Physiology Flashcards
Explain the phases of the myocardial action potential (non-pacemaker cells)
Cells are polarized meaning that there is an electrical voltage across the cell membrane. In a resting cell the resting membrane potential is usually negative (non-pacemaker cell -90mV).
1. Resting membrane potential - more Na+ and Ca2+ outside the cell and more K+ inside the cell.
2. Depolarization (rapid change in the membrane voltage) due to a large influx of Na+ into the cell, rapidly increasing the voltage to +50 mV.
3. Phase 1 - rapid closure of NA+ channels and brief opening of the K+ channels allow for brief K+ entrance into the cell.
4. Phase 2 - “plateau phase” K+ leaves slowly the cell and Ca2+ slowly enters the cell, near balance of charge moving in and out of the cell.
5. Phase 3 “rapid depolarisation” - Ca2+ channels close and K+ gradually enters the cell
Explain the action potential of pacemaker cells.
Explain the two cardiac cell refractory periods and correlate them with the cell action potential phases.
Cardiac cells have two refractory periods, the first from the beginning of phase 0 until part way through phase 3; this is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential
What is Fontan procedure and when is it performed?
Fontan procedure is performed to correct cyanotic congenital heart disease. Fontan procedure entails in the first stages the anastomosis of SVC and IVC to the RPA (via BTT shunt). To do a complete repair, the surgeon closes the VSD and opens the RVOT by removing some thickened muscle below the pulmonary artery, repairing or removing the pulmonary valve and enlarging the peripheral pulmonary arteries that go to the lungs. Sometimes a tube is placed between RV and PA (Rastelli repair).
What is Tetralogy of Fallot?
Tetralogy of Fallot consists of four key features: a VSD, pulmonary stenosis (atresia), RV hypertrophy, the aorta overrides (sits just above) the ventricular septal defect.
Physiologic blood flow is determined by the severity of RVOTO:
A large VSD → equal pressures in the right and left ventricles → blood flow along the path of least resistance
Severe RVOTO → flow from RV to LV → desaturated blood entering the circulation via the aorta.
What is the typical pacemaker lead position following a Fontan procedure?
Initial epicardial RV lead followed by subsequent intraveous RA lead.
What is transposition of the great arteries?
Consists of the anatomical reversal of the aorta and the pulmonary artery.
Other cardiac defects associated with TGV:
VSD
Left ventricular outlet obstruction
Abnormal valves and/or coronary arteries
Pathophysiology:
Failed spiraling of the aorticopulmonary septum → RV emptying into the aorta and LV into the pulmonary artery → complete isolation of the pulmonary and systemic circuits → ↓ oxygenated blood entering the systemic circulation
Fatal, unless mixing occurs via an intracardiac shunt (e.g., PFO, VSD, ASD) or via an extracardiac connection (e.g., PDA)
Treatment:
Initial postnatal management: Initiate mixing between the two parallel circulations to ensure adequate systemic oxygenation.
Infusion of PGE1 to prevent closure of the PDA
Balloon atrial septostomy
Objective: to enhance atrial mixing if PGE1 administration is insufficient, and to alleviate hypoxemia
Procedure: right heart catheterization with the creation or enlargement of an existing ASD
Surgical repair: recommended within the first two weeks of life
Arterial switch procedure: reversal of the aorta and pulmonary artery with insertion into the anatomically correct ventricle as well as correction of coronary artery supply
Rastelli procedure:
Indication- TGV with concurrent large VSD and LVOTO repair
Procedure: creation of a conduit from the LVOTO through the VSD to the aorta and creation of a conduit from the RV to the pulmonary artery
What is hypoplastic left heart syndrome (HLHS)?
Definition: spectrum of disease consisting of severe hypoplasia of the left ventricle with possible stenosis and/or atresia of the mitral valve, aortic valve, or aortic arch.
Pathophysiology:
The hypoplastic left ventricle is nonfunctional, resulting in the RV becoming the primary supply for pulmonary and systemic circulations.
Survival depends on the presence of a PDA (right-to-left shunt) and an ASD.
Treatment:
Initial medical management: continuous PGE1 infusion prior to heart surgery
Surgical repair: Palliative surgery is used in single-ventricular cardiopathologies.
Three-step staged surgical correction
Norwood procedure (stage I): performed while the patient is a neonate
Glenn procedure (stage II): performed at ∼ 3–6 months of age
Fontan procedure (stage III): performed after 2–3 years of age
Alternative: heart transplant
What is the physiology of the neurocardiogenic syncope/ carotid sinus reflex?
Pressure exerted on the carotid sinuses (stress, exertion, pain) -> activation of the barroreceptors in the carotid sinuses -> discharge from vagal efferents -> increased parasympathetic tone and sympathetic withdrawal-> vasodilation -> decreased venous return -> decreased LV filling (“empty venctricle” -> hypotension + decreased HR (cardiac slowing) -> syncope.
The reflex has two components: cardio-inhibitory and vasodepressor. Cardio-inhibitory results from increased parasympathetic tone -> results in HR slowing (sinus arrest, sinus bradycardia, PR prolongation, AV block). Vasodepressor response results from sympathetic withdrawal and secondary hypotension.
Decreased venous return -> decrease in LV filling
