Cardiovascular

Question 1

A person with horrendous arteries has their left coronary artery obstructed at time 0. How long until the muscle fibers that receive oxygen from that artery stop contracting? How long until irreversible damage occurs?

Answer 1

The muscle fibers will pretty much immediately stop contracting when ischemia begins. It switches from aerobic to anaerobic, and the amount of ATP greatly diminishes. However, all damage is reversible until after about 30 minutes.
Moral of the story? In heart attack, get the vessel open quick to avoid major permanent damage.

Question 2

What are the first and second line drug choices for ventricular arrhythmia post-MI?

Answer 2

1) Amiodarone (increases AP duration, ERP, and QT interval)

2) Class IB sodium channel blockers (lidocaine, mexiletine)-these preferentially affect ischemic tissue

Question 3

You have a patient on long-term isosorbide dinitrate. What is an important instruction you should give this patient?

Answer 3

Make sure to have a nitrate-free period (ie don’t take it at night) to avoid nitrate tolerance. It’s easy to gain tolerance to nitrates, something you don’t want to happen.

Question 4

In which vessel will blood be MOST deoxygenated in the body? (Even more so than the pulmonary artery)

Answer 4

The coronary sinus. Heart muscle needs the most oxygen, so it takes the most. Also, remember that heart muscle is perfused during DIASTOLE.

Question 5

What are the 4 components of the Tetralogy of Fallot?

Think PROVe

Answer 5

1) Pulmonary stenosis
2) Right Ventricular Hypertrophy (boot-shaped heart)
3) Overriding Aorta
4) Ventricular-Septal Defect (VSD)

Question 6

Why are Adenosine and Dipyridamole not good drugs to give when a heart is under ischemic conditions?

Answer 6

When the heart is ischemic, the blocked vessels are already dilated maximally trying to get blood into there. Normally, blood goes to those vessels through collaterals. However, these 2 drugs cause coronary vessel dilatation, which results in the blood flowing more towards the unblocked vessels, and shunting away from ischemic areas. This is bad.

Question 7

What is Beck’s triad, and what diagnosis does it indicate? What are common causes?

Answer 7

Diagnosis=Cardiac Tamponade.
Triad=Pulsus paradoxus (BP decreases on inspiration >10mmHg), elevated JVP (ie JVD), and diminished heart sounds.
Causes: Malignancy, Infection, Drugs (hydralazine, isoniazid, Connective Tissue diseases (lupus, RA).

Question 8

What is a prolonged QT interval involved with, and what are drugs that commonly can cause this syndrome?

Answer 8

Torsades de Point.
Drugs: Class IA and III Antiarrhythmics (sotolol, quinidine), Antipsychotics (haloperidol), and Antibiotics (macrolides, fluoroquinolones).

Question 9

What is the mechanism of digoxin?

Answer 9

It blocks the Na/K ATPase, which raises intracellular Na. This in turn slows down activity of the Na/Ca exchanger, so intracellular Ca increases and contractility in turn increases.

Question 10

What occurs in Phase 0 of myocardial AP?

Answer 10

Rapid depolarization (resting membrane potential reaches threshold)-voltage gated Na gates open, Na INflux.

Question 11

What occurs in Phase 1 of myocardial AP?

Answer 11

Initial repolarization-voltage gated Na gates close, Voltage gated K gates open, K EFflux.

Question 12

What occurs in Phase 2 of myocardial AP?

Answer 12

Plateau phase. Ca INflux through voltage gated Ca channels matches K EFflux. The Ca influx triggers Ca release from SR–>myocyte contraction.

Question 13

What occurs in Phase 3 of myocardial AP?

Answer 13

Rapid repolarization. Massive K efflux due to opening of voltage gated K slow channels. Ca channels close.

Question 14

What occurs in Phase 4 of myocardial AP?

Answer 14

Resting potential (between -80 and -95 mV). High K permeability through K channels. Sodium then leaves and K enters via the Na/K ATPase pump. (Digoxin blocks the Na/K ATPase pump)

Question 15

You are looking to prescribe a calcium channel blocker to someone who has sinus bradycardia and a prolonged QR (>200 msec). What type of calcium channel blocker should you give?

Answer 15

You should give a DIHYDROPYRIDINE (-ipine).
These only affect peripheral arteries (dilation), and thus won’t worsen the existing heart problems.
Nondihydropyridines (Verapamil, diltiazem) act more on the heart and will slow HR and AV conduction. (Verapamil>Diltiazem for heart effects)

Question 16

If a DVT ends up in the carotid artery, what can you assume? What murmur would be likely?

Answer 16

This is called a paradoxical embolism. You can assume that there must be some sort of defect that allowed for the embolus to cross from the right chamber to the left chamber (ie PFO, ASD or VSD).
Shunts cause wide and fixed splitting of S2.

Question 17

Somebody comes in with a dilated coronary sinus. What process is most likely causing this issue? Why?

