Heart failure

Suchithra .p.v

1st year Msc Nursing

College of Nursing

Heart failure

• Heart Failure is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients.

• It is otherwise known as Congestive Cardiac Failure.

• Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion.

causes

• Reduced ventricular contractility • Ventricular outflow obstruction (pressure

overload )• Ventricular inflow obstruction• Ventricular volume overload• Arrhythmia • Diastolic dysfunction

Acute causes

• Acute myocardial infarction• Dysrrhythmias• Pulmonary emboli• Thyrotoxicosis• Hypertensive crisis• Rupture of papillary muscle( eg: mitral valve)• Ventricular septal defect• Myocarditis

Chronic causes• Coronary artery disease• Hypertension• Rheumatic heart disease• Congenital heart disease• Cor pulmonale• Cardiomyopathy• Anemia • Bacterial endocarditis• Valvular disorders•  

RISK FACTORS

• Advancing age• Hypertension • Diabetes • Obesity• High serum cholesterol • Cigarette smoking

PRECIPITATING CAUSES

• Anemia• Infection• Hypothyroidism• Bacterial endocarditis• Paget’s disease• Nutritional deficiencies• Hypervolemia

PATHO PHYSIOLOGY

Compensatory mechanism

• 1. Hemodynamic alterations• 2. Neurohormonal responses • 3. Ventricular dilation • 4. Ventricular hypertrophy

Alterations in Beta-adrenergic Receptor pathway

• Increased NE concentration cause down regulation of beta-1 adrenergic receptors in the ventricles.

• Beta- adrenergic receptor kinase(BARK) enzyme level increases.

Role of Arginine Vasopressin (AVP)

• Circulating AVP is elevated. This leads to salt and water retention and systemic vasoconstriction.

Role of cytokinine

• They have crucial roles in mediating the changes in myocardial structure and function in CHF.

Cellular and Molecular Mechanisms

• Role of calcium• Calcium plays a central role in myocardial

contraction and relaxation. In CHF, there is prolonged elevation of intracellular calcium during relaxation

• Role of free radicals and apoptosis

• Altered mitochondrial oxygen metabolism results in formation of free radicals.

• Free radicals produced by various mechanisms have been shown to result in apoptosis of cardiac myocytes in CHF.

DECOMPENSATED HEART FAILURE

• Ventricular remodeling• Sustained neurohumoral activation

Counter regulatory mechanism

• ANP and BNP are hormones produced by the heart muscle .

• ANP is released in response to stretch or increased volume in the chambers.

• Levels of circulating ANP can be correlate with functional class prognosis and hemodynamic state.

• Inhibit renin, aldosterone and ADH secretion and results in excretion of sodium and water

• Promotes venous and arterial vasodilatation.

• BNP is released in response to an increase in wall stress or triggered by pressure.

TYPES OF HEART FAILURE

• Left –sided heart failure or left ventricular dysfunction

• Right sided heart failure or right ventricular failure

• Biventricular heart failure• Diastolic and systolic dysfunction

High output versus low output failure

High output failure occurs when the heart despite normal output to high output levels is simply not able to meet the accelerated needs of the tissues

Low output failure occurs in most forms of heart disease resulting in hypoperfusion of tissue cells .

Backward versus forward failure

• Backward failure focuses on the ventricles inability to eject completely ,which increases ventricular filling pressures ,causing venous and pulmonary congestion .

• Forward failure is a problem of inadequate perfusion. It results when reduced contractility produces a decrease in stroke volume and cardiac output

• Acute versus chronic heart failure

CLINICAL MANIFESTATIONS

• Left Sided HeartFailure• Acute LVF presents with a sudden onset of

dyspnoea at rest.• progresses to acute respiratory distress,

orthopnoea and prostration.• appears agitated ,pale and clammy• Rapid pulse

• Cool periphery• High BP• Elevated JVP if associated with RVF.• Auscultaition – crepitations,triple gallop

rhythm.• Displaced apex beat.

Respiratory system

• Tachypnea• Capillary refill > 3 seconds• Orthopnea• Dyspnea on exertion• Nocturnal dyspnea• Cough with frothy sputum (indicative of

pulmonary edema)

• Basilar crackles or rhonchi• Cyanosis• Hypoxia (respiratory acidosis)• Kussmaul’s sign• Cheyne stokes respiration

Cardiovascular system• Diaphoresis• Audible S3 and S4 heart tones• Murmur or mitral insufficiency• Enlarged left ventricle on X-ray• Enlarged left atrium on X-ray• Narrowing pulse pressure• Pulses alternans (alteration of weak and strong

beats)

