Cardiology Flashcards
1
Q
What should be asked in the evaluation of a patient with Chest Pain?
A
- Know quality (i.e. sharp, dull, burning, etc), severity (1-10), radiation, frequency, duration, associated symptoms (n/v, sob, diaphoresis).
- What he/she is doing when it comes on – is it effort induced, and if so how much (types of activity, walking distance/time).
- Know what he/she does to make it go away – is it relieved by rest? Nitroglycerin?
- If history of coronary artery disease (CAD), ALWAYS ask if this is the same as their prior chest pain (“index chest pain”).
2
Q
What should be asked in the evaluation of a patient with likely or diagnosed CHF?
A
- Always ask about dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, unexpected weight gain, medication compliance, dietary (salt) indiscretion.
- Ask about exercise capacity (walking, climbing stairs, yard work, formal exercise) - document as New York Heart Association (NYHA) Class I-IV.
3
Q
What should be asked in the evaluation of a patient with Dizziness/Syncope?
A
- Ask about true loss of consciousness, injuries, ictal features (incontinence, tongue biting).
- Ask about prodrome – nausea, chest pain, dyspnea, diaphoresis, palpitations.
- Ask about recovery – fatigue, post-ictal state.
- Ask about witness accounts – shaking, color (blue, pale, etc).
4
Q
What diagnosis may prohibit a patient from being a candidate for CABG?
A
Severe COPD
5
Q
Questions to ask patients with Peripheral Vascular Disease
A
History of: amputations, surgeries, stents, angiograms, ulcers, claudication
6
Q
Cardiology patients with Renal failure are at risk of what adverse outcome?
A
Increased risk of contrast-induced nephropathy from catheterization
7
Q
Cardiology patients with Cerebrovascular Accident/Transient Ischemic Attack are at risk of what adverse outcome?
A
Increased risk of intracranial bleeding
8
Q
Cardiology patients with Liver disease are at increased risk of what adverse outcome?
A
Increased risk of bleeding.
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.
10
Q
Medications for treatment of general chest pain
A
Aspirin Beta blocker ACE inhibitor for HTN or DM Statin \+/- Proton Pump Inhibitor (PPI)
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)
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)
13
Q
Medications for treatment of STEMI
A
Aspirin Beta blocker ACE inhibitor for HTN or DM Statin Treatment dose heparin or lovenox \+/- Nitrates
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!!
15
Q
Main finding of the RALES Trial?
A
Pts with HFrEF who took spironolactone had reduced rates of hospitalizations and mortality.
16
Q
Spironolactone initiation criteria?
A
- Already on BB and ACEi/ARB
- LVEF less than or equal to 35% and NYHA class III-IV
- Cr less than 2.5 (males) or 2 (females); GFR > 30
- K+ < 5, no hx of severe hyperK
17
Q
Describe the heart sound: S1
A
Mitral and tricuspid valves close
Start of systole, heard at apex
18
Q
Describe the heart sound: S2
A
Pulmonic and aortic valves close
end of systole, heard at base
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
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)
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
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
23
Q
Describe the sound of Aortic Stenosis
A
Systolic, Crescendo-Decrescendo
Right 2nd intercostal space, base –> carotids
24
Q
Describe the sound of Mitral Regurgitation
A
Holosystolic, apex
25
Describe the sound of Aortic Insufficiency
Diastolic, decresendo
| Right 2nd intercostal space
26
Describe the sound of Mitral Stenosis
Diastolic
Opening snap, diastolic rumble
apex with bell
27
Describe the sound of Mitral Valve Prolapse
Systolic
midsystolic click, apex
standing- smaller LV, longer louder murmur
squatting- larger LV, shorter mild murmur
28
What is the most common congenital heart defect in the U.S.?
Bicuspid aortic valve
*Screen 1st degree relatives with echo
29
Describe the sound of Pulmonary stenosis
Crescendo- decresendo
Left 2nd intercostal space
radiates to shoulder and neck
30
Management of aortic stenosis?
No meds, including statins, slow progression
If asymptomatic repeat echo q3-5 years
TAVR if symptomatic
*PE does not correlated with grading severity
31
What is the etiology of Acute Coronary Syndrome?
Reduced myocardial perfusion due to reduced oxygen supply or increased oxygen demand
32
What is the most common cause of Acute Coronary Syndrome?
Plaque rupture
Thrombus develops on disrupted plaque
33
What characteristics make an arterial plaque more likely to rupture?
Thin fibrous cap
Large, soft fatty core
*Size of plaque does not correlate with severity
34
What are some non plaque etiologies of Acute Coronary Syndrome?
