heart failure, shock and hemodynamics howard sacher d.o. long island cardiology

Heart Failure, Shock and Hemodynamics

Howard Sacher D.O.Long Island Cardiology

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.

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.

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

Generally Pt’s dying from HF have either sudden cardiac death 2nd to: Fatal Arrhythmias

Electrolyte Abnormalities Inc. serum catacholamines Ischemia

Developing significant systemic hypoperfusion

Congestion Low Cardiac Output

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

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

The flat stroke volume index curve is pathopneumonic of heart failure

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

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

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

The failing heart has fewer receptors

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

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

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

Same patient showing non-sustained V-tach

45min after his K+ was brought down

Cardiac transplantation

Implantable ventricular assist device

The wave of the future:

Fully contained mechanical heart