• Basilar crackles or rhonchi• Cyanosis• Hypoxia (respiratory acidosis)• Kussmaul’s sign• Cheyne stokes respiration• Elevated pulmonary artery pressures• Elevate pulmonary artery occlusive pressures

Central nervous system• Mental confusion

Generalized symptoms• Weight gain. • Fatigue/weakness/lethargy

Right sided heartfailure

Gastro intestinal system• Hepatomegaly• Splenomegaly• Hepatojugular reflux• Ascites

• Weight gain

• Weight loss and emaciation as a result of inadequate intake of food and wasting of tissues. This picture is termed as cardiac cachexia

Cardiovascular system

• Arrhythmias• Elevated CVP• Elevated right atrial pressure• Elevated right ventricular pressure• Narrowing pulse pressure• Murmur or tricuspid insufficiency

• Audible S3 and S4 heart tones• Enlarged right atrium on X-ray• Enlarged right ventricle on X-ray• Dependant pitting edema• Venous distention

• Urinary system• Oliguria• Nocturia

Chronic heart failure

• Fatigue• Dyspnea• Orthopnea • Paroxysmal nocturnal dyspnea• Tachycardia • Edema

• Nocturia • Skin changes

Chronic swelling result in pigment changes causing the skin to appear brown

• cool and damp to the touch• Behavioral changes• Chest pain • Weight changes

COMPLICATIONS

• Pleural effusion • Dysrhythmias

EF less than 35%have a high risk of fatal dysrhythmias and sudden cardiac death.

• Renal failure • Impaired liver function & Cardiac cirrhosis• Thromboembolism

Hypokalemia & Hyperkalemia

DIAGNOSTIC STUDIES

• History• Physical Examination

• Electrocardiogram• Laboratory data(cardiac enzymes, BNP,serum

chemistries ,liver function studies ,thyroid function studies and complete blood count). In severe CHF dilutional hyponatremia occurs. BUN and creatinine are moderately elevated.

• BNP levels are used to assess the HF.• BNP<100pg/ml - heart failure very

improbable• BNP100-500pg/ml -HF probable• BNP>500pg/ml -HF very probabl

• Echocardiogram : EF less than 40% accepted as evidence of systolic dysfunction.

• Asessment of myocardial viability

This can be done by using dobutamine or dipyridamole stress echocardiography, nuclear imaging using thallium or sestamibi and positron emission tomography

Identify patients who will benefit from long term therapy with drugs such as ACE inhibitors

• Stress testing,(treadmill test, stress echocardiography and nuclear perfusion studies)

• Cardiac catheterization and coronary angiography:

• Endomyocardial biopsy

This is indicated in patients with clinical indication of myocarditis and systemic disease with possible cardiac involvement such as hemochromatosis, amyloidosis, sarcoidosis and those who have received adriamycin chemotherapy.

MANAGEMENT OF ACUTE PULMONARY EDEMA

• Sit the patient up• Give oxygen(high flow ,high concentration ).

non invasive positive pressure ventilation (CPAP-5-10 mmhg)

• IV glceryl trinitrate 10-200 microgram /minute until clinical improvement occurs or systolic blood pressure falls to ˂110mmHg.

• loop diuretic such as frusemide 50-100mg IV

• continuous monitoring• Ionotropic agents • Intra aortic balloon pump

Management

• General measures• Pharmacologic therapy• Devices• Surgery• Newer evolving therapies

General measures

• Rest• Correction of aggravating factors• Salt restriction – sodium intake should be

limited to ˂ 2g/day• Fluid restriction- to 1-2l/day is advisable in

patients with dilutional hyponatremia.• Smoking cessation• Avoid alcohol• Management of co morbidities

Pharmacologic therapy

To Reduce workload • Angiotensin converting enzyme inhibitors • Angiotensin II receptor blockers• Vasodilators • Diuretics• Beta blockers

ACE inhibitors

• Interrupts the vicious cycle of neurohumoral activation

• Prevents salt and water retension ,peripheral arterial and venous vasoconstriction

• Also increase the concentrations of the vasodilator bradykinin.

• Decreases SVR and improves myocardial performance.

