HEART FAILURE. blood goes round and round, and sometimes it doesn t. PGIM EM Teaching Colombo, November 2015

Transcription

1 HEART FAILURE blood goes round and round, and sometimes it doesn t PGIM EM Teaching Colombo, November 2015 Dr Nick Taylor MBBS FACEM Visiting Emergency Specilaist ETU, Teaching Hospital Karapitiya Senior Specialist and Co-DEMT, The Canberra Hospital

2 Goals Understand basic circulation physiology Describe the cause and effects of left and right heart failure Classify Left Ventricular Failure Learn the principles to treat acute left ventricular failure and cardiogenic shock

3 The Physiology of the Circulation Blood goes round and round...

4 Schematic of circulation

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7 Fully labelled...all you ll ever need

8 A few equations CO= BP=

9 CO=HR x SV BP=CO x TPR

10 What is preload? Preload is the initial stretch of myocytes before they contract It is often described by a surrogate: the volume of blood in the left ventricle at the end of diastole (LVEDV)

11 What is afterload? Afterload is the Left ventricular wall stress [the wall tension (pressure x radius) divided by wall thickness] It is often thought about as the pressure the LV must overcome to eject blood It is closely related to Aortic pressure

12 What is inotropy? Inotropy is a preload independent increase in the rate of force and pressure generated by the LV It leads to higher velocity of ejection It increases stroke volume by decreasing End systolic volume

13 Ahh. Messers Frank and Starling Increased inotropy, decreased afterload Stroke Volume Increased afterload, decreased inotropy RVEDP/V//LVEDP/V//preload

14 Increasing SV Increasing preload and inotropy and decreasing afterload increase stroke volume Raising afterload decreases stroke volume Only preload is free

15 CO=HR x SV BP=CO x TPR

16 Heart Failure blood goes round and round, and sometimes it doesn t

17 Right heart failure: Causes Pulmonary Disease Right Heart Machinery failure: Valves, Muscle, Circulation Left Heart Failure

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19 Right heart failure: Effects Raised JVP Congested liver, pulsatile liver, ascites, portal hypertension Peripheral oedema

20 Left Heart Failure: Causes PRELOAD problems AFTERLOAD problems Left Heart machinery dysfunction: Muscle, valves, circulation

21 Left Heart Failure: Effects Right heart failure Acute Pulmonary Oedema End Organ Dysfunction: shock

22 Left Heart Failure: 3 types Hypertensive: SBP>140 Normotensive: SBP Hypotensive: SBP<90

23 CARDIAC FAILURE vs VASCULAR FAILURE

24 CARDIAC FAILURE PATHOPHYSIOLOGY Patients with CHF represent the old school textbook A patient with chronic heart failure who develops intravascular volume overload through a variety of mechanisms (eg, medication noncompliance, dietary noncompliance, acute kidney injury). Their weak LV/RV cannot tolerate increases in intravascular volume, so oedema develops in the lungs and periphery In general, symptoms develop gradually in the patient with this type of ADHF.

25 Normotensive Left Heart Failure CLASSIC CHF Fluid overload. Some LV dysfunction Often iatrogenic, non compliant, another cause eg RF Rx with diuretics, preload reduction (venodilators eg nitrates), NIV The inpatient granny on ortho

26 VASCULAR FAILURE PATHOPHYSIOLOGY Patients with vascular failure have an sudden increase in vasoconstriction and afterload. This sharp increase in afterload occurs via neurohumoral pathways involving the sympathetic and renin angiotensin aldosterone axes. Patients with vascular failure typically present acutely often lack the classic signs of peripheral edema, and generally have preserved cardiac function. These patients are frequently hypertensive upon ED presentation and can be either euvolemic or hypovolemic.

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29 Hypertensive Left Heart Failure LVEF relatively preserved Redistributive Too much afterload Rx with veno/arteriodilators eg GTN, SNP, Hydrallazine; NIV Generally don t need much diuretic (Frusecide) unless obviously overloaded The elderly female, stiff ventricle, diastolic dysfunction, most common

30 TREATMENT of ADHF

31 Morphine Available evidence is weak but shows higher rates of ventilation and ICU and mortality No trials have shown benefit Review: Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema. Emerg Med Australas 2008;20: Weak dilator: resp depressant, sedative why use??

