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01 Family Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What should be asked in the evaluation of a patient with Chest Pain?

A
  1. Know quality (i.e. sharp, dull, burning, etc), severity (1-10), radiation, frequency, duration, associated symptoms (n/v, sob, diaphoresis).
  2. What he/she is doing when it comes on – is it effort induced, and if so how much (types of activity, walking distance/time).
  3. Know what he/she does to make it go away – is it relieved by rest? Nitroglycerin?
  4. If history of coronary artery disease (CAD), ALWAYS ask if this is the same as their prior chest pain (“index chest pain”).
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2
Q

What should be asked in the evaluation of a patient with likely or diagnosed CHF?

A
  1. Always ask about dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, unexpected weight gain, medication compliance, dietary (salt) indiscretion.
  2. Ask about exercise capacity (walking, climbing stairs, yard work, formal exercise) - document as New York Heart Association (NYHA) Class I-IV.
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3
Q

What should be asked in the evaluation of a patient with Dizziness/Syncope?

A
  1. Ask about true loss of consciousness, injuries, ictal features (incontinence, tongue biting).
  2. Ask about prodrome – nausea, chest pain, dyspnea, diaphoresis, palpitations.
  3. Ask about recovery – fatigue, post-ictal state.
  4. Ask about witness accounts – shaking, color (blue, pale, etc).
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4
Q

What diagnosis may prohibit a patient from being a candidate for CABG?

A

Severe COPD

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5
Q

Questions to ask patients with Peripheral Vascular Disease

A

History of: amputations, surgeries, stents, angiograms, ulcers, claudication

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6
Q

Cardiology patients with Renal failure are at risk of what adverse outcome?

A

Increased risk of contrast-induced nephropathy from catheterization

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7
Q

Cardiology patients with Cerebrovascular Accident/Transient Ischemic Attack are at risk of what adverse outcome?

A

Increased risk of intracranial bleeding

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8
Q

Cardiology patients with Liver disease are at increased risk of what adverse outcome?

A

Increased risk of bleeding.

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9
Q

Cardiology patients with Recent Trauma or Surgery (< 30 days) may not be able to receive which medication?

A

may be a contraindication to thrombolytics and/or other anticoagulants.

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10
Q

Medications for treatment of general chest pain

A 
Aspirin
Beta blocker
ACE inhibitor for HTN or DM
Statin
\+/- Proton Pump Inhibitor (PPI)
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11
Q

Medications for treatment of Unstable Angina

A 
Aspirin
Beta blocker
ACE inhibitor for HTN or DM
Statin
Treatment dose heparin or enoxaparin
\+/- Nitrates
\+/- Proton Pump Inhibitor (PPI)
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12
Q

Medications for treatment of NSTEMI

A 
Aspirin
Beta blocker
ACE inhibitor for HTN or DM
Statin
Treatment dose heparin or lovenox
\+/- Nitrates
\+/- Proton Pump Inhibitor (PPI)

GP IIbIIIa inhibitor (fellow determination)

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13
Q

Medications for treatment of STEMI

A 
Aspirin
Beta blocker
ACE inhibitor for HTN or DM
Statin
Treatment dose heparin or lovenox
\+/- Nitrates
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14
Q

Medication contraindications for patients with inferior/posterior MI?

A

No beta blockers, nitrates, or diuresis.

These are PRELOAD-dependent patients, so give fluids!!

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15
Q

Main finding of the RALES Trial?

A

Pts with HFrEF who took spironolactone had reduced rates of hospitalizations and mortality.

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16
Q

Spironolactone initiation criteria?

