By: Darryl Jamison NREMT-PMacon County EMS Training Coordinator
– Approximately 30-40% of – The most common cause of patients with CHF are death is progressive heart hospitalized each year. failure, but sudden death Leading diagnosis-related may account for up to 45% group over 65. The 5 year mortality after Dx was of all deaths. reported as 60% in men and – Patients with coexisting 45% in women in 1971. In IDDM have a significantly 1991, data from the higher mortality rate. 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.
– Effects an estimated – Responsible for 5-10% of 4.9 million Americans all hospital admissions– 1% of adults 50-60 – Causes or contributes to approximately 250,000– 10% adults over 80 deaths per year– Over 550,000 new cases annually– $28.7 million committed in research dollars each year– $132 million for lung cancer, affecting 390,000 Americans
– An imbalance in pump function in which the heart fails to maintain the circulation of blood adequately.
♦ 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
– Preload— – Afterload— • The amount of blood the • The pressure that must be heart must pump with each overcome for the heart to beat pump blood into the • Determined by: arterial system. – Venous return to heart • Dependent on the systemic – Accompanying stretch vascular resistance of the muscle fibers • With increased afterload, • Increasing preload the heart muscles must increase stroke volume in work harder to overcome normal heart the constricted vascular • Increasing preload bed chamber impaired heart enlargement decreased SV. Blood is • Increasing the afterload trapped chamber will eventually decrease enlargement 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.
– Left Ventricular Failure with Pulmonary Edema • Aka—systolic heart failure– Right Ventricular Failure • Aka—diastolic heart failure
– Occurs when the left – When pressure ventricle fails as an effective forward pump becomes to high, the back pressure of blood fluid portion of the into the pulmonary blood is forced into the circulation alveoli. pulmonary edema– Cannot eject all of the decreased blood delivered from the oxygenation capacity right heart. of the lungs– Left atrial pressure rises increased pressure in the – AMI common with pulmonary veins and LVF, suspect capillaries
– Severe resp. distress– – Diaphoresis— • Evidenced by • Results from orthopnea, dyspnea sympathetic stimulation • Hx of paroxysmal – Pulmonary congestion nocturnal dyspnea. • Often present– Severe apprehension, • Rales—especially at the bases. agitation, confusion— • Rhonchi—associated • Resulting from hypoxia with fluid in the larger • Feels like he/she is airways indicative of smothering severe failure • Wheezes—response to– Cyanosis— 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— – Pathophysiology— • Acute MI— • Decreased right-sided – Inferior MI cardiac output or • Pulmonary disease increased pulmonary – COPD, fibrosis, HTN vascular resistance increased right vent. • Cardiac disease Pressures. involving the left or • As pressures rise, this both ventricles increased pressure in • Results from LVF 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 – Often will be on Lasix,– Clear chest Digoxin,– Hypotension – Have chronic pump– Marked peripheral failure edema– Ascites, hepatomegaly– Poor exercise tolerance – The first three are for an inferior MI, describe cardiac tamponade.
– 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 PneumoniaCough Frequent Occasional FrequentWheeze Frequent Occasional FrequentSputum Thick Thin/white Thick/yellow/ brownHemoptysis Occasionally Pink frothy occasionallyPND Sometimes after Often within 1 Rare a few hours hourSmoking Common Less common Less commonPedal edema Occasional Common with none chronic
COPD CHF PneumoniaOnset Often URI with Orthopnea at Gradual with cough night fever, coughChest Pain pleuritic Substernal, Pleuritic, often crushing localizedClubbing Often Rare RareCyanosis Often and severe Initially mild but May be present progressesDiaphoresis May be present Mild to heavy Dry to moistPursed Lips Often Rare Rare unless COPD
COPD CHF PneumoniaBarrel Chest Common Rare Rare unless COPDJVD May be present Mild to severe Rare with RVFBP Usually normal Often high NormalDysrhythmia Occasional May precipitate Common CHFWheeze Common Less common CommonCrackles Coarse, diffuse Fine to coarse, Localized to begin in gravity diffuse, coarse dependent areas
– Aimed at diminishing the compensatory mechanisms of low cardiac output and also improving contractility– Vasodilators—ACE inhibitors– Diuretic agents– Inotropic agents
– Dilate blood vessels – Common ACE– Often constricted due inhibitors to activation of the • Captopril sympathetic nervous • Lisinopril system and the renin- • Vasotec angiotensin- • Monopril aldosterone system. • Accupril– Aka—ACE inhibitors – 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
– Nifedipine – Used to dilate blood– Diltiazem vessels– Verapamil – Used mostly with CHF– Amlodipine in the presence of ischemia– Felodipine
– Metoprolol – Useful by blocking the– Atenolol beta-adrengergic– receptors of the Propanolol sympathetic nervous– Amiodarone 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