4 Function of the heart
- generate BP
- route for blood: pulmonary & systemic circulation
- one-way blood flow
- provide blood supply for metabolic needs
describe how heart gets its own blood supply
blood supply to myocardium
- R&L coronary arteries @ ascending aorta
- > large arteries travel in sulci on <3 surface, small branches penetrate myocardium
- > cardiac veins -> coronary sinus (posterior <3) -> R atrium
3 Purpose of CT ring around 4 valves
- anchorage
- structural stability
- electrical insulation b/w atria & ventricles
2 Properties of cardiac muscle that allow it to function
- functional synctium= very fast electrical conduction w/in muscle fibres
- myocardinal fibres very aerobic w/ many mitochondria, oxidise FA & glucose for energy
location of <3
mediastinum
coverings of heart
- Fibrous pericardium: anchor & protection
- Serous pericardium: parietal + viseral = pericardial cavity
wall layers of <3
- epicardium (/visceral pericardium)
- myocardium (cardiac muscle)
- endocardium (simple squamous)
What is the cardiac cycle?
One complete <3 beat = atrial sys & dias + ventricular sys & dias. Note: depolarise => contract, repolarise => relax
Describe depolarisation sequence (7 steps)
- SA node (cause auto rhythmicity)
- Atrial muscle
- AV node
- Atrioventricular bundle
- R&L bundle branches
- Purkinje fibres
- Ventricular muscles
Does the pacemaker have a stable RMP?
No because after repolarisation it SLOWLY DEPOLARISE again
Describe AP of cardiac muscle fibres
AP initiated by adjacent current flow & fibres remain depolarised»_space; prevent premature re-excitation & tetany (spasm)
* myocardial fibres stable RMP = return to normal RMP
What is an ECG & function
Electrocardiogram: sum of all electrical events during cardiac cycle measured on surface of body.
» determine heart health, identify heart attack
waves of an ECG
- P: atrial depol
- QRS: ventricular depol (behind it atrial repol)
- T: ventricular repol
Describe mechanical phases of cardiac cycle
- Atrial depol -> atrial sys: pushes out 20% blood remaining
- Ventricular depol -> ventricular sys: isovolumetric ventricular contraction = hi pressure (AV valves close & semilunar valves open) -> ventricular ejection
- Ventricular repol. followed by ventricular dias: semilunar valve close -> isovolumetric ventricular relaxation -> AV valves open = rapid passive ventricular filling (80%)
How Neural factor affects <3 rate?
- note: SA & AV innervated by para&sympathetic nerves from cardiovascular centre in medulla oblongata
- Para (via VAGUS): acetylcholine= slow <3 rate ,innervate SA & AV nodes.
- Symp (via thoracic spinal cord): noradrenaline = increase <3 rate, innervate SA node
Other factors (except neural) that affect <3 rate
- Hormones: nor&adrenaline, thyroid hormones
- Tb
- drugs
- sleep
3 factors that affect SV (stroke volume)
- preload (intrinsic effect): force on ventricular muscle @ EDV & venous return
- contractility (extrinsic effect): inotropic state of heart- strength of ventricular contraction (by [Ca2+])
- afterload: force developed by ventricles -> eject blood in arteries (RV is lo, LV is hi)
Cardiac volumes (3)
- End diastolic vol. (EDV): vol of ventricle @ end of filling (120-130mL)
- End systolic vol. (ESV): vol of ventricle @ end of emptying (50-60mL)
- stroke vol. (SV): vol blood ejected per beat (70mL). SV = EDV - ESV
What is Starling’s law of the heart? (type of effect)
Relationship b/w stretch of ventricles as blood fills it and the contraction required to eject blood out. More filling = more force to empty (intrinsic effect)
What is extrinsic effect (affects contractility)?
Para/sympathetic NS involved in <3 function.
- Contractility increase= Sympathetic NS innervate ventricular muscle -> nor+adrenaline act on beta 1 receptors (+ve inotropic effect)
- Contractility decrease= decrease stimulation -> decrease nor+adrenaline and beta blockers
