Cardiac failure - terms

O2 DELIVERY = O2 content x cardiac

output
O2 CONTENT = O2 sat x Hb x 1.39 x10ml/
L (1gm Hb carries 1.39 ml O2 at 100%
saturation)
CARDIAC OUTPUT = HR X Stroke
volume

CF Terms
STROKE VOLUME depends on preload,
afterload and contractility (inotropic state)
PRELOAD (the load before contraction)
equates to the filling volume of the heart
AFTERLOAD (the load after the
contraction of the heart) the resistance the
ventricles face on ejection of blood e.g.BP

CF terms
CONTRACTILITY (inotropic state) the efficiency (greater velocity) and force
of contraction of heart muscle
MYOCARDIAL O2 DEMAND increases with HR, wall stress (afterload
and preload), and contractility
WALL STRESS = pressure x radius /
2 x wall thickness

CF terms
Myocardial hypertrophy in response to
PRESSURE overload acutely -> increase wall
stress -> replication of myofibrils in parallel,
thickening of individual myocytes, &
CONCENTRIC HYPERTROPHY
Response to ventricular VOLUME overload ->
replication of sarcomeres in series, elongation of
myocytes & DILATATION -> moderate increase
sys stress ->moderate ECCENTRIC hypertrophy

Cardiac failure
A state in which there is inadequate cardiac
output to meet the bodys metabolic needs
at normal physiologic venous pressures.
Due to
Primary abnormality of the myocardium
Excessive workload e.g. VSD or AV
regurgitation.

Acute Cardiac Failure

is acute functioning uncoupling between
compensatory mechanisms and decreased
myocardial function -> homeostatic
imbalance and overt symptoms

Chronic CF

Cardiac pump dysfunction with activation of

compensatory responses that ultimately ->
silent and progressive deterioration of
myocardial function

SHOCK
Acute circulatory dysfunction with completely
overwhelmed physiological compensatory
mechanisms. This results in death if not
treated promptly.

Cardiac failure
Compensatory mechanisms

Increased heart rate.

Frank Starling Mechanism.
Sympathetic nervous system activation.
Increased 2-3 DPG.
Increased natruretic peptide.
Myocardial hypertrophy.

CF - Haemodynamic changes
Increase in - heart rate
- ventricular E.D. volume
- ventricular E.D. pressure
- atrial pressure
- systemic vascular resistance
Decrease in - systemic blood flow

CF Compensatory mechanisms
Starlings Law of the Heart
The force of contraction (ventricular) and
the volume of ejected blood increase
directly with an increase in the initial
volume of ventricle at the time of systole
(EDV).

Frank-Starlings Law of the Heart

Maximum Capacity
To Produce SV

Stroke
Volume

Normal Range:
SV increases with EDV
End-Diastolic Volume
Mechanism: Length-Force Relations of Muscle Contraction

Family of Ventricular Function Curves

Sympathetic stimulation
increases heart rate and
contractility
Cardiac
Output

Parasympathetic stimulation
decreases heart rate

Increase in
Cardiac
Contractility
or
Increase in
Heart Rate

Atrial Pressure (Preload)

Family of Frank-Starling Curves

At a given EDV, SV increases
With cardiac contractility
High
Stroke
Volume

Increase in
Cardiac
Contractility
Low

Preload (End-Diastolic Volume)

CF Compensatory mechanisms
Effects of catecholamines
Increased contractility -> increased CO, BP
Increased heart rate
Decreased renal perfusion, renin
production,angiotensin II & aldosterone,
systemic vasoconstriction, Na and H2O
retention -> increase in CO

CF Compensatory mechanisms
2,3-Diphosphoglycerate is increased in CF
resulting in a shift to the right of the oxygen
dissociation curve which facilitates oxygen
unloading to the tissues.
Atrial Natruretic peptide (ANP) is released from
the atrial wall in response to atrial stretch ->
urinary loss of Na and water. ANP is a vasodilator
and reduces tachycardia.

CF - compensatory mechanisms
Sympathetic NS stimulation
In the NORMAL STATE state inhibitory
impulses from arterial & cardiopulmonary
baroceptor afferent nerves control
sympathetic outflow. Parasympathetic
outflow is under baroceptor (+) control.
In CF- inhibitory (-) input decreases,
excitatory (+) increases -> Sympathetic NS
stimulated. Parasympathetic blunted.

