The Heart As An Electrical Pump Flashcards
How are cardiac myocytes arranged? Why?
Into syncytium of cells which branch + interdigitate
Intercalated disks provide mechanical + electrical interconnection between myocytes
-> low threshold all or nothing response with rapid propagation of electrical activity
What makes up myocytes?
Composed of myofibrils which contain myofilaments (actin + myosin)
Myofilament interdigitation forms repeating microanatomical units (sarcomeres)
What aspect of myocytes is responsible for contraction? How does contraction occur?
Sarcomeres
Slide along each other shortening the muscle during contraction
What is a sarcomere?
Region of myofibril between 2 Z lines
What is a sarcomere made up of?
Thick (myosin) + thin (actin) myofilaments which interdigitate
What aspects of the heart are involved in the conduction system in order of where electrical activity begins in the left atrium?
Sino-Atrial (SA) node Atrio-ventricular (AV) node Bundle of His L bundle branch R bundle branch
Why is the Sinoatrial (SA) node important?
Source of action potential that drives cardiac contraction in normal individuals
Why is the Atrio Ventricular (AV) node important?
Delays the passage of electrical activity between atria + ventricles to ensure coordinated chamber contraction
What happens if the Sinoatrial (SA) node stops working?
Another conductor will take over; AV node -> Bundle of His etc.
The lower you get in the conduction system, the slower the replacement rhythm generator is
What is the Sinoatrial (SA) node?
Primary pacemaker but any muscle cell can take over this role
What are the features of Sinoatrial (SA) node cells?
Modified muscle cells characterized by:
- No true resting potential
- Generation of regular + spontaneous APs
What is pacemaker activity usually like?
Spontaneously generated
What can modify pacemaker activity?
Autonomic nerves (e.g. SNS), hormones or drugs
Ions, ischaemia or hypoxia
What ion movements occur during an action potential (AP)?
- Slow influx of Na+ from adjacent AP (prepotential)
- Threshold membrane potential reached
- Rapid influx of Ca2+ (depolarization)
- Outflow of K+ (repolarization)
- Membrane potential drops below threshold
- Refractory period in this cell + cycle starts again in next adjacent muscle cell
How are the ion concentrations of Na+ and K+ maintained in the ECF and ICF?
Na+/K+ return Na+ to the ECF and K+ to ICF returning concentrations back to baseline after an AP
How are action potentials (APs) propagated?
- Change in potential difference across the cell surface
- Reaches AP threshold
- AP modifies adjacent membrane by cytosolic ion flux (movement facilitated by desmosomes) in direction opposite to refractory zone
Why is it not possible for action potentials (APs) to move backwards along the muscle cells?
Refractory period where cells that have just experienced an AP, cannot have another one for a short period of time
What is the difference between refractory periods in skeletal and cardiac muscle?
Skeletal: does not extend long or much into contraction so APs + contractions can occur rapidly causing a build-up of muscle taut (sustanic state)
Cardiac: longer extending to end of contraction i.e. cannot contract muscle until one contraction is done
What are the 2 myocardial syncytia and what separates them?
Atrial + ventricular
Separated by AV node
What is excitation-contraction coupling?
Excitation: AP originates in SA node pacemaker cells + passes along myocyte syncytium membranes
Coupling: membrane depolarization initiates release of Ca2+ into myocyte cytoplasm
-> Ca2+ facilitates CONTRACTION
How does the coupling process increase intracellular calcium concentration?
AP propagates along sarcolemma + enter cells via T tubule system -> Ca2+ enters sarcoplasm from T-tubules, SR + cell membrane = increased [Ca2+]ic
How can increased intracellular calcium concentration cause muscle contraction?
- Ca2+ binds troponin on thin actin filament
- Tropomyosin moves revealing an actin binding site for myosin heads
- ATP is bound + hydrolysed to ADP via ATPase in myosin head providing energy
- ATP hydrolysis drives repeated cycle of interaction between myosin heads + actin
- Conformational changes in myosin result in movement of myosin heads along actin filaments
- Movement causes muscle fibre shortening
What is calciums role within the heart?
