Cardiac physiology (Block 3) Flashcards
Drugs and the Heart
Drugs can affect the efficiency for the heart pump (HR, force of contraction, rhythm, etc)
Drugs can affect blood vessels (altering blood pressure, etc)
Average weight of human adult heart
250-350g
Approx size dimensions of human adult heart
12cm long by 9cm wide
Typical resting heart rate
60-80 bpm
Typical HR during exercise
140-180 bpm
How much blood is on average pumped by the heart?
70ml per heartbeat
5L per minute
Anatomically, the heart consists of what tissues?
Endocardium
Myocardium
Epicardium
Pericardium
What is endocardium made of?
Endothelial cells
What is myocardium made of?
Specialised muscle cells called myocytes
What is epicardium composed of?
A thin layer of mesothelioma cell and connective tissue
What is pericardium?
A fibrous sac that encloses the heart
Myocardium structure
Cardiac muscle is striated, BUT:
single nucleus
under autonomic control
all cardiac cells contract together (skeletal - selective recruitment of motor units)
high oxygen demand
structure permits coordinated contraction (acts as a syncytium)
Cardiac myocytes do not regenerate
Automaticity
Ability to initiate an electrical impulse
Excitability
Ability to respond to an electrical impulse
Conductivity
Ability to transmit an electrical impulse from one cells to another
Physiology of cardiac conduction
Cardiac electrical activity is the result of ion movement across the cell membrane. In resting state, cardiac muscles cells are polarised (an electrical difference exists between the negatively charged inside of the cell and the positively charged outside of the cell membrane)
Sinoatrial (SA) ode
Primary pacemaker of the heart
Located at the junction of the superior vena cava and the right atrium
15mm long x 5mm wide
Cells spontaneously depolarise ~100 times per min
Atrioventricular (AV) node
Impulses from SA node are conducted to AV node
AV node co-ordinates incoming electrical impulses after slight delay
Relays the impulse via His/Purkyne fibres to the ventricles
Sinus rhythm
Normal heartbeat rhythm
Atrial arrhythmia
Without rhythm
Action potential
The pattern of repolarisation and depolarisation
The Nernst equation
Predicts where the electrochemical gradient will balance
** write equation in notes bc you can’t type it here
Key cardiomyocyte pump
Na/K pump
Key cardiomyocyte transporte
Na/Ca exchanger
Drug action of the SA node
SAN contains autorhythmic fibres that initiate an action potential (100-110 per minute)
• Nerve impulses from the autonomic nervous system (ANS) and hormones (e.g. adrenaline) modify the timing and strength of each heartbeat, but they do not establish the fundamental rhythm.
• Vagus nerve innervates SA node, reducing rate to 60-80bpm (through acetylcholine action on muscarinic receptors)
• Higher (>100 bpm) = tachycardia; Lower (<50 bpm) = bradycardia
• Acetylcholine decreases slope of phase 4 and therefore extends time to reach threshold ( through increased K+ efflux, reduced Ca++ and Na+ influx)
• Atropine will block effect of acetylcholine
• Sympathetic activity releases noradrenaline (norepinephrine), increasing bpm (reduced vagal tone) via action at -adrenoreceptors
Non-pacemaker action potentials
Non-pacemaker cells have true resting potential (phase 4)
e.g. ventricular myocytes, Purkinje cells
• Depolarisation to -70mV (from an incoming action potential) causes rapid influx of Na+ (phase 0)
• Partial repolarisation occurs as the Na+ current is inactivated (Phase 1) and transient K+ efflux
• Slow Ca++ influx (plateau phase 2) via slow L-type calcium channels (open at ~ -40 mV)
• Repolarization (phase 3) is caused by increased K+ efflux and decreased influx of Na+ and Ca++
• Phase 4 - resting state
Phases of non-pacemaker action potentials
0 Depolarisation (Na+ channels open: fast)
1 Early repolarisation (Na+ channels close, some K+ efflux)
2 Plateau (Ca++ influx: slow)
3 Repolarisation (K+ out)
4 Resting (restoration of normal ionic balance by pumps)
Refractory periods in non-pacemaker cells
The refractory period of cardiac muscle is dramatically longer than that of skeletal muscle.
• This prevents tetanus from occurring and ensures that each contraction is followed by enough time to allow the heart chamber to refill with blood before the next contraction.
ARP
Absolute Refractory Period
During this time a second stimulus will not cause any response
ERP
Effective refractory period
After the end of of the ERP a second stimulus will cause a propagated action potential
Cardia Rhythm
Electrocardiogram (ECG) is measured from electrodes placed on the skin
It therefore shows a summation of cardiac electrical activity
Changes in the ECG are used to diagnose heart disrhythmias
Properties of cardiac muscle
Excitation of the heart is triggered by intrinsic electrical impulse rather than neural transmitters.
Contraction of the heart is triggered by
elevation of intracellular calcium influx.
Myocyte contraction
Excitation-contraction coupling (ECC) causes myocyte contraction in phase 2 of action potential
• L-type Ca++ channels in sarcolemma open. Calcium influx then activates ryanodine receptors (RyR) on sarcoplasmic reticulum (SR), increasing intracellular Ca++ from 10-7 to 10-5M
• Ca++ binds troponin C, changing its conformation and allowing myosin-actin cross-bridging and contraction
• At the end of phase 2, Ca++ is sequestered by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase) m influx.
