What is the best treatment for a patient with MASH (Multifocal Acquired Shunt Hyperkinosis) cirrhosis experiencing sustained tachycardia?

Treatment of Sustained Tachycardia in the 110s in MASH Cirrhosis

In a patient with MASH cirrhosis presenting with sustained tachycardia in the 110s, immediately assess for underlying precipitants (infection, bleeding, hypovolemia) and circulatory dysfunction patterns before initiating treatment, as the tachycardia likely represents compensatory response to the hyperdynamic circulation or decompensation rather than a primary cardiac arrhythmia. 1, 2

Initial Assessment and Hemodynamic Evaluation

Perform bedside echocardiography immediately to distinguish between hypovolemic, vasodilatory, and cardiogenic shock patterns, evaluating left and right ventricular function, inferior vena cava for volume status, and stroke volume variation to determine fluid responsiveness. 1 This is critical because:

• Decompensated cirrhosis typically presents with hyperdynamic circulation characterized by high cardiac output and low systemic vascular resistance, where tachycardia is a compensatory mechanism. 1
• Cirrhotic cardiomyopathy (CCM) prevents adequate cardiac output compensation in advanced decompensation, leading to effective hypovolemia despite the hyperdynamic state. 1, 3, 4
• Cold extremities indicate peripheral vasoconstriction, which is atypical for pure vasodilatory shock and suggests either severe hypovolemia, cardiogenic component from CCM, or mixed shock with inadequate cardiac compensation. 1

Assess for specific precipitants that commonly cause tachycardia in cirrhosis:

• Spontaneous bacterial peritonitis or other infections (perform diagnostic paracentesis if ascites present, checking cell count, culture, albumin, and Gram stain). 2
• Active gastrointestinal bleeding (check hemoglobin, assess for melena/hematemesis). 5
• Hypovolemia from over-diuresis or large volume paracentesis without albumin replacement. 1, 2
• Electrolyte abnormalities, particularly hypokalemia or hypomagnesemia from diuretics. 2
• Hepatic encephalopathy or other metabolic derangements. 2

Hemodynamic Management Strategy

Target a mean arterial pressure (MAP) of 65 mmHg as the primary goal, not heart rate reduction. 1, 2 A retrospective study of 273 critically ill cirrhotic patients showed mortality in ICU increased below a MAP threshold of 65 mmHg. 1

Volume Resuscitation

Use balanced crystalloids (Ringer's lactate) as first-line for fluid resuscitation if hypovolemia is suspected, as balanced crystalloids are associated with lower mortality compared to normal saline in critically ill patients. 1

Administer albumin 20% in specific cirrhosis-related scenarios:

• For sepsis-induced hypotension in cirrhosis: albumin 20% achieves faster reversal of hypotension compared to crystalloids, with one randomized study showing albumin 5% versus normal saline improved one-week survival (43.5% vs 38.3%). 1
• For large volume paracentesis (>5L): give 8g albumin per liter of ascites removed. 1
• If hepatorenal syndrome suspected: albumin 1 g/kg (up to 100g) over 2-4 hours for plasma volume expansion. 2

Monitor dynamic changes in stroke volume, stroke volume variation, and pulse pressure variation during fluid resuscitation to avoid over-resuscitation. 1

Vasopressor Support

Initiate norepinephrine as the first-line vasopressor if hypotension persists despite adequate volume resuscitation, with concurrent ongoing fluid management. 1, 2

Add vasopressin as a second-line agent when escalating doses of norepinephrine are required. 1

Relative Adrenal Insufficiency

Consider empiric hydrocortisone 50 mg IV every 6 hours (or 200 mg infusion over 24 hours) for 7 days or until ICU discharge if shock remains refractory despite high-dose vasopressors, as relative adrenal insufficiency is common in cirrhosis and associated with increased mortality. 1

Medications to Absolutely Avoid

Do not use beta-blockers for rate control in this setting. 2, 6 Here's why:

• Beta-blockers may compromise renal function and hemodynamic stability in advanced decompensation. 2
• In cirrhotic patients, propranolol clearance is reduced with plasma concentrations increased 2.5-fold, and half-life prolonged from 2.9 to 7.2 hours. 6
• Beta-blockers should be immediately discontinued if acute kidney injury develops. 2

Avoid ACE inhibitors and angiotensin antagonists as they aggravate hypotension and have not been clinically useful in cirrhosis. 1, 3

Absolutely avoid NSAIDs as they precipitate renal failure in cirrhotic patients. 2

Specific Cardiac Considerations in MASH Cirrhosis

Recognize that cirrhotic cardiomyopathy is prevalent in approximately 50% of cirrhotic patients and comprises systolic dysfunction, diastolic dysfunction, and electrophysiological abnormalities. 4 Key features include:

• Diastolic dysfunction occurs in 64% of cirrhotic patients (grade I in most, grade II in some), and is more prevalent in those with ascites (77% vs 56%). 7
• Prolongation of QTc interval is common and may indicate poor outcome; agents that prolong QT should be used cautiously. 5
• Cardiac dysfunction is clinically latent but can be unmasked by physical or pharmacological stress. 3

Assess for diastolic dysfunction using recent ASE guidelines: average E/e' >14, tricuspid velocity >2.8 m/s, and left atrial volume index >34 ml/m². 5 However, note that cardiac load conditions in cirrhosis are confounding factors in this diagnosis. 7

Monitoring Parameters

Monitor the following at least twice weekly initially, then weekly once stable: 2

• Complete blood count, comprehensive metabolic panel, liver function tests
• Daily weight, vital signs, mental status, intake/output, volume status
• Electrolytes (particularly sodium, potassium, magnesium)

Avoid rapid correction of hyponatremia if present (target <10-12 mEq/L increase in 24 hours) to prevent central pontine myelinolysis. 1

Common Pitfalls to Avoid

• Do not treat the heart rate number in isolation without addressing the underlying hemodynamic derangement or precipitant. The tachycardia is compensatory in most cases. 1, 3
• Do not assume the hyperdynamic circulation is protective – CCM can prevent adequate cardiac compensation despite high baseline cardiac output. 1, 4
• Do not use traditional rate-control agents (beta-blockers, calcium channel blockers) as they worsen hemodynamics in decompensated cirrhosis. 2, 6
• Do not overlook infection as a precipitant – perform diagnostic paracentesis liberally in any patient with ascites and clinical deterioration. 2

Transplant Considerations

Refer immediately for liver transplant evaluation if this represents new decompensation, as median survival with decompensated cirrhosis is approximately 1 year without transplantation. 2 Liver transplantation is the only treatment that can reverse cirrhotic cardiomyopathy. 3, 4