[Ca2+]ec determines strength of cardiac muscle contraction
What happens to calcium concentration in the extracellular fluid at the end of an action potential?
Ca2+ flow reversed (back into SR + T-tubules via Ca/Mg ATPase) which stops actin-myosin interaction causing relaxation
How does blood pass through the heart?
SVC -> R atrium -> tricuspid valve -> R ventricle -> pulmonary valve -> pulmonary artery -> pulmonary system (lungs) -> pulmonary vein -> L atrium -> mitral valve -> L ventricle -> aortic valve -> aorta -> systemic system
What are the steps of the cardiac cycle?
- Ventricular pressure falls below atrial pressure
- MV + TV open
- Passive ventricular filling
- Atrial systole (corresponds to ‘a’ wave on JVP + P ECG wave)
- Small ‘hump’ in L ventricular pressure due to volume increase
- Ventricular + atrial pressure equalize so MV + TV close
- QRS ECG complex
- Isovolumic ventricular contraction causes big increase in ventricular pressure above that of great vessels
- AV + PV open so blood flows into aorta + PA
- ‘c’ wave on JVP (tricuspid bulging back due to pressure)
- Ventricular contraction finishes + pressure falls
- Aortic pressure follows ventricular
- T ECG wave (ventricular repolarisation)
- Ventricular pressure falls below aortic pressure
- AV + PV shut at beginning of dichrotic notch
- Ventricular isovolumic relaxation
- Ventricular pressure falls below atria which has been slowly rising due to venous return
- ‘v’ wave on JVP (atrial filling)
- MV + TV open
- ‘y’ descent (atrial emptying)
What does a pressure volume loop of left ventricular pressure (y-axis) and volume (x-axis) show?
- Initial diastole when the MV is closed + L atrium is filling
- Ventricular isovolumetric relaxation
- When ventricular pressure < atrial pressure MV opens
- Initial rapid ventricular filling + sharp increase in volume
- Diastasis
- Atrial contraction
- Ventricular isovolumetric contraction
- When ventricular > atrial pressure MV closes
- AV opens when ventricular > aortic pressure
- Rapid ejection of blood accounting for 1st 1/3rd of ejection time
- Blood flow slows as potential energy stored in elastic walls of aorta
- Aortic > ventricular pressure so AV closes
What does valve stenosis cause? What is its compensation?
Ventricular outflow obstruction (i.e. restriction to forward flow into systemic circulation) + fixed CO placing pressure load on the ventricle so ventricles hypertrophy
What does regurgitation cause? What is its compensation?
Increased volume load (due to backflow) so there is increased sarcomere length + cavity volume, increases SV + eccentric hypertrophy to compensate for further wall stress
What happens to the affected ventricle as valvular pathology worsens?
Will functionally decompensate + dilate
What are the 4 heart sounds and what causes them?
S1: MV + TV closure
S2: AV + PV closure
S3: Rapid passive phase of ventricular filling (coincides with ‘y’ descent in JVP)
S4: Atrial contraction phase of ventricular filling (coincides with ‘a’ atrial systole wave in JVP)
What will mitral stenosis sound like?
Opening snap + loud 1st heart sound that both quieten as valve becomes rigid
Low frequency diastolic rumble
Does not radiate but palpable thrill at apex in severe disease
What can cause mitral stenosis?
Rheumatic fever
Sclerosis
Endocarditis
Congenital disease
What can occur in mitral stenosis?
Reduction in flow + increased ventricular filling time -> pulmonary hypertension -> L atrium increases in size -> increased tendency for atrial arrhythmia
What can exacerbate mitral stenosis?
Increased HR
Why can atrial fibrillation by catastrophic in stenotic patients?
As they are dependent for atrial kick for ventricular filling
What can cause mitral regurgitation?
Degenerative
Rheumatic
Congenital prolapse (esp. Marfans syndrome)
MI + chordae tendinae rupture (acute emergency)
What sound can occur in aortic stenosis?
Midsystolic murmur may radiate to carotid pulse
What causes aortic regurgitation?
Endocarditis Marfan's disease Ankylosing spondylitis Dissection Trauma
What will aortic regurgitation sound like?
Early diastolic murmur + high pitched