CF- Compensatory mechanisms

Sympathetic NS stimulation
Norepinephrine (NE) released and with
endothelin-1 and vasopressin -> BP rise,
vasoconstriction-> AFTERLOAD up.
Cyclic AMP increased -> Influx Ca into
myocytes -> CONTRACTILITY & CO
up.
Heart rate increased
Decreased renal perfusion -> renin -> Na &
H2O retention ->PRELOAD up.

CF Compensatory mechanisms
Myocardial hypertrophy . The myocytes
respond to changes in loading conditions in
CF by hypertrophy.
Angiotensin II -> myocyte hypertrophy.
Aldosterone -> collagen synthesis

CF- Sympathetic NS stimulation

- harmful effects
Myocyte injury and necrosis
Accelerated apoptosis (normal process of
programmed cell death).
Increase HR and contractility & increase
wall stress -> increase O2 consumption
Hypertrophy -> O2 demand up, myocyte
damage and fibrosis-> decrease CO.
ACUTE improvement, CHRONIC decline.

CF Causes - categories
Increased blood VOLUME - AI, MI, TI, L to R
shunts, overtransfusion & hypervolaemia.
Increased PRESSURE load, AS, HOCM, CoA,
hypertension.
Myocardial DYSFUNCTION - Cardiomyopathy,
myocarditis, dysrhythmias, toxic.
FILLING disorders.
Increased METABOLIC demands

CF Causes age groups

FOETAL or CONGENITAL - SVT,
erythroblastosis foetalis, AV malformation
CF IN THE FIRST WEEK - Duct
dependent ( Hypoplastic LHS, Severe AS
and CoA)and non duct dependent(TAVR,
AV malform, myocardial dysfunction
syndrome, SVT, sepsis).

CF Causes age groups

INFANCY
Obstructive lesions severe CoA & AS
L to R shunts
Mixing lesions TAPVR, TGA, truncus
Myo/pericardial SVT, myocarditis,
cardiomyopathy, purulent pericarditis.

CF Causes - age groups

CHILD & ADOLESCENT
Acquired myocarditis, cardiomyopathy,
AIDS, cardiotoxic drugs and
substance abuse.
Factors complicating congenital lesions anaemia, infective endocarditis, surgery,
myocardial deterioration.

CF NY Classification
Class I - no limitation of ordinary activity
Class II - slight limitation, no symptoms at
rest, symptoms on ordinary activity
Class III marked limitation of physical
activity, no symptoms at rest, symptoms on
< ordinary activity.
Class IV symptomatic at rest.

CF Clinical manifestations
TACHYCARDIA (except primary bradycardia or
complete heart block)
SYSTEMIC VENOUS CONGESTION
hepatomegaly, raised JVP, oedema (facial in
infants), pleural effusions,ascites
PULMONARY VENOUS CONGESTIONincreased RR, retractions, nasal flaring, grunting,
creps, wheeze, pulm. oedema, irritability(low O2)

CF Clinical manifestations
LOW CO fatigue, pallor, sweating, cool
extremities, low pulse volume, decreased
capillary refill.
VOLUME OVERLOAD cardiac
enlargement, gallop , regurgitant murmur
Low urine output.
Growth failure and weight loss.

CF -Evaluation
History
Physical examination.
Investigations Cxray, ECG, 2DE, pulse
oximetry, blood gases, O2 challenge, U &E,
CBC, urinalysis, blood culture, serum Ca,
blood glucose, others indicated by history
and P.E.

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CF History
Poor feeding in small infants
SOB worse on feeding (exertional
dyspnoea), respiratory symptoms in infants
Sweating increased on feeding
Poor weight gain and linear growth
In older child fatigue, exertional
dyspnoea, orthopnoea, oedema of face and
legs

CF Treatment
Identify and treat underlying cause
Correct aggravating factors e.g. anaemia
and sepsis, arrhythmias, hypertension
NON-PHARMACOLOGICAL
PHARMACOLOGICAL

CF Treatment
Non-pharmacological
SEVERE bed rest, prop-up, O2, fluid
restriction, salt restriction, adequate
calories.
AMBULANT No added salt
mild exercise

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CF Treatment
Pharmacological

Diuretics
Vasodilators
ACE inhibitors
Beta adrenergic blockade
Digoxin
Beta agonists used in ICU setting
dobutamine, dopamine, isoprenaline

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