Cardiology

Question 1

In patients receiving a stent (bare-metal or DES) during PCI for NSTE-ACS, P2Y12 inhibitor therapy should be given for at least?

Answer 1

12 months

Question 2

P2Y12 inhibitor therapy options include:

Answer 2

• Clopidogrel (plavix): 75 mg daily • Prasugrel (effient): 10 mg daily • Ticagrelor (Brillinta): 90 mg twice daily

Question 3

ACS: STEMI on EKG

Answer 3

• Anterior/anteroseptal – LAD – Leads V1 – V4 • Lateral – Circumflex – Leads V5 – V6 • Inferior – RCA – Leads II, III, aVF

Question 4

Which medications improves survival post-MI?

Answer 4

ACE-inhibitors, ß-blockers, statins, and ASA improve survival post MI.

Question 5

4 statin benefit groups

Answer 5

1. Individuals with clinical ASCVD 2. With primary elevations of LDL-C > 190 mg/dL 3. 40-75 yrs with diabetes and LDL-C 70-189 4. Without clinical ASCVD or diabetes, age 40-75, LDL-C 70-189, and estimated 10-year ASCVD risk of 7.5% or higher

Question 6

What is correct regarding the addition of nonstatin therapy to existing statin therapy?

Answer 6

Current RCT data shows event reduction with maximum tolerated statin intensity rather than with the addition of non-statin therapy: niacin, fibrates, omega3 fatty acids. While each of these may (numerically) improve components of the lipid profile, none has data demonstrating improvement in cardiovascular outcomes.

Question 7

“ATP IV” Basics on systolic heart failure and patients on hemodialysis

Answer 7

There are no good RCTs to support (or refute) the use of statins in: • Patients with NYHA Class II-IV ischemic systolic heart failure • Patients on maintenance hemodialysis

Question 8

ATP IV versus III for hypertriglyceridemia

Answer 8

• ATP IV makes no specific recommendations on the management of hypertriglyceridemia. • ATP III recommended treatment of triglycerides >500 mg/dL prior to initiation of statin therapy, with initiation of statin therapy after triglycerides were brought to <500 mg/dL, in order to decrease the risk of pancreatitis.

Question 9

High-intensity Statins

Answer 9

High-intensity (> 50% LDL-C reduction) Atorvastatin 40-80 mg Rosuvastatin 20 mg

Question 10

Moderate-intensity statins

Answer 10

Moderate-intensity (30% to < 50% LDL-C reduction) Atorvastatin (lipitor) 10-20 mg Rosuvastatin (crestor) 5-10 mg Simvastatin (Zocor) 20-40 mg Pravastatin (pravachol) 40-80 mg

Question 11

Heart failure with reduced ejection fraction (HFrEF)

Answer 11

EF <40% Also referred to as systolic HF RCTs have mainly enrolled patients with HFrEF, and it is only in these patients that efficacious therapies have been demonstrated to date

Question 12

Heart failure with preserved ejection fraction (HFpEF)

Answer 12

– EF >50% – Also referred to as diastolic HF – To date, efficacious therapies have not been identified.

Question 13

HFrEF / Systolic HF Treatment

Answer 13

Low cardiac output triggers neurohormonal activation, which ultimately results in premature apoptosis of cardiac myocytes. Preload reduction – Diuretics, nitrates Afterload reduction – ACEI, ARB, hydralazine, nitrates Sympathetic blockade – ß-blockers Aldosterone-antagonist therapy – Spironolactone, eplerenone

Question 14

Most common cause of Heart failure with preserved ejection fraction (HFpEF)

Answer 14

Hypertensive LV hypertrophy is the most common cause

Question 15

HFpEF Treatment

Answer 15

Careful decrease in heart rate, using ß-blocker (or non-dihydropyridine CCB) is appropriate. • If rapid atrial fibrillation/flutter is present, digoxin is indicated for rate control. – Larger doses of ß-blocker or non-dihydropyridine CCB may have excessive negative inotropic effect.

Question 16

BNP and Heart Failure

Answer 16

BNP is secreted from the ventricles in response to ventricular volume expansion and pressure overload. correlates with end-diastolic pressure. BNP undergoes partial renal excretion; levels are inversely proportional to creatinine clearance.

Question 17

BNP values and Heart Failure

Answer 17

BNP < 100 excludes CHF as a cause of dyspnea BNP > 400 confers a 95% likelihood of CHF

Question 18

ACE-Inhibitors and Heart Failure

Answer 18

ACEIs are preferred for HFrEF because they offer the greatest reduction in mortality.

