Cardiac Failure

7/21/2019 Cardiac Failure

http://slidepdf.com/reader/full/cardiac-failure-56d98b5bb63b3 1/12

1

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 (afterloadand preload), and contractility

• WALL STRESS = pressure x radius /2 x wall thickness



2

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 body’s 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 -> homeostaticimbalance and overt symptoms



3

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.



4

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

• Starling’s 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-Starling’s Law of the Heart

End-Diastolic Volume

Stroke

Volume

Normal Range:

SV increases with EDV

Maximum Capacity

To Produce SV

Mechanism: Length-Force Relations of Muscle Contraction



5

Family of Ventricular Function Curves

Atrial Pressure (Preload)

Cardiac

Output

Increase in

Cardiac

Contractility

or

Increase in

Heart Rate

Sympathetic stimulation

increases heart rate andcontractility

Parasympathetic stimulation

decreases heart rate

Family of Frank-Starling Curves

Stroke

Volume

Preload (End-Diastolic Volume)

Increase in

Cardiac

Contractility

At a given EDV, SV increases

With cardiac contractility

Low

High



6


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


•

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.



7

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.


• Myocardial hypertrophy . The myocytes

respond to changes in loading conditions in

CF by hypertrophy.

•

Angiotensin II -> myocyte hypertrophy.

• Aldosterone -> collagen synthesis



8

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 ASand CoA)and non duct dependent(TAVR,

AV malform, myocardial dysfunction

syndrome, SVT, sepsis).



9

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.



10

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 CONGESTION-

increased 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.



11

CF – History

• Poor feeding in small infants

• SOB worse on feeding (exertionaldyspnoea), respiratory symptoms in infants

• Sweating – increased on feeding

• Poor weight gain and linear growth

• In older child – fatigue, exertionaldyspnoea, orthopnoea, oedema of face andlegs

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



12

CF Treatment

Pharmacological

• Diuretics

• Vasodilators

• ACE inhibitors

• Beta adrenergic blockade

• Digoxin

• Beta agonists – used in ICU setting

dobutamine, dopamine, isoprenaline

Documents

Cardiac Failure