A
  1. Already on BB and ACEi/ARB
  2. LVEF less than or equal to 35% and NYHA class III-IV
  3. Cr less than 2.5 (males) or 2 (females); GFR > 30
  4. K+ < 5, no hx of severe hyperK
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17
Q

Describe the heart sound: S1

A

Mitral and tricuspid valves close

Start of systole, heard at apex

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18
Q

Describe the heart sound: S2

A

Pulmonic and aortic valves close

end of systole, heard at base

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19
Q

Describe the heart sound: S3

A

Impaired rapid early filling, follows S2

low pitched diastolic extra sound

ok in youth/athletes

S3 need to pee- volume overload

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20
Q

Describe the heart sound: S4

A

Atrial gallop, precedes S1

late diastolic low pitched extra sound

Always pathological (except in kids)

decreased compliance, pressure overload

(LVH, aortic stenosis, HOCM, dilated CM)

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21
Q

Describe the heart sound: Physiological S2 splitting

A

During inspiration, increased RV filling, longer RV emptying, delayed closure of pulmonic valve

S1 A2 P2

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22
Q

Describe the heart sound: Wide fixed splitting of S2

A

Atrial septal defect

Increased RV filling from VCs and left atria, delayed emptying and P2 closure

During inspiration and expiration

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23
Q

Describe the sound of Aortic Stenosis

A

Systolic, Crescendo-Decrescendo

Right 2nd intercostal space, base –> carotids

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24
Q

Describe the sound of Mitral Regurgitation

A

Holosystolic, apex

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25
Q

Describe the sound of Aortic Insufficiency

A

Diastolic, decresendo

Right 2nd intercostal space

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26
Q

Describe the sound of Mitral Stenosis

A

Diastolic
Opening snap, diastolic rumble

apex with bell

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27
Q

Describe the sound of Mitral Valve Prolapse

A

Systolic
midsystolic click, apex

standing- smaller LV, longer louder murmur

squatting- larger LV, shorter mild murmur

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28
Q

What is the most common congenital heart defect in the U.S.?

A

Bicuspid aortic valve

*Screen 1st degree relatives with echo

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29
Q

Describe the sound of Pulmonary stenosis

A

Crescendo- decresendo
Left 2nd intercostal space
radiates to shoulder and neck

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30
Q

Management of aortic stenosis?

A

No meds, including statins, slow progression

If asymptomatic repeat echo q3-5 years
TAVR if symptomatic

*PE does not correlated with grading severity

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31
Q

What is the etiology of Acute Coronary Syndrome?

A

Reduced myocardial perfusion due to reduced oxygen supply or increased oxygen demand

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32
Q

What is the most common cause of Acute Coronary Syndrome?

A

Plaque rupture

Thrombus develops on disrupted plaque

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33
Q

What characteristics make an arterial plaque more likely to rupture?

A

Thin fibrous cap

Large, soft fatty core

*Size of plaque does not correlate with severity

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34
Q

What are some non plaque etiologies of Acute Coronary Syndrome?

A

Spasm at site of plaque

Spasm in normal coronary arteries
-Prinzmetal’s angina, arterial inflammation (Kawasaki’s disease)

Cocaine induced

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35
Q

What is the treatment for Cocaine induced Acute Coronary Syndrome?

A

Nitroglycerin

Benzodiazepines

*Avoid Beta blockers

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36
Q

How do you differentiate Unstable angina from NSTEMI?

A

NSTEMI - elevated troponin levels

*Both may have ST depression on EKG

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37
Q

How soon can troponin be detected after ischemia and how long does it remain elevated?

A

Detected 3-6 hours after onset of ischemia

Can remain elevated 7 to 14 days post-MI

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38
Q

What are some non-ischemic causes of troponin elevation?

A

Chronic kidney disease

Heart Failure

Pulmonary Embolism

Sepsis

Stroke

Myocarditis

Cardiac toxicity from chemotherapy

Subarachnoid hemorrhage

Amyloidosis, sarcoidosis

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39
Q

In low risk patients presenting with NSTEMI what three medications should be started?

A

Aspirin 162-325 mg (chewable)

P2Y12 inhibitor (clopidogrel)

Anticoagulation (Heparin)

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40
Q

In high risk patients presenting with NSTEMI what four medications should be started?

A

Aspirin 162-325 mg (chewable)

P2Y12 inhibitor (clopidogrel)

Anticoagulation (Heparin)

*Glycoprotein IIb/IIIa receptor blockers (before cath lab)

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41
Q

Patients with NSTEMI and what characteristics are higher risk and may benefit from early invasive strategies?

A

Symptoms or ischemia despite adequate medical therapy

Hx of PCI or CABG

Hx of significant cardiac disease

High TIMI or GRACE scores

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42
Q

What is the role of fibrinolytic therapy in NSTEMI management?