32 Frusemide Traditional mainstay of pharmacologic therapy for patients with ADHF. Because the majority of acutely ill ED patients with ADHF are not volume overloaded, indiscriminate administration of diuretics could be harmful. Adequate renal perfusion is necessary for these medications to be effective. As a result, the role of diuretics in the ED management of patients with ADHF is limited. No difference between bolus vs infusion, high dose vs low dose

33 Digoxin Has little to no effect on systemic blood pressure and renal function, and has many protective neurohormonal effects. It has not been shown to reduce in heart failure, despite symptom relief and improvement in hemodynamics.

34 ACE- I ACE inhibitors are effective at reducing afterload and have been used in the ED treatment of patients with ADHF. Several small studies on ACE inhibitors in patients with ADHF demonstrated improvement in hemodynamic markers. A single- center study demonstrated reduced rates of intubation and intensive care unit admission for patients who received sublingual captopril in ED Current ACEP guidelines include ACE inhibitors in the treatment options for ED patients with ADHF Captopril or enalapril

35 Nitrates.At low doses, nitroglycerin reduces preload primarily through its dilatory effects on the venous system. At higher doses, nitroglycerin causes arterial dilation, thereby also reducing afterload. Initially, nitroglycerin can be given SL route (400 mcg every 5 minutes) The infusion often begins at 20 mcg/min, It is critically important to titrate the infusion rapidly to clinical improvement. In general, the dose of GTNcan be increased by 40 mcg/min every 5 minutes to a maximum of 200 mcg/min.

36 SNP Sometimes needed for afterload reduction in severe HTN Nitroprussideis given IV at a starting dose of to mcg/kg per minute. The infusion can be increased by 0.1 mcg/kg per minute every 5 minutes until a maximum dose of 400 mcg/min is reached. Importantly, nitroprussideis metabolized to cyanide, which can accumulate rapidly in patients with renal dysfunction. It is associated with increased mortality in AMI

37 NIV NPPV reduces afterload by reducing the transmural pressure across the left ventricle. In addition, NPPV increases intrathoracic pressure, thereby reducing venous return and preload Through these mechanisms, NPPV reduces the work of breathing and improves oxygenation. Cochrane review :compared with standard medical therapy alone, NIV resulted in significant reductions in the rates of in- hospital mortality and intubation in patients with ADHF. Neither CPAP nor BiPAP has been shown to be superior.

38 Treating the patient with APO Sit up High flow O2, monitor, arrange CXR/USS IV access, 12 lead ECG ASAP S/L GTN mcg unless hypotensive CPAP start with PEEP 5-10, max 15cm H2O Frusemide IV if obviously overloaded (20-40mg) No morphine GTN infusion start low and increase rapidly; titrate to response and blood pressure Rx for ACS if required

39 CARDIOGENIC SHOCK/HYPOTENSIVE HF

40 PATHOPHYSIOLOGY The primary insult is typically an infarct causing either reversible ischemia or irreversible injury to the LV Coronary perfusion decreases, followed by cardiac output. The drop in cardiac output results in hypoperfusion, triggering catecholamine release to improve contractility and blood pressure. This increases myocardial oxygen demand. The result is a vicious cycle of decreasing myocardial blood supply with increasing myocardial oxygen demand, that can manifest as rapid clinical deterioration.

41 REMEMBER We can cause shock by injudicious use of medications Be particularly cautious with negative inotropes in arrhythmias with LV dysfunction and diuretics and dilators with RHF

42 TREATMENT OF CARDIOGENIC SHOCK: revascularise ASAP Revascularization addresses the underlying pathology by restoring coronary blood flow to perfuse myocardial tissue that is still viable. Time is of the essence: animal models have demonstrated that nearly 50% of salvageable myocardium is lost within the first hour of coronary artery occlusion, and two- thirds within 3 hours.