• Enalapril: 2.5 mg 12 hrly• Lisinopril 2.5 mg daily • Ramipril :1.25 mg daily• Captopril :50 mg tds

Adverse effects

• Persistant cough • Hypotension• Hyperkalemia• \deteriorating renal function• Loss of taste

Angiiotensin II receptor blockers

• Similar hemodynamic effects to ACE inhibitors

• Do not affect bradykinin metabolism• Losartan, Valsartan, Irbesartan and Eprosartan• Losartan :25 mg daily• Candesartan:4 mg daily • Valsartan : 40 mg daily

Vasodialators

• Venous dialation blood is trapped in the veins ,and venous return to the heart is decreased .This reduces preload

• eg: nitroglycerin and isosorbide dinitrate• Dilation of arterioles: arteriolar vasodilators

decreases peripheral vascular resistance and afterload

• Eg:ACE inhibitors

Combined action on veins and arterioles• decrease both preload and afterload• sodium nitroprusside relaxes the smooth

muscle of both veins and arterioles.it does not directly affect the heart muscle or heart rate

Beta blockers

• Directly block the direct effects of the SNS • Cardio selective agents block beta 1 adrenergic

receptors.non selective agents block beta 1 and beta 2 adrenergic receptors.

• Eg: atenolol,metoprolol , bisoprolol, bucindolol, labetalol,carvedilol,esmolol (25-50 mg bd)

Diuretics

• To mobilize edematous fluid , reduce pulmonary venous pressure ,and reduce preload

• Thiazide diuretics may be the first choice in chronic HF

• Eg;benzthiazide,chlorothiazide,chlorthalidone,metolazone

• Loop diuretics • eg.Frusimide ,torsemide• Spironolactone is an inexpensive ,potassium

sparing diuretic.

Human b-type natriuretic peptide

Nesiritide is a synthetic form of human BN

Beta adrenergic agonists

• short term treatment • E.g.:-dopamine, dobutamine

Cardiac glycosides• Eg ; Digoxin• Slow the ventricular rate, improves cardiac

function• Optimum therapeutic level os digoxin in serum

is 1-1.5 ng/ml• Toxic level is above 2ng/ml

Calcium channel blockers• Vasodilator• Anti ischemic effects• Eg: Verapamil, diltiazem, amlodipine

• Phosphodiesterase inhibitors:-

Eg: amrinone,milrinone• Antidysrhythmic drugs

e.g.adenosine, digoxin, ibutilide, magnesium

Devices

• Implantable cardiac defibrillators and resynchronization therapy

Ventricular assist devices

Extracorporeal membrane oxygenator

Surgery

• Heart transplantation • Coronary revascularization • Dynamic cardiomyoplasty• Partial left ventriculectomy( Batista

procedure)• Aneurysmectomy• Mitral annuloplasty and mitral valve repair

Newer evolving therapies

• Gene therapy• To increase the myocardial contractility at

molecular level• Genes expressing SERCA2a are increased by

using adenovirus transfection of myocytes

• NURSING ASSESSMENT

Nursing diagnosis

Decreased cardiac output r/t heart failure ,dysrhythmia or both

• Assess blood pressure for hypotension or hypertension

• Assess heart rate and rhythm • Document rhythm strips q8h • Auscultate heart rate q2h • Monitor lung sounds

• Monitor intake and output • Assess for change in mental status • Administer prescribed medications • Encourage physical and mental support • Encourage client to eat small frequent feeds

• Excess fluid volume related to cardiac failure as evidenced by edema ,dyspnea on exertion ,increased weight gain

• Monitor intake and output chart • Assess for presence of peripheral edema • Assess for jugular vein distention • Follow low sodium or fluid restriction• Auscultate breath sounds • Administer diuretic therapy

Impaired gas exchange related to increased preload, mechanical failure or immobility as evidenced by increased respiratory rate, shortness of breath, and dyspnea on exertion

• Auscultate breath sounds q2h• Assess respiratory rate • Asses for cyanosis • Monitor pulse oximetry• Position the client to facilitate breathing • Administer diuretic therapy

Ineffective tissue perfusion related to decreased cardiac output

• Note colour and temperature of the skin q4h• Monitor peripheral pulsesq4h• Provide a warm environment • Encourage active rang of motion • Monitor urine output

• Activity intolerance related to fatigue secondary to cardiac insufficiency and pulmonary congestion as evidenced by dyspnea,shortness of breath ,weakness, increased in heart rate on exertion

• space nursing activities • Schedule rest periods • Monitor the clients response to activities • Instruct the client to avoid activities that

increase cardiac workload

• Anxiety r/t to dyspnea or perceived threat of death as evidenced by restlessness, irritability

• Deficient knowledge related to disease process as evidenced by questions about the disease and prognosis

References

• KV Krishnadas. Text book of Medicine. 5th edition.Jaypee publications.New Delhi.2008

• Marscall S. Runge. Georege A.Netter’s Cardiology .2nd ed. USA .2014

• Nicki R.Colledge,Brian R. Walker,Stuart H.Ralston.Davidson’s Principles and Practice of Medicine 21st edition 2010 Churchil Living stoneElsevier page no 542-550

• Richard Hatchett, David R Thompson. Cardiac Nursing. Elsevier publications. USA.2007