Thiamine Cardiomyopathy (Cardiac Beriberi) 

Thiamine cardiomyopathy is a reversible cause of heart failure due to deficiency of vitamin B1 (thiamine). In ICU and emergency practice, it is crucial because:

  • It mimics septic shock
  • It mimics dilated cardiomyopathy
  • It may present as refractory lactic acidosis
  • It dramatically improves within hours after IV thiamine

Why Is It Called “Beri-Beri”?

The term “beriberi” comes from the Sinhala language of Sri Lanka.

In Sinhala, “beri”  means:

“I cannot” or “weakness” .When repeated — “beri-beri” — it conveys:

“I cannot, I cannot”

This describes the profound muscle weakness and fatigue seen in thiamine deficiency.


Historical Context


  • The disease was common in 19th-century Sri Lanka and Southeast Asia.
  • It was strongly associated with populations consuming polished white rice.
  • Milling removes the thiamine-rich outer husk (bran layer).
  • As polished rice consumption increased, beriberi epidemics appeared.

Later, in the late 19th century, researchers like Christiaan Eijkman demonstrated that polished rice caused a deficiency disease in chickens, leading to the discovery of vitamin B1 (thiamine).


ICU Clinical Scenario

A malnourished alcoholic presents with:

  • Hypotension
  • Lactate 8 mmol/L
  • EF 25%
  • No infection source

Given IV thiamine lactate drops to 3 mmol/L in 12 hrs BP improves.

Diagnosis: Shoshin Beriberi


1. Thiamine: Biochemical Foundation

Thiamine (Vitamin B1) is converted to Thiamine Pyrophosphate (TPP), a cofactor for:TCA cycle,Amino acid metabolism,Pyruvate dehydrogenase

Core Concept:

Thiamine deficiency impaired aerobic metabolism ATP lactate myocardial energy failure.


2. Causes of Thiamine Deficiency (ICU-Relevant)

1. Chronic alcoholism

Commonest cause.

2. Malnutrition

  • Cancer
  • Chronic illness
  • Elderly
  • Post bariatric surgery

3. Prolonged parenteral nutrition without supplementation

4. Dialysis patients

5. Sepsis (increased utilization)

6. Hyperemesis gravidarum


3. Pathophysiology of Thiamine Cardiomyopathy

Stepwise Mechanism:

  1. Impaired PDH activity
  2. Pyruvate accumulates converts to lactate
  3. Cellular ATP falls
  4. Myocardial contractility declines
  5. Peripheral vasodilation develops
  6. Neurohormonal activation (RAAS, SNS)
  7. High-output heart failure later low-output failure


4. Clinical Presentation

Early

  • Fatigue
  • Dyspnea
  • Tachycardia
  • Peripheral edema

Advanced

  • Cardiomegaly
  • Hypotension
  • Pulmonary edema
  • Lactic acidosis
  • Shock

Associated Findings

  • Peripheral neuropathy
  • Wernicke encephalopathy


5. Types of Cardiac Beriberi

A. Wet Beriberi (Classic Form)

  • Peripheral edema
  • Tachycardia
  • Wide pulse pressure
  • Warm extremities
  • High-output cardiac failure

B. Shoshin Beriberi (Fulminant Form)

“Shoshin” = acute, severe, rapidly fatal form.

Features:

  • Severe hypotension
  • Cardiogenic shock
  • Severe lactic acidosis
  • Rapid collapse
  • Multiorgan failure

ICU pearl:
Refractory shock + high lactate + malnourished patient Give thiamine immediately.


5. Hemodynamic Profile

Parameter

Early Stage

Late Stage

Cardiac Output

High

Low

SVR

Low

Variable

PCWP

Normal/slightly

Lactate

↑↑

BNP

Mild

Mechanism of high-output state:

  • Peripheral vasodilation due to metabolic failure
  • Reduced SVR compensatory tachycardia




7. Echocardiography Findings

  • Dilated LV
  • Global hypokinesia
  • Reduced EF
  • No coronary artery disease

Important: Reversible after thiamine therapy


8. Laboratory Features

Test

Finding

Mechanism

Serum lactate

Impaired PDH

ABG

Metabolic acidosis

Lactate

Troponin

Mild

Myocardial stress

BNP

HF

Thiamine level

Diagnostic

RBC Transketolase Activity

Gold standard (rarely available)


9. Diagnostic Clue in ICU

The most important diagnostic tool:

Therapeutic trial of IV thiamine

If:

  • Lactate decreases within 12–24 hrs
  • BP improves
  • Inotrope requirement falls

Diagnosis strongly supported.


10. Management (Guideline-Oriented Critical Care Approach)

1. Immediate Thiamine

  • 100–200 mg IV stat
  • Severe shock: 200–500 mg IV TDS
  • Continue for 3–5 days
  • Then oral 100 mg/day

Always give thiamine before glucose in malnourished patients

Why?
Glucose infusion increases pyruvate worsens lactic acidosis.


2. Heart Failure Management

  • Oxygen
  • Diuretics
  • Vasopressors (if shock)
  • Inotropes if low EF

But dramatic response often seen after thiamine.



11. Differential Diagnosis

Condition

How to Differentiate

Septic shock

Infection source, procalcitonin

Dilated cardiomyopathy

No rapid reversal

Myocarditis

Troponin ↑↑

Takotsubo

Regional wall motion abnormality