43 Inotropes Endogenous catecholamine release itself is part of the vicious cycle of cardiogenic shock. When using inotropes to treat cardiogenic shock, need to find a balance between excessive myocardial oxygen demand and total cardiovascular collapse

44 DOPAMINE Dopamine acts via ß- adrenergic receptors to increase inotropy and heart rate, and at higher doses induces peripheral vasoconstriction via alpha- activation. Downsides are its propensity to cause arrhythmia and increase myocardial work

45 DOBUTAMINE Dobutamine is a synthetic agent that was developed to activate ß- adrenergic receptors without causing peripheral vasoconstriction or triggering the release of endogenous catecholamines. Dobutamine can effectively increase cardiac output and reduce left ventricular end- diastolic pressure, but hypotension may result because of unopposed peripheral ß2 stimulation, Tachycarida and proarrhythmic, and tolerance is observed with pro- longed infusions

46 Noradrenaline Norad is an endogenous adrenergic agent that acts at A- and B- receptors, and causes an increase in inotropy, chronotropy, and peripheral vasoconstriction. When compared with dopamine in cardiogenic shock, norepinephrine was found to be as effective as dopamine in improving hemodynamic parameters, but carried less risk of adverse arrhythmias and improved 28- day mortality. Based on the available evidence, norepinephrine is the preferred first- line adrenergic agent in cardio- genic shock. De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010;362:

47 Phosphodiesterase Inhibitors Milrinoneis a noncatecholamineinotropic agent that inhibits the breakdown of cyclic AMP and promotes an increase in intracellular calcium in cardiac myocytes. Similar to dobutamine, milrinoneimproves contractility and cardiac output at the risk of increased systemic hypotension. It has not been shown to improve outcomes when routinely used in acute exacerbations of congestive heart failure.

48 Calcium Sensitizers As the name implies, calcium sensitizers, such as levosimendan, enhance cardiac contractility without actually increasing intracellular calcium levels. Levosimendan has been shown to improve cardiac output, increase lactate clearance, and reduce norepinephrine requirements in decompensated heart failure. At least one meta- analysis has suggested it may reduce overall mortality in critically ill patients, although the data are mixed. The SURVIVE trial compared levosimendanwith dobutamine in acute decompensated heart failure, and found no difference in all- cause mortality at 6 months.

49 Intra- aortic Balloon Pump The IABP uses the principle of counterpulsationto augment systolic function and promote myocardial oxygen delivery.. In principle, IABP seems like a logical way to manage cardiogenic shock. The SHOCK- II trial, among others, failed to demonstrate benefit when routinely used in the setting of cardiogenic shock and acute MI However, the BCIS- 1 trial showed a long- term mortality benefit in patients with severe cardiomyopathy under- going PCI.

50 LVAD Several different ventricular- assist devices (VADs) have been developed, The most common type in current practice involves a continuous- flow pump that enhances output from the left ventricle (LVAD). The relatively small INTrEPID trial demonstrated signif- icant morbidity and mortality benefits for patients ineligible for transplant who underwent LVAD placement versus medical therapy alone.

51 Extracorporeal Membrane Oxygenation Extracorporeal membrane oxygenation (ECMO) combines a centrifugal pump, a heat exchanger, and an oxygenator to provide cardiac and respiratory support. Veno- venous and venoarterial forms exist; the former provides only pulmonary support, whereas the latter is true cardiopulmonary bypass. ECMO has been used in a variety of settings, including cardiogenic shock, acute respiratory distress syndrome, and the periarrest period. There is evidence to suggest that ECMO may improve short- and long- term survival compared with conventional CPR in the setting of in- hospital cardiac arrest, particularly for patients with primary heart disease

52 Hypotensive Left Heart Failure/Cardiogenic shock Pump failure (poor LVEF) Rx with inotropes/volume challenge Rx with NIV/IPPV eg LAD infarct, myocarditis

53 SUMMARY Hypertensive: SBP>140: Vascular Failure Most common mode of ED presentation Not Volume overloaded; Thus Dilate Normotensive: SBP Chronic LV dysfunction with volume overload Targeted diuresis/dilatation Hypotensive: SBP<90 Difficult clinical problem Revascularization is key Inotropic balance

54 References Michael C. Scott, MDa,b, Michael E. Winters Congestive Heart Failure Emerg Med Clin N Am 33 (2015) Joshua B. Moskovitz, MD, MPH, MBA*, Zachary D. Levy, MD, Todd L. Slesinger, Cardiogenic Shock. Emerg Med Clin N Am 33 (2015) Susan R. Wilcox, MD*; Christopher Kabrhel, MD, MPH; Richard N. Channick, MD. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Annals of Emergency Medicine Volume 66, no. 6 : December 20 David M Viau, Javier A Sala- Mercado,Marty D Spranger, Donal S O Leary, Phillip D Levy. The pathophysiology of hypertensive acute heart failure Heart 2015;101:

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