Acute Heart Failure

When there are no sign of congestion or hypoperfusion. (baseline patient, no acute symptoms)

When there are signs of congestion (orthopnea, edema, ect.) but no signs of hypoperfusion. (Most common presentation of HF)

When there are signs of hypoperfusion (cool extremities, narrow pulse pressure, ect.) but not signs of congestion

When there are signs of congestion (orthopnea, edema, ect.) and signs of hypoperfusion (cool extremities, narrow pulse pressure, ect.) (highest rate of mortality)

The cardiac output of a patient normalized against their BMI, provides a normalized reference range for all body types

Afterload

Preload, they wedge a capillary into the pulmonary vasculature to measure vascular wall pressure at diastole

PCWP <18 mmHg, dry patients

PCWP >18 mmHg, wet patients

CI <2.2 L/min/m^2, cold patients

CI >2.2 L/min/m^2, warm patients

The signs and symptoms are being caused by something besides heart failure

give IV loop diuretics up to 2.5x greater than their dose prior to administration
Diuretics and GDMT should be titrated (optimized) to resolve clinical evidence of congestion after acute congestion cleared
For refractory (stubborn) symptoms, loop diuretic dose may be increased or second (thiazide) diuretic may be added
In the absence of hypotension, an IV vasodilator may be considered for dyspnea

1:1

2:1

20:1

20:1

2:1

Intercardiac pressure drop within 5-15 minutes, patients start to feel better. 20-30 minutes is when diuresis occurs.

Ototoxicity, hearing loss or ringing, more common with furosemide than bumetanide, not very common when IV is administered over a length of time, but can happen
Musculoskeletal toxicity (pain), more common with bumetanide than furosemide, fairly common with the doses used for acute heart failure

Decreased gut absorption / renal perfusion, may be caused by gut wall edema or gut wall hypoperfusion (or taking with food leading to decreased bioavailability), leading to decreased absorption of the drug. If there is insufficient renal perfusion, the loop diuretics won't be able to work as effectively. Often it will start working again once fluid volume is reduced, may need temporary dose increase.

Compensatory sodium reabsorption, since loop diuretics block sodium reabsorption in the acending loop of henle, the sodium concentration is much higher once it reaches the distal convoluted tubule. This over time may lead to increased expression of sodium channels in the distal convoluted tubule, leading to increased reabsorption there to compensate. Can use a sequential nephron bloccaide by adding a thiazide diuretic, which will then act to block reabsorption in the distal convoluted tubule as well.

hydrochlorothiazide
chlorthalidone
metolazone
indapamide
chlorothiazide

Norephinephrine
Epinephrine
Dopamine

Drugs that increase heart contractility (positive inotropic) and constrict the blood vessels

Dobutamine
Milrinone

Drugs that increase heart contractility (positive inotropic) and dilate the blood vessels.

Phenylephrine
Vasopressin

Drugs that constrict the blood vessels

Nitroglycerin
Nitroprusside

Drugs that dilate the blood vessels

Venodilator, decreases preload, may decongest organs

venous and arterial vasodilation, decreases pre and afterload, increases cardiac output

hepatically metabolized to thiocynate, which is renally elminated. If too high a dose is given, or there is renal dysfunction, may see signs of cyanide poisoning.

B1 agonist with slight peripheral vasodilation, not renally excreted so better for kidney disease

PDE3 inhibitor, augments Ca utilization and causes moderate peripheral vasodilation

Blood pressure, heart rate, ECG (to monitor for arrythmias), consider PAC (Pulmonary Artery Catheterization) monitoring, renal function with milrinone

When there is a patient with hypoperfusion