Newman Review Flashcards

1
Q

How could you raise the stroke volume?

A

Increase preload or contractility

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2
Q

Most important equation

A

Pressure (MAP) = Flow (CO = HR x SV) x R (TPR)

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3
Q

What is the ejection fraction?

A

SV/EDV

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4
Q

What do you do when you encounter heart failure with low ejection fraction? How do you do it?

A

Reduce the afterload via 1 of 2 determinants: left ventricular size or SBP

Dilated ventricle is a big part of this (afterload)

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5
Q

What does aortic regurgitation cause?

A

Volume overload leading to eccentric hypertrophy

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6
Q

What are the 2 mechanisms of dysrhythmias?

A

Automaticity and reentry

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7
Q

What things alter automaticity?

A

Digoxin, hypoxia, CO2, acidosis, hypokalemia, low magnesium

Alter phase 4 of the AP such that it reaches threshold

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8
Q

What are the prerequisitites for reentry?

A

Two continuous pathways with different conduction velocities

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9
Q

What does it mean if you have JVD, barely palpable BP, and pulse that goes away with inhale (i.e., pulsus paradoxus)?

A

IV septum has received inspiratory volume, ventricle has tried to expand, but can’t, so IV septum imposes on LV, decreasing stroke volume

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10
Q

What are the signs of heart failure with a low EF? How do you fix this?

A

Laterally displaced PMI, larger than a dime or nickel, S3

Renin, angiotensin up

ACEI: decreases afterload (have to check serum potassium in 1 week b/c worried about hyperkalemia) -> should increase CO

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11
Q

What is the stress-exercise test for?

A

Test to diagnose CAD

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12
Q

What is stable CAD? How does it progress?

A

Supply-demand mismatch due to coronary narrowing

2 major determinants of O2 demand: HR and SBP (both of which INC during exercise; this is why you do a stress test)

Coronary angiogram: stable, fixed stenosis (usually about 70%)

3 MONTHS LATER: elephant sitting on chest -> rupture of plaque, leading to MI

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13
Q

How do you confirm aortic regurgitation?

A

Confirm via echo

LV will adapt via eccentric hypertrophy

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14
Q

How do you detect aortic stenosis?

A

Bell of stethoscope right underneath right clavicle

Concentric hypertrophy og LV

Echo

Risk for CAD development

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15
Q

How do you determine if person with mitral stenosis needs to be sent to sx?

A

Gradient: difference b/t LA and LV in diastole (normal is 0); can be measured via Doppler echo

Flow across valve: echo (flow affects CO)

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16
Q

How do you tell if mitral regurgitation is acute?

A

Echo, cath to look for lack of adaptation (eccentric hypertrophy) and/or marked elevation of pressure upstream (i.e., LA, pulmonary vein or capillary)

17
Q

What are the big risks with bacterial endocarditis?

A

Embolism (tricuspid to lungs; mitral to brain, kidneys, legs, coronary/MI)

Acute regurgitant lesions (i.e., chew up chordae tendineae)

18
Q

How do you detect pericarditis?

A

Feel better when they lean forward

Friction rub

19
Q

What causes sudden cardiac death? What if they survive?

A

Ventricular fibrillation

ICD

20
Q

What does mitral regurg sound like? Most common cause?

A

Systolic blowing murmur at the apex

Mitral valve prolapse (often has a distinctive click)

21
Q

Asymptomatic mitral regurg patient with no eccentric hypertrophy about to have dental procedure? What do you do?

A

Give her 4 amoxicillin an hour before

22
Q

What are some causes of ST elevation in absence of CAD?

A

Cocaine, vasospasm, hematocrit of 12 (anemia), aortic stenosis (not enough blood to coronary arteries), coronary emboli