E.4 ADHF Treatment Flashcards
In ADHF should we discontinue any medications?
We try not to due to rebound adrenergic output or vasoconstriction which could actually worsen the patients condition.
What is our goal for treatment of ADHF?
To maintain or achieve Class I. This means the patient is warm and dry. In other words they are perfusing well and are not congested.
What is the primary problem in a patient with class II ADHF?
Congestion (they are fluid overloaded but perfusing well.)
How do we treat Class II ADHF?
We need to dry them out using diuretics to reverse the fluid overload.
Patients with class ______ should receive diuresis that is _______ the home dose as IV.
If they are loop diuretic naive, they should be initiated on _____.
1) Class II ADHF
2) 1.5-2.5 X the home dose.
3) Furosemide 40 mg or equivalent IV.
After initiating a patient with congestion on a loop diurectic, what is our goal respnse?
What should we do if they do not achieve the goal?
1) At least 500 mL of urine per hour over the first 6 hours.
2) Double the dose.
In ADHF with congestion, what is our goal urine output?
1-2 liters negative/day. (losing 2 liters essentially)
In class III ADHF, what is the primary physiological problem?
Hypoperfusion.
What is the goal of treatment in class III ADHF?
Increase perfusion.
In class III ADHF, what methods can be used to increase perfusion?
1) Vasodilators
2) Positive Inotropic Agents
How does vasodilation increase perufsion?
Arterial vasodilation makes it easier to move blood from the LV to the aorta due to decrease afterload.
In Class III ADHF, _____ is best for patients who are hemodynamically stable.
Vasodilators.
What vasodilators are used in Class III ADHF?
1) ARNI/ACEi/ARB
2) Hydralazine
3) IV vasodilators
What do positive inotropic agents do?
They increase the squeeze of the LV to move blood forward.
Positive inotropic agents are best for what patients?
Class III ADHF with low BP that are not in shock.
What positive inotropic agents are used in Class III ADHF?
1) Dobutamine
2) Milrinone
The mechanism of action of this vasodilator is to form nitric oxide. this leads to the activation of cGMP in smooth muscle leading to dephophorylation of myosin light chains —> leads to smooth muscle relaxation.
This smooth muscle relaxation leads to a vasodilator effect on the peripheral veins and arteries. It should be noted that there is a more prominent effect on the veins.
Nitroglycerin