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