A

No role in NSTEMI

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43
Q

On EKG what does ST elevation indicate?

A

Myocardial injury

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44
Q

On EKG, what does resolution of ST elevation indicate?

A

Reperfusion

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45
Q

On EKG, what does persistent ST elevation indicate?

A

Possible aneurysm formation

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46
Q

On EKG, what does ST depression indicate?

A

myocardial ischemia

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47
Q

On EKG, what do Q waves indicate?

A

Dead myocardium

*Develops about 12 hours after plaque rupture

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48
Q

Leads V1- V4 on EKG represent what area of the heart?

A

Anterior, anteroseptal

Left anterior descending artery

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49
Q

Leads V5-V6 on EKG represent what area of the heart?

A

Lateral

Circumflex artery

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50
Q

Leads II, III, aVF on EKG represent what area of the heart?

A

Inferior

Right coronary artery

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51
Q

In patients with STEMI, how soon should reperfusion occur?

A

Within 12 hours

PCI preferred

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52
Q

In patients with STEMI, when is fibrinolytic therapy indicated?

A
  1. If onset of symptoms plus transport time to PCI capable hospital is greater than 12 hours
  2. If transport time from first contact at non PCI capable hospital to arrival in cath lab of PCI capable hospital is greater than 2 hours
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53
Q

What is the difference between Bare metal stents and Drug-eluting stents?

A

BMS- increased risk of in-stent thrombosis due to endothelialization

DES- delays endothelialization, reduces rate of in-stent stenosis
(Sirolimus, tacrolimus, paclitaxel)

54
Q

What comprises Dual Antiplatelet Therapy?

A

Aspirin 81 mg

plus one of these P2Y12 inhibitors:

Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)

55
Q

How long do patients with Acute Coronary Syndrome treated with drug-eluting or bare metal stents need dual antiplatelet therapy?

A

12 months

After one year, okay to discontinue the P2Y12 inhibitor

*Keep ASA indefinitely

56
Q

How long do patients with Stable Coronary disease treated with drug-eluting or bare metal stents need dual antiplatelet therapy?

A

(scheduled cath not in setting of ACS)

Bare metal stents- 1 month of DAPT

Drug-eluting stents- 6 months of DAPT

57
Q

How does the antiplatelet activity of clopidogrel compare to aspirin?

A

Slower onset compared to aspirin

Comparable to ASA in reducing ischemic events

58
Q

Should dual antiplatelet be continued after one year from myocardial infarction?

A

Can decrease the risk of major cardiovascular event without increasing likelihood of major bleeding event

“This treatment may be reasonable”

-Shared decision making

59
Q

What conditions may benefit from CABG over PCI?

A

Improved survival in:

  • Left main coronary artery stenosis
  • 3 vessel disease with LVEF <50%
  • 2-3 vessel disease with >75% stenosis of proximal LAD
60
Q

How long do patients need dual anti-platelet therapy after CABG?

A

At least one year to reduce graft occlusion

61
Q

Which medications improve survival post myocardial infarction?

A

ACE inhibitor

Beta-blockers

Statins

Aspirin

62
Q

Which medications only improve symptoms post myocardial infarction (not survival)?

A

Calcium channel blockers

Digoxin

Nitrates

63
Q

A patient presents with crushing chest pain, EKG shows Left bundle branch block. What is the next step in management?

A

Determine need for reperfusion considering, clinical picture, troponin level, echo and EKG interpreted using Sgarbossa criteria

64
Q

What is Sgarbossa criteria used for?

A

Determining presence of ischemia, infarction on EKG in patients with Left bundle branch block

LBBB- usually not new, and not caused by ACS

65
Q

How does pericarditis typically present?

A

Young adult presenting with chest pain (happens with older adults too)

Relieved by sitting forward

66
Q

What is the most common cause of pericarditis?

A

Viral or idiopathic

Pain is due to inflammation

67
Q

What is the treatment for pericariditis?

