Congestive heart failure

Heart Failure

MAGDI AWAD SASI 2013

1 MAGDI AWAD SASI HEART FAILURE 2013

DEFINITION

Heart (or cardiac) failure: pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure

According to AHA,

HF is a clinical syndrome including circulatory congestion or inadequate tissue perfusion , due to abnormal heart function and associated neurohormonal abnormalities.

An inadequate or decreased cardiac output which causes an increase in the blood volume within the vascular system. The resulting congestion within the venous system interferes with the movement of body fluids, resulting in fluid accumulation in the tissue spaces, causing edema

Frequency : United States

• More than 3 million people have congestive heart failure (CHF), and more than 400,000 new patients present yearly. The prevalence rate is 1-2%.

Race

Blacks are 1.5 times more likely to die of CHF than whites are. Nevertheless, black patients appear to have similar or lower in-hospital mortality rates than white patients.

Sex

Prevalence is greater in males than in females in patients aged 40-75 yrs. No sex predilection is noted among patients older than 75 years.

Age

Prevalence of CHF increases with increasing age and affects about 10% of the population older than 75 years


Mortality/Morbidity

Approximately 30-40% of patients with congestive heart failure (CHF) are hospitalized every year. CHF is the leading diagnosis-related group (DRG)

among hospitalized patients older than 65 years. 35% will die within one year of diagnosis. Less than 50% of patients with HF have typical physical signs. Less than 50% of patients being correctly identified during the initial consultation. 50% readmission rate within 6 months

50% of HF patients will die 5 years after the diagnosis The most common cause of death is progressive heart failure, but sudden

death may account for up to 45% of all deaths.

Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality rate.

Cardiac Physiology

(remember this?)

• CO = SV x HR

• HR: parasympathetic and sympathetic tone

• SV: preload, afterload, contractility

Preload

• Def: Passive stretch of muscle prior to contraction

• Measurement: Swan-Ganz

– LVEDP( venous return)

• Really a function of diastole


• Affected by compliance

– Low compliance = higher LVEDP with lower LVEDV

Afterload

• Def: Force opposing/stretching muscle after contraction begins

• Measurement: SVR

Contractility

• Def: Normal ability of the muscle to contract at a given force for a given stretch, independent of preload or afterload forces

• In other words:

– How healthy is your heart muscle?

• Ischemia,infarction, Hypertrophy (?), Muscle loss

Pathophysiology

• Hemodynamic changes

• Neurohormonal changes

• Cellular changes

1.Hemodynamic changes:

• HF can be secondary to systolic dysfunction or diastolic dysfunction

• 2. Cellular changes

• Changes in Ca+2 handling• Changes in adrenergic receptors:

Slight in α1 receptors


β1 receptors desensitization ® followed by down regulation • Changes in contractile proteins• Program cell death (Apoptosis)• Increase amount of fibrous tissue

• 3. Neurohormonal changes

Classifying Heart Failure

• Forward Vs Backward

• Rt. Vs Lt. sided HF

• Acute Vs Chronic HF

• Low Vs High output HF

• Systolic Vs Diastolic HF



• A etiology It is a common end point for many diseases of cardiovascular system

1. Vascular –

Ischemic heart disease, myocardial infarction

2. Valvular

–stenosis/regurgitation( RHD, infective endocarditis)

3. Preesure- hypertension

4.Muscle- cardiomyopathy

5. Rhythm- atrial fibrillation

Symptoms:

Left ventricular failure-

The patient present with chest symptoms which may delay the diagnosis and keep the patient to seek chest consultants advice.

Failure of forward flow from left ventricle into the aorta result into pulmonary congestion with chest symptoms.


Since the left ventricle does not empty completely, it cannot accept blood returning from the lungs via the pulmonary veins. The pulmonary veins become engorged and fluid seeps out through the veins and collects in the lungs.

LVF can be acute or chronic depending on the underlying cause of heart disease

LVF= CHEST SYMTOMS= D/D OF ALL LUNG DISEASES= CHEST FINDING

LVF symptoms are:

Dyspnea at rest Dyspnea upon exertion: This has been found to be the most sensitive

symptom reported, yet the specificity for dyspnea is less than 60%. Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms

are observed; however, the sensitivity for orthopnea and PND is only 20-30%.

Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF).The sputum is whitish , soap like , watery.

Wheezing= new onset of wheezing above age of 60 years or wheezing in elder diabetic or wheezing all of a sudden in HTN patient is cardiac asthma until prove other wise.

Palpitation in arrhythmia Chest pain or tightness especially if the cause is vascular(IHD/ACS).

