▪️Definition and diagnosis
▫️ADHF is a clinical syndrome of new or worsening signs and symptoms of HF.
Consider ADHF when a patient(with chronic HF) presents with fluid retention and exertional dyspnea. It is essential to rule out other causes.
🔺Pulmonary edema has been observed in 16 percent or more of admitted ADHF
▪️Clinical features
▫️Acute dyspnea, orthopnea, tachypnea, tachycardia, and hypertension.▪️Etiologies
🔺Hypotension reflects severe disease, and arrest may be imminent
CHAMPIT:▪︎ICU admission:
(ACS, Hypertension, Arrhythmia, Mechanical causes, Pulmonary embolus, Infection, and Tamponade)
any of the following:
• SpO2 ≤90 percent) despite supplemental oxygen.
• using accessory muscles and respiratory rate is ≥25.
•Signs and symptoms of hypoperfusion and/or sys BP <90 mmHg.
•HR <40 or >130 .
▪️DDXs
Pulmonary embolism, acute asthma, pneumonia, noncardiogenic pulmonary edema (eg, adult respiratory distress syndrome), pericardial tamponade or constriction.
▪️Supplemental oxygen:
▫️treat the hypoxemia (SpO2 <90 ).
▫️Oxygen is not recommended as routine therapy in patients without hypoxemia, as it may cause vasoconstriction and reduction in cardiac output.
▪️Diuretics (Furosemide)
▫️Adding a thiazide diuretic may
potentiate the effect, but hypokalemia should be avoided.
▫️The onset: 30 minutes with peak diuresis usually at one to two hours.
▫️after administration.
Monitor the Volume status, evidence of congestion, oxygenation, daily weight, fluid intake, and output .
▫️Monitoring the side effects (electrolyte abnormalities(esp decrease in K and Mg and muscle cramping), symptomatic hypotension, worsening renal function and metabolic alkalosis).
▫️Diuretic can precipitate attacks of gout.
▫️Management of worsening renal function⤵️
🔹Patients with severe symptoms or signs of congestion, particularly pulmonary edema, require continued fluid removal independent of changes in GFR.
🔹If the BUN rises and the serum Cr is stable or increases minimally, and the patient is still fluid overloaded, the diuresis can be continued with careful monitoring of renal function.
🔹If increases in serum Cr appear to reflect intravascular volume depletion, then reduction in or temporary discontinuation of diuretic and/or ACE inhibitor/ARB should be considered. Adjunctive inotropic therapy may be needed .
▪️Vasodilator therapy (nitroglycerin/ nitroprusside) indications
🔹Patients with (HFrEF) and severe hypertension.
🔹Patients with HFrEF or HFpEF who do not respond to diuretics.
🔹Patients with refractory HFrEF and low cardiac output.
▫️nitroglycerin is suggested when the initial response to diuretics is not sufficient to alleviate respiratory distress.
▫️Tachyphylaxis may develop within 24 to 48 hours of continuous nitroglycerin.
▫️Potential adverse effects of nitroglycerin include hypotension and headache. Nitrate therapy should be
avoided or used with caution in settings in which hypotension could result in serious decompensation such as RV infarction or aortic stenosis.
▫️Nitrate is contraindicated after use of PDE-5 inhibitors(sildenafil.)
▫️Early IV vasodilator therapy (eg, nitroprusside) is suggested in severe hypertension, acute Mitral regurgitation, or acute AR.
▫️The limitation of nitroprusside is its metabolism to cyanide.
🔺The routine use of vasodilators should be avoided.
▪️Opiates
generally avoiding
▪️Inotropes(dobutamine and/or milrinone)
▫️may be required as a temporizing measure in patients with severe (LV) systolic dysfunction and low output syndrome.
▫️Patients with HFpEF presenting with hypotension should not receive
inotropes and may require a vasopressor in addition to diuretic therapy.
▪️Vasopressor therapy (norepinephrine)
▫️In patients with ADHF and marked hypotension.
▪︎یه سری نکات تکمیلی هم در اوردر آورده شده است.