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FA notes > CV Resp > Flashcards

CV Resp Flashcards

1
Q

How does the ductus arteriosus normally close?

A

when baby takes first breath theres an increase in O2 which causes a decrease in prostaglandin production > closure of DA

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2
Q

What are the energy sources of the heart?

A
  1. Fatty oxidation (60%)
  2. Glucose oxidation
  3. Glycolysis
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3
Q

what is the most posterior part of the heart?

A

left atrium

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4
Q

calculate CO using rate of o2 and such

A

= rate of O2 consumption/arterial O2 content - venous O2 content

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5
Q

What happens when theres a wide splitting of A2/P2?

A

seen in conditions that delay RV empyting: pulmonic stenosis and right bundle branch block

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6
Q

What happens when theres a paradoxical splitting of A1 and P2?

A

seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block), normal valve closure is reversed since LV is trying to empty for a longer period of time

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7
Q

When can you hear an S3 the best?

A

left lateral decubitus position during exhalation

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8
Q

What murmurs are heard better w valsalva?

A

MVP and hypertrophic cardiomyopathies
(it decreases preload and afterload)
- decreases the intensity of most other murmurs

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9
Q

How does hand grip affect murmurs?

A

it increases afterload: increases intensity of MR, AR, VSD, MVP

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10
Q

How does the murmur of MVP change w position?

A

Standing up: decreases preload, click closer to S1

Lying down: increases preload, click and murmur closer to S2

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11
Q

Marfans pt dies slowly bc of a heart issue, what is it?

A

MVP- leading to conductive issue

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12
Q

left infraclavicular murmur loudest at S2

A

PDA: congenital rubella or prematurity

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13
Q

what phase of the cardiac AP does cardiac muscle contractoin occur?

A

phase 2

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14
Q

How do ACh and adenosine act on the pacemaker AP?

A

they decrease the rate of diastolic depolarization and decrease HR

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15
Q

Speed of conduction?

A

purkinje, atria, ventricle, AV node

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16
Q

how do T waves relate to K?

A 
Hyperkalemia = peaked T waves
Hypokalemia = flat T waves
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17
Q

how do you treat A flutter?

A
  1. Class IA, IC, or III antiarrhythmics

2. Rate control: betal blocker or Ca channel blocker

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18
Q

What can cause a first degree AV block?

A

lyme disease- but more likely causes third degree heart block if not treated

19
Q

where does ANP act in the kidney?

A

causes decreased Na reabsorption at the medullary collecting tubule

  • constricts efferent arteriole and dilates afferent arteriole via cGMP
  • contributes to the escape from aldosterone
20
Q

delta wave on ECG

A

wolf parkinson white syndrome: acessory conduction pathway that bypasses the AV node leading to early ventricle depolarization

  • also see a slurred upstroke of QRS
    tx: Procainamide or amiodarone
21
Q

where do the aortic arch and carotid sinus receptors send their info?

A

to solitary nucleus of medulla

22
Q

What happens in supine hypotension?

A

supine or right lateral decubitus position > compression of IVC > reduced venous return, reduced preload, reduced CO and hypotension

23
Q

Tricuspid atresia: what is it?

A

absence of tricuspid valve and hypoplastic RV

- requires both ASD and VSD for viabiliity

24
Q

boot shaped heart

A

tetrology of fallot

25
Q

how do pts with tetrology of fallot relieve cyanotic spells?

A

they squeat to increase PVR and decrease the right to left shunt

26
Q

why are beta blockers the drug of choice for aortic dissections?

A

decrease the slope of rise in BP

27
Q

how do you diagnose prinzmetals angina?

A

ergonovine challenge!

28
Q

how do you reverse a hibernating myocardium?

A

CABG revascularization!

29
Q

Time course microsopically of MI: contraction bands from reperfusion injury, release of necrotic cell content into blood, beginning of neutrophil migration

A

12-24 hrs

30
Q

Time course of MI: early coagulative necrosis, wavy fibers

A

4-12hrs

31
Q

Time course of MI: extensive coagulative necrosis, tissue shows acute inflammation, neutrophil migration

A

1-3days

32
Q

Time course of MI: macrophage infiltration followed by granulation tissue at the margins

A

3-14 days

33
Q

when is an MI pt most at risk for fibrinous pericarditis?

A

1-3days

34
Q

when is an MI pt most at risk of free wall rupture or papillary muscle rupture?

A

3-14days

35
Q

When is an MI pt most at risk for Dresslers syndrome?

A

~6 weeks

36
Q

tx of dresslers syndrome?

A

nonsteroidals

37
Q

treatment of MI?

A 
MONA
morphine
oxygen
nitrates
Aspirin
38
Q

inheritance of hypertrophic cardiomyopathy?

A

Autosomal dominant

39
Q

mutation of hypertrophic cardiomyopathy?

A

beta myosin heavy chain mutation

40
Q

What drugs reduce mortality in CHF?

A
  1. ACE inhibitors
  2. Beta blockers
  3. Angiotensin receptor antagonists
  4. Spironolactone
41
Q

how does syphilis affect the heart?

A

it disrupts the vasa vasorum, leading to atrophy of the vessel wall and dilation fo the aorta

42
Q

electrical alternans: alternating amplitude of QRS segment

A

cardiac tamponade

43
Q

most common heart tumor?

A

metastases from melanoma or lymphoma

FA notes (11 decks)

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