement when EF <60% or LV end systolic diameter >40mm, regardless of symptoms

151
Q

What are the INR goals for mechanical valves in the mitral vs aortic positions?

A

Mitral: 2.5-3.5
Aortic: 2-3

152
Q

What medication should be used in conjunction w/ warfarin to prevent clots in pts w/ metal heart valves?

A

Aspirin

153
Q

How do pts w/ ventricular septal defect present?

A

Holosystolic murmur at lower L sternal border + SOB in larger defects
- murmur worsened w/ exhalation, squatting, leg raise

154
Q

What are the best initial and most accurate diagnostic tests for ventricular septal defect?

A

Initial: Echo
Accurate: Cath (shows extent of left-to-right shunting)

155
Q

How do atrial septal defects present?

A

Small: asymptomatic
Large: signs of R ventricular failure (SOB, parasternal heave)

  • a/w fixed S2 split due to differing pressure on either side of the heart
156
Q

How do you treat atrial septal defect?

A

Percutaneous or catheter device when shunt ratio exceeds 1.5:1

157
Q

How does dilated cardiomyopathy present and how is it managed?

A

Presents and is managed the same way as CHF
- ACE/ARB/ARNI, beta blockers, spironolactone (MRAs)
- digoxin for symptomatic relief (doesn’t prolong survival)

158
Q

What are the most common causes of dilated cardiomyopathy?

A

Ischemia, EtOH, doxorubicin, radiation, and Chagas disease

159
Q

What is the most accurate test to determine ejection fraction?

A

MUGA or nuclear ventriculography

160
Q

How does hypertrophic cardiomyopathy present?

A

DOE and S4 gallop (sign of decreased compliance of ventricle)
- normal EF on echo

161
Q

What is the treatment for hypertrophic cardiomyopathy?

A

MRAs (spironolactone/eplerenone)

162
Q

How does restrictive cardiomyopathy present?

A

Hx of sarcoidosis, amyloidosis, hemochromatosis, cancer, myocardial fibrosis, or glycogen storage diseases
- SOB
- Kussmaul sign (increased JVP on inhalation)

163
Q

What are the diagnostic tests for restrictive cardiomyopathy?

A

Cardiac cath showing rapid x and y descent (lol whatever that is)
EKG w/ low voltage
Echo

** Endomyocardial bx is most accurate test to determine etiology **

164
Q

How do you treat restrictive cardiomyopathy?

A

By treating the underlying cause

(also diuretics)

165
Q

What is tokotsubo cardiomyopathy?

A

Rare, sudden systolic dysfunction brought on by extreme emotions
- often a/w post-menopausal women w/ sudden psychological stress

Presents like MI w/ ventricular dysfunction but coronary arteries are normal

166
Q

How is tokotsubo cardiomyopathy treated?

A

ACEs, diuretics, beta-blockers

Pt will recover w/in a few weeks if they survive the initial attack

167
Q

How does pericarditis present?

A

Brief, sharp chest pain that is both pleuritic and positional (relieved by sitting up and leaning forward)
- only 30% of pts have friction rub
- no pulsus paradoxus, tenderness, edema, or Kussmaul sign
- normal BP, no JVD or organomegaly

168
Q

What is the best initial test for pericarditis?

A

EKG
- ST segment elevation in all leads
- PR segment depression in lead II is pathognomonic but may not be present

169
Q

What is the treatment for pericarditis?

A

NSAID plus colchicine to prevent recurrent episodes
- oral prednisone can be added if pain persists after 1-2 days of tx

170
Q

How does pericardial tamponade present?

A

-SOB, hypotension, JVD w/ clear lung sounds
- pulsus paradoxus (BP drops more than 10mmHg on inhalation)
- electrical alternans on EKG (variation of QRS complex height from heart moving forward and backward in the chest)

171
Q

What is the treatment of pericardial tamponade?

A

Pericardiocentesis

(pericardial window in long-term conditions)

  • do NOT use diuretics
172
Q

How does constrictive pericarditis present?

A

SOB and signs of chronic R heart failure
- edema
- JVD
- hepatosplenomegaly
- ascites

Unique features: Kussmaul sign (increased JVP on inhalation) and pericardial knock (extra diastolic sound from heart hitting calcified pericardium)

173
Q

What are the diagnostic tests and relevant findings for constrictive cardiomyopathy?

