Treatment for Hypotension, Congestive Cardiac Failure, and Hypoalbuminemia
The optimal treatment for patients with hypotension, congestive cardiac failure, and hypoalbuminemia requires careful management of fluid status with intravenous albumin for volume expansion, cautious use of inotropic agents for hypotension, and judicious diuretic therapy once adequate perfusion is established.
Initial Management of Hypotension
- In patients with hypotension (SBP <90 mmHg) and signs of hypoperfusion, short-term intravenous inotropic agents should be administered to maintain systemic perfusion and preserve end-organ function while more definitive therapy is considered 1
- Norepinephrine is the preferred vasopressor for patients with cardiogenic shock who remain hypotensive despite treatment with another inotrope 1
- Intravenous albumin should be administered to address hypoalbuminemia, as it will expand plasma volume by three to four times the volume actually administered by withdrawing fluid from interstitial spaces 2
- The initial albumin dose should not exceed 2g per kg body weight in the absence of active bleeding 2
- Inotropic agents should be used with caution and are not recommended unless the patient is symptomatically hypotensive due to safety concerns 1
Management of Hypoalbuminemia
- Hypoalbuminemia is common in heart failure patients and is associated with increased mortality, especially in elderly patients 3, 4
- According to Starling's law, low plasma oncotic pressure related to hypoalbuminemia induces fluid shift from intravascular to interstitial space, facilitating cardiogenic pulmonary edema 3
- Intravenous albumin administration is indicated to support colloid osmotic pressure of the plasma and improve intravascular volume 2, 5
- The volume effectiveness of intravenous albumin solution appears to be greater when serum albumin levels are low 5
- Monitoring of serum albumin levels during hospitalization is important as levels commonly decrease during treatment, with nadir levels associated with increased risk of acute worsening of renal function 6
Diuretic Therapy (After Adequate Perfusion is Established)
- Diuretics should be avoided in patients with acute heart failure and signs of hypoperfusion until adequate perfusion is attained 1
- Once perfusion is adequate, intravenous loop diuretics should be administered to patients with evidence of fluid overload 1
- The initial intravenous diuretic dose should be at least equal to the pre-existing oral dose used at home 1
- For diuretic resistance, options include dual nephron blockade by combining loop diuretics with thiazide diuretics or mineralocorticoid receptor antagonists (MRAs), with careful monitoring to avoid hypokalemia, renal dysfunction, and hypovolaemia 1
- Monitor renal function and electrolytes 1-2 weeks after initiation and after any increase in diuretic dose 1
Management of Beta-Blockers and ACE Inhibitors/ARBs
- Beta-blockers should be used cautiously if the patient is hypotensive 1
- If beta-blockade is thought to be contributing to hypotension with subsequent hypoperfusion, an intravenous infusion of levosimendan or a phosphodiesterase III inhibitor may be considered to reverse the effect 1
- For patients with symptomatic hypotension, reconsider the need for nitrates, calcium-channel blockers, and other vasodilators and reduce dose or stop if possible 1
- If no signs or symptoms of congestion are present, consider reducing diuretic dose 1
Monitoring and Follow-up
- Monitor ECG and blood pressure when using inotropic agents and vasopressors, as they can cause arrhythmia, myocardial ischemia, and in the case of levosimendan and PDE III inhibitors, hypotension 1
- Carefully measure fluid intake and output, vital signs, body weight, clinical signs and symptoms of systemic perfusion and congestion 1
- Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or active titration of heart failure medications 1
- For patients with hypoalbuminemia, a dietary survey should be performed, and renutrition may be indicated 3
Special Considerations
- Hypoalbuminemia in heart failure may be caused by malnutrition, inflammation, cachexia, hemodilution, liver dysfunction, protein-losing enteropathy, increased transcapillary escape rate, and nephrotic syndrome 3
- Tricuspid regurgitation can worsen hypoalbuminemia by enhancing liver dysfunction and reducing enteral protein absorption due to increased stasis in mesenteric system 4
- Hypoalbuminemia contributes to the progression of heart failure by favoring myocardial edema, volume overload, and diuretic resistance 4
- Midodrine should be used cautiously in patients with heart failure who are using other negative chronotropic agents such as beta-blockers and digoxin 7