Cardio 2 Flashcards

1
Q

What happens with Myocardial Hybernation?

A

There is chronic myocardial ischemia due to reduced cardiac metabolism and function to match a reduction in coronary blood flow (stenosis) to prevent necrosis. As a result, there is disorganization and dec. expression of contractile and cytoskeletal proteins, leading to dec. contractility and LV systolic dysfunction.

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2
Q

What is the pathogenesis leading to aortic dissection?

A

A tear in the tunica intima is the primary event. As more blood is forced through the tear, a hematoma develops b/w the intimal flap and the medial wall, creating a false lumen.
*HTN is the most important RF.

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3
Q

W/ right heart failure, why is it that sometimes a patient will not present w/ peripheral edema?

A

RHF causes inc. central venous pressure, w/c leads to inc. capillary hydrostatic pressure and inc. interstitial fluid pressure. As interstitial fluid pressure rises, so does lymphatic drainage, w/c can compensate for moderate CVP elevations. Large CVP elevations result in overt edema.

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4
Q

What is the recommended treatment for acute obstructive pulmonary exacerbations (like in Asthma, COPD)?

A

Beta-agonists (B2 receptor) usually treat these exacerbations by activating adenylyl cyclase to inc. intracellular cAMP, thus relaxing bronchial smooth muscles.

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5
Q

In absence of a pericardial disease, what may cause a patient to have pulsus paradoxus?

A

Asthma and COPD exacerbations are the most frequent causes of pulsus paradoxus in absence of pericardial disease. The significant drop in intrathoracic pressure upon inspiration is transmitted to extrathoracic structures, leading to an inc. drop in BP upon inspiring.

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6
Q

What determines the amount of deO2 blood entering the systemic circulation in Tetralogy of Fallot?

A

The degree of right ventricular outflow tract obstruction (via pulmonary stenosis). Significant RVOT obstruction means more deO2 blood is shunted into aorta and the patient appears cyanotic.

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7
Q

How do “tet spells” happen in TOF?

A

The degree of RVOT obstruction by pulmo stenosis is dynamic and can increase suddenly, leading to episodes of profound cyanosis. Squatting can relieve tet spells by inc. SVR while PVR remains the same.

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8
Q

How would you treat the hemodynamic instability caused by mitral regurgitation?

A

MR has inc. preload and inc. afterload. Preload can be reduced w/ Diuretics, therefore decreasing LVEDV. Afterload can be reduced by vasodilators to decrease the intraventricular systolic pressure needed to generate a given stroke volume.

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9
Q

Why may aortic regurgitation present w/ a sense of pounding or uncomfortable heartbeat sensation?

A

AR causes inc. LVEDV and wall stress. The resulting chamber enlargement and eccentric hypertrophy causes inc. total SV, w/c may present w/ the pounding sensation and head bobbing.

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10
Q

What is the MOA of Nitrates to cause vascular smooth muscle relaxation?

A

Nitrates activate guanylate cyclase and inc. cGMP, w/c dec. intracellular Ca and activates myosin light chain phosphatase. This promotes myosin dephosphorylation and vascular smooth muscle relaxation.

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11
Q

B-blockers may be used in acute MI to dec. HR, CO, and myocardial O2 demand. Which B-blockers are safe in obstructive lung dses and which are not?

A

> Safe: Cardioselective – metoprolol, atenolol, bisoprolol, nebivolol.
Unsafe: Noncardioselective – propanolol, nadolol.
Well-tolerated: Combined Beta and alpha-blockers – Carvedilol, Labetalol.

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12
Q

Concurrent use of w/c drugs would increase the risk of Statin-induced myopathy?

A

The risk of severe myopathy is increased if Statins are given w/ fibrates (Gemfibrozil), w/c impair hepatic clearance of statins. Concurrent use of Niacin or Ezetimibe also increases the risk, but to a lesser extent.

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13
Q

What is the most important endogenous factor responsible for autoregulation of coronary blood flow?

A

Nitric oxide mediates vascular dilation in large arteries and pre-arteriolar vessels (ex. exercise inc. cardiac O2 demand, so blood flow needs to increase). NO is synthesized from arginine and O2 by endothelial cells via eNOs.

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14
Q

During what stage of the cardiac cycle is coronary blood flow minimal?

A

During ventricular systole, the myocardial blood vessels are compressed by the surrounding muscle. Systolic reduction in blood flow is greatest in the subendocardial region where wall pressures are highest, making it most prone to ischemia and MI.

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15
Q

What sarcomere contractile proteins are most involved in Hypertrophic cardiomyopathy?

A

Hypertrophic cardiomyopathy can be due to an AD mutation involving sarcomere genes encoding proteins like B-myosine heavy chain and myosin-binding protein C.

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16
Q

How are phosphodiesterase-3 inhibitors (Milrinone, Inamrinone) useful in refractory HF?

A

PDE-3 inhibitors dec. rate of degradation of cAMP in cardiac tissues, thus promoting Ca influx and increasing contractility.
But this inc. cAMP also causes systemic vasodilation, w/c limits use of PDE-3 inhibitors in patients w/ severe hypotension.