A

CXR: calcification
EKG: low voltage
CT/MRI: thickening of pericardium

174
Q

What is the best initial treatment of constrictive cardiomyopathy? What’s the most effective tx?

A

Initial: diuretic
Best: surgical removal of pericardium

175
Q

How does dissection of the thoracic aorta present?

A
  • “Ripping” chest pain radiating to back b/tw scapulae
  • difference in BP b/tw R and L arms
  • widened mediastinum on CXR (best initial test; CTA is most accurate)
176
Q

How do you manage dissection of the thoracic aorta?

A
  • beta-blockers + nitroprusside to control BP
  • EKG, CXR, CTA
  • transfer to ICU and consult surgery
177
Q

What are the screening criteria for AAA?

A

Screening US for men 65-75 who are current or former smokers

178
Q

At what size does a AAA require surgical repair?

A

> 5cm

179
Q

How does PAD present?

A
  • Claudication (pain in calves on exertion)
  • smooth, shiny skin w/ loss of hair and sweat glands
  • loss of pulses in feet
180
Q

What’s the best initial test to diagnose PAD? Most accurate?

A

ABIs

Most accurate: angiogram (MRA/CTA)

181
Q

What is the best initial therapy of PAD?

A
  • ASA or clopidogrel
  • ACEs
  • exercise as tolerated
  • cilostazol
  • statins w/ target LDL <70

*CCBs are ineffective

182
Q

How do you mange PAD when pain persists despite initial pharmacological tx?

A

Revascularization by catheter or surgically, followed by DAPT (aspirin + clopidogrel)

183
Q

How does acute arterial embolus present?

A

Very sudden onset of loss of pulse and cold extremity w/ severe pain
- aortic stenosis and A-fib may be in the PMHx

184
Q

What defines an unstable pt w/ A-fib and how do you treat them?

A

Instability: SBP <90mmHg, congestive failure, AMS due to hemodynamic instability, or chest pain

Tx: immediate synchronized electrical cardioversion

185
Q

How should stable pts w/ A-fib be managed?

A

Rate control (metoprolol, atenolol, carvedilol, diltiazem, or digoxin)

Anticoagulation w/ DOACs (dabigatran, rivaroxaban, edoxaban, apixaban)

186
Q

How can you reverse bleeding a/w warfarin?

A

Prothrombin complex concentrate (PCC) or FFP

187
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

188
Q

What is the reversal agent for factor Xa inhibitors?

A

Andexanet

189
Q

When should warfarin be used to treat A-fib instead of DOACs?

A

When pt has mitral valve stenosis or metallic heart valves

190
Q

What is the CHADSVASC used for?

A

To indicate need for anticoagulation.
0-1: aspirin or nothing
2+: DOACs

191
Q

What are the components of a CHADSVASC score?

A

C: CHF
H: HTN
A: Age >75
D: Diabetes
S: Stroke/TIA
V: Vascular dz
A: Age 65-74
SC: Sex Category

Age>75 and Stroke/TIA give 2 pts if positive

192
Q

Which A-fib/A-flutter pts should receive CCBs for rate control?

A

Pts w/ asthma or migraines

193
Q

Which A-fib/A-flutter pts should receive digoxin for rate control?

A

Pts w/ borderline hypotension ~90

194
Q

How does multifocal atrial tachycardia present?

A

Like an atrial arrhythmia in association w/ COPD/emphysema
- EKG w/ polymorphic P waves
- HR >100
- chaotically irregular rhythm on EKG

195
Q

How do you treat multifocal atrial tachycardia?

A

O2, then diltiazem (NOT beta blockers)

196
Q

How does Wolff-Parkinson-White Syndrome present?

A

As SVT that can alternate w/ VT
- worsening SVT after use of calcium blockers or digoxin

197
Q

What is the initial diagnostic test for WPW? What’s the most accurate test?

A

First: EKG (shows delta wave)
Accurate: electrophysiologic study

198
Q

How do you treat WPW?

A

Procainamide, sotalol, or amiodarone for SVT or VT
- radiofrequency catheter ablation can be used for long-term treatment

199
Q
A

Step 3 (3 decks)

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