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EMS overview of Congestive Heart Failure.pptx
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- 2. CHF numbers • FromAHA report in 2013 – 5.1 million Americans • .3/1000 <45 yo • 8/1000 45-65 yo • 10/1000 65-85 yo • 66/1000 >85yo • 5.4% of the National Health Care budget
- 3. CHF Epidemiology • Eachyear: – 500,000 new cases – 1-2 million hospitalizations – 20% of admits in pts >65yo – $17.8 billion spent annually • 5-year death rate – Males 62% Females 42% • 6-year death rate – Both sexes 75%
- 4. CHF Epidemiology • Hospitalizationrate – Initial episode ~14% – Repeat visit ~76% • Hospital Readmission – 2% within 2 days – 20% within 1 month – 50% within 6 months – 18% after 6 months
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- 6. CHF Definition • Clinicalsyndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood • AHA / ACC guidelines 2001 • Clinical symptoms / signs secondary to abnormal ventricular function • ESC HF Guidelines 2001
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- 8. CHF Pathophysiology • Cardiacoutput is key
- 9. CHF and PulmonaryEdema
- 10. CHF Pathophysiology • CHFand pulmonary edema
- 11. CHF Pathophysiology • CHFand pulmonary edema – Distance across interstitial space increased – Affects O2 transport more than CO2 diffusion
- 12. CHF Pathophysiology • Cardiacoutput is key CO = SV X HR Bad Pump –Valvular disease –Poor squeeze –Inability of ventricle to relax
- 13. CHF Pathophysiology • Cardiacoutput is key CO = SV X HR Pump out of sync –New onset or poorly controlled atrial fibrillation or flutter
- 14. CHF Pathophysiology • Cardiacoutput is key CO = SV X HR Increased peripheral vascular resistance –Arterial contraction PVR
- 15. Theory and Treatment •Old Theory: “Bag of Water” – Volume overload in the vasculature causes fluid to “back up into the lungs”
- 16. Theory and Treatment •New Theory: Cycle of Dysfunction • Decrease in cardiac output causes compensatory response in effort to maintain perfusion – Stimulates a negative feedback cycle that leads to decompensation
- 17. Compensatory Mechanisms Cardiac Output VEDP Tachycardia Sympathetic Discharge Blood VolumeAldosterone Angiotensin II Cardiac Output Heart Failure
- 18. Compensatory Mechanisms • Increasedheart rate – Sympathetic stimulation = norepinephrine • Dilation = “Stretch of the ventricle wall” – Frank Starling Curve = contractility • Neurohumeral – Redistribution of blood to the brain
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- 20. Theory and Treatment •New Theory: Cycle of Dysfunction
- 21. Theory and Treatment •New Theory: Cycle of Dysfunction • Body response to decreased CO from HF – Renin-angiotensin, aldosterone levels – Peripheral vascular resistance – Sympathetic tone
- 22. Theory and Treatment •New Theory: Cycle of Dysfunction • Leads to: – Worsening heart function – Cardiac output – Hypoxia and work of breathing
- 23. Effect of HF( CO) in Lungs • Fluid ‘backs up’ into pulmonary veins causing increase in hydrostatic pressure inside vessel • Fluid crosses capillary membrane into interstitial space • Fluid enters alveolar space • Fluid filled alveoli inhibit gas exchange
- 24. Effect of Cycleof Dysfunction • Systolic Failure – Most studied and easily recognized – Reduced ejection fraction – Symptoms? • Diastolic dysfunction – Failure of filling – Ventricular wall size and thickness
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- 26. Causes of SystolicFailure • Chronic – Hypertension – Damage to ventricle – Thickened ventricle • Acute – Arrhythmia – MI – Medication non-compliance
- 27. New York HeartAssociation Classification • Class I – No limitation of physical activity • Class II – Slight limitation of structural activity • Class III – Marked limitation of structural activity • Class IV – Symptoms occur at rest, discomfort with any physical activity
- 28. Making the Diagnosis •EMS correct only about 50% of the time – Don’t take adequate history – Don’t recognize presence of risk factors – Don’t understand new theories on causes of CHF • Differential diagnosis?
