. 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..
1. By: Darryl Jamison
Macon County EMS Training Coordinator
2. 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.
3. 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
4. An imbalance in pump function in which the heart fails to maintain the circulation of blood adequately.
5. 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.
6. 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
7. Coronary artery disease--chronic
Valvular heart disease (especially aorta and mitral disease)--chronic
The amount of blood the heart must pump with each beat
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.
9. 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
10. Uncontrolled HTN doubles the chances of failure
With HTN, the chambers of the heart enlarge and weaken.
11. Can result from disease, infection, or be congenital
Don’t open and/or close completely ? increased workload ? failure
12. Tachycardias ?decreased diastolic filling time ? decreased SV.
Atrial dysrhythmias ? as much as 30% reduction in stroke volume
13. 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.
14. Tend to be overweight
15. Types of Rhythms Associated with CHF
16. Left Ventricular Failure with Pulmonary Edema
Aka—systolic heart failure
Right Ventricular Failure
Aka—diastolic heart failure
18. 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
19. 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
Results from sympathetic stimulation
Rales—especially at the bases.
Rhonchi—associated with fluid in the larger airways indicative of severe failure
Wheezes—response to airway spasm
20. Jugular Venous Distention—not directly related to LVF.
Comes from back pressure building from right heart into venous circulation
Significant increase in sympathetic discharge to compensate.
Pulse rate—elevated to compensate for decreased stroke volume.
Respirations—rapid and labored
Depends on the level of hypoxia
May in the presence of MI
Can be masked by the RDS.
22. REMEMBER LEFT VENTRICULAR FAILURE IS A TRUE LIFE THREATENING EMERGENCY
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
24. 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
25. Marked JVD
Marked peripheral edema
Poor exercise tolerance
The first three are for an inferior MI, describe cardiac tamponade. Often will be on Lasix, Digoxin,
Have chronic pump failure
26. Neurohormonal system
27. Stimulated by decreased perfusion ? secretion of hormones
Increases rate and pressure
Vasoconstriction ? SVR
Mild vasoconstriction, renal water retention
28. Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released ? increase in Na+ retention ? water retention
29. Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
33. Aimed at diminishing the compensatory mechanisms of low cardiac output and also improving contractility
34. 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
These inhibit reabsorption of Na+ into the kidneys
Increases the contractility of the heart ? increasing the cardiac output
Used to dilate blood vessels
Used mostly with CHF in the presence of ischemia
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
39. The prehospital goals for managing CHF
Promotion of rest
Relief of anxiety
Decreasing cardiac workload
Attainment of normal tissue perfusion
40. 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
41. 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
O2—High flow O2
44. ACE Inhibitors
45. Prevent the production of the chemicals that causes blood vessels to narrow
Resulting in blood pressure decreasing and the heart pumping easier
46. Inotropic effects on the heart
Negative chronotropic effects
47. Decrease the body’s retention of salt and water
Reduces blood pressure
Probably will be on potassium
48. Widens the blood vessels, therefore allowing more blood flow
49. Relaxation of smooth muscle
Widens blood vessels
Lowers systolic blood pressure
50. Particularly difficult in elderly
Predominant symptoms include:
51. Bubbling Rhonchi