A

NSAIDs

  • Indomethacin
  • High dose ASA (2-4 g per day)
68
Q

Name four groups of people who benefit from statin therapy

A
  1. Hx of atherosclerotic disease or cardiovascular disease (ASCVD)
  2. LDL 190 or greater (typically familial)
  3. Ages 45-75 with diabetes and LDL 70 or greater
  4. Ages 40-75, LDL 70 to 189, no hx of diabetes, atherosclerotic or cardiovascular disease and estimated 10 year-ASCVD risk 7.5% or greater
69
Q

Of the four groups of people who benefit from statin therapy, who needs high intensity statin therapy?

A
  1. Hx of atherosclerotic disease or cardiovascular disease (ASCVD)
  2. LDL greater than or equal to 190 (typically familial)
  3. Ages 45-75 with diabetes and LDL 70 or greater (could also do moderate intensity therapy)
70
Q

For patients with hx of ASCVD or aged 45-75 with diabetes and LDL 70 or greater, what is the goal of statin therapy?

A

To reduce LDL by 50% or greater

71
Q

Of the four groups of people who benefit from statin therapy, who needs moderate intensity statin therapy?

A
  1. Ages 45-75 with diabetes and LDL 70 or greater
    (could also do high intensity therapy)
  2. Ages 40-75, LDL 70 to 189, no hx of diabetes, atherosclerotic or cardiovascular disease and estimated 10 year-ASCVD risk 7.5% or greater
    (Shared decision making to start statin therapy)
72
Q

What are the high intensity statins? How do they affect LDL?

A

50% or greater LDL reduction

Atorvastatin 40-80 mg

Rosuvastatin 20 mg

73
Q

What are the moderate intensity statins? How do they affect LDL?

A

30-50% LDL reduction

Atorvastatin 10-20 mg

Rosuvastatin 5-10 mg

Simvastatin 20-40 mg

Pravastatin 40-80 mg

Lovastatin 40 mg

Fluvastatin 40 mg BID

74
Q

What components go into ASCVD risk calculation?

A

Age, race, gender

Total cholesterol, HDL

Hx of diabetes

Systolic BP, use of antihypertensive medications

Smoking status

75
Q

What is the USPSTF guideline for starting statin therapy in patients without a history of atherosclerotic or cardiovascular disease?

A

Ages 40-75 with one risk factor (DM, HTN, Smoking, LDL 130 or greater, HDL less than 40)

If ASCVD risk 10% or greater: start moderate statin therapy

If ASCVD risk 7.5-10%: shared decision making to state moderate or low statin therapy

76
Q

Should adults over 75 years be started on statin therapy?

A

Insufficient evidence on benefits and harms

77
Q

When discussing starting statin therapy with a patient, what factors make them higher risk, and would push the decision towards starting a statin?

A

Family hx of early ASCVD (male <55, female <65)

LDL persistently above 160, Triglycerides above 175

Metabolic syndrome, CKD, chronic inflammatory disorders

Hx of pre-eclampsia or early menopause

ABI <0.9

*Consider lifestyle changes, side effects, cost, patient preference

78
Q

What additional testing (other than lipid profile) can help with the decision to start statin therapy?

A

Coronary artery calcium testing
(CT scan)

-Degree of calcium indicates need for statin

79
Q

In high risk patients with ASCVD and LDL greater than 70 on maximally tolerated statin, what is the next step in managment?

A

Add Ezetimibe

If LDL still greater than 70, add PCSK9 inhibitor

80
Q

What are PCSK9 inhibitors?

A

Protein that destroys LDL receptors in liver to lower LDL levels

Very expensive injectable drug

81
Q

What is the difference between myalgia, myositis and rhabdomyolysis?

A

Myalgia- Muscle pain without CK elevations

Myositis- Muscle pain with CK elevations

Rhabdomyolysis- Elevated CK and creatinine

82
Q

What medical conditions increase the risk of statin-related myopathy?

A

Liver or renal failure

Hypothyroidism

Diabetes mellitus

83
Q

What medications increase the risk of statin-related myopathy?

A

Macrolides

-azoles

Cyclosporine

Gemfibrozil

Niacin

HIV protease inhibitors

Nefazodone

Verapamil, Diltiazem

Amiodarone

84
Q

What ejection fraction is considered reduced ejection fraction in heart failure?

A

40% or less

85
Q

What is the most common cause of heart failure with reduced ejection fraction?