Spasm at site of plaque
Spasm in normal coronary arteries
-Prinzmetal's angina, arterial inflammation (Kawasaki's disease)
Cocaine induced
35
What is the treatment for Cocaine induced Acute Coronary Syndrome?
Nitroglycerin
Benzodiazepines
*Avoid Beta blockers
36
How do you differentiate Unstable angina from NSTEMI?
NSTEMI - elevated troponin levels
*Both may have ST depression on EKG
37
How soon can troponin be detected after ischemia and how long does it remain elevated?
Detected 3-6 hours after onset of ischemia
Can remain elevated 7 to 14 days post-MI
38
What are some non-ischemic causes of troponin elevation?
Chronic kidney disease
Heart Failure
Pulmonary Embolism
Sepsis
Stroke
Myocarditis
Cardiac toxicity from chemotherapy
Subarachnoid hemorrhage
Amyloidosis, sarcoidosis
39
In low risk patients presenting with NSTEMI what three medications should be started?
Aspirin 162-325 mg (chewable)
P2Y12 inhibitor (clopidogrel)
Anticoagulation (Heparin)
40
In high risk patients presenting with NSTEMI what four medications should be started?
Aspirin 162-325 mg (chewable)
P2Y12 inhibitor (clopidogrel)
Anticoagulation (Heparin)
*Glycoprotein IIb/IIIa receptor blockers (before cath lab)
41
Patients with NSTEMI and what characteristics are higher risk and may benefit from early invasive strategies?
Symptoms or ischemia despite adequate medical therapy
Hx of PCI or CABG
Hx of significant cardiac disease
High TIMI or GRACE scores
42
What is the role of fibrinolytic therapy in NSTEMI management?
No role in NSTEMI
43
On EKG what does ST elevation indicate?
Myocardial injury
44
On EKG, what does resolution of ST elevation indicate?
Reperfusion
45
On EKG, what does persistent ST elevation indicate?
Possible aneurysm formation
46
On EKG, what does ST depression indicate?
myocardial ischemia
47
On EKG, what do Q waves indicate?
Dead myocardium
*Develops about 12 hours after plaque rupture
48
Leads V1- V4 on EKG represent what area of the heart?
Anterior, anteroseptal
Left anterior descending artery
49
Leads V5-V6 on EKG represent what area of the heart?
Lateral
Circumflex artery
50
Leads II, III, aVF on EKG represent what area of the heart?
Inferior
Right coronary artery
51
In patients with STEMI, how soon should reperfusion occur?
Within 12 hours
PCI preferred
52
In patients with STEMI, when is fibrinolytic therapy indicated?
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
53
What is the difference between Bare metal stents and Drug-eluting stents?
BMS- increased risk of in-stent thrombosis due to endothelialization
DES- delays endothelialization, reduces rate of in-stent stenosis
(Sirolimus, tacrolimus, paclitaxel)
54
What comprises Dual Antiplatelet Therapy?
Aspirin 81 mg
plus one of these P2Y12 inhibitors:
Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)
55
How long do patients with Acute Coronary Syndrome treated with drug-eluting or bare metal stents need dual antiplatelet therapy?
12 months
After one year, okay to discontinue the P2Y12 inhibitor
*Keep ASA indefinitely
56
How long do patients with Stable Coronary disease treated with drug-eluting or bare metal stents need dual antiplatelet therapy?
(scheduled cath not in setting of ACS)
Bare metal stents- 1 month of DAPT
Drug-eluting stents- 6 months of DAPT
57
How does the antiplatelet activity of clopidogrel compare to aspirin?
Slower onset compared to aspirin
Comparable to ASA in reducing ischemic events
58
Should dual antiplatelet be continued after one year from myocardial infarction?
Can decrease the risk of major cardiovascular event without increasing likelihood of major bleeding event
"This treatment may be reasonable"
-Shared decision making
59
What conditions may benefit from CABG over PCI?
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
How long do patients need dual anti-platelet therapy after CABG?
At least one year to reduce graft occlusion
61
Which medications improve survival post myocardial infarction?
ACE inhibitor
Beta-blockers
Statins
Aspirin
62
Which medications only improve symptoms post myocardial infarction (not survival)?
Calcium channel blockers
Digoxin
Nitrates
63
A patient presents with crushing chest pain, EKG shows Left bundle branch block. What is the next step in management?
Determine need for reperfusion considering, clinical picture, troponin level, echo and EKG interpreted using Sgarbossa criteria
64
What is Sgarbossa criteria used for?
Determining presence of ischemia, infarction on EKG in patients with Left bundle branch block
LBBB- usually not new, and not caused by ACS
65
How does pericarditis typically present?
