L7 - Cardiovascular Physiology Flashcards
what is meant by the heart is ‘autonomous’
- that it can beat without signals from the brain (has its own internal pacemaker)
- atrial relaxation - atria filling - atrial contraction - ventricular relaxation - ventricular filling - ventricular contraction (same events are always happening)
- well coordinated effort
describe the heart’s electrics: excitation and conduction
- Sinoatrial (SA) node: generates action potential and determines heart rate (~100min -1)
Conducts through atria - Atrioventricular (AV) node: (slow conduction) allows atria to complete contraction before the ventricles excite/contract (‘gate keeper’)
- Bundle of His: bundle branches - (fast conduction, 5min-1) to the apex
Apex depolarises first and then spread upwards from the base (0.5m s -1) via - Purkinje fibres: causing synchronous depolarisation, moving blood upwards to the aortic/pulmonary semilunar valves
describe the action potentials of the SA node and the ventricular cells (how they differ/same) - look at graphs in slides for clarification
- SA node causes automaticity (‘spontaneous beats’)
- Ca2+ plateau in ventricular cells prolongs refractory period, preventing tetanic contraction of the heart
Excitation depends on ion concentrations, permeabilities and movements across the cell membrane
SA node: (pacemaker, ‘leader’)
- resting membrane potential at ~60mV (way higher than ventricular)
- unstable pacemaker potential: funny Na+ channels (slow Na+ influx), T-type Ca2+ channel (TTCC; influx of Ca2+)
- fast depolarisation: L-type Ca2+ channel LTCC (Ca2+ influx)
- repolarisation: K+ channels (slow K+ efflux)
Ventricular cells (‘followers’):
- rest membrane potential (~90mV) and stable
- very fast depolarisation: Na+ channels (fast Na+ influx)
- depolarisation plateau: LTCC (Ca2+ influx)
- repolarisation: K+ channels (fast K+ efflux)
why do action potential differ between cells?
- different action potentials in conduction system, depend on function and localisation
- due to localisation -> shape
- but also timing -> when - overall electrical cardiac activity (spatial and temporal changes in potential) can be measures and represented as an electrocardiogram (ECG)
P wave - atrial depolarisation
QRS complex - atrial repolarisation and ventricular depolarisation
T wave - ventricular repolarisation
how is the ECG a powerful tool?
monitoring the electrical activity of the heart
a) standard ECG limb leads
- Einthoven’s triangle: tries to show the electrical activity of the heart and understand its electrical axis
- lead II shows: P, QRS, T
describe cardiac excitation and conduction in dental practice
Sudden cardiac arrest (SDA):
- heart stops beating due to arrhythmia (impaired excitation/conduction)
- one of the deadliest medical emergencies in dental practice
- 1:500 dentist in UK, possibly more in other countries
Cardia arrhythmias: (2 types)
- atrial fibrillation (AF, most common, mostly non-lethal
- ventricular fibrillation (VF, less common, but mostly lethal)
–> both result in/are uncoordinated contraction, impaired ejection of blood (output)
describe the two types of cardiac fibrillation in more detail and why they are mostly lethal/non-lethal
Atrial fibrillation (AF):
- when arythmia occurs in atria. P wave is not as it should be on ECG but QRS is normal so blood still gets pumped out of the heart (why its mostly non-lethal)
- gate keeper of electrical signal to ventricles
- AF is non-lethal but can lead to blood clots in atria (stroke) - bc blood not all moving out of that space, builds up
Ventricular fibrillation (VF):
- less common, but lethal, almost no filling, no proper contraction, no cardiac output
- no blood to brain and other organs so die
- the big difference is that it is happening in the ventricle
- no QRS complex, ECG looks really scrambled
what are some things to know about cardiac arrest/how/when to look out for it in dent
- over age of 35, heart failure is the most common underlying pathology of cardiac arrest with diabetes, obesity, hypertension and high cholesterol as risk factors (ie. age is a massive risk factors and these other things also increase risk)
- in young people, mostly congenital cardiac structural abnormalities (cardiac protein or ion channel mutations)
- less than give mins to act before permanent neurological damage
Dent staff:
- should be trained in CPR
- should have defibrillator and kit to deal with this
describe excitation-contraction coupling (maybe go over cross bridge cycle to refresh) + go over diagram on slide to confirm understanding (could watch YouTube vid on slide)
1. how does this excitation spread through the myocardium?
2. how does escitation cause cardiac muscle contraction?
- how does this excitation now spread though the myocardium?
- the depolarisation wave spreads through myocardium via gap junctions in intercalated disks (membrane proteins known as gap junctions connect cells and that allows signal to go from one cell to another) - how does excitation cause cardiac muscle (myocardium) contraction?
- depolarisation causes Ca2+ induced Ca2+ release
- Ca2+ binds troponin on myofilament -> cross bridge cycle sliding of myofilaments
descibe the cardiac cycle (periods, pressure, volumes, electrical events, heart sounds) + go over wiggers diagram make sure to understand
Periods:
- diastole - relaxation, filling (0.5s - 63%)
- systole - contraction, ejection (0.3s - 37%)
- ie. spends more time in diastole than systole
Pressures:
- LV, aortic and LA pressurs
- pressure differences create flow, and open valves (no muscle or anything opening valves)
Volumes:
- stroke volume (SV, 70ml) = end-diastolic volume (EDV, 135 ml)
- end-systolic volume (ESV, 65 ml)
- SV = EDV-ESV
- isovolumetric - volume remains the same
Electrical events (ECG):
- P wave, QRS complex, T wave
Heart sounds:
- 1st lub - AV valves closure
- 2nd dub - semilunar valves closure
Electrical activity usually happens a little bit before mechanical changes because it’s the electricity that controls all of these things.
how do we control cardiovascular function?
CO = HR x SV
5.0 L min-1 = 70 bpm x 70 mL
Average sized adult with 5.5L total blood volume, nearly all blood is pumped around the circulation in one minute
During excersise increases to 20-25 L min-1 in untrained individuals, and 35 L min-1 in trained individuals
Autonomic nervous system!
HR - Preload - Afterload - Contractility
describe how heart infections can be causes in dentistry
- caused by an infection with bacteria, virus, fungi or parasites
- enter the bloodstream and travel to the heart
Endocarditis: infection/inflammation
-> heart valves
-> inner linings of heart chambers
Myocarditis: inflammation mostly caused by virus (eg. COVID or influenza)
-> affecting the myocardium (whole heart or parts)
In dentistry endocarditis will be more common since it deals with bacteria
describe how heart infection and dental practice are related/may cross over + risk factors for endocarditis
Poor dental health:
- a healthy mouth and healthy gums are essential for good health
- not brushing or flossing regularly, might cause bacteria to grow inside the mouth, which can enter the bloodstream through a cut on the hums
- certain dental procedures that cut the gums might also allow bacteria to get in the bloodstream
- preventative antibiotics might be needed
Risk factors for endocarditis:
- artificial implanted heart valves
- damaged heart valves
- implanted heart devices
- ‘illegal’ IV drug use
- long-term catheter use