Non specific symptoms of low COP

Malaise, Weakness,Light headedness, fatigue, dizziness ,sweating ,lose of effort.



Right ventricular heart failure

The patient present with abdominal symptoms which may delay the diagnosis and keep the patient to seek gastroenterologist advice.

Failure of forward flow from right ventricle into the pulmonary artery results into systemic congestion with abdominal symptoms.

Failure of the right ventricle to maintain a normal output of blood.

Since the right ventricle does not empty completely, it cannot fully accept blood returning from the body. Pressure builds in the veins of the body causing fluid to seep out and collect in the cells of the body – especially the extremities.

Engorgement of the systemic veins produces pitting edema, enlargement of the

liver, and ascites.


RVF can be acute or chronic depending on the underlying cause of heart disease

RVF= ABDOMENAL SYMTOMS= D/DOF ABDOMENAL DISEASES= ABD FINDING.

Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side. When the right side loses pumping power, blood backs up in the body's veins. This usually causes swelling in the legs and ankles.

RVF symptoms are:

Abdominal distention Right hypochondrial pain Epigastric fullness, early satiety , nausea , vomiting(stomach congestion) Change of bowel habit –constipation, diarrhea, malabsorption Bilateral leg swelling Yellowish coloration of sclera Change of urine frequency and colour

These symptoms are caused by internal abdominal organs congestion

And can be mistaken for local abdominal pathology.

RVF is caused by:

1. Left ventricular failure - most common cause- mitral stenosis

2. Pulmonary hypertension caused by chronic lung disease

(cor pulmonale)

3. Cardimyopathies and myocarditis


SIGNS:

General appearance Patients with mild heart failure appear to be in no distress after a

few minutes of rest, but they may be obviously dyspneic during and immediately after moderate activity. Patients with LV failure may be dyspneic when lying flat without elevation of the head for more than a few minutes. Those with severe heart failure appear anxious and may exhibit signs of air hunger in this position.

Patients with recent onset of heart failure are generally well nourished, but those with chronic severe heart failure are often malnourished and sometimes even cachectic.

Chronic marked elevation of systemic venous pressure may produce exophthalmos and severe tricuspid regurgitation and may lead to visible pulsation of the eyes and of the neck veins.

Central cyanosis, icterus, and malar flush may be evident in patients with severe heart failure.

In mild or moderate heart failure, stroke volume is normal at rest; in severe heart failure, it is reduced, as reflected by a diminished pulse pressure and a dusky discoloration of the skin.

With very severe heart failure, particularly if cardiac output has declined acutely, systolic arterial pressure may be reduced. The pulse may be weak, rapid, and thready; the proportional pulse pressure (pulse pressure/systolic pressure) may be markedly reduced. The proportional pulse pressure correlates reasonably well with cardiac output.

Evidence of increased adrenergic activity Increased adrenergic activity is manifested by tachycardia,

diaphoresis, pallor, peripheral cyanosis with pallor and coldness of the extremities, and obvious distention of the peripheral veins secondary to venoconstriction.

Diastolic arterial pressure may be slightly elevated.Pulmonary rales =LVF

Rales heard over the lung bases( bilateral basal end inspiratory) are characteristic of heart failure of at least moderate severity.

The absence of rales certainly does not exclude elevation of pulmonary capillary pressure due to LV failure.


Protodiastolic (S3) gallop: This is the earliest cardiac physical finding in decompensated heart failure in the absence of severe mitral or tricuspid regurgitation or left-to-right shunts.

LVF=CHEST-B/L BASAL INSPIRATORY CREPITATION + HEART-S3Systemic venous hypertension: This is manifested by jugular venous distention. Normally, jugular venous pressure declines with respiration; however, it increases in patients with heart failure, a finding known as the Kussmaul sign. This reflects an increase in right atrial pressure and therefore right-sided heart failure.Hepatojugular reflux: This represents distension of the jugular vein induced by applying manual pressure over the liver. The patient's body should be positioned at a 45 º angle. This is found in patients with elevated left-sided filling pressures and reflects elevated capillary wedge pressure and left-sided heart failure.

Edema Bilateral pitting pedal odema. Usually, a substantial gain of extracellular fluid volume (ie, a

minimum of 5 L in adults) must occur before peripheral edema is manifested.

Edema, in the absence of dyspnea or other signs of LV or RV failure, is not solely indicative of heart failure and can be observed in many other conditions, including chronic venous insufficiency, nephrotic syndrome, or other syndromes of hypoproteinemia or osmotic imbalance.