Question 19

β-blockers and Heart Failure

Answer 19

Three have sufficient data to support their use: – Metoprolol succinate – Carvedilol – Bisoprolol Mortality rates are improved in HF patients who receive ß-blockers in addition to ACEIs and diuretics. ß-blockers decrease mortality in patients with prior MI, regardless of NYHA classification

Question 20

Contraindications to ß-blocker use include

Answer 20

– Hemodynamic instability – Heart block – Bradycardia – Severe asthma

Question 21

Good and Bad Drugs for HF

Answer 21

ACEIs, β-blockers, and aldosterone antagonists (spironolactone and eplerenone): – Reduce all-cause mortality – Improve ejection fraction in systolic HF Verapamil, due to its negative inotropic effect, is associated with worsening heart failure and an increased risk of adverse cardiovascular events.

Question 22

BP and Cardiovascular Risk

Answer 22

HTN is an independent risk factor for ischemic cardiovascular events. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressure, the risk of major cardiovascular events and stroke doubles

Question 23

What is recommended by the American Heart Association as a first-line agent for managing hypertension in patients with stable ischemic heart disease?

Answer 23

β-blockers and/or ACEIs for hypertensive patients with stable ischemic heart disease

Question 24

Hypertension plus: Diabetes: CKD: Clinical CAD: Stroke history: CHF:

Answer 24

Hypertension plus: Diabetes: ACEI or ARB CKD: ACEI or ARB Clinical CAD: β-blocker plus ACEI or ARB Stroke history: ACEI or ARB CHF: β-blocker plus ACEI or ARB, plus diuretic, plus spironolactone, regardless of BP

Question 25

most common cause of secondary hypertension in the middle-aged population

Answer 25

Primary hyperaldosteronism Diagnosis is based on the aldosterone/renin ratio.

Question 26

Renal Artery Stenosis

Answer 26

Most common cause: – Age < 30: fibromuscular disease – Age > 30: atherosclerotic disease Diagnosis: – MRA of renal arteries (or CT angiogram) – Elevated renin level alone is not diagnostic

Question 27

Treatment-Induced Decline in Renal Function

Answer 27

A 20-30% increase in creatinine, which then stabilizes, represents a hemodynamic change, and not a structural change. • Slight rise in creatinine serves as an indirect indicator that intraglomerular (IG) pressure has been reduced. • ACEI/ARB also dilate efferent arteriole, exaggerating decline in IG pressure. If creatinine increases by more than 30%, agent should be discontinued and other causes of renal dysfunction should be evaluated

Question 28

Thiazide Diuretics in HTN causes

Answer 28

Reduce excretion of: – Calcium (may slow bone demineralization) – Uric acid (increasing likelihood of gout) – Lithium (increasing risk of lithium toxicity) • Increase excretion of: – Potassium (average decrease of 0.3-0.4 mmol/L; dietary salt restriction can minimize thiazide-induced K loss) – Magnesium (complicates correction of hypo-K)

Question 29

Antihypertensive effect of HCTZ comparison to that of ACEIs, ARBs, CCBs, and β-blockers

Answer 29

Antihypertensive effect of HCTZ was significantly inferior to that of ACEIs, ARBs, CCBs, and β-blockers

Question 30

HCTZ Dose Titration

Answer 30

There was no significant difference in systolic or diastolic 24-hour BP reduction between HCTZ 12.5 mg and 25 mg. • With HCTZ 50 mg, the reduction in 24-hour BP was significantly higher and was comparable to that of other agents. • Adverse biochemical effects and risk of sudden cardiac death increase in a dose-dependent fashion with HCTZ doses that exceed 25 mg/d

Question 31

Resistant Hypertension

Answer 31

Persistent HTN despite > 3 drugs Spironolactone is an appropriate choice for treating resistant HTN

Question 32

Mobitz Type I Second Degree AV Block (Wenckebach)

Answer 32

The PR interval progressively lengthens until a P wave fails to conduct and a beat is “dropped.”

Question 33

What is the most likely pathological cause of Mobitz type I second degree AV block?

Answer 33

Almost always represents disease of the AV node In the acute setting, inferior wall ischemia is likely. – Inferior wall is supplied by RCA, which also supplies the AV node. – Anterior wall is supplied by the left coronary artery, which supplies the His-Purkinje system

Question 34

Mobitz Type II Second Degree AV Block

Answer 34

Characterized by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening Almost always represents disease of the distal conduction system, below the AV node: His-Purkinje system

Question 35

Mobitz Type II Second Degree AV Block treatment

Answer 35

Treatment: permanent pacemaker

Question 36

Third Degree AV Block (Complete Heart Block)

Answer 36

Characterized by a regular rhythm with complete AV dissociation. Impulses generated by the SA node do not propagate to the ventricles. Two independent rhythms can be noted on the EKG.

