Cardiac Cycle Flashcards
Where is the sa node located and what is its role
Group of cells Found in the walls of the right atrium
Spontaneously produce action potential that travels through the heart via electrical conduction system
Sets rhythm of heart
Role of the av node
Electrically connects right atrium and right ventricle delaying impulses so atria have enough time to eject their blood into ventricles before ventricular contraction
Hyperpolarisation
Membrane repolarises below threshold, it is unstable
Phases of atrial and ventricular muscle action potentials
0-voltage gated sodium channels open , na influx , voltage gated ca channels open slowly
1- sodium channels close , cells begin to repolarise
2-calcium voltage gated channels fully open , calcium influx halts repolarisation, voltage gated potassium channels start to open
3-calcium ion channels close and potassium ion channels open fully, potassium ion efflux
4-stable na/k pump , 3na out 2k in
Electrical conduction of heart stages
1-electrical activity generated in SA node spreads out via gap junctions in to atria
2- av node conduction is delayed so there is a correct filling of ventricles
3- conduction occurs through bundle of His into ventricules
4-conduction through purkinje fibres , spreads quickly throughout ventricles
What happens at the p wave
Atrial depolarisation and contraction
What happens at the PR segment
Av nodal delay
What happens at the QRS complex
Ventricular depolarisation contraction, atria are repolarising simultaneously
What happens at the ST segment
Ventricles contracting and emptying
T wave
Ventricular repolarisation
What happens at the TP interval
Ventricles relaxing and filling
What creates pressure changes in the heart chambers
Electrical activity is converted into myocardial contractions
What is cardiac diastole
Relaxation of heart muscles
Blood returns to the heart and fill the chambers
Low pressure in ventricles, mitral and tricuspid valves open and ventricles fill with blood
Atrial systole
Ventricles are in diastole at low pressure
Atrial contraction causes blood to move into relaxed ventricles,
Mitral and tricupsid valve close
Ventricular systole
Atrial diastole
Period if isovolumetric contraction
Pressure rises sufficiently, forces open aortic and pulmonary valves
Blood pushed out of ventricles
Left ventricular pressure changes
-contraction of left atrium pushes blood into ventricle, pressure of ventricle rises
-mitral valve close
-pressure rises in isovolumetric contraction
-ventricular pressure highe than aortic , aortic valve pushed open blood is ejected from ventricle
-when ventricular pressure is less than aortic , aortic valve close
-isovolumetric relaxation
When does isovolumetric contraction occur
Ventricular systole
Ventricular pressure volume loop
-ventricule relaxed , pressure low , volume increased
- mitral valve closes ,ventricles contract , pressure increases
-pressure high enough to force aortic valve to open and blood leaves ventricle
- as ventricle empties ,aortic valve closes so pressure deals
What creates the lub sound
Close of mitral valve at beginning of ventricular diastole
What creates the dub sound
Close of aortic valve at end of ventricular systole
What causes occasional sound
Turbulent blood flow into ventricles
Cardiac output
CO=HR x SV
Amount of blood ejected from heart per volume
What is preload
Stretching of heart at rest , increases stroke volume due to starlings law
More blood in = ,more blood out
After load
Opposes ejection reduces stroke volume due to Laplace law
Opposes contraction that ejects blood from the heart, stress through wall of heart prevents muscle contraction
Equation for wall stress
Stress = tension / wall thickness
How is afterload increased
Increasing pressure and radius
Why does radius affect wall stress/afterload
Small ventricle radius has more wall stress directed to the centre of the chamber so less afterload and better ejection
Large ventricle radius will have less wall stress directed to the centre of the chamber so more afterload and less ejection
Acute rises in blood pressure offset by ?
-starling law - increased stretch give increases contraction and increased stroke volume
Local positive inotropes eg noradrenaline
Baroreflex - decreased sympathetic tone which decreases blood pressure
What causes volume overload
The heart doesn’t contract properly, so blood is left in the ventricle
Increased pressure or radius leads to
Increase in wall stress which opposes ejection
How does the heart compensate for wall stress ?
Ventricular hypertrophy, greater myocyte size and more sarcomeres , thus increases wall thickness , which decreases wall stress
What is the downside of ventricular hypertrophy
It requires more energy as more sarcomeres are used so also a greater oxygen, eventually contractility will decrease and produce more heart failure
What happens during exercise
- increased venous return , which leads to increased preload and higher EDV
- the ventricle while eject blood to the same ESV so there is an increase in stroke volume
What happens during hypertension
Longer time spend in isovolumetric contraction to increase pressure in chamber above that I’m aorta to open the valve
-more energy used and lowers force of contraction which reduces stroke volume and increased esv