A

Ischemic heart disease

86
Q

What ejection fraction is considered preserved ejection fraction in heart failure?

A

50% or greater

87
Q

What is the most common cause of heart failure with preserved ejection fraction?

A

Hypertension -> left ventricular hypertrophy

-> Ventricular stiffness and diastolic dysfunction

88
Q

What would you call an ejection fraction of 41-49%?

A

Borderline heart failure with preserved ejection fraction

Similar to HFpEF

89
Q

What would you call an ejection fraction that went from less than 40% to greater than 40%?

A

Heart failure with preserved ejection fraction

Previously HF with reduced EF

90
Q

What type of heart failure does primary cardiomyopathy typically cause?

A

HF with reduced EF

91
Q

What is takotsubo cardiomyopathy?

A

“Octopus trap”

Also called broken heart syndrome

  • Left ventricle balloons out
  • Stress induces chest pain, EKG changes, elevated troponin
  • Normal coronary arteries
  • Most common in women 62-76 (postmenopausal)
92
Q

What is hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy without LV dilation

Autosomal dominant

Usually asymptomatic

Systolic murmur, increases with valsalva

93
Q

What is the treatment of hypertrophic cardiomyopathy?

A

Beta blockers or Non-dihyropyridine calcium channel blockers
-Reduce dyspnea, chest pain and prevent sudden death

No competitive sports

Consider implantable cardioverter- defibrillator

94
Q

Define NYHA functional classification class 1

A

No limitation of physical activity.

Normal physical activity does not cause symptoms of HF

95
Q

Define NYHA functional classification class 2

A

Slight limitation of physical activity.

No symptoms at rest, but normal physical activity does cause symptoms of HF

96
Q

Define NYHA functional classification class 3

A

Marked limitation of physical activity.

No symptoms at rest, but less than normal activity causes symptoms of HF

97
Q

Define NYHA functional classification class 4

A

Unable to do any physical activity without symptoms of HF

or

Symptoms of HF at rest

98
Q

From where and why is BNP released?

A

Secreted from ventricles

In response to ventricular volume expansion and pressure

Correlates with end diastolic pressure

Increases in HFrEF and HFpEF

99
Q

How is BNP excreted?

A

Partial renal excretion

BNP levels inversely proportional to creatinine clearance

100
Q

At what levels of BNP can you rule in or rule out heart failure as the cause of dyspnea?

A

BNP <100: excludes HF as cause

BNP >400: 95% likelihood that HF is cause

BNP 100 - 400: need further investigation

101
Q

What other diseases can cause elevated BNP?

A

Lung cancer

Cor pulmonale

Chronic hypoxia

OSA

Pulmonary embolus

Cirrhosis with ascites

Primary hyperaldosteronism

Cushing disease

Anemia

Renal failure

102
Q

In heart failure, low cardiac output triggers sympathetic (fight or flight) response, with this in mind, what are the goals of HF treatment?

A

Preload reduction

Afterload reduction

Sympathetic blockade

Aldosterone- antagonist therapy

103
Q

In heart failure what drug classes reduce preload?

A

Diuretics

Nitrates

104
Q

In heart failure what drug classes reduce afterload?

A

ACEi or ARB

Hydralazine

Nitrates

105
Q

In heart failure what drug classes block sympathetic response?

A

Beta- blockers

106
Q

In heart failure what drug classes inhibit aldosterone response?

A

Spironolactone

Eplerenone

107
Q

What is the role of ACE inhibitors in HFrEF?

A

Reduce morbidity and mortality

Use in mild to severe HF

108
Q

What are the side effects of ACE inhibitors?

A

Angioedema risk

Cough (elevated bradykinin)

Hyperkalemia

Hypotension

*Caution in patients with renal insufficiency

109
Q

What is the role of ARBs in HFrEF?

A

Reduce morbidity and mortality

  • Use if ACEi intolerant
  • Less risk of cough or angioedema

*Caution in patients with hypotension, renal insufficiency, hyperkalemia

110
Q

What is the role of beta blockers in HFrEF?

A

Improved mortality in combination with ACEi and diuretics

Decreases mortality in patients with prior MI

*Only start when patient is euvolemic and stable

111
Q

Which patients with HFrEF should not be on a beta blocker?

