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74 Cards in this Set

  • Front
  • Back
Are the number of hospitalizations for HF increasing or decreasing?
increasing, 1 million annually
What stage are refractory HF pts?
stage D, typically class III or IV
persistent symptoms despite optimal tx with ACEI and BB
What is decompensated HF or exacerbation of HF?
pt with ne or worsening signs or symptoms, which are usually caused by volume overload and/or hypoperfusion and lead to additional medical care
What is acute HF?
pt with a sudden onset of s/s of HF in setting of previously normal cardiac function
What clinical syndromes are seen in decompensated HF?
systemic volume overload, low output, acute pulmonary edema
What can cause decompensation?
dietary indiscretion, medical noncompliance, noncardiac concurrent illness (infection), recurrent MI, atrial fibrillation, myocarditis, or acute valvular insufficiency,
large MI or sudden increase in BP in setting of LV dysfunction
severe LV systolic dysfunction associated with progressive worsening of cardiac output and refractoriness to tx
What are predictors of in hospital mortality in acute decompensated HF?
best: BUN greater than or equal to 43mg/dL
SBP less than 115mmHg, serum Cr 2.75mg/dL or higher
others: hyponatremia, elevations in troponin I, ischemic etiology, poor functional capacity, additional negative prognostic factors
What is goal of tx in decompensated HF?
relieve congestive symptoms or optimize volume status as well as tx symptoms of low CO, so pt is discharged in compensated state on PO drug
minimize risk of drug tx
What risks from drug tx?
diuretic induced electrolyte depeletion, hypotension from vasodilators, myocardial ischemia and arrhythmias from positive inotropes
What is the more common presentation of HF?
congestion
What is the main symptom of fluid overload that best correlates with elevated pulmonary pressures?
orthopnea
What is the most reliable indicator of the pts volume status?
jugular venous pressure: follow during hospitalization as an indicator of the efficacy of diuretic tx
What is S3 gallop?
represents ventricular filling, high diagnostic specificity for HF decompensation
Dose pulmonary crackles and lower extremity edema have high specificity and sensitivity for the diagnosis of decompensated HF?
no
Is BNP used in diagnosis of acute decompensated HF?
aid in diagnosis: plasma BNP is positively correlated with the degree of LV dysfunction and HF (used in differential diagnosis: asthma, COBD, or infection)
low BNP has a 96% predictive value for excluding HF
elevated prehospital discharge BNP associated with increased risk of worse long term outcome
What is required to elevate BNP?
any disease process that increases right heart pressures: pulmonary emboli, chronic obstructive lung disease, primary pulmonary HTN
mild increase: increasing age, female, renal dysfunction
What is associated with a lower BNP?
obesity
When is admission to ICU required?
hemodynamic instability requiring frequent monitoring of vital signs, invasive hemodynamic monitoring, or rapid titration of IV meds with concurrent monitoring to assure safe and effective outcomes
When is hospitalization recommended?
severely decompensated HF: hypotension, worsening renal function, altered mentation
dyspnea at rest: resting tachypnea, oxygen saturation less than 90%
hemodynamically significant arrhythmia: new onset of rapid atrial fibrillation
acute coronary syndromes
When should hospitalization be considered?
worsened congestion: even without dyspnea, wt gain 5kg or more
s/s pulmonary or systemic congestion: even in absence of wt gain
major electrolyte disturbance
comorbid conditions: pneumonia, pulmonary embolus, DKA, TIA/stroke
repeated implantable cardioverter defibrillator firings
previous undiagnosed HF with s/s of systemic or pulmonary congestion
What is first step in management of decompensated HF?
ascertain that optimal tx with PO meds has been achieved
What is tx if fluid retention is evident?
aggressive diuresis: IV diuretic may be necessary
Is ACEI and BB continued in decompensated HF?
yes, d/c BB if dose initiation or up titration was responsible for the decompensated state
d/c ACEI or BB if cardiogenic shock or symptomatic hypotension
What tx are held in renal dysfunction, especially oliguria or hyperkalemia?
ACEI, ARB, aldosterone antagonist
What is target trough for digoxin in decompensated HF?
0.5-1ng/mL
What is essential for assuming optimal response to tx while avoiding AE in decompensated HF?
close monitoring
daily: wt, strict fluid I & O, HF s/s, orthostatic BP
frequently: electrolyte depletion, symptomatic hypotension, renal dysfunction
vital signs: multiple times/day
Is foley catheter placement recommended in decompensated HF?
only if close monitoring of urine output is needed
When should wt be measured?
after voiding in the morning, account for possible increased food intake
What signs of decompensated HF should be monitored daily?
edema, acites, pulmonary rales, hepatomegaly, increased jugular venous pressure, hepatojugular reflux, liver tenderness
What symptoms of decompensated HF should be monitored daily?
orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough, dyspnea, fatigue
What electrolytes should be monitored daily?
K, Mg, Na
What is wet HF?
s/s of fluid overload: orthopnea, dyspnea with minimal exertion, systemic congestion (GI discomfort, ascites, peripheral edema)
What is dry HF?
s/s of low cardiac output: extreme fatigue and tiredness, poor appetite, nausea, early satiety,
worsening renal function and decline in serum Na
Do most pts present with wet or dry HF?
wet
Can pt present with s/s of dry and wet HF?
yes: low output symptoms may not be obvious until congestion is optimally treated
What is the minimal noninvasive standard of care for critically ill pts with cardiopulmonary decompensation?
