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Acute decompensated heart failure

What stage are patients with persistent/refractory symptoms despite oral therapy based on ACC/AHA staging system? Stage D
What class are patients that experience symptoms with mild or moderate exercise based on NYHA functional class? III(mild)-IV(moderate)
What are possible causes for ADHF? -Lifestyle/Medication non-adherence -Acute insult(AFib, acute coronary syndrome) -Disease progression
What is the body response to ADHF? Activation of RASS(increase in sodium & water retention -> preload) and SNS(incrase in SVR->afterload); arginine vasopressin secretion -> free water retention -> hyponatremia
How is ADHF diagnosed? -Dyspnea -BNP > 100 pg/mL
Reasons for false BNP elevation(2) -Pneumonia -Pulmonary embolism
Use of pulmonary artery catheter/swan ganz catheter help improveoutcomes) T/F) False
What are indications for PAC(3)? -Patients not responding to initial therapy -Pts whose volume status cannot be determine by hx of physical examination -Pts experiencing hemodynamical instability during tx
How are pts with CI < 2.2 L/min/m2 classified? Cold
How are pts with CI> 2.2 L/min/m2 classified? Warm
How are pts with PCWP of > 18 mmHg classified? Wet
How are pts with PCWP of 15 - 18 mmHg classified? Dry/Euvolimic
What is a normal PCWP? 6-12
What is a normal value for SVR measured using PAC? 800-1200 dyne*sec*cm5
What values of SVR are considered a vasoconstricted state? >1200 dyne*sec*cm5
What values of SVR are considered a vasodylated state? <800 dyne*sec*cm5
Clinical presentation of pulmonary edema? Crackles, hypoxemia, dyspnea, orthopnea, elevated PCWP
Clinical presentation of peripheral edema? Ascites, hepatomegaly/hepatojugular reflux
Goal of treatmet of ADHF? Restoration of hemodynamical stability and correction of fluid overload
When should beta blockers be d/c in the setting of ADHF? Cardiogenic shock or clinically significant hypotension
If a pt presents with ADHF and acute kideny injury which medications should be discontinued? RAAS, digoxin(renally excreted --> acumulation)
Why might ACE/ARBs and MRA be stopped? Decreased urine output might mean higher risk for hyperkalemia if already hyperkalemic upon admission.
What are three common vasodilators? Nitroglycerin, nitroprusside, nesiritide
What is the place in therapy of IV vasodilators? Persistent ADHF despite aggressive treatment with diuretics in the absence of hypotension(SBP < 90 mmHg)
Nitroglyerin effect at high vs low dose? Low dose: Venous dilation --> decreased preload High dose: Arterial dilation --> decreased SVR --> increased CI MOA: Nitric oxide donor
When should we expect tolerance development from Nitroglycerin? After 12 hours(might need to increase dose)
What is Nesiritide MOA? Recombinant BNP which promotes natriuresis, venous and arterial vasodilation.
What is Nitroglycerin MOA? Nitric oxide donor
Place in therapy of IV ionotropes Diuretic refractory patients with low CO or symptoms of hypo perfusion.
Mechanism of action of Dobutamine? Non-selective beta agonist with alpha 1 adrenergic agonist effects.
Mechanism of action of Milrinone? PDE3 inhibitor
What are major cardiovascular concerns with ionotropes? Arrhythmias: Sinus tachycardia, ventricular tachycardia, Afib
Created by: olimac



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