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



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