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Pathophysiology of
Congestive heart failure
Sirilak Surachetpong
DVM MS PhD DTBVM AiCVIM (cardiology)
Departement of Veterinary Science
Chulalongkorn University

Definition of heart failure

• A complex clinical syndrome that results from structural or functional
impairment of ventricular filling or ejection of blood.
• A state where cardiac output fails to meet the metabolic needs of the
peripheral tissues

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Classification of heart failure (human)

• Modified New York Heart Association (NYHA) functional classification

Class Details
I Patients with asymptomatic with heart disease (no clinical
signs even with exercise)
II Patients with clinical signs only strenous exercise
III Patients with clinical signs with rountine daily activites
IV Patients with clinical signs even at rest
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Classification of heart failure

• ACVIM consensus statement of valvular heart disease (dogs)

Stage Details
A Patients with high risk for developing heart disease
B1 Asymptomatic patients without evidence of cardiac remodeling
B2 Asymptomatic patients with evidence of heart enlargement
C Patients with part or current clinical signs of heart failure
D Patients that are refractory to “standard therapy”

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Phases of heart failure

Phase Details
1 Initial insult
Slow progression without clinical signs (eg. valvular disease, feline cardiomyopathies)
May produce life-threatening signs (eg. cardiac mass, thromboembolism)
2 Compensatory phase
Short term-activate within seconds to minutes
activation of several neurohormonal systems
utilization of the Frank-Starling mechanism
Long term-myocardial remodeling/hypertrophy
3 Transtition to heart failure

Short-term activation
• Sympathetic nervous system
• Renin angiotensin aldosterone
• Vasopressin
• Aldosterone

Modified from Schrier RW, Abraham WT: Hormones and 6

hemodynamics in heart failure. N Engl J Med 341:577, 1999.

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Sympathetic nervous system (SNS)

Hypotension Release norepinephrine
Low blood pressure from terminal neurons to
systemic vasculature
Release norepinephrine
from terminal neurons to
SA, AV nodes and cardiomyocytes
Catecholamines + alpha 1 receptors

Release norepinephrine and epinephrin

from adrenal glands to
circulation
Vasoconstriction

Catecholamines + beta receptors

Arterial vasoconstriction
Increase contractility and heart rate >> maintain systemic blood pressure
increased cardiac output Venoconstriction-promote increased venous return
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Renin-Angiotensin-Aldosterone System (RAAS)

Decrease cardiac output
Effects of AII
Vasodilation Norepinephrine
Anti-remodeling ADH
Natriuresis-diuresis Necrosis/fibrosis

Bradykinin Increase blood pressure

Inactive peprides

ACE acts as a regulator between

vasoconstrictive/sodium retension and Increase blood volume/preload
Vasodilatory/natriuretic mechanisms
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Arginine vasopressin (AVP)/antidiuretic hormone (ADH)

• Release from the pituitary gland in response to
• Increased plasma osmolarity
• Hypovolemia
• SNS an RAAS also promote release of vasopressin

V1AR
Vasoconstriction
Weak inotropic action
AVP
V2AR Free water resorption

Long-term adaptive response

• Laprace’s law
• Wall stress=pressurexradius Normal Concentric Eccentric
2xwall thickness hypertrophy hypertophy

• Normalization of wall stress via increased left ventricular wall thickness

• Concentric hypertrophy
• Volume overload increases wall dimension
• Eccentric hypertrophy
Phase Details
Initial Exceed workload
Compensatory Work-induced growth of the myocardium normalizes wall stress
Exhaustion Cardiomyocyte death, myocardial fibrosis and ventricular dilation 10

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Transition to heart failure

Decrease ventricular performance
1. Ventricular performance declines
2. Short- and long-term compensatory mechanism
3. Maladaptive and decompensatory mechanism

Balmer, 2020

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Compensatory mechanisms
• Neuroendocrine (SNS, RAAS, AVP, aldosterone)
• Cardiac changes (hypertrophy, dilatation)
• Counter-regulatory
• Congestive heart failure

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Counter-regulatory mechanisms
• Increased prostagrandin E and I release
• Increased atrial and brain natriuretic peptide release
Renal and cardiac flow Myocardial stretch
Heart rate
Norepinephrine
RAAS
Vasopressin ANP & BNP

PGE &PGI

Vasodilatation Diuresis

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Compensatory mechanisms

ANP

ANP RAAS

RAAS

Compensate Decompensate

Maintenance of euvolemia Systemic hypertension

Compensation Decompensation
Asymptomatic Symptomatic
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Transition of Heart Failure

