1. Heart Failure, Shock and Hemodynamics Howard Sacher D.O. Long Island Cardiology

2. Learning Objectives To gain insight into the definition of, epidemiology of, pathophysiology of, changes in treatment recommendations for, clinical trials pertaining to, and prevention of ventricular dysfunction and heart failure. To understand the pathophysiology of heart failure with specific reference to the syndrome's molecular biodynamics, humoral, neurohumoral, and cytokine milieu.

3. Learning Objectives (cont.) To place in proper perspective the clinical trials that have shaped our contemporary heart failure therapeutic philosophies. To understand alternatives to pharmacologic therapies of heart failure.

10. Hemodynamic Abnormalities of HF trigger many subsequent compensatory mechanisms designed to augment peripheral organ perfusion Increased sympathetic tone increases: Contractility HR Venous and Arterial Tone Pressure RAA system is upregulation Ventricular dilation and hypertrophy are compensatory mechanisms designed to augment SV and peripheral organ flow

13. Generally Pt’s dying from HF have either sudden cardiac death 2 nd to: Fatal Arrhythmias Electrolyte Abnormalities Inc. serum catacholamines Ischemia Developing significant systemic hypoperfusion Congestion Low Cardiac Output

18. Study shows that HF patients have lower oxygen carrying capabilities (VO2), decreasing exercise tolerance

19. HF patients are noted to have an inappropriate increase in PCWP and increased EDV

20. The flat stroke volume index curve is pathopneumonic of heart failure

21. HF Pt’s shows an increase in LVEDV consistently with a concomitant rise in PCWP with exercise

34. Studies On LV Dysfunction (SOLVD) looks at vasoactive peptides norepi, renin, arginine vasopressin, and atrial natriuretic hormone

37. Importance of neuroendocrine receptors B1, B2, Alpha 1, and Angiotensin II specific receptors all play a key role in signal transductance at the myocyte surface generating specific proteins Adenyl Cyclase (AC) Ang II Ang I ATP cAMP

38. The failing heart has fewer receptors

60. 12lead of an acute myo/pericarditis (confirmed at autopsy)

61. 22 yoa previously healthy female now presenting with acute myo/pericarditis (confirmed with autopsy)

62. 35yoa male presenting with severe SOB. PMHx of a dialated cardiomyopathy and hyperkalemia

63. Same patient showing non- sustained V-tach

64. 45min after his K + was brought down

130. Cardiac transplantation

147. Implantable ventricular assist device

148. The wave of the future: Fully contained mechanical heart