Session 4 - Congenital Heart Defects & Electrical Mechanisms

Question 1

What are 2 main types of congenital heart lesions?

Answer 1

Cyanotic

Acyanotic

Question 2

What is cyanosis?

Answer 2

Blue-purple discoloration of skin and mucous membranes caused by elevated blood concentration of deoxygenated hemoglobin

Question 3

What direction does blood shunt in for acyanotic lesions?

Answer 3

Left to right

Question 4

What direction does blood shunt in for cyanotic lesions?

Answer 4

Right to left

Question 5

What is atrial septal defect?

Answer 5

Persistent opening in the interatrial septum after birth that allows direct communication between left and right atria

Question 6

What are 2 locations where atrial septum defect can occur?

Answer 6

Ostium secondum and ostium primum

Question 7

What is patent foramen ovale?

Answer 7

Foramen ovale doesn’t close and seal after birth

Question 8

What happens during atrial septal defect?

Answer 8

Oxygenated blood from left atrium is shunted into right atrium

Question 9

What are the 4 haemodynamic effects of ASD?

Answer 9

Increased pulmonary blood flow
RV volume overload
Right ventricle and right atrium enlarge
Right heart might fail

Question 10

What is a ventricular septal defect?

Answer 10

Abnormal opening in the interventricular septum

Question 11

What happens during VSD?

Answer 11

Flow is shunted from left to right ventricle, increased blood flow to left side, causes enlargement of LA and LV

Question 12

What is patent ductus arteriosus?

Answer 12

Ductus connecting pulmonary artery to descending aorta fails to close after birth

Question 13

What happens during patent ductus arteriosus?

Answer 13

Flows from aorta to pulmonary artery, increases blood return to left side of heart, enlargement of LA, LV and aorta

Question 14

What is congenital aortic stenosis?

Answer 14

Abnormal structural development of valve leaflets, biscuspid instead of tricuspid causing narrower opening for blood to flow

Question 15

What is the effect of congenital aortic stenosis?

Answer 15

Left ventricle systolic pressure increases to pump blood, LV hypertrophies

Question 16

What is coarctation of aorta?

Answer 16

Discrete narrowing of aortic lumen

Question 17

What is the effect of aorta coarctation?

Answer 17

LV faces increased after load, LV hypertrophy, dilation of collateral blood vessels

Question 18

What is the effect of Tetralogy of Fallot?

Answer 18

Ventricular septal defect
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy

Question 19

What is transposition of the great arteries?

Answer 19

Each great vessel inappropriately rises from the opposite ventricle - aorta from RV and pulmonary artery from LV

Question 20

What is the effect of transposition of great arteries?

Answer 20

Separates pulmonary and systemic circulations, no oxygen delivered to body at all

Question 21

What is Eisenmenger syndrome?

Answer 21

Severe pulmonary vascular obstruction that results in chronic left to right shunting through congenital cardiac defect

Question 22

How is the resting membrane potential of cardiac cells generated?

Answer 22

K+ ions move out of the cell down their concentration gradient, making the inside negative with respect to outside, until equilibrium potential is reached and there is no nett movement of K+

Question 23

What happens during a cardiac action potential?

Answer 23

RMP due to background K+ channels
Upstroke due to opening of voltage gated Na+ channels and influx of Na+
Initial repolarization due to transient outward voltage gated K+ channels
Plateau due to opening of voltage gated Ca2+ channels and influx of Ca2+ balancing with efflux of K+
Repolarisation due to efflux of K+ through voltage gated K+ channels

Question 24

What happens during a pacemaker potential?

Answer 24

Hyperpolarization activated Cyclic Nucleotide gated channels allows influx of Na+ ions, depolarizing cells and forming funny current
Depolarization opens V-gated Ca2+ channels
V-gated K+ channels opens causing repolarisation

Question 25

How does excitation-contraction coupling work in cardiac myocytes?

Answer 25

When action potential is fired, depolarization opens L-type Ca2+ channels in T-tubule system, localized Ca2+ entry opens calcium-induced calcium release channels in SR, Ca2+ binds to troponin C, conformational change shifts tropomyosin to reveal myosin binding site on actin filament, causing contraction

Question 26

How do cardiac myocytes relax?

Answer 26

Ca2+ pumped back into SR through SERCA or exits across cell membrane through PMCA and NCX

Question 27

What is the effect of hyperkalaemia on heart?

Answer 27

High plasma K+, Ek less negative, membrane depolarizes, inactivating some voltage gated Na+ channels, causing a slower upstroke and shorter action potential as repolarisation is faster, can cause asystole

Question 28

What is the effect of hypokalaemia on the heart?

Answer 28

Plasma K+ lower, lengthens action potential as efflux of K+ slower and delays repolarisation can lead to early after depolarisations, oscillations in membrane potential and ventricular fibrillation

Question 29

What kind of action potentials lead to bradycardia?

Answer 29

Action potentials fire too slowly

Question 30

What happens to action potentials during asystole?

Answer 30

Fail

Question 31

What happens to action potentials during tachycardia?

Answer 31

Fire too quickly

Question 32

How does excitation contraction coupling work in smooth muscle cells?

Answer 32

Depolarization opens VGCC, influx of Ca2+, binds to calmodulin
Noradrenaline activates alpha1 receptors, produces IP3 and DAG
IP3 activates IP3R on SR, releasing more Ca2+, binds to calmodulin
Calmodulin activates myosin light chain kinase, phosphorylates myosin light chain to allow interaction with actin

Question 33

How do VSM relax?

Answer 33

Ca2+ levels decline, myosin light chain phosphatase dephosphorylates myosin light chain