Young adult presenting with chest pain (happens with older adults too)
Relieved by sitting forward
66
What is the most common cause of pericarditis?
Viral or idiopathic
Pain is due to inflammation
67
What is the treatment for pericariditis?
NSAIDs
- Indomethacin
- High dose ASA (2-4 g per day)
68
Name four groups of people who benefit from statin therapy
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
Of the four groups of people who benefit from statin therapy, who needs high intensity statin therapy?
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
For patients with hx of ASCVD or aged 45-75 with diabetes and LDL 70 or greater, what is the goal of statin therapy?
To reduce LDL by 50% or greater
71
Of the four groups of people who benefit from statin therapy, who needs moderate intensity statin therapy?
3. Ages 45-75 with diabetes and LDL 70 or greater
(could also do high intensity therapy)
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
(Shared decision making to start statin therapy)
72
What are the high intensity statins? How do they affect LDL?
50% or greater LDL reduction
Atorvastatin 40-80 mg
Rosuvastatin 20 mg
73
What are the moderate intensity statins? How do they affect LDL?
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
What components go into ASCVD risk calculation?
Age, race, gender
Total cholesterol, HDL
Hx of diabetes
Systolic BP, use of antihypertensive medications
Smoking status
75
What is the USPSTF guideline for starting statin therapy in patients without a history of atherosclerotic or cardiovascular disease?
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
Should adults over 75 years be started on statin therapy?
Insufficient evidence on benefits and harms
77
When discussing starting statin therapy with a patient, what factors make them higher risk, and would push the decision towards starting a statin?
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
What additional testing (other than lipid profile) can help with the decision to start statin therapy?
Coronary artery calcium testing
(CT scan)
-Degree of calcium indicates need for statin
79
In high risk patients with ASCVD and LDL greater than 70 on maximally tolerated statin, what is the next step in managment?
Add Ezetimibe
If LDL still greater than 70, add PCSK9 inhibitor
80
What are PCSK9 inhibitors?
Protein that destroys LDL receptors in liver to lower LDL levels
Very expensive injectable drug
81
What is the difference between myalgia, myositis and rhabdomyolysis?
Myalgia- Muscle pain without CK elevations
Myositis- Muscle pain with CK elevations
Rhabdomyolysis- Elevated CK and creatinine
82
What medical conditions increase the risk of statin-related myopathy?
Liver or renal failure
Hypothyroidism
Diabetes mellitus
83
What medications increase the risk of statin-related myopathy?
Macrolides
-azoles
Cyclosporine
Gemfibrozil
Niacin
HIV protease inhibitors
Nefazodone
Verapamil, Diltiazem
Amiodarone
84
What ejection fraction is considered reduced ejection fraction in heart failure?
40% or less
85
What is the most common cause of heart failure with reduced ejection fraction?
Ischemic heart disease
86
What ejection fraction is considered preserved ejection fraction in heart failure?
50% or greater
87
What is the most common cause of heart failure with preserved ejection fraction?
Hypertension -> left ventricular hypertrophy
-> Ventricular stiffness and diastolic dysfunction
88
What would you call an ejection fraction of 41-49%?
Borderline heart failure with preserved ejection fraction
Similar to HFpEF
89
What would you call an ejection fraction that went from less than 40% to greater than 40%?
Heart failure with preserved ejection fraction
| Previously HF with reduced EF
90
What type of heart failure does primary cardiomyopathy typically cause?
HF with reduced EF
91
What is takotsubo cardiomyopathy?
"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
What is hypertrophic cardiomyopathy?
Left ventricular hypertrophy without LV dilation
Autosomal dominant
Usually asymptomatic
Systolic murmur, increases with valsalva
93
What is the treatment of hypertrophic cardiomyopathy?
Beta blockers or Non-dihyropyridine calcium channel blockers
-Reduce dyspnea, chest pain and prevent sudden death
No competitive sports
Consider implantable cardioverter- defibrillator
94
Define NYHA functional classification class 1
No limitation of physical activity.
Normal physical activity does not cause symptoms of HF
95
Define NYHA functional classification class 2
Slight limitation of physical activity.
No symptoms at rest, but normal physical activity does cause symptoms of HF
96
Define NYHA functional classification class 3
Marked limitation of physical activity.
No symptoms at rest, but less than normal activity causes symptoms of HF
97
Define NYHA functional classification class 4
Unable to do any physical activity without symptoms of HF
or
Symptoms of HF at rest
98
From where and why is BNP released?
