Cardiac Physiology Flashcards
What is the primary mechanism of class I antiarrhythmics? What drugs are in each subclass? Effect on AP? Notable uses, contraindications, side effects.
No Bad Boy Keeps Clean
Class I = Na+ channel blockers
Decrease phase 0 slope in ventricular cells.
Class Ia -> I, A Queen, Proclaim Diso’s Pyramid.
Class Ia = Quinidine, Procainamide, Disopyramide
Increase AP duration and ERP -> prolong QT
Quinidine SE: cinchonism (headache, tinnitus)
Procainamide SE: reversible SLE like syndrome (anti-histone Ab)
Disopyramide SE: Heart failure
Class Ia SE: thrombocytopenia, Torsades de pointes (both of these are esp. by quinidine)
Class Ib -> I’d Buy Lidy’s Mexican Tacos and Phenytoin
Class Ib = Lidocaine, Mexiletine, Tocainamide, Phenytoin
Decrease AP duration. Best post MI and digitalis induced arrhythmias. Safe for long QT patients.
Class Ic -> I Coordinate Proper Flexion
Class Ic= Propafenone, Flecainide
No effect on AP duration. Contraindicated post MI and structural heart disease. Last resort. Ventricular tachycardias that progress to Vfib and intractable SVT.
What is the primary mechanism of class II antiarrhythmics?
No Bad Boy Keeps Clean
Class II = beta blockers
Decrease phase 4 slope in nodal cells (current by funny sodium channels -> diastolic depolarization). They also decrease cAMP and Ca++ in AV and SA node (decreasing activity). Incr PR interval.
What is the primary mechanism of class III antiarrhythmics? What drugs are in this class?
No Bad Boy Keeps Clean
Class III = K+ channel blockers
Class III affects phase III in ventricular cells. Blocking K+ channels prevents K+ efflux, prolong Ca++ plateau phase. This increase AP duration and ERP-> prolonged QT.
Class III -> AIDS
Amiodarone, Ibutilide, Dofetilide, Sotalol
Amiodarone SE: “Make sure to check the LFTs, TFTs, PFTs.” Pulmonary fibrosis, hypo/hyperthyroidism (40% iodine by weight), hepatotoxicity, corneal deposits, blue/grey skin deposits resulting in photosensitivity (SAT 4 photo), Neurologic side effects.
Sotalol SE: torsades, excess Beta blocker activity
Ibutilide SE: torsades
What is the primary mechanism of class IV antiarrhythmics? What drugs are in this class?
No Bad Boy Keeps Clean
Class IV= Ca++ blockers (non-dihydropyridine)
Decreases phase 0 slope in nodal cells. Incr ERP and PR interval.
Class IV= verapamil and diltiazem
SEs: constipation, flushing, edema, CV SE
How does increasing the diameter of a vessel by two times effect the resistance of that vessel?
R = (8 x viscosity x length) / (pi x r^4). 2^4 = 16. This would reduce the resistance by a factor of 16.
Describe the phases of a myocardial action potential and which ions are responsible for each phase
Phase 0 -> rapid upstroke. Voltage gated Na+ channels open
Phase 1: Initial repolarization. Voltage gate Na+ channels close and voltage gated K+ channels begin to open.
Phase 2: Plateau. Ca++ influx through voltage gated Ca++ channels balances K+ efflux. (This triggers Ca++ release from SR)
Phase 3: Rapid repolarization. Massive K+ efflux do to opening of slow voltage gated Na+ channels and closure of the voltage gated Ca++ channels.
Phase 4: Resting potential. High K+ permeability thru K+ channels.
What is the pulse pressure in a patient with a systolic BP of 150 and a MAP of 90?
MAP = 2/3 diastolic + 1/3 systolic 90 = 2/3 diastolic + 1/3 (150) 90 = 2/3 diastolic + 50 40 = 2/3 diastolic 60 = diastolic Pulse pressure = 150 -60 = 90
What is the basic equation for cardiac output? What is the Fick principle?
CO = SV x HR
CO = O2 consumption / (Arterial O2 content - Venous O2 content)
What factors effect stroke volume?
Contractility- Decreased by beta blockers, heart failure, acidosis, hypoxia, verapamil. Increased by catecholamines, digitalis (blocks Na+/K+ exchanger thereby limiting gradient for Na+/Ca++ exchanger and increasing intracellular Ca++
Preload: Increased w/ exercise, increased blood volume, transfusion, pregnancy. Decreased w/ nitrates
Afterload: increased whenever you squat. Decreased with ACE inhibitors, Hydralazine
What heart sound heart sound is a/w dilated congestive heart failure? What heart sound is a/w chronic HTN.
Dilated- S3 heart sound
Chronic HTN -> stiffened LV -> S4 heart sound
What gives rise to jugular a, c and v waves?
“At carters crossing (X) vehicles yield”
A wave = atrial contraction
C wave = RV contraction (tricuspid pushes back into RA)
V = increased right atrial pressure d/t filling against closed tricuspid valve
What is the heart ejection fraction?
It is an index of ventricular contractility. EF = SV/ EDV = (EDV - ESV) / EDV. Normally > 55%
What physiology accounts for the automaticity of the AV and SA nodes?
Primarily phase 4 gradual sodium conductance.
With what type of congenital heart defect would increasing afterload be beneficial?
Squatting or knees to the chest. Any type of R -> L shunt will benefit from increased afterload. Tetralogy, truncus, transposition, Eisenmeinger syndrome with PDA, ASD, VSD
Where does the QRS complex fall in relation to valvular dynamics?
At mitral valve closure