Question 37

VT versus sinus tachy and AVNRT

Answer 37

VT is a wide-complex rhythm

Sinus tachycardia and AVNRT (SVT is a more general term) are narrow complex tachycardia

Question 38

Narrow Complex Tachycardia treatment

Answer 38

Options to quickly slow AV conduction include

-Vagal maneuvers: Valsalva, unilateral carotid massage

– IV adenosine: 6 mg bolus; follow with 12 mg if ineffective

Electrical cardioversion is appropriate if hypotensive or ongoing chest pain. • Long-term therapy with digoxin, diltiazem, or ß-blocker. • Ablation of the reentrant pathway is an increasinglyemployed alternative.

Question 39

Atrial Flutter atrial rate

Answer 39

300

Vagal maneuver (arrow) slows AV conduction and makes the flutter waves more apparent (arrowheads)

Question 40

Answer 40

MAT is an irregular narrow-complex rhythm with 3 or more P waves of variable morphology.

• Most commonly seen in patients with lung disease; can occur post-MI or with hypokalemia or hypomagnesemia.
• Rate may be reduced with IV verapamil.

Question 41

Atrial Fibrillation: CHA 2DS 2-VASC

Answer 41

Atrial Fibrillation: CHA 2DS 2-VASC Congestive heart failure = 1 point Hypertension = 1 point Age = 65-74 = 1 point Age > 75 = 2 points Diabetes = 1 point Prior Stroke or TIA = 2 points VAScular disease = 1 point Female = 1 point

Question 42

Ventricular Tachycardia (VT)

Answer 42

• > 3 beats in a row that originate from the ventricle at a rate of more than 100 bpm
• Self-termination within 30 seconds: non-sustained VT
• Duration > 30 seconds: sustained VT (even if it ultimately self-terminates)

Question 43

Torsades de Pointes

Answer 43

Usually nonsustained; may evolve into ventricular fibrillation.

• Associated with hypomagnesemia, hypokalemia and medications or conditions that prolong the QT interval

Question 45

Abdominal Aortic Aneurysm (AAA)

Answer 45

Aneurysm is > 50% in vessel diameter

Normal aorta diameter is 1.8-2.0 cm

Location: 95% are infra-renal (Thoracic and supra-renal aneurysms do occur think Marfan’s, Ehlers-Danlos, syphilis)

Pathogenesis: Atherosclerosis

Rupture: 60% of patients die before arrival

Only 50% that do arrive alive, survive

Question 46

Screening for AAA

Answer 46

One-time screening for men ages 65-75, who have ever smoked

Question 47

You identified an abdominal aortic aneurysm (AAA) in your patient. At what size (in centimeters) should you refer your patient for surgical intervention?

Answer 47

5 - 5.5 cm

Question 48

Your patient’s AAA diameter is 4.5 cm. He leaves your practice and returns 4 yrs later where you meet him in the ED complaining of severe right flank/ abdominal pain.

Vitals: 120/60, P = 90, afebrile Labs: H/H = 13/39, Urine = 10-20 RBC’s/hpf

Which of the following should be performed?

Answer 48

STAT non-contrasted abdominal CT scan

Question 49

AAA versus Aortic disection

Answer 49

Aortic dissections are NOT aneurysms The pathophysiology is different!!!!

Question 50

Aortic Dissection: Location

Answer 50

• Ascending Aorta (60-65%) Type A
• Descending Aorta (30-35%) Type B (After origin of subclavian artery)

Question 51

Aortic Dissection: Diagnosis

Answer 51

Echocardiography

1. Transthoracic (TTE) 2. Transesophageal (TEE)

CT scanning (with contrast)

• MRI
• Aortography

All are acceptable, depends on what you have available!

Question 52

Aortic Dissection: Management

Answer 52

2 Goals:

• Lower blood pressure to BP sys 90-110 – IV nitroprusside
• Lower velocity of LV ejection – IV esmolol

Pearl: Start with your B-Blocker

Question 53

Arterial Occlusive Disease chronic versus acute

Answer 53

• Chronic due to: Atherosclerosis => Claudication
• Acute due to: Thromboembolic => 5 “P’s

Question 54

Claudication: Definition

Answer 54

Reproducible ischemic muscle pain - that occurs with exercise, - relieved with rest

It’s stable angina…of the legs!!!

Question 55

Chronic Arterial Occlusive Disease Screening

Answer 55

An ABI >1.4 indicates noncompressible arteries (calcified vessels)

Bottom Line: “Normal” ABI = 0.9 - 1.4

Question 56

PAD: Management

Answer 56

Question 57

Acute Arterial Occlusion

Answer 57

• Thromboembolic
• Heart is most common source: 80-90%
• Presentation: The 5 “ P’s ”

– “ P ”ain

– “ P ”allor

– “ P ”aresthesia

– “ P ”ulselessness

– “ P ”aralysis

Question 58

Acute Arterial Occlusion Management

Answer 58

Start heparin and immediately consult a vascular surgeon