Hepatomegaly Hepatomegaly is prominent in patients with chronic right-sided

heart failure, but it may occur rapidly in acute heart failure. When occurring acutely, the liver is usually tender. In patients with considerable tricuspid regurgitation, a prominent

systolic pulsation of the liver, attributable to an enlarged right atrial V wave, is often noted. A presystolic pulsation of the liver, attributable to an enlarged right atrial A wave, can occur in tricuspid stenosis, constrictive pericarditis, restrictive cardiomyopathy involving the RV, and pulmonary hypertension (primary or secondary).


Hydrothorax (pleural effusion) Hydrothorax is most commonly observed in patients with

hypertension involving both systemic and pulmonary systems. Hydrothorax is usually bilateral, although when unilateral, it is usually confined to the right side of the chest.

When hydrothorax develops, dyspnea usually intensifies because of further reductions in vital capacity.

Ascites This finding occurs in patients with increased pressure in the

hepatic veins and in the veins draining into the peritoneum. Ascites usually reflects long-standing systemic venous

hypertension.Pulsus alternans ( one strong and one weak beat)Pulsus alternans occurs most commonly in heart failure due to increased resistance to LV ejection, as occurs in hypertension, aortic stenosis, coronary atherosclerosis, and dilated cardiomyopathy.

It is usually associated with an S3 gallop, signifies advanced myocardial disease, and often disappears with treatment of heart failure.

Accentuation of P2 heart sound, S3 gallop, and systolic murmurs This accentuation is a cardinal sign of increased pulmonary artery

pressure. It disappears or improves after treatment of heart failure. Mitral and tricuspid regurgitation murmurs are often present in

patients with decompensated heart failure because of ventricular dilatation. These murmurs often disappear or diminish when compensation is restored. Note that correlation between the intensity of the murmur of mitral regurgitation and its significance in patients with heart failure is poor. Severe mitral regurgitation may be accompanied by soft murmur.

The presence of an S3 gallop in adults is important, pathologic, and often the most apparent finding on cardiac auscultation in patients with significant heart failure.

Cardiac cachexia Cardiac cachexia is found in long-standing heart failure, particularly

of the RV, because of anorexia from hepatic and intestinal congestion and sometimes because of digitalis toxicity. Occasionally, impaired intestinal absorption of fat and (rarely) protein-losing enteropathy occur.



Precipitating Factors

• Infection Sodium Intake

• Medications!!! Anemia

• Thyroid disorders Endocarditis

• Pulm Embolus Noncompliance

• Arrhythmia Myocardial Infarction

• Stress reaction

Diagnosis of CHF / Routine Tests:

CBC count INVESIVE Electrolytes 1. Exercise stress test

Renal function tests 2. Cardiac catheterization Liver function tests 3. Holter monitor B-type natriuretic peptide ECG Chest x-ray Echocardiogram

CXR

Cardiomegaly Vascular redistribution Kerley B lines Interstitial edema Peri-bronchial “cuffing” Effusions



Chest radiographs in patients with abrupt onset are usually helpful but can be limited because a delay of as long as 12 hours is possible from the onset of dyspnea due to acute heart failure to the development of classic abnormal findings on radiographs.

Classic radiographic findings demonstrate cardiomegaly (in patients with underlying CHF) and alveolar edema with pleural effusions and bilateral infiltrates in a butterfly pattern. The other signs are loss of sharp definition of pulmonary vasculature, haziness of hilar shadows, and thickening of interlobular septa (Kerley B lines).

In long standing biventricular chronic heart failure, chest radiographs may only show cardiomegaly without alveolar edema or pleural effusions due to adaptive lung mechanism with increased arterial vasoconstriction and lymphatic drainage.


Electrocardiography o The presence of left atrial enlargement and LV hypertrophy is

sensitive (although nonspecific) for chronic LV dysfunction.o ECG may suggest an acute tachyarrhythmia or bradyarrhythmia.o ECG may aid in the diagnosis of acute myocardial ischemia or

infarction as the cause of heart failure or may suggest the likelihood of prior myocardial infarction or presence of coronary artery disease as the cause of heart failure.

o ECG is of limited help when an acute valvular abnormality or LV systolic dysfunction is considered to be the cause of heart failure; however, the presence of left bundle branch block (LBBB) on an ECG is a strong marker for diminished LV systolic function

Echocardiogram

Chamber enlargement Wall motion abnormalities Diminished ejection fraction Possible LVH Possible valvular problems Assess diastolic dysfunction


Treatment Goals

• Improve symptoms

A. Enhance well-being and quality of life

B. Increase exercise tolerance

• Improve survival

A. Prevent progressive heart failure

B. Prevent sudden death

C. Prevent thromboembolic episodes

• Treatment ::


