Heart failure lecture 3

By Dr sharmeen talpur

– Approximately 30-40% of patients with CHF are hospitalized each year. Leading diagnosis-related group over 65. The 5 year mortality after Dx was reported as 60% in men and 45% in women in 1971. In 1991, data from the Farmington heart study showed the 5 year mortality rate remaining unchanged, with a median survival of 3.2 years for men, and 5.4 years for women, post dx.

– 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 IDDM have a significantly higher mortality rate.

– Effects an estimated 4.9 million Americans

– 1% of age 50-59– 10% age over 80 89

years– In the UK most

patients admitted to hospital with heart failure are >70 years and remain hospitalised for a week or more.

– Heart failure describes the clinical syndrome that develops when the heart can not maintain an adequate cardiac output,or can do so only at the at the exposure of an elevated filling pressure.

– In mild to moderate form of heart failure ,cardiac output is adequate at rest and only becomes inadequate when the metabolic demand increases during exercise or some other forms of stress

♦ Summarized as an imbalance in Starlings forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in the ensuing contraction.

♦ Or basically like a rubber band, the more it is stretched, the greater the releasing velocity.

– Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs.

– However, when the capacity of the lymphatic drainage is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, this creating CHF.

– When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema

– Coronary artery disease--chronic

– HTN--both– Valvular heart disease

(especially aorta and mitral disease)--chronic

– Inc metabolic demand– ASD,VSD

– Dysrhythmias--acute

– Diabetes—chronic

– Preload—• The amount of blood the

heart must pump with each beat

• Determined by:– Venous return to heart– Accompanying stretch

of the muscle fibers

• Increasing preload increase stroke volume in normal heart

• Increasing preload impaired heart decreased SV. Blood is trapped chamber enlargement

– Afterload—• The pressure that must be

overcome for the heart to pump blood into the arterial system.

• Dependent on the systemic vascular resistance

• With increased afterload, the heart muscles must work harder to overcome the constricted vascular bed chamber enlargement

• Increasing the afterload will eventually decrease the cardiac output.

– When cholesterol and fatty deposits build up in the heart’s arteries, less blood reaches the heart muscle. This damages the muscle, and the healthy heart tissue that remains has to work harder

– Uncontrolled HTN doubles the chances of failure

– With HTN, the chambers of the heart enlarge and weaken.

– Can result from disease, infection, or be congenital

– Don’t open and/or close completely increased workload failure

– Tachycardias decreased diastolic filling time decreased SV.

– Atrial dysrhythmias as much as 30% reduction in stroke volume

– The ischemic tissue is basically taken out of the equation, leaving a portion of the heart to do the work of the entire heart decreased SV CHF.

– Tend to be overweight– HTN– Hyperlipidemia

Types of Rhythms Associated with CHF

– Left Ventricular Failure with Pulmonary Edema

– Right Ventricular Failure

The smooth, glistening pleural surface of a lung is shown here. This patient had marked pulmonary edema, which increased the fluid in the lymphatics that run between lung lobules. Thus, the lung lobules are outlined in white.

– Occurs when the left ventricle fails as an effective forward pump

back pressure of blood into the pulmonary circulation

pulmonary edema– Cannot eject all of the

blood delivered from the right heart.

– Left atrial pressure rises increased pressure in the pulmonary veins and capillaries

– When pressure becomes to high, the fluid portion of the blood is forced into the alveoli.

decreased oxygenation capacity of the lungs

– AMI common with LVF, suspect

– Severe resp. distress– • Evidenced by

orthopnea, dyspnea

• Hx of paroxysmal nocturnal dyspnea.

– Severe apprehension, agitation, confusion—

• Resulting from hypoxia

– Cyanosis—

– Diaphoresis—• Results from

sympathetic stimulation

– Pulmonary congestion• Often present• Rales—especially at the

bases.• Rhonchi—associated

with fluid in the larger airways indicative of severe failure

• Wheezes—response to airway spasm

– Jugular Venous Distention—not directly related to LVF.

• Comes from back pressure building from right heart into venous circulation

– Vital Signs—• Significant increase in

sympathetic discharge to compensate.

• BP—elevated• Pulse rate—elevated to

compensate for decreased stroke volume.

• Respirations—rapid and labored

– LOC—• may vary.• Depends on the level of hypoxia

– Chest Pain• May in the presence of MI• Can be masked by the RDS.

♦ REMEMBER LEFT VENTRICULAR FAILURE IS A TRUE LIFE THREATENING EMERGENCY

– Etiology—• Acute MI—

– Inferior MI

• Pulmonary disease – COPD, fibrosis, HTN

• Cardiac disease involving the left or both ventricles

• Results from LVF

– Pathophysiology—• Decreased right-sided

cardiac output or increased pulmonary vascular resistance increased right vent. Pressures.

