HEART FAILURE

Harmeet Kaur Kang

Lecturer

Definition

• Heart failure is the term used when heart is unable to pump enough blood to meet the metabolic needs of body at rest or during exercise even though filling pressures are adequate.

Key words

• Preload: stretch of myocardial fibres at end diastole.

• Afterload: force that the ventricle must develop to eject the blood during each contraction.

Key words

• Cardiac output: stroke volume X heart rate.

• Stroke volume: the amount of blood ejected from the ventricle with each contraction.

Etiology & risk factors

• Abnormal load on heart.

• Abnormal muscle function.

• Other conditions that exacerbate heart failure.

Abnormal load on heart

Overloading of the heart

Excessive stretch

Decreased contraction

Decreased cardiac output

Abnormal muscle function

• Muscles replaced by scar tissue eg: MI

• Externally compress the heart

• Decreased diastolic relaxation and diastolic blood pressure

• Hampers forward flow through heart.

Other factors

• Emotional stress

• Dysrhythmias

• Infections

• Anemia

• Thyroid disorders

• Pregnancy

• Paget’s disease.

Other factors

• Nutritional deficiency.

• Pulmonary disease.

• Hypovolemia.

Pathophysiology Diseased Normal

myocardium myocardium

Unable to meet the demands

Activation of compensatory system

(sympathetic stimulation fails )

Increased residual volume in left ventricle

Pathophysiology (contd..)• Decreased ability to receive blood from

left atrium • Left atrium work hard to eject blood

• Dilation and hypertrophy

• Pulmonary edema and congestion

Pathophysiology (contd…)

Increased pressure in pulmonary vascular

system

Right ventricular dilation&hypertrophy

Fails

Engorgement of systemic venous system

Congestion in GIT,Liver viscera,Kidneys,Legs,sacrum

Pathophysiology (contd..)

Conditions that causes RVF - Pulmonary diseases (PAH,Pulmonary embolism,COPD,cor pulmonale) - Constrictive Pericarditis - Tricuspid and pulmonary valvular disorders - RV infarction

Pathophysiology (contd..)

• Cardiac reserve (Hearts ability to increase the output in response to stress(5 the times the normal)

• But in the diseased heart, it fails to respond to body’s increased demands

• Compensatory mechanism will be initiated

Pathophysiology contd..• Compensatory mechanisms are

-Ventricular dilation: Lengthening of the muscle fibers Increased volume of heart chambers Increased preload and cardiac out put leads to reduced contractibility when stretched beyond capacity Increased oxygen demand hypoxia

Pathophysiology (contd..)• Ventricular hypertrophy-Increase in the

diameter of muscle fibers

Size and weight of heart increases

Increased oxygen demand

Hypoxia and reduced contractibility

Pathophysiology(contd..)• Increased sympathetic stimulation

Increased heart rate and peripheral vascular resistance

Reduced renal flow and increased renal conservation of water and sodium

Fluid overload and increased workload

Forms of heart failure• Systolic versus diastolic failure

Systolic-Inability to contract normally

Diastolic-Inability to relax or fill normally

• High output versus low output

Low output-IHD, HT,cardiomyopathy,pericardial diseases

Highoutput-Hyperthyroidism,anemia,pregnancy,paget disease

Forms (contd..)

• Acute versus chronic Acute –Acute large MI• Chronic-Dilated cardiomyopathy

multivalvular heart disease• Right sided versus left sided RVF-PAH,Pulmonary

stenosis,pulmonary embolism, LVF-Aortic stenosis,Post MI

Types (contd..)

• Backward versus forward H F

backward-ventricles fail to fill normally Increased pressure in the atrium and venous system sodium and water retention edema

• Forward-Inadequate discharge of blood in to the arterial system

Pathophysiology

• Ventricular dilatation.

• Ventricular hypertrophy.

• Increased sympathetic nervous stimulation.

Clinical features

• LVF-Dyspnea(PND)

Orthopnea

cough(frothy&blood tinged sputum)

chyne stoke respiration

pulmonary edema (extreme

breathlessness,anxiety,frothy sputum,

nasal flarring)

C/F Contd

• Cardiovascular signs –

Enlarged left laterally displaced apical

impulse, Heart gallop(S3 & S4)pulses alternas

• Cerebral hypoxia- Anxiety,Irritability,Restlesness,confusion,Impaired memory, Insomnia

• Renal changes-Oliguria,fatigue and muscular weakness

C/F Contd

• RVF-Peripheral edema and venous congestion,

• Hepatomegaly and abdominal pain • Cardiac cirrhosis and ascitis• Anorexia,nausea and bloating• cardiac cachexia• Pitting edema• Jugular vein distention, Increased CVP• Anxiety and depression

Diagnostic tests

• X-ray

• ECG

• Echocardiography

• Blood tests

• ABG analysis

• Pulse oximetry.

Medical management

• Removal of precipitating factors

• Correction of underlying causes

• Prevention of deterioration of cardiac function

• Control of CHF state

Immediate management

• Positioning – high fowlers position

• Oxygen administration(8–10 Lts,40-70%)

Medical management

• Oxygen inhalation.

• Digitalis.

• Diuretics.

• Inotropic agents.

Management contd

• Digitalis-Increases ventricular emptying,slow conduction of impulses through AV node,Increases stroke volume and cardiac output

-Effective in systolic heart failure -0.25 6 hourly for adults,for elderly 0.125 mg 6

hourly -Reduce dose in renal impairment -Should not be given in heart failure with high

output - Digitalis toxicity should be monitored

Management contd

• Dopamine and dobutamine Low output failure Dopamine-2-10 microgram/kg/mt Dobutamine-2.5-10 microgram/kg/mt• Phosphodiesterase inhibitors:Amrinone, Milrinone• Anticoagulants• Antiarrythmics • ACEI• Aldosterone antagonist;spironolactone25mg /day• Beta adrenergic blockers

Dietary management

• Fluid restriction.

• Sodium restriction.

• Potassium supplementation with diuretics.

Other management

• Assist devices.

• Intra- aortic balloon pump.

Palliative management

• Heart transplantation.

Nursing management

• Decreased cardiac output.

• Fluid volume overload.

• Impaired gas exchange.

• Altered peripheral tissue perfusion.

• Risk for activity tolerance.

• Impaired skin integrity.

• Risk for digitalis toxicity.