Conducting system of the heart Flashcards
Describe the conduction system of the heart from SA node to purkinje fibres?
SA node-> 3 antrial internodal pathways -> AV node-> bundle of HIS -> R and L bundle branches -> Purkinje fibres
Which are the only fibres to traverse fibrous cardiac skeleton?
Bundle of His
Why are purkinje fibres necessary?
Convey electrical activities to the muscles-> normal myocardial cells cannot themselves spontaneously generate an action potential
Where is the SA node located?
Wall of RA, below SVC
How fast is depolarisation through the SA node, muscle and internodal pathway?
Depolarisation through node is 0.05m/s
Atrial muscle 0.3m/s
Through internodal pathway at 1m/s
AV node 0,05m/s
Why is conduction through the AV node so slow?
AV node is in posterior interatrial septum, behind tricuspid valve
Delay of 0.1 to 0.13 seconds
This delay allows completion of atrial systole before ventricles begin to contract
Which direction does the interventricular septum get activated?
From left to right
Which are the last parts of the heart to be depolarised?
Spreads from apex to base of heart
From endocardium to epicardium
Finally; pulmonary conus, top part of interventricular septum, basal posterior parts of LV
Describe how parasympathetic activation affects HR
Vagus nerve-> releases Ach and SA and AV node
Ach binds to M2 muscarinic receptors-> +G protein -> opens special K+ channels -> hyperpolarisation of membrane -> so it takes longer for cell to reach threshold -> reduces HR
Describe how sympathetic activation affects HR via SA node
Noradrenaline binds to B1-> increased cellular cAMP -> increased permeability of sarcolemma to Na + Ca ->depolarisation +steeper prepotential -> cells reach threshold more quickly
How does contraction of atria compare to contraction of ventricles from left to right?
RA systole precedes LA systole
LV contracts before RV
RV ejection begins before LV ejection (as pulmonary arterial pressure is lower than aortic pressure)
How does the timing of valve closer vary with respiration?
Inspiration: aortic valve closes before pulmonary valve
Expiration: aortic + pulmonary valve close simultaneously
How does the cardiac cycle correspond to an ECG?
P wave: ventricular diastole
R wave: ventricular contraction
QTinterval: period of ventricular depolarisation and repolarisation
T wave: ventricular relaxation with falling ventricular pressure
What are the key features of atrial flutter?
Sawtooth pattern
HR 200-350
There is a large counterclockwise circus movement in RA
Almost always associated with 2:1 or greater AV block because the AV cannot conduct >230/min
Ventricular rate can be slowed by carotid sinus pressure
Where in the heart is the issue in WPW syndrome?
Aberrant connection between atria and ventricles
(bundle of Kent)
Circus movement tachycardia is usually initiated by an atrial premature beat
What are the ECG manifestations of WPW syndrome?
Short PR interval
Wide slurred QRS complex (J wave)
Normal PJ interval
Paroxysmal atrial tachycardia
Why is AF life threatening in WPW syndrome?
Frequently degenerates into VT or VF
What is a normal QT interval?
0.35-0.42 seconds
What are the key facts about QT interval?
Corresponds with ventricular action potential
Varies inversely with HR
NOT prolonged with hypokalemia
What is normal EF, EDV and SV?
EF: 65%
EDV: 130mL
SV: 70-90mL
50mls remains in ventricle at end of systole
What are systolic and diastolic pressures?
Systolic: peak pressure in ventricles during contraction
Diastolic: lowest pressure in ventricles during relaxation
Pulse pressure=systolic-diastolic
Which section of the cardiac cycle has the most rapid change in pressure per unit time?
Isometric contraction of left ventricle
How do the pressures in the ventricles differ?
Left V: 120 systole 80 diastole
Right V: 25 systole 15 diastole
When aortic valve closes the pressure in RV is 15mmHg
What is Starling’s law of the heart?
Increased venous return, increased cardiac output
Up to a point. No change in contractility.
What is the Frank-Starling curve?
Relationship between EDV and SV
Curve shifts up and to the left -> with increased contractility (inotropes)
Shifts down and to the right -> decreased contractility
Describe the different parts of the jugular venous wave?
a: atrial systole
c: rebound of triscuspid valve into RA during isovolumetric contraction
v: rise in atrial preessure before tricuspid valve opens in diastole
What are the 2 heart sounds?
1st: closure of mitral and tricuspid valves
2nd: closure of aortic/pulmonary valves
3rd: rapid ventricular filling
4th: pathological-stiff ventricle
What is the general function of inotropes?
reduce afterload and preload as well as increasing cardiac output and ejection fraction (widening pressure volume loop)
Safe use requires monitoring to be available
What is the mechanism of action by which adrenaline, dopamine and NA are inotropes?
Act on b1 receptors-> + adenylyl cylase -> increased cAMP -> influx of calcium-> stronger contraction
What is the mechanism of action by which glucagons are inotropes?
Forms cAMP in cardiac muscles-> influx of calcium-> stronger contraction
What is the mechanism of action by which caffeine and theophylline are inotropes?
Inhibit breakdown of cAMP-> influx of calcium->stronger contraction
What is the mechanism of action by which digoxin is an inotrope?
Inhibitory effect on Na K ATPase in myocardium-> influx of calcium
What are some negative inotropes?
Hyoercapnia
Heart failure
Beta blockers, calcium channel blockers and many anaesthetics
Which conditions have no effect on cardiac output?
Sleep
moderate changes in environmental temperature
Which conditions increase cardiac output?
Anxiety/excitement eating exercise high environmental temperature pregnancy adrenaline
What conditions decrease cardiac output?
Sitting or standing from lying position
Rapid arrhythmias
Heart disease
How does diastolic dysfunction and systolic dysfunction affect the volume pressure curve?
Systolic: shifts curve up and to the right, decreases SV
Diastolic: shifts curve up and to the left, decreases SV
How is cardiac output maintained in exercise in dennervated vs normal hearts?
Denervated: Cardiac output increases by frank starling mechanism, ie SV increases
Normal: HR increases
Why is angina more likely to increase with aortic stenosis than aortic regurgitation?
Myocardial O2 requirement increases more with increased pressure than volume
Which factors increase and decrease end diastolic volume?
Decreases in MI, pericardial effusion and reduced venous return to heart (standing)
Increases with stronger atrial contraction, negative intrathoracic pressure during inspiration, increased venous return to the heart
Which parameters are decreased in a failing LV?
Ejection fraction
Rate of rise of pressure at the commencement of systole
Stroke-volume at a given filling pressure
Systolic shortening of myocardial fibres
What are the features of pressure overload seen in aortic stenosis?
Hypertrophy, fibrosis, vascular insufficiency and changes in myosin isoform expression
Surgery fixes cardiac status but not pressure changes
What makes cardiac function worse in aortic stenosis?
Increased pressure gradient across the aortic valve
Increased reflux through the aortic valve
Increased aortic systolic pressure
Rapid HR
When does backflow in the proximal aorta occur?
Transiently during the initial phase of diastole
What happens to blood flow in the coronary arteries during systole?
Still flows to RA and RV
Flow to LV decreases
Flow to subendocardial portion of LV stops
What is happening to the pressure in the aorta during the isometric contraction phase of the ventricles?
The aortic pressure is falling until the aortic valve opens again