• Oxygen – nasal, BiPAP, intubation

• Fluid Balance

Restrict fluid- 1000ml daily/ salt intakeMonitor Input/Outputs and daily weightDialysis if needed -Critical renal failure patientsAspirin 75mg

Promoting Rest and Activity Bed rest or limited activity may be necessary during the acute

phase Provide an overbed table close to the patient to allow resting the

head and arms Use pillows for added support. Gradual ambulation is encouraged to prevent risk of venous

thrombosis and embolism due to prolonged immobility Activities should progress through dangling, sitting up on a chair

and then walking in increased distances under close supervision. Assess for signs of activity intolerance (dyspnea, fatigue and

increased pulse rate that does not stabilize readily) Providing Skin Care

Edematous skin is poorly nourished and susceptible to pressure sores

Change position at frequent intervals Assess the sacral area regularly Use protective devices to prevent pressure sores

Promoting Elimination Advise to avoid straining at defecation which involves Valsalva

manoeuvre. Administer laxative as ordered Encourage use of bedside commode


Preload Reduction

– Loop diuretics Lasix 20-200mg IV (q 6-8 hours)

– Nitrates -Nitroglycerin IV:10-200 mcg/min

– ACEi / ARB Captopril 6.25-50mg PO q8h

Enalapril 2.5-20mg PO BID

Afterload Reduction

– IV NTG, Nitroprusside

– Hydralazine 10-100mg PO q6-8 h

– ACE-I / ARB

Ionotropic Support

– Dopamine / Dobutamine 500mg in 250cc D5W

3-10 cg/kg/min


– Amrinone / Milrinone n Digoxin (chronic)

– Mechanical (ABP) Cardiogenic shock unresponsive to above tx

A.-----------Diuretics

• volume overload , sodium overload , preload reduction

Advantages

• Highly effective in most classes

• Essential with fluid retention

• Well tolerated, simple to use

Disadvantages

• Electrolyte abnormalities Na, k ,Ca ,Mg

• Hypovolemia, hypotension, renal dysfunction

• Activation of neurohormaonal system

AIM----Elimination of symptoms and/or signs of congestion

• Avoid volume depletion

A. Postural hypotension B. Increase in heart rate

C. Increase in BUN/Cr D. Neuroendocrine activation

Thiazide Diuretics-----Hydrochlorothiazide, Chlorthalidone , Metolazone

Loop Diuretics----------Furosemide , Torsemide

Potassium Sparing Diuretics---Spironolactone , Triamterene , Amiloride

Spironolactone :

Aldosterone inhibition minimize potassium loss, prevent sodium and water retention, endothelial dysfunction and myocardial fibrosis.


B-------------ACE Inhibitors

ACE inhibitors should be the initial treatment for heart failure

• Improve hemodynamic status

• Attenuate neurohumoral abnormalities

• Improve symptoms, left ventricular ejection fraction .

• Reduce incidence of hospitization

• Slow progression

• Reduce mortality

Neurohormonal Changes

• Decreased angiotensin II.

• Reduction in arterial resistance (afterload).


• Reduction in venous tension (preload).

• Inhibition of cardiac and vascular remodeling .

• Increased bradykinin

• Decreased or no change in aldosterone

• Decreased norepinephrine

Reduction in Sudden Death/Potential Mechanisms

• Increase in serum/total body potassium

• Decreased adrenergic stimulation

• Reduced heart size and decrease in ventricular hypertrophy

• Prevention of myocardial ischemia

• Prevention of progressive myocardial damage

FDA Approved

• Captopril ,Enalapril ,Lisinopril ,Quinapril ,Trandolapril ,Fosinopril

Adverse effects :

Dry irritating persistent cough

Hyperkalemia

Angioedema

Fetal toxicity


C---------------Beta Blockers

• Primary mechanism is inhibition of down regulation of beta receptors

• Additional mechanisms

A. Restore receptor density

B.Protect against cardiotoxicity of catecholeamines

C. Improve systolic/diastolic function in ischemic myocardium

• First Generation: Beta 1 and Beta 2

Propranolol/Timolol

• Second Generation: Beta 1

Metoprolol/Atenolol

• Third Generation: Vasodilating Properties

Carvedilol

Improve symptoms and clinical class


• Degree of benefit appears to relate to degree of disability before treatment

• Should be used in all stable Class II/III patients unless contraindicated

• Treatment should not be initiated in patients with acutely decompensated CHF

• Clinical response may take 2 to 3 months

Risks of Treatment

• Hypotension Fluid retention and worsening CHF

• Bradycardia and heart block


Start at low dose and monitor for bradycardia

Carvedilol and Metoprolol are the most commonly used for CCF amongst beta blockers

D------------Angiotensin Receptor AT-1 blockers (ARB) :

Losartan, Irbesartan, Candesartan

Competitive antagonists of Angiotensin II (AT-1).

