Cardiovascular Critical Care I
Box 4. Non-ischemic Cardiomyopathies
Non-ischemic Cardiomyopathies
| • | Amyloidosis |
|---|---|
| • | Sarcoidosis |
| • | Drug induced |
| • | Alcohol |
| • | Anabolic steroids |
| • | Chemotherapy |
§ Anthracyclines
§ Cyclophosphamide
§ Fluorouracil
§ Bevacizumab
§ Trastuzumab
§ Tyrosine kinase inhibitors
| • | Cocaine |
|---|---|
| • | Methamphetamine |
| • | Tricyclic antidepressants |
| • | Anorexigens |
| • | Familial |
| • | Hypertension |
| • | Hyper/hypothyroidism |
| • | Hypertrophic obstructive (HOCM) |
| • | Idiopathic |
| • | Myocarditis |
| • | Autoimmune |
| • | Eosinophilic |
| • | Giant cell |
| • | Viral |
| • | Other infectious cause |
| • | Non-compaction |
| • | Peripartum |
| • | Obesity |
| • | Stress induced (Takotsubo) |
Heart Fail 2010;3:340-6; Anesth Analg 2009;108:422-33; Anesth Analg 2009;108:407-21)
Less well characterized than LV HF
RV physiology
The RV normally has only about one-sixth the myocardial mass of the LV. Primary means of
compensation is heart rate increase.
Normal RV ejection fraction is 40%–45%.
Conduit to a low pressure system in the pulmonary vasculature (normally) and capable of
accommodating for increased stroke volume but not able to compensate for acute pressure
fluctuations.
| d. | Physiologic deficits: |
|---|
Preload dependent
ii.
Interdependent on LV and septal contribution to contraction
iii.
Highly sensitive to acute increases in afterload. PVR elevations may be:
| (a) | Drug induced (e.g., α1 agents, protamine) |
|---|---|
| (b) | Caused by ventilator settings (high positive end-expiratory pressure [PEEP], high tidal |
volumes)
| (c) | Caused by hypoxia |
|---|---|
| (d) | Caused by hypercarbia |
| (e) | Caused by pulmonary embolism |
iv.
Poor elastic response to acute preload increases compared with LV
Atypical geometric form contributes to:
| (a) | Difficulty in objective assessment of RV function by ECHO |
|---|---|
| (b) | Increases susceptibility to further inefficiency/dysfunction when severely dilated |