100714 acute heart failure Flashcards
heart failure is
any cardiac disorder that impairs ability of ventricle to fill or eject blood
NOT necessiarly “congestive” heart failure
tachycardia influences cardiac output how?
it decreases diastolic filling time
for acute heart failure, what should we do?
identify cause of acute heart failure
appropriately treat to achieve stable hemodynamic equilibrium
reverse the exacerbating stimulus
what is very important to do in a pt w/ acute heart failure?
physical exam
what assessments are done of a pt with acute heart failure
hx and PE
labs
echo
swan-ganz catheter (invasive hemodynamics)-to measure heart fxn and blood flow
important things to ask for hx for acute hearth failure
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)
PE findings for acute heart failure
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!)
S3 is caused by
early rapid diastolic filling of ventricle
seen in congestive heart failure, dilated cardiomyopathy
S4 is caused by
increased atrial contraction into noncompliant ventricle (stiff)
what labs would you want to look at for acute heart failure?
brain natiuretic peptide (made in response to stretch in heart)
troponin
BMP-assess renal fxn
CBC-anemia?
CXR-pulmonary edema?
mixed venous oxygen saturation
pulmonary wedge pressure
reflex left atrium and (if there’s no obstruction) left ventricular pressures
normal RA, RV, pulmonary artery, and pulmonary wedge pressures
5, 25, 20, 12
when would you consider a pulmonary artery catheter?
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
wet
volume overload
cold
low perfusion at rest
symptoms of low perfusion
narrow pulse pressure sleepy low serum sodium cool extremities hypotension with ACE inhibitor renal dysfxn (one cause)
SVR
systemic vascular resistance
dry-what would measurements be?
PCWP under 18
and
RA pressure under 8
wet-what would measurements be?
PCWP greater than 18
or RA pressure greater than 8
warm-measurements?
cardiac index greater than 2.2
cold
cardiac index under 2.2
holosystolic murmur could suggest
mitral regurg
SVO2 indicates (if low)
more oxygen extraction from blood due to blood moving slowly (b/c heart doesn’t pump as well)
normal should be 70 or higher
cold and wet-how prevalent
less than 3 percent of pts present w cardiogenic shock
tx for cold and wet
diuretics
vasodilators
inotropes
what to consider in tx for cold and wet
SVR?
BP?
if high SVR, you need to give vasodilator
if normal SVR, give inotropic drugs
requirements for inotrope use
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
why are inotropes double edged swords?
increases in calcium leads to increased work and arrhythmia
inotropes ex
dobutamine
milrinone
dopamine
milrinone MOA
phosphodiesterase inhibitor
inodilator-inotrope and vasodilator
inotropes work how?
by increasing intracellular calcium
side effects of milrinone
hypotension
arrhythmia
tachycardia
dopamine MOA
stimulates release of catecholamines
dobutamine MOA
predominantly is a beta1 agonist with weak beta2 activity
weak beta2 activity means mild vasodilation
side effects of dobutamine
arrythmia
angina
hypertension
tachycardia
levosimendan MOA
calcium sensitizer and vasodilator
acts on troponin C to increase sensitivity to Ca
what’s wrong with inotropes in acute decompensated heart failure?
arrhytmias hypotension increased troponin release increase in-hospital and 6 month mortality does not shorten hospitalization
diuretics side effects
electrolyte abnormalities (hypokalemia, hypomagnesemia, hyponatremia)
hypotension
gout exacerbation hearing loss increased incidence of digoxin toxicity renal insufficiency muscle cramps
wet and warm prevalence
most pts with acute decompensated heart failure fall in this category
goal for wet and warm
to decrease filling pressures (LVEDP, PCWP)
for majority-IV diuretics. may also require vasodilators
nitroglycerin MOA
venodilator. arterial vasodilator at high doses
limitations of nitroglycerin
headache hypotension prolonged hypotension and bradycardia (rare) tachyphylaxis 20% are nonresponders
nitroprusside MOA
balanced vasodilator
major limitations of nitroprusside
cyanide toxicity
accumulation of thiocyanate
warm and wet tx
diuretics mainly
inotropes are not indicated
