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100714 acute heart failure Flashcards

1
Q

heart failure is

A

any cardiac disorder that impairs ability of ventricle to fill or eject blood

NOT necessiarly “congestive” heart failure

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2
Q

tachycardia influences cardiac output how?

A

it decreases diastolic filling time

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3
Q

for acute heart failure, what should we do?

A

identify cause of acute heart failure

appropriately treat to achieve stable hemodynamic equilibrium

reverse the exacerbating stimulus

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4
Q

what is very important to do in a pt w/ acute heart failure?

A

physical exam

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5
Q

what assessments are done of a pt with acute heart failure

A

hx and PE
labs
echo
swan-ganz catheter (invasive hemodynamics)-to measure heart fxn and blood flow

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6
Q

important things to ask for hx for acute hearth failure

A

any recent changes to meds? (too much beta blocker?)

what do you eat for meals? (too much salt?)

do you weight yourself everyday (in terms of Na and water intake)

do you have chest pain? (MI)

how far can you walk?

how many pillows do you sleep with? do you wake up SOB? (correlates with L ventricular pressure)

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7
Q

PE findings for acute heart failure

A 
mitral regurg (b/c don't want to rule out papillary rupture)
crescendo-decrescendo murmur of aortic stenosis
S3 gallop (due to high overload)
P2 knock-suggests right ventricle volume or pressure overload

distended jugular veins

pulmonary-tachypnea, inspiratory crackles

lower extremity edema

hypotension (if less than 115 mmHg, is predictive of increased mortality in the context of heart failure)

decreased pulses, cold clammy skin –these two go along with shock

tachycardia (even rates of 110 should you make you think!)

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8
Q

S3 is caused by

A

early rapid diastolic filling of ventricle

seen in congestive heart failure, dilated cardiomyopathy

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9
Q

S4 is caused by

A

increased atrial contraction into noncompliant ventricle (stiff)

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10
Q

what labs would you want to look at for acute heart failure?

A

brain natiuretic peptide (made in response to stretch in heart)

troponin

BMP-assess renal fxn

CBC-anemia?

CXR-pulmonary edema?

mixed venous oxygen saturation

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11
Q

pulmonary wedge pressure

A

reflex left atrium and (if there’s no obstruction) left ventricular pressures

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12
Q

normal RA, RV, pulmonary artery, and pulmonary wedge pressures

A

5, 25, 20, 12

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13
Q

when would you consider a pulmonary artery catheter?

A

when you are unsure of fluid status, perfusion, systemic or pulmonary vascular resistance

if giving empiric therapy and pt gets hypotension or worsening renal fxn,

etc

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14
Q

wet

A

volume overload

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15
Q

cold

A

low perfusion at rest

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16
Q

symptoms of low perfusion

A 
narrow pulse pressure
sleepy
low serum sodium
cool extremities
hypotension with ACE inhibitor
renal dysfxn (one cause)
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17
Q

SVR

A

systemic vascular resistance

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18
Q

dry-what would measurements be?

A

PCWP under 18
and
RA pressure under 8

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19
Q

wet-what would measurements be?

A

PCWP greater than 18

or RA pressure greater than 8

20
Q

warm-measurements?

A

cardiac index greater than 2.2

21
Q

cold

A

cardiac index under 2.2

22
Q

holosystolic murmur could suggest

A

mitral regurg

23
Q

SVO2 indicates (if low)

A

more oxygen extraction from blood due to blood moving slowly (b/c heart doesn’t pump as well)

normal should be 70 or higher

24
Q

cold and wet-how prevalent

A

less than 3 percent of pts present w cardiogenic shock

25
Q

tx for cold and wet

A

diuretics
vasodilators
inotropes

26
Q

what to consider in tx for cold and wet

A

SVR?
BP?

if high SVR, you need to give vasodilator
if normal SVR, give inotropic drugs

27
Q

requirements for inotrope use

A

advanced systolic heart failure and low output syndrome and hypotension

vasodilators either ineffective or contraindicated (check BP?)

fluid overloaded and reponsive to diuretics or manifest deteriorarting renal fxn

28
Q

why are inotropes double edged swords?

A

increases in calcium leads to increased work and arrhythmia

29
Q

inotropes ex

A

dobutamine
milrinone
dopamine

30
Q

milrinone MOA

A

phosphodiesterase inhibitor

inodilator-inotrope and vasodilator

31
Q

inotropes work how?

A

by increasing intracellular calcium

32
Q

side effects of milrinone

A

hypotension
arrhythmia
tachycardia

33
Q

dopamine MOA

A

stimulates release of catecholamines

34
Q

dobutamine MOA

A

predominantly is a beta1 agonist with weak beta2 activity

weak beta2 activity means mild vasodilation

35
Q

side effects of dobutamine

A

arrythmia
angina
hypertension
tachycardia

36
Q

levosimendan MOA

A

calcium sensitizer and vasodilator

acts on troponin C to increase sensitivity to Ca

37
Q

what’s wrong with inotropes in acute decompensated heart failure?

A 
arrhytmias
hypotension
increased troponin release
increase in-hospital and 6 month mortality
does not shorten hospitalization
38
Q

diuretics side effects

A

electrolyte abnormalities (hypokalemia, hypomagnesemia, hyponatremia)

hypotension

gout exacerbation
hearing loss
increased incidence of digoxin toxicity
renal insufficiency
muscle cramps
39
Q

wet and warm prevalence

A

most pts with acute decompensated heart failure fall in this category

40
Q

goal for wet and warm

A

to decrease filling pressures (LVEDP, PCWP)

for majority-IV diuretics. may also require vasodilators

41
Q

nitroglycerin MOA

A

venodilator. arterial vasodilator at high doses

42
Q

limitations of nitroglycerin

A 
headache
hypotension
prolonged hypotension and bradycardia (rare)
tachyphylaxis
20% are nonresponders
43
Q

nitroprusside MOA

A

balanced vasodilator

44
Q

major limitations of nitroprusside

A

cyanide toxicity

accumulation of thiocyanate

45
Q

warm and wet tx

A

diuretics mainly

inotropes are not indicated

CV (34 decks)

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