Secreted from ventricles
In response to ventricular volume expansion and pressure
Correlates with end diastolic pressure
Increases in HFrEF and HFpEF
99
How is BNP excreted?
Partial renal excretion
BNP levels inversely proportional to creatinine clearance
100
At what levels of BNP can you rule in or rule out heart failure as the cause of dyspnea?
BNP <100: excludes HF as cause
BNP >400: 95% likelihood that HF is cause
BNP 100 - 400: need further investigation
101
What other diseases can cause elevated BNP?
Lung cancer
Cor pulmonale
Chronic hypoxia
OSA
Pulmonary embolus
Cirrhosis with ascites
Primary hyperaldosteronism
Cushing disease
Anemia
Renal failure
102
In heart failure, low cardiac output triggers sympathetic (fight or flight) response, with this in mind, what are the goals of HF treatment?
Preload reduction
Afterload reduction
Sympathetic blockade
Aldosterone- antagonist therapy
103
In heart failure what drug classes reduce preload?
Diuretics
Nitrates
104
In heart failure what drug classes reduce afterload?
ACEi or ARB
Hydralazine
Nitrates
105
In heart failure what drug classes block sympathetic response?
Beta- blockers
106
In heart failure what drug classes inhibit aldosterone response?
Spironolactone
Eplerenone
107
What is the role of ACE inhibitors in HFrEF?
Reduce morbidity and mortality
Use in mild to severe HF
108
What are the side effects of ACE inhibitors?
Angioedema risk
Cough (elevated bradykinin)
Hyperkalemia
Hypotension
*Caution in patients with renal insufficiency
109
What is the role of ARBs in HFrEF?
Reduce morbidity and mortality
* Use if ACEi intolerant
- Less risk of cough or angioedema
*Caution in patients with hypotension, renal insufficiency, hyperkalemia
110
What is the role of beta blockers in HFrEF?
Improved mortality in combination with ACEi and diuretics
Decreases mortality in patients with prior MI
*Only start when patient is euvolemic and stable
111
Which patients with HFrEF should not be on a beta blocker?
Hemodynamically unstable
Hx of heart block or bradycardia
Severe asthma or COPD (could use 2nd generation BB)
112
Which beta blockers are used in the treatment of HFrEF?
Metoprolol succinate
Carvedilol
Bisoprolol
113
What is the role of aldosterone antagonists in HFrEF?
Reduce mortality
Improve injection fraction
114
What are contraindications to aldosterone antagonist use?
GFR < 30
Potassium > 5
*Avoid use with NSAIDs and COX-2 inhibitors
115
What is a side effect of spironolactone? Which medication would you use instead?
Gynecomastia
Use Eplerenone instead
116
What is the role of Digoxin in HFrEF?
Decreases hospitalizations
NO reduction in mortality
117
What is the role of furosemide in HFrEF?
Improves symptoms
Reduces hospitalizations
*May decrease mortality
118
What is the role of Nesiritide (BNP) in HFrEF?
Causes hypotension
No effect on hospitalizations or deaths
119
What is the role of Hydralazine and Isosorbide in HFrEF?
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
Which patients with HFrEF would benefit from an ARNI (ARB + neprilysin inhibitor)?
Patients NYHA class II/III, who are symptomatic despite adequate medical therapy
Must be able to tolerate ACEi or ARB
121
Compare ANRI to ACEi in HFrEF treatment
ARNI: Valsartan + sacubitril (Entresto)
- Reduced death from CV or overall causes
- Reduced hospitalizations
- Expensive
122
In patients with HFrEF on an ACEi, how long do they need to wait after stopping the ACEi before switching to an ARNI?
36 hours
123
What is the role of Ivabradine (Corlanor) in the treatment of HFrEF?
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
Which medications should be avoided in HFrEF?
Verapamil, Diltiazem
Antiarrhythmics
NSAIDs
- glitazones
* anything that causes water retention, edema or negative inotropic effect
125
How does HFpEF treatment compare to HFrEF treatment?
HFpEF
- evidence based treatment guidelines are limited
- Priority is symptom relief and managing comorbidities
126
In treatment of HFpEF, what medication effects should be carefully monitored?
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
Should digoxin be used in HFpEF treatment?
Only if atrial fibrillation or flutter is present
128
What is the role of aldosterone antagonists in HFpEF treatment?
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
What is the role of an implantable cardioverter defibrillator in heart failure management?
- 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
What is the role of cardiac resynchronization therapy (CRT) in heart failure management?
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
What is the role of Left ventricular assist devices in heart failure management?
Used as a bridge to recovery or transplant or other care decisions
-Patients with 1 year survival of less than 50%
