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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Systolic dysfunction is AKA

A

HFrEF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Patients with which conditions MUST be on a statin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

> 7.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

All patients with ACS should be on…

A

A statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When/why might icosapent be added to statins?

A

When triglycerides are elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does carvedilol work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Dobutamine is less effective for patients on what cardiology med?

A

Beta-blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the mechanism of respiratory alkalosis in CHF?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are three positive inotropes used IV in the ICU?

A

Dobutamine, inamrinone, milrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When is unsynchronized cardioversion used?

A

V-fib or V-tach without a pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

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

A

Metoprolol, carvedilol, bisoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the benefit of SGLT2 inhibitors in HFrEF?

A

Lower mortality; decrease progression of renal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the role/utility of digoxin in HFrEF?

A
  • Decreases symptoms and frequency of hospitalizations
  • Does NOT lower mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Do diuretics lower mortality in CHF?

A

Nope, sorry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What CHF med causes transient excess brightness of vision?

A

Ibavradine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What agents offer mortality benefit for CHF?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the most common cause of death in CHF?

A

Arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

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

A

<35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

When do patients with CHF need warfarin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

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

A

beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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

A

Mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What valvular dz is more common in healthy young athletes?

A

HOCM (hypertrophic obstructive cardiomyopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

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

A

Mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

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

A

Bicuspid aortic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

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

A

Mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which murmurs are systolic?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Which murmurs are diastolic?

A

Aortic regurgitation, mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A

Coronary artery disease

*CAD kills more women than breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

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

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Which valve problem causes holosystolic blowing murmur?

A

Mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is an S3 gallop? What causes it?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Which cardiac enzyme rises first in ischemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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