ECG monitoring, continuous pulse oximetry, urine flow monitoring, and automated BP recording
What is used for continuous and acurate assessment of arterial pressure?
peripheral or femoral arterial catheters
When is invasive hemodynamic monitoring considered?
pts who are refractory to initial tx, whose volume status is unclear, or who has clinically significant hypotension such as SBP less than 80mmHg, or worsening renal function despite therapy
What is invasive hemodynamic monitoring usually performed with?
a flow directed pulmonary artery or Swan-Ganz catheter placed percutaneously through a central vein and advanced through the right side of the heart and into the pulmonary artery
How is the pulmonary artery occlusion pressure measured?
inflation of a balloon proximal to the end port allow the catheter to "wedge" yielding the pulmonary artery occlusion pressure
What does the pulmonary artery occlusion pressure estimate?
pulmonary venous pressure and, in the absence of intracardiac shunt, mitral valve disease or pulmonary disease, the LV diastolic pressure
What is risk of death at 1 year for wet warm and wet cold compared to dry warm?
wet warm: 2 fold risk
wet cold: 2.5 fold risk
What is subset I pts?
CI and pulmonary artery occlusion pressure within generally acceptable ranges, lowest mortality of any subset
What tx for subset I?
maximize PO tx and monitoring
Can pt with significant LV dysfunction still present in subset I?
yes
Who are subset II pts?
adequate CI but pulmonary artery occlusion pressure is greater than 18mmHg
likely to have pulmonary congestion (wet HF)
What is goal in subset II?
reduce pulmonary congestion by lowering pulmonary artery occlusion pressure
reduce filling pressures without reducing CO, increasing HF, or further activating neurohormones
What result if decrease pulmonary artery occulusion pressure excessively?
significant decrease in CI
What should pulmonary artery pressure be lowered to?
normal is 5-12mmHg, higher pressures of 15-18mmHg needed for HF pt to optimize CI while avoiding pulmonary congestion
Why can pulmonary artery occlusion pressure be lowered to 15-18mmHg with little decrease in CI?
Frank-Starling curve is flatter at higher pulmonary artery occlusion pressure values
What tx for goal in subset II?
IV agents that reduce preload: loop, nitroglycerin, nesiritide
very rapid decrease in preload, may take longer for s/s of pulmonary congestion to resolve
What is 1st line tx for pt admitted with fluid overload?
loop diuretic: achieve desirable volume status without causing a rapid reduction in intravascular volume resulting in symptomatic hypotension or renal dysfunction
How much fluid if hyponatremic (less than 130mEq/L)?
less than 2L/day
When are IV vasodilators considered in addition to diuretics for rapid symptoms resolution?
acute pulmonary edema or severe HTN, as well as in pts who fail to respond to aggressive tx with diuretics
When should vasodilators be avoided?
symptomatic hypotension, low left heart filling pressure
What is considered if pt doesn't respond to diuretics or vasodilators?
IV inotropic tx
What is considered subset III?
CI less than 2.2L/min/m2 and normal pulmonary artery occlusion pressure
How does subset III present?
no evidence of pulmonary congestion
s/s of peripheral hypoperfusion: decreased urine output, weakness, peripheral vasoconstriction, weak pulses
What is mortality rate of subset III compared to pt without hypoperfusion?
4x higher
What is goal of subset III tx?
alleviate s/s of hypoperfusion by increasing CI and perfusion to essential organs
What is tx for subset III?
mild LV dysfunction: IV fluid may be all that is needed to achieve CI above 2.2L/min/m2
IV positive inotropic agens: dobutamine, milrinone
and/or arterial vasodilators: nitroprusside, NTG
When are IV inotropes recommended?
symptom relief of end organ dysfunction in pts with LV dysfunction and low cardiac output syndrome
What monitoring for inotropes?
frequen BP monitoring and continuous monitoring for arrhythmias (d/c or lower dose)
Who should avoid inotropes?
low left heart filling pressures
Should inotropes or vasodilators be considered first?
vasodilators
Should inotropic tx be used in the broad decompensated HF population?
no
What is used to "bridge" pts with cardiogenic shock to heart transplantation or left ventricular assist device?
inotropes
What is subset IV pt?
CI less than 2.2L/min/m2 and pulmonary artery occlusion pressure higher than 18mmHg
worst prognosis of any subset
How does subset IV pt present?
symptoms of "wet" and low output HF
What are tx goal in subset IV?
alleviate s/s by increasing CI above 2.2L/min/m2 and reducing pulmonary artery occlusion pressure to 15-18mmHg while maintaining and adequate MAP
What is tx for subset IV?
diuretic plus positve inotrope
nitroprusside is particularly useful because of mixed arterial venous vasodilating effects
significant hypotension: inotropic agent with vasopressor activity
Is subset II pulmonary congestion of hypoperfusion?
pulmonary congestion
Is subset III pulmonary congestion or hypoperfusion?
hypoperfusion
fig 16-8 16-10 pg 203
203