electrolytes and ECG
K+ Nernst equation shows that hypoK = hyperpolarization and hyperK = hypopolarization
Major effect, hower, is due to changes in ion currents
Mg++
hypoMg++ similar to hypoK+ for ECG changes
Ca++
hyperCa++
- shortens QT
- ST segment abolished
Ischemia
- depolarization of resting membranes
- inactivates fast Na channels = slows phase 0 = slows conduction cell to cell
- local acidosis
- K leakage from cell
- arrythmias due to dispersion of refractoriness in different parts of heart
- ST segment elevation in infarct zones and depression in reciprocal leads
Arrhythmia mechanisms associated with ischemia
- A-V Block, Bundle Branch & Fascicular Blocks
- Bradyarrhythmias
- Enhanced Automaticity
- PVCs
- Triggered Activity
- Polymorphic VT
- Reentry
- Monomorphic VT
- Ventricular Fibrillation
Hypothermia
- Osborn or J wave: A hump-like elevation of the J-point at the onset of ST segment.
- Caused by dispersion of endocardial to epicardial phase 1 repolarization.
- Shivering (muscle) artifact.
- QT prolongation.
Pressure - Volume loops
Positive inotropic agents (digoxin, dopamine, dobutamine, eicosanoids, epinephrine, inamrinone, isoprenaline, milrinone, norepinephrine, phosphodiesterase inhibitors, theophylline)
Negative inotropic agents (beta-blockers, calcium channel blockers, disopyramide, flecainide, procainamide, quinidine)
Reflex control of the heart
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Of these two sites for arterial baroreceptors, the carotid sinus is quantitatively the most important for regulating arterial pressure. The carotid sinus receptors respond to pressures ranging from 60-180 mmHg
important to know that carotid baroreceptor activity is proportional to blood pressure.
switch from sympathetic stimulation to sympathetic inhibition due to GABA release by CVLM
summary figure P = QR
MABP = CO x TPR
memory tool: alphabet rule ABC
PQR or P = QR
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