No inhibition of ACE or Cough.


E--------------Vasodilators :

Isosorbide dinitrate and hydralazine also used specially in patients who cannot tolerate ACE inhibitors.

Amlodipine and prazosin are other vasodilators can be used in CCF.


F-------Cardiac glycosides : Digoxin :

Inhibition of Na/K ATPase pump increase intracellular sodium concentration – eventually increase cytosolic calcium.

It restores the vagal tone and abolishes the sympathetic over activity.

Has positive inotropic (strengthens force of cardiac contractility) and negative chronotropic effects (decreases heart rate.

Increase the refractoriness of AV node thus decrease ventricular response to atrial rate.


Digoxin is used as a first-line drug in patients with congestive heart failure who are in atrial fibrillation.

Adverse effects / Precautions :

Nausea, vomiting, gynecomastia, visual disturbances and psychosis.

Ventricular bigeminy, AV block and bradycardia. Antidote for Toxicity: Digibind Nursing Responsibilities

Assess heart rate before administration; if below 60 bpm or above 120 bpm, withhold the drug.

Monitor serum potassium Assess for signs of Digitalis toxicity

- Bradycardia- GI manifestations (anorexia, nausea, vomiting and

diarrhea)- Dysrrhythmias- Altered visual perceptions- In males: gynecomastia, decreased libido and

impotence Amiodarone and verapamil can increase the plasma concentration of

digoxin by inhibiting its excretion

IN DIASTOLIC FAILURE;

USE B-BLOCKER, ACE-I , CALCIUM CHANNEL BLOCKER RATE LIMITING

• Difficult to treat

• Diuretics for volume overload. Avoid volume depletion

• Prevent tachycardia

• Rate-limiting calcium channel blockers first choice

• Beta 1 beta blockers second choice


ADVERSE PROGNOSTIC MARKERS IN CHRONIC HEART FAILURE

• Old Age,

• Severity of heart failure (NYHA class)

• Left ventricular dysfunction,

• Diabetes Mellitus,

• Raised creatinine,

• Hyponatremia , Hypoalbuminaemia,Anaemia

• Presence of arrhythmia : AF / VT

Causes of Mortality in Heart Failure

• Pump failure

• Arrhythmia

• Severe Anaemia

• Associated serious co-morbidities i.e. Renal failure

Cardiac Inotropes =

• Dopamine acts at a variety of receptors (dose dependant)

• Rapid elimination- can only be administered as a continuous infusion

Dobutamine

• Stimulates beta-adrenergic receptors and produces a positive inotropic response

• Unlike the vasoconstriction seen with high doses of dopamine, dobutamine produces a mild vasodilatation .


PDE Phosphodiesterase inhibitors

• Inamrinone (amrinone) and Milrinone (bipyridines)

• Acts by inhibiting the enzyme Phosphodiesterase

• Thus lead to increase of intracellular concentrations of cAMP

• cAMP is responsible for the conversion of inactive protein kinase to active form

• Protein kinases are responsible for phosphorylation of Ca channels

• Thus causing increased Ca entry into the cell.

MECHANISM OF ACTION:

• Increase myocardial contractility by increasing the Ca influx during AP

• Also have vasodilating effect

• Selective for PDE isoenzyme-3 (found in cardiac and smooth muscle)

ADVERSE RECTIONS

• Inamrinone: nausea, vomiting, arrhythmias, thrombocytopenia and liver enzyme changes

• Withdrawn in some countries

• Milrinone: arrhythmias, less likely to cause other ADR

Niseritide

• Brain (B-type) natriuretic peptide (BNP) is secreted constitutively by ventricular myocytes in response to stretch

• BNP binds to receptors in the vasculature, kidney, and other organs, producing potent vasodilation with rapid onset and offset of action by increasing levels of cGMP


• Niseritide is recombinant human BNP approved for treatment of acute decompensated CHF.

• It reduces systemic and pulmonary vascular resistances, causing an indirect increase in cardiac output and diuresis.

• Effective in HF because cause reduction in preload and afterload

• ADR- hypotension

OTHERS;

Implantable cardioverter-defibrillator

Pacemakers, Biventricular pacemaker

Heart transplant

Cardiac Resynchronisation Therapy



Health & Medicine

Congestive heart failure