- 29. Making the Diagnosis •History – Onset of dyspnea • Sudden versus gradual? – Chest pain • Present or absent? – Paroxysmal nocturnal dyspnea • Waking up at night short of breath? – Positional shortness of breath – History of previous MI
- 30. Making the Diagnosis •History – Coronary artery disease or prior MI – New dysrhythmia – Use of Digitalis – Use of Diuretics
- 31. Making the Diagnosis •History – History of COPD or Asthma • BIGGEST FOOLER!! Not all wheezing is asthma!
- 32. Signs and Symptoms •Slowly progression over days to weeks – Can be very fast if due to rapidly elevated BP – “Flash” pulmonary edema • Associated with shortness of breath with exertion or lying down • Hypertension and tachycardia – why?? • Peripheral edema • Wheezing – why??
- 34. Old Treatment Theory •Based on body as a ‘Bag of water’ – Phlebotomy – blood letting – Rotating tourniquets – Massive dose of Lasix
- 35. New Treatment Theory •CO = SV x HR • Fundamental to recognize role of pre-load and after-load and effect on stroke volume – Pre-load is amount of ventricular volume just prior to systole – After-load is amount of resistance against which the ventricle is pumping during systole
- 36. New CHF Management •Identify CHF correctly • High flow O2 • Identify cause if possible • Provide respiratory support • Reduce left ventricular pre-load • Reduce left ventricular after-load • Provide inotropic (contraction) support
- 37. New CHF Management •Oxygen!! • High dose Nitroglycerin – Reduces pre-load – Reduces after-load – Dilated coronary arteries • Repeat doses of nitroglycerine optimal – IV preferred but not necessary
- 38. Hemodynamic Effect ofNitroglycerine Venous Vasodilation Pre-load Pulmonary congestion Coronary Vasodilation Blood flow to heart muscle Oxygen and glucose to heart muscle Arterial Vasodilation Afterload Cardiac Output
- 39. How much NTG? Asmuch as they can tolerate!!
- 40. Continuous Positive AirwaySupport CPAP • Increases alveolar pressure – Redistributes interstitial fluid – Increases alveolar exchange of oxygen and CO2 • Provides ventilatory support by reducing work of breathing • Significantly reduces need for intubation • Buys time for other therapies to work
- 41. ACE Inhibitors • AngiotensinI converted to Angiotensin II – Angiotensin converting enzyme (ACE) • Angiotensin II – Helps controls the cardiovascular system • Causes vasoconstriction which raises blood pressure – Causes the body to release chemicals to retain sodium and fluid – Causes the body to release vasopressin(ADH) • Causes even more fluid retention
- 42. ACE Inhibitors • Inthe acute patient: – Reduces after-load by blocking vasoconstriction thus causing vasodilation • Captopril – Oral versus Sublingual • Enalapril – Intravenous
- 43. Inotropic Support • Inthe presence of cardiogenic shock there is a role for the use of inotropes such as – Dopamine – Dobutamine • Very tricky to monitor in the pre-hospital setting – More use for prolonged interfacility transport
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- 45. Furosemide • Inhibits sodiumre-absorption – Takes at least 4-6 hours to have effect • Neruohumeral effect initially causes vasodilation – good • Secondary neurohumeral effect causes increased peripheral vascular resistance -- bad
- 46. Morphine • No datato support that it improves outcomes • Lowers anxiety • Vasodilatory effect is mediated through histamine release which negatively effects the heart
- 47. Bronchodilators • Not allthat wheezes is asthma or COPD • Alpha-adrenergic effect increases cardiac workload – bad • Does not treat underlying problem • If no wheezing in CHF patient, avoid
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