Answer 17

Pulmonary hypertension, which increases right heart pressure. The coronary sinus empties into the right atrium. So anything causing backup in the right atrium would also cause backup of the coronary sinus.

Question 18

What is the effect of nitroprusside on preload, afterload, and stroke volume?

Answer 18

Nitroprusside is a balanced vasodilator of both arteries and veins, so it reduces both preload and afterload equally, and as a result the stroke volume remains the same.

Question 19

How can you differentiate between eccentric and concentric cardiac hypertrophy, and what are common causes of each?

Answer 19

Concentric: Thickening of ventricle wall, narrowing of ventricular cavity. Due to increased afterload (ie chronic hypertension)
Eccentric: Reduced ventricular wall thickness, increase in chamber size. Associated with volume overload (ie mitral regurgitation, dilated cardiomyopathy, myocardial infarction)

Question 20

Heart/Chest pain that is worse with inspiration, gets better by sitting up.
Diagnosis? What would you expect to hear?

Answer 20

Acute pericarditis.

You would hear a friction rub.

Question 21

Patient has bad jaw pain, along w/ history of diabetes, hyperlipidemia, hypertension. >50 yrs old. Arterial biopsy shows giant cells w/ elastic membrane fragmentation. Diagnosis? Complications?

Answer 21

Giant cell arteritis (most common vasculitis).

Ischemic optic neuropathy is a complication, and very dangerous. Need to treat immediately with glucocorticoids.

Question 22

Where is the AV node located?

Answer 22

Endocardial surface of RA. Near septal leaflet of tricuspid valve and orifice of coronary sinus.

Question 23

A patient is on an anthracycline (-‘rubicin’) to treat their AML. They have exertional dyspnea. What’s the underlying problem?

Answer 23

Dilated cardiomyopathy–>these drugs produce free radicals in the myocardium that cause dilated cardiomyopathy. Present with signs of R and L ventricular HF.

Question 24

Bounding femoral pulses, as well as carotid pulses that cause head bobbing. What’s the diagnosis?

Answer 24

Aortic regurgitation. There’s a big LVSV, so the heart really has to crank it out. It’s an incompetent aortic valve, you’ll also see increased pulse pressure (and end diastolic volume in the LV).

Question 25

A patient presents with acute angina that radiates tot he back and unequal elevated BPs in both arms (L>R). What is the likely cause?

Answer 25

Aortic dissection (intimal tear)

Question 26

What are the symptoms of digoxin toxicity?

Answer 26

Think cholinergic-N/V, diarrhea, blurry yellow vision, ARRHYTHMIAS.
Also hyperkalemia.

Question 27

You prescribe a nitrate to someone. What is the general mechanism of action?

Answer 27

They are vasodilators (veins»>arteries).

The INCREASE the capacitance of the veins, and thus DECREASE the amount of blood delivered to the heart.

Question 28

You start a patient on aspirin for their angina, but they have shortness of breath and wheezing. Which drug should you switch them to?

Answer 28

An ADP receptor inhibitor (ie Clopidogrel, prasugrel, ticagrelor, ticlodipine).
The reason for this is because they prevent cardiovascular events in patients with coronary artery disease as effectively as aspirin.

Question 29

What are the negatives of using a medication that ONLY causes vasoconstriction in arteries (ie hydralazine, minoxidil)?

Answer 29

They temporarily reduce systemic vascular resistance, but eventually they lead to activation of the sympathetic NS. This results in increased HR, contractility, output, and ACTIVATES RENIN-ANGIOTENSIN-ALDOSTERONE axis, which increases sodium and fluid retention, and thus offsets the meds’ desired effect.
Thus, they’re usually given with sympatholytics and diuretics.

Question 30

What is the mechanism of action of statins?

Answer 30

Statins inhibit the rate-limiting enzyme of hepatic cholesterol synthesis, thus causing the hepatocytes to increase their expression of LDL receptors to increase cholesterol uptake.

Question 31

A patient has an increased pulmonary capillary wedge pressure, in fact it is greater than the LV end diastolic pressure. What does the PCWP typically approximate, and what would cause it to be increased?

Answer 31

It typically approximates the left atrial pressure.
If it is greater than the LVEDP, it means that there is mitral stenosis. This is because there is resistance to blood flow from the LA to the LV. This increased pressure is then registered in the pulmonary veins.

Question 32

You give a drug that results in vasodilation of the coronary vessels due to nitric oxide. Which amino acid is necessary since it is the precursor to nitric oxide?

Answer 32

Arginine. Nitric oxide is synthesized from arginine by nitric oxide synthase.
Arginine supplementation may play some sort of role in the treatment of conditions that improve with vasodilation.

Question 33

A patient had an MI over a year ago, and they just died. Upon autopsy, what type of cartilage would you expect to see in the scar on their heart?
What type would you have seen within the first week of the MI?

Answer 33

Type 1 collagen–the same found in tendons.
It is the primary collagen in mature scars.
Within the first week you would’ve seen Type 3 collagen (granulation tissue).