A

Hemodynamically unstable

Hx of heart block or bradycardia

Severe asthma or COPD (could use 2nd generation BB)

112
Q

Which beta blockers are used in the treatment of HFrEF?

A

Metoprolol succinate

Carvedilol

Bisoprolol

113
Q

What is the role of aldosterone antagonists in HFrEF?

A

Reduce mortality

Improve injection fraction

114
Q

What are contraindications to aldosterone antagonist use?

A

GFR < 30

Potassium > 5

*Avoid use with NSAIDs and COX-2 inhibitors

115
Q

What is a side effect of spironolactone? Which medication would you use instead?

A

Gynecomastia

Use Eplerenone instead

116
Q

What is the role of Digoxin in HFrEF?

A

Decreases hospitalizations

NO reduction in mortality

117
Q

What is the role of furosemide in HFrEF?

A

Improves symptoms

Reduces hospitalizations

*May decrease mortality

118
Q

What is the role of Nesiritide (BNP) in HFrEF?

A

Causes hypotension

No effect on hospitalizations or deaths

119
Q

What is the role of Hydralazine and Isosorbide in HFrEF?

A

Combination called BiDil

Vasodilator

Reduces mortality

Improves symptoms

Use if diuretics, beta blocker, ACEi/ARB do not control symptoms

*Benefits mainly seen in black patients with NYHA class III or IV

120
Q

Which patients with HFrEF would benefit from an ARNI (ARB + neprilysin inhibitor)?

A

Patients NYHA class II/III, who are symptomatic despite adequate medical therapy

Must be able to tolerate ACEi or ARB

121
Q

Compare ANRI to ACEi in HFrEF treatment

A

ARNI: Valsartan + sacubitril (Entresto)

  • Reduced death from CV or overall causes
  • Reduced hospitalizations
  • Expensive
122
Q

In patients with HFrEF on an ACEi, how long do they need to wait after stopping the ACEi before switching to an ARNI?

A

36 hours

123
Q

What is the role of Ivabradine (Corlanor) in the treatment of HFrEF?

A

Sinus node modulator

Reduces hospitalizations

Patients NYHA class II or III, on guideline directed management, including beta blocker at maximum tolerated dose and in normal sinus rhythm with heart rate of 70 or greater

124
Q

Which medications should be avoided in HFrEF?

A

Verapamil, Diltiazem

Antiarrhythmics

NSAIDs

  • glitazones
  • anything that causes water retention, edema or negative inotropic effect
125
Q

How does HFpEF treatment compare to HFrEF treatment?

A

HFpEF

  • evidence based treatment guidelines are limited
  • Priority is symptom relief and managing comorbidities
126
Q

In treatment of HFpEF, what medication effects should be carefully monitored?

A

Preload reduction- lower preload leads to reduced ventricular filling and therefore decreased cardiac output

Heart rate reduction- no clear evidence showing benefit or improvement in diastolic filling with lowered heart rate

127
Q

Should digoxin be used in HFpEF treatment?

A

Only if atrial fibrillation or flutter is present

128
Q

What is the role of aldosterone antagonists in HFpEF treatment?

A

Use only if:

  • EF 45% or greater
  • Elevated BNP or 1 HF admission in the past year
  • GFR > 30
  • Creatinine < 2.5
  • Potassium < 5.0

*May decrease hospitalizations

129
Q

What is the role of an implantable cardioverter defibrillator in heart failure management?

A
  • Reduces risk of sudden death due to ventricular tachyarrhythmias
  • For patients with EF 35% or less, NYHA class II or III symptoms on meds, life expectancy more than 1 year
130
Q

What is the role of cardiac resynchronization therapy (CRT) in heart failure management?

A

Biventricular pacing

-For patients with EF 35% or less, NYHA class II, III, IV with symptoms on meds, QRS 150 ms or greater, life expectancy greater than 1 year

131
Q

What is the role of Left ventricular assist devices in heart failure management?

A

Used as a bridge to recovery or transplant or other care decisions

-Patients with 1 year survival of less than 50%

01 Family Medicine (16 decks)

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