Usmle - Cardio

Front 1

a wave

Back 1

atrial contraction

Front 2

c wave

Back 2

RV contraction (tricuspid value bulging into the atrium)

Front 3

v wave

Back 3

inc atrial pressure due to filling against close tricuspid valve.

Front 4

Normal S2 splitting happens because? Split gets wider when?

Back 4

the aortic valve closes before the pulmonic valve. Wider on inspiration

Front 5

When is the period of highest O2 consumption?

Back 5

During isovolumetric contraction

Front 6

What disease states cause wide splitting?

Back 6

Pulmonic stenosis or RBBB

Front 7

What disease states cause paradoxical splitting?

Back 7

Aortic stenosis or LBBB

Front 8

What effect does expiration have on the heart?

Back 8

increases LA return.

Front 9

What effect does inspiration have on the heart?

Back 9

Inc RA return

Front 10

Causes a wide pulse pressure

Back 10

Aortic regurg

Front 11

What are the phases of the pacemaker action potential?

Back 11

Phase 0, 3, 4, there is no phase 1 or 2 (plateau)

Front 12

What in the SA node potential determines HR?

Back 12

The slope of phase 4

Front 13

Aortic arch vs. Carotid sinus: which responds to inc/dec BP and which responds only to inc BP?

Back 13

The aortic arch only responds to inc BP

Front 14

What is the Cushing's triad associated with cerebral ischemia?

Back 14

HTN, bradycardia, respiratory depression

Front 15

What causes Tetrology of Fallot?

Back 15

Anterosuperior displacement of the infundibular septum

Front 16

preductal vs. postductal coarctation of the aorta

Back 16

Preductal: INfantile form, IN towards the heart

Postductal: aDult: Distal to the Ductus

Front 17

Monckeberg arteriosclerosis

Back 17

Calicification in the media of arteries, especially in the radial or ulnar. Usually benign; "pipestem" arteries. Does not obstruct bloodflow; intima not involved

Front 18

Atherosclerosis happens in what layer?

Back 18

In the intima

Front 19

Aortic dissection is most associated with what disease state?

Back 19

HTN

Front 20

ECG changes with stable angina

Back 20

ST depression

Front 21

ECG changes with Prinzmental angina? Sx?

Back 21

ST elevation. Coronary spasm happens AT REST

Front 22

ECG changes with unstable angina

Back 22

ST depression

Front 23

What is the most common cause of sudden cardiac death?

Back 23

a lethal arrhythmia

Front 24

Complications of MI:

First day:

2-4 days:

5-10 days:

7 weeks:

Back 24

First day: Risk for arr.

2-4 days: Risk for arr.

5-10 days: Risk for free wall rupture, tamponade, papillary muscle rupture, interventricular septal rupture

7 weeks: Risk for ventricular aneurysm. Also Dressler's syndrome

Front 25

Cardiac troponin I

Back 25

Rises after 4 hours and is elevated for 7-10 days. More specific than other markers.

Front 26

CK-MB

Back 26

Peaks at one day then drops

Predominantly found in myocardium but can also be released from skeletal muscle

Front 27

MI: what does ST elevation imply?

Back 27

transmural infarct

Front 28

MI: what does ST depression imply?

Back 28

Subendocardial infarct

Front 29

Frideich's ataxia is assoc w what type of cardiomyopathy?

Back 29

hypertrophic

Front 30

Loffler's syndrome

Back 30

endomyocardial fibrosis with a prominent eosinophilic infiltrate (causes a restrictive cardiomyopathy)

Front 31

Beta blockers are contraindicated in what disease state?

Back 31

In DEcompensated CHF

Front 32

What cardiac drug can cause cyanide poisoning?

Back 32

Nitroprusside

Front 33

Fendolopam

Back 33

Dopamine D1 receptor agonist - relaxes renal vascular smooth muscle.

Txt for malignant hypertension.

Front 34

Diazoxide

Back 34

K+ channel opener - hyperpolarizes and relaxes renal vascular smooth muscle. Can cause hyperglycemia (reduces insulin release)

Will maintain euglycemia in most patients with an insulinoma

Txt for malignant hypertension

Front 35

How do beta-blockers affect EDV and ejection time?

Back 35

EDV: inc

Ejection time: in

Everything else decs

Front 36

How do nitrates affect EDV and the ejection time?

Back 36

EDV: down

Ejection time: down

Front 37

What is a notable side effect of niacin?

Back 37

Can cause hyperuricemia and can thus exacerbate gout

Front 38

What is the effect of Fibrates (gemfibrozil, clofibrate, bexafibrate, fenofibrate)? MOA?

Back 38

Fibrates upregulate LPL causing increased TG clearance. TGs go way down.

Front 39

What is digoxin contraindicated with?

Back 39

With re-entrant arrhythmias. Digoxin can enhance transmission through accessory pathways --> V tach/V fib

Front 40

Indications:

Class IA:
Class IB
Class IC

Back 40

Class IA: a fib, v fib, esp reentrant and ectopic supraventricular tachycardia

Class IB: Acute v arr, esp post MI


Class IC: Useful in v tachs that progress to v fib and in intractable svt. Contraindicated post-MI

Front 41

Treat beta-blocker overdose with what?

Back 41

glucagon

Front 42

Check what when using amiodarone?

Back 42

Check LFTs, PFTs, and TFTs

Front 43

Effects of adenosine blocked by what other drug?

Back 43

Theophylline

Front 44

Left parasternal heave

Back 44

RVH

Front 45

Sustained apical heave

Back 45

AS --> LVH

Front 46

Cardiac issue that causes weak peripheral pulses

Back 46

AS

Front 47

Decreased S2

Back 47

AS

Front 48

Heart murmurs: ASD vs VSD

Back 48

ASD: a loud systolic ejection murmur over the midsternal border

VSD: A harsh holosystolic murmur over hte lower left sternal border.