Cardiac and systemic haemodynamic complications of liver cirrhosis

Figures & data

Table I.  Circulatory changes in different vascular beds in cirrhosis.

Systemic circulation
Plasma volume ↑
Total blood volume ↑
Non-central blood volume ↑
Central and arterial blood volume? (→)
Arterial blood pressure ? (→)
Systemic vascular resistance ↓
Heart
Heart rate ↑
Cardiac output ↑
Left atrial volume ↑
Left ventricular volume↓ (↑)
Left ventricular end-diastolic pressure →
Total vascular compliance ↑
Arterial compliance ↑
Hepatic and splanchnic circulation
Hepatic venous pressure gradient ↑
Postsinusoidal resistance ↑
Renal circulation
Renal blood flow ?
Pulmonary circulation
Pulmonary blood flow ↑
Pulmonary transit time ?
Pulmonary arterial pressure → ↑

↑ → ↓ denote: increased, unchanged, and decreased.

Arrows in parentheses describe less typical changes.

Table II.  Evidence of reduced central and arterial filling in patients with cirrhosis [19], [25].

	Cirrhosis	Controls
CBV/BV^#	0.25±0.04^a (n = 60)	0.34±0.10 (n = 22)
CBV/CO^+	11.8±2.9^a (n = 60)	19.4±4.4 (n = 22)
PV/PRA*	3.41^a (n = 89)	7.6 (n = 32)

a Cirrhosis vs controls: p < 0.001. Mean±SD

# CBV/BV: central and arterial blood volume relative to blood volume (fraction)

+CBV/CO: central and arterial blood volume relative to cardiac output (min)

* PV/PRA: plasma volume relative to plasma renin activity (10⁻¹⁵ ml²/pg²)

In most clinical cases an increased plasma renin activity will be taken as evidence of reduced arterial filling in patients with cirrhosis.

Figure 1.  Vasodilatators and vasoconstrictors in the pathogenesis of a hyperdynamic systemic circulation in patients with cirrhosis.

Figure 2.  Cardiovascular hyporeactivity in cirrhosis may originate in the central nervous system, the autonomic nervous system, from local mediators, or within the heart muscle cell. The balance between vasodilatators and vasocontrictors is different in different vascular beds. Abbreviations: CGRP: Calcitonin gene-related peptide; ANP: atrial natriuretic peptide; CNP: C-type natriuretic peptide, TNFα: tumor necrosis factor-alpha; ET: endothelin; SNS: systemic nervous system.

Table III.  Diagnostic and supportive criteria for cirrhotic cardiomyopathy.

Definition of cirrhotic cardiomyopathy:

A cardiac dysfunction in patients with cirrhosis characterised by impaired contractile responsiveness to stress and/or altered diastolic relaxation with electrophysiological abnormalities in the absence of other known cardiac disease.

Diagnostic criteria

Systolic dysfunction

Blunted increase in cardiac output on exercise, volume challenge or pharmacological stimuli Resting ejection fraction < 55%

Diastolic dysfunction

E/A ratio < 1.0 (age-corrected) Prolonged deceleration time (>200 ms) Prolonged isovolumetric relaxation time (>80 ms)

Supportive criteria

Electrophysiological abnormalities Abnormal chronotropic response Electromechnical uncoupling/dyssynchrony Prolonged Q-Tc interval Enlarged left atrium Increased myocardial mass Increased BNP and pro-BNP Increased troponin I

BNP: brain natriuretic peptide; E/A ratio: ratio of early to late atrial phases of Left ventricular filling.

Figure 3.  Potential pathophysiological mechanism involved in the development of cirrhotic cardiomyopathy. Abbreviations: cAMP: cyclic adenosine monophosphate; pro-ANP: N-terminal propeptide of atrial natriuretic peptide; pro-BNP: pro-brain natriuretic peptide: N-terminal propeptide of brain natriuretic peptide, QTc: frequency adjusted Q-T interval; SR: sacroplasmic reticulum; TC: cardiac troponin C; G-prot: signal protein of G-type.

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