Congestive Heart Failure and Congestive Heart Failure and Pulmonary EdemaPulmonary Edema

– 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.

Mortality/MorbidityMortality/Morbidity

– Effects an estimated 4.9 million Americans

– 1% of adults 50-60– 10% adults over 80– Over 550,000 new cases

annually– $28.7 million committed

in research dollars each year

– $132 million for lung cancer, affecting 390,000 Americans

– Responsible for 5-10% of all hospital admissions

– Causes or contributes to approximately 250,000 deaths per year

BackgroundBackground

– An imbalance in pump function in which the heart fails to maintain the circulation of blood adequately.

CHF DefinedCHF Defined

¨ 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.

PathophysiologyPathophysiology

– 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

– Infections--acute– Dysrhythmias--acute

– Alcohol--chronic– MI--acute– Diabetes—chronic

Etiologies

– 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 à increase

stroke volume in normal heart• Increasing preload à impaired

heart à decreased SV. Blood is trapped àchamber 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 à chamber enlargement

• Increasing the afterload will eventually decrease the cardiac output.

Important TerminologyImportant Terminology

– 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

CADCAD

– Uncontrolled HTN doubles the chances of failure– With HTN, the chambers of the heart enlarge and

weaken.

HypertensionHypertension

– Can result from disease, infection, or be congenital

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

Valvular Heart DiseaseValvular Heart Disease

– Tachycardias àdecreased diastolic filling time à decreased SV.

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

Disrhythmias

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

MI--Acute and Past

– Tend to be overweight– HTN– Hyperlipidemia

Diabetes

Types of Rhythms Associated with CHF

–Left Ventricular Failure with Pulmonary Edema•Aka—systolic heart failure

–Right Ventricular Failure•Aka—diastolic heart failure

Types of CHFTypes of CHF

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

– àback pressure of blood into the pulmonary circulation

– à pulmonary edema– Cannot eject all of the blood

delivered from the right heart.– Left atrial pressure rises à

increased pressure in the pulmonary veins and capillaries

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

– àdecreased oxygenation capacity of the lungs

– AMI common with LVF, suspect

Left Ventricular Failure with PELeft Ventricular Failure with PE

– Severe resp. distress– • Evidenced by orthopnea,

dyspnea• Hx of paroxysmal

nocturnal dyspnea.

– Severe apprehension, agitation, confusion—• Resulting from hypoxia• Feels like he/she is

smothering

– 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

Signs and Symptoms of LVF

– 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 àincreased right vent. Pressures.

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

• Higher right atrium pressures à JVP

Right Heart Failure

– 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– Poor exercise tolerance

– The first three are for an inferior MI, describe cardiac tamponade.

– Often will be on Lasix, Digoxin,

– Have chronic pump failure

Signs and SymptomsSigns and Symptoms

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

Compensatory Mechanisms in CHFCompensatory Mechanisms in CHF

–Stimulated by decreased perfusion à secretion of hormones

•Epi—– Increases contractility– Increases rate and pressure– Vasoconstriction à SVR

•Vasopressin—– Pituitary gland– Mild vasoconstriction, renal water retention

Neurohormonal SystemNeurohormonal System

– Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys•Aldosterone is released à increase in Na+ retention à

water retention•Preload increases•Worsening failure

Renin-Angiotensin Mechanism

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

skeletal muscle

Ventricular Ventricular HypertrophyHypertrophy

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

Comparison of COPD, CHF PneumoniaComparison of COPD, CHF Pneumonia

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

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

–Vasodilators—ACE inhibitors–Diuretic agents– Inotropic agents

Drug TherapyDrug Therapy

– 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

Vasodilators

–Lasix–Hydrochlorothiazide(HCTZ)–Spironolactone

•These inhibit reabsorption of Na+ into the kidneys

DiuretiDiureticscs

–Digoxin–Lanoxin

• Increases the contractility of the heart à increasing the cardiac output

Inotropic AgentsInotropic Agents

– Nifedipine– Diltiazem– Verapamil– Amlodipine– Felodipine

– Used to dilate blood vessels

– Used mostly with CHF in the presence of ischemia

Calcium Channel Calcium Channel BlockersBlockers

– 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 àcould actually worsen CHF

Beta Blockers

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

Prehospital Treatment

– 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

Promotion of RestPromotion of Rest

– 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

Relief of AnxietyRelief of Anxiety

– NTG– MS– Lasix– O2—High flow O2

Decreasing Cardiac Workload

– ACE Inhibitors– Digitalis– Diuretics– Hydralazine– Nitrates

Common Heart Failure Medications

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

– Resulting in blood pressure decreasing and the heart pumping easier

ACE Inhibitors

– Inotropic effects on the heart– Negative chronotropic effects

DigitalisDigitalis

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

DiureticsDiuretics

– Widens the blood vessels, therefore allowing more blood flow

Hydralazine

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

NitratNitrateses

– Particularly difficult in elderly– Atypical presentations – Predominant symptoms include:•Anorexia•Generalized weakness•Fatigue•Mental disturbances •Anxiety

Diagnostic Challenges

– Bubbling Rhonchi– Coarse Crackles– Fine Crackles– Gurgling Rhonchi– Rales

Lung Sounds Associated with CHF