• Myocyte loss
• Necrosis, apoptosis and autophagy
• Promote by norepinephrine, AII and other mediators
• Reduce myocardial contractile function
• Altered contractile proteins
• Particularly, proteins that involved with contractile function
• Altered excitation-contraction coupling
• Alteration in proteins responsible for Ca cycling
• Slower Ca delivery to contractile proteins during systole
• Excessive cytosolic Ca during diastole

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Transition of Heart Failure

• Changes within the extracellular matrix
• Concentric hypertrophy -collagen accumulation
• Increase ventricular stiffness
• Reduce compliance Concentric
hypertrophy
• Impaired ventricular filling
• Eccentric hypertrophy-increase extracellular matrix turnover
• Increase matrix metalloproteinase (MMPs)/inhibitors ratio
• Shifting type I to III collagen –degradation of collagen
Eccentric
hypertophy

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Transition of Heart Failure

• Alterations in cardiac metabolism
• Oxidation of fatty acids account for 70-90% of ATP production.
• Decreased cardiac energy production
• Impaired substrate use or altered mitochrondiral function
• Impaired fatty acid transport and utilization
• Alteration in glucose oxidation
• Mitochondrial damage mediate autophargy

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Hemodynamics of heart failure

Systemic and
Systolic and diastolic Elevated venous
pulmonary venous
dysfunction pressure
congestion

Increased plasma
Reduced venous
volume Congestive heart
capacitance
via sodium and water failure
via venoconstriction
retention

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Clinical signs from hemodynamic disturbance

Decreased cardiac output Increased ventricular filling pressure
Weakness/lethargy Dyspnea (left)
Syncope Coughing (left)
Hypothermia Ascites (right)
Pale mucous membrane Hepatomegaly (right)
Jugular dystension (right)

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Terminology

• Systolic dysfunction
• Heart fails to pump bloods
• Disease (eg. DCM)
• Drugs (eg. beta blockers)
• Diastolic function
• Heart fails to relax and stiff
• Disease (eg. HCM)

Image Courtesy: med.uc.edu 20

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Terminology
Right sided heart failure Left sided heart failure
Increased central venous pressure Increased left atrial pressure
-Pleural effusion -Pulmonary venous congestioin
-Ascites -Pulmonary edema
-Hepatomegaly -Ocasionally pleural effusion (cat)
-Jugular distension

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Etiology
Myocardial failure Contractility failure
Restrited ventricular filling Diastolic dysfunction
Volume overload Shunt, valve regurgitation
Pressure overload Increased outflow resistiance

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Koko mixed 13 years old MC4 kg

• CC: Cough dyspnea and weakness
• PE: HR 180 RR 48 Temp 100F
Systolic murmur 4/6 regular rhythm
Crackle lung sound
Pale pink mm CRT >2 s
Variable pulse quaility
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload
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Yumi Persian 5 months old FI 2.4kg

• CC: Dyspnea/abdominal enlargement
• PE: HR >200 RR 48 Temp 100 F
Systolic murmur 4/6
Regular rhythm
Dull lung sound at lower thorax
Increased lung sound at upper thorax
Abdominal fluctuation
Soft pulse
Pale pink mm CRT 2 S
Jugular pulsation and distension
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload 24

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Thong DSH FI 4 years old 4 Kg

• CC: Dyspnea/tachypnea
• PE: HR >200 RR 100 Temp 101 F
Normal heart sound increased lung sound
Pale pink mm CRT 2 s strong pulse
Dehydrate 5%
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload

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Joker Bulldog 1 year old MI 25.5Kg

• CC: Abdominal enlargement
• PE: HR 180 RR 32 Temp 101 F
Systolic murmur 3/6 at left base
Normal lung sound
Pale pink mm CRT 2 s strong pulse
Normal hydration
Fluctuation abdomen
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload
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Tigger Persian 8 years old MC 4 Kg

• CC: Dyspnea/tachypnea
• PE: HR 180 RR 60 Temp 101 F
Normal heart sound regular rhythm
Increased lung sound
Pink mm CRT 1-2 s strong pulse
Normal hydration
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload

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Am Pittbull 3 years old MI 20 Kg

• CC: Dyspnea
• PE: HR 120 RR 40 Temp 102
Normal heart sound
Normal lung sound
Pink mm CRT 1-2 s
Strong pulse
Normal hydration
Cough induce negative
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload 28

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Euro 13 year old MI LAB 28.5 Kg

• CC: Tachypnea/dyspnea anorexia
• PE: HR 120 RR 60 Temp 102
Muffle heart sound
Increased lung sound
Pale pink mm CRT 2 s
Soft pulse
Dehydration 5%
Abdominal enlargement (Ping/flutuation)
Question
• CHF?
• Forward or backward failure
• Left or right sided heart failure
• Etiology: Myocardial failure/restricted filling
Volume overload/pressure overload
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Question

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