ITE OpenAnesthesia Flashcards
Signs of malignant hyperthermia (x5)
- Rigidity
- Increased EtCO2
- Hyperthermia
- Increased MV
- Increased CO, HR, SBP +/- arrhythmias
- Increased O2 consumption
- Following volatile anesthetics or suxx
Lab results of malignant hyperthermia (x8)
- Mixed metabolic and respiratory acidosis
- Increased serum potassium, sodium, calcium, phosphate
- Increased myoglobin and creatine kinase
- Lactic Acidosis
Malignant hyperthermia vs thyroid storm
MH: intra-op, rigid, hyperkalemia, elevated CK and lactic acid (LA)
TS: post-op, hypokalemia, not rigit, normal CK and LA
Type and Screen determines and test for…
ABO-Rh of the patient and screens for the presence of the most commonly found unexpected antibodies
ABO-RH testing (“Type”) is done by…
The patient’s blood cells are mixed with serum known to have antibodies against A or against B to determine blood type.
The patient’s blood cells are also treated with anti-D antibodies to determine Rh.
Antibody Screen (“Screen”) is done by…
The patient’s serum is mixed with red cells of known antigenic composition
Test = Indirect Coombs test
Crossmatching (“Cross”) is done by…
The donor cells are mixed with the recipient’s serum so check for lysis
Differentiating decreased cardiac function vs decreased afterload as the cause of hypotension with TEE
decreased afterload: manifests as a hypercontractile ventricle
decreased cardiac function: manifests as a hypocontractile ventricle with/without wall motion abnormalities +/- increased LVEDA
Etiologies of Hypotension Easily Identifiable by TEE (x5)
Poor LV function Decreased LV afterload Decreased LV preload Pericardial tamponade Acute valvular dysfunction
Ketamine’s effect on EEG
Characterized by the abolition of alpha rhythm and the dominance of theta activity
Ketamine’s effect on the CNS
Generally considered to increase cerebral blood flow (CBF), cerebral metabolism (CMRO2), and intracranial pressure (ICP)
Recent data: does not increase ICP and has little impact on cerebral hemodynamics
Ketamine’s effect on the cardiovascular system (x5)
Dose dependent direct stimulation of the CNS that leads to increased sympathetic nervous system outflow although direct negative inotropic effects.
- Increased systemic and pulmonary blood pressures, 2. Increased heart rate
- Increased cardiac output
- Increased cardiac work
- Increased myocardial oxygen requirements
Ketamine’s effect on the cardiovascular system in critically ill patients
critically ill patients may occasionally respond to ketamine with unexpected decreases in blood pressure and cardiac output
depletion of endogenous catecholamines and exhaustion of sympathetic compensatory mechanisms, unmasking ketamine’s direct negative inotropic effects.
Ketamine’s effect on the pulmonary system
Bronchodilatory activity but has been shown to increases salivary and tracheobronchial mucous gland secretions
unchanged ventilation
Ketamine’s effect on the renal and hepatic systems
No change