• As pressures rise, this increased pressure in the right atrium and venous system

• Higher right atrium pressures JVP

– In the peripheral veins, pressures rise and the capillary pressures increase, hydrostatic pressure exceeds that of interstitial pressure

– Fluid leaks from the capillaries into the surrounding tissues causing peripheral edema

– Lungs are clear due to left ventricular pressures are normal

– Marked JVD– Clear chest– Hypotension– Marked peripheral

edema– Ascites, hepatomegaly

– Often will be on Lasix, Digoxin,

– Have chronic pump failure

– Neurohormonal system– Renin-angiotensin-aldosterone system– Ventricular hypertrophy

– Stimulated by decreased perfusion secretion of hormones

• Epi—– Increases contractility

– Increases rate and pressure

– Vasoconstriction SVR

• Vasopressin—– Pituitary gland

– Mild vasoconstriction, renal water retention

– Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys

• Aldosterone is released increase in Na+ retention water retention

• Preload increases

• Worsening failure

– Long term compensatory mechanism– Increases in size due to increase in work load ie

skeletal muscle

COPD CHF Pneumonia

Cough Frequent Occasional Frequent

Wheeze Frequent Occasional Frequent

Sputum Thick Thin/white Thick/yellow/ brown

Hemoptysis Occasionally Pink frothy occasionally

PND Sometimes after a few hours

Often within 1 hour

Rare

Smoking Common Less common Less common

Pedal edema Occasional Common with chronic

none

COPD CHF Pneumonia

Onset Often URI with cough

Orthopnea at night

Gradual with fever, cough

Chest Pain pleuritic Substernal, crushing

Pleuritic, often localized

Clubbing Often Rare Rare

Cyanosis Often and severe Initially mild but progresses

May be present

Diaphoresis May be present Mild to heavy Dry to moist

Pursed Lips Often Rare Rare unless COPD

COPD CHF Pneumonia

Barrel Chest Common Rare Rare unless COPD

JVD May be present with RVF

Mild to severe Rare

BP Usually normal Often high Normal

Dysrhythmia Occasional May precipitate CHF

Common

Wheeze Common Less common Common

Crackles Coarse, diffuse Fine to coarse, begin in gravity dependent areas

Localized to diffuse, coarse

– RENAL FAILURE– HYPOKAELEMIA– HYPERKAELIMIA– HYPONATRAEMIA– IMPAIRED LIVER FUNCTION– THROMBOEMBOLISM– ATRIAL AND VENTRICULAR

ARRHYTHMIAS

– Aimed at diminishing the compensatory mechanisms of low cardiac output and also improving contractility

– Vasodilators—ACE inhibitors– Diuretic agents– Inotropic agents

– Dilate blood vessels– Often constricted due

to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system.

– Aka—ACE inhibitors

– Common ACE inhibitors

• Captopril• Lisinopril• Vasotec• Monopril• Accupril

– Nitrates

– Lasix– Hydrochlorothiazide(HCTZ)– Spironolactone

♦ These inhibit reabsorption of Na+ into the kidneys

– Digoxin– Lanoxin

♦ Increases the contractility of the heart increasing the cardiac output

– Metoprolol– Atenolol– Propanolol– Amiodarone

– Useful by blocking the beta-adrengergic receptors of the sympathetic nervous system, the heart rate and force of contractility are decreased could actually worsen CHF

– The prehospital goals for managing CHF– Promotion of rest– Relief of anxiety– Decreasing cardiac workload– Attainment of normal tissue perfusion

– DO NOT make these patient’s walk– Could start a fluid “rush” into the alveoli– Try to get them to sit still if they appear

agitated and hypoxic

– Often experienced– Leads to increase in O2 demand and cardiac

workload– Explain what you are doing– MS 2 mg for treatment of anxiety and for

decreasing preload

– ACE Inhibitors– Digitalis– Diuretics

– Hydralazine– Nitrates

– Prevent the production of the chemicals that causes blood vessels to narrow

– Resulting in blood pressure decreasing and the heart pumping easier

– Inotropic effects on the heart– Negative chronotropic effects

– Decrease the body’s retention of salt and water– Reduces blood pressure– Probably will be on potassium

– Widens the blood vessels, therefore allowing more blood flow

– Relaxation of smooth muscle – Widens blood vessels– Lowers systolic blood pressure

– Particularly difficult in elderly– Atypical presentations – Predominant symptoms include:

• Anorexia• Generalized weakness• Fatigue• Mental disturbances • Anxiety