Unsorted Review

Question 1

How do PDE-5 inhibitors mediate an increase in Nitric Oxide?

Answer 1

PDE5 inhibitors block the breakdown of cGMP.
So, there is an increase in cGMP.

Higher intracellular cGMP = inhibit Calcium entry into cell.
So, decrease in intracellular calcium concentration.
So, Smooth muscle relaxation = dilation.
—————————

Nitric Oxide enhances guanyl cyclase, so enhances the breakdown of GTP to cGMP.
So, NO also increases cGMP.

PDE5= increase cGMP by inhibiting enzyme that breaks down cGMP.

NO = increase cGMP by enhancing enzyme that forms cGMP.

Nitroglycerin–>nitrate–>NO

So, if taking a PDE-5 inhibitor (incr cGMP by reduced breakdown), then take a nitrate (enhance cGMP by breaking down GTP faster), then there can be an excess of cGMP-mediated vasodilation.

=BAD
NO

Clinical Relevance: Patient who had taken sildenafil then was given nitroglycerin for chest pain. Causes severe hypotension.

Question 2

Which vasoactive effect in pulmonary circulation, vasoconstriction or vasodilation?
Endothelin 1 (ET1)

Answer 2

Vasoconstrictor

ET1 is a potent vasoconstrictor

Question 3

Which vasoactive effect in pulmonary circulation, vasoconstriction or vasodilation?
PGI2

Answer 3

Vasodilator

PGI2 and eNOS are vasodilators.

Question 4

Which vasoactive effect in pulmonary circulation, vasoconstriction or vasodilation?
eNOS pathway

Answer 4

Vasodilator
PGI2 and eNOS are vasodilators.
(ET1 is the potent vasoconstrictor)

Question 5

What are the 3 pathways in the pulmonary circulation which control the balance between vasoconstriction/vasodilation and affecting proliferation/anti-proliferation?

Answer 5

1. Prostacyclin
2. Endothelin
3. Nitric Oxide

Question 6

In a patient with mitral stenosis, if the symptoms are out of proportion to the resting hemodynamics on echocardiography, what is the next diagnostic step?

Answer 6

Remeasure hemodynamics during exercise.
If increase in mean gradient over 15mmHg or PA pressure over 60mmHg, patient would benefit from valve intervention.
(Exercise testing in MS with discrepancy is a Class IC recommendation)

Question 7

S/p thrombolytic therapy for inferior STEMI, sudden severe SOB and hypotension. Sitting bolt upright, rales in lung fields, no murmur.
What is going on and what are next steps?

Answer 7

Acute papillary muscle rupture resulting in severe acute mitral regurgitation.
Echo for diagnosis and urgent surgery.
(The pap muscle most involved is the posteromedial pap muscle due to single blood supply by PDA).
(remember: post MI- sitting upright: acute MR. Lying flat- VSD)

Question 8

70’s female, remote MI, EF 33%, ICD in place. Presenting with sustained palpitations, found to have wide complex tachycardia requiring shock. What is the preferred antiarrhythmic?

Answer 8

Amiodarone.
If an ICD is already in place, recurrent scar based VT is best treated with amiodarone.
(if fails, VT ablation, then finally neuroaxial blockade).

Question 9

First option of choice for acutely thrombosed mechanical mitral valve?

Answer 9

Emergency Operation. (esp with heart failure)

Distant 2nd option for left sided valves is thrombolytic therapy (long onset of action and high risk of embolic events)

Question 10

Acute severe aortic regurgitation.

What is the treatment of choice?

Answer 10

Urgent surgical intervention.

Question 11

For acute severe aortic regurgitation, urgent surgical intervention is the clear recommendation.
What medical therapy can be helpful while waiting for surgery?

Answer 11

Nitroprusside for afterload reduction

cannot use B-blocker, pressor, or IABP because will increase the AR severity

Question 12

What is the name for the process to help determine procedures such as ICD implantation?

Answer 12

Shared Decision Making

Question 13

Severe chronic AI, asymptomatic, nondilated, EF normal. What is the next step in management?

Answer 13

Continued observation with serial echocardiograms every 6 months.
Operate for symptoms, EF<50%, ESD>50mm, or EDD >65.

Question 14

What testing modality is indicated in a patient with syncope and structural heart disease without source identified with noninvasive testing?

Answer 14

Electrophysiology Study

Question 15

What are the 2 most common causes for a long RP interval tachycardia?

Answer 15

Sinus Tachycardia
Atrial Tachycardia
(if terminates after a QRS, indicative of an AT)

Question 16

S/P heart transplant, onset of low grade fever, palpitations, and shortness of breath within past 48 hours, intermittent high grade block, no syncope. Emergency biopsy shows T-cell infiltration. Next management step?

Answer 16

High Dose IV steroids is the immediate treatment.

This is T-cell mediated cardiac rejection.
Heart block will likely resolve with therapy.

Question 17

Patient with Left Bundle Branch block, able to walk well. Exercise testing or Pharmacologic stress?

Answer 17

Pharmacologic Stress.

High likelihood of false positive during exercise testing due to dyssynchronous contraction of septum.

Question 18

What are the order of treatment for SVT in pregnancy>

Answer 18

1. Vagal maneuvers
2. Adenosine
3. IV beta blocker metoprolol/propranolol
4. IV Verapamil
   (can cardiovert, but concern for fetal bradycardia

Question 19

In patients with a high likelihood of AMI and normal ECG, what kind of ECG should you get?

Answer 19

Supplemental leads V7-V9.

Aid in diagnosis of STEMI due to circumflex artery occlusion.

Question 20

In cirrhosis, which oral anticoagulants to avoid?

Answer 20

All of the novel anticoagulants.

Warfarin also has a risk, but with careful monitoring it is the safest of all anticoagulants

Question 21

What are the ECG characteristics of RVOT tachycardia?

Answer 21

1. LBBB
2. Positive forces in the inferior leads during tachycardia.

These are responsive to beta blockers or calcium channel blockers.
If intolerant to medical therapy, can undergo ablation