- Cardiac physiology
- CO
- Fick principle
- uptake of a substance = amount entering an organ - the amount leaving
- O2 substituted in and rearranged: CO = VO2 / arterio-venous difference
- VO2 can be measured by alveolar Vm(Fi - Fe) or by spirometry
- CvO2 must be measured from the pulmonary artery
- cardiac cycle
- pressure volumes loops
- first draw P-V graph, with ESPVR and EDPVR lines
- LV compliance curve basic
- increased preload
- decreases slope of curve at LVEDV
- lines remain the same
- fatter box
- LV compliance curve increased preload
- increased afterload
- increases gradient of LVEDV to LVESV line
- ESPVR line shifted to right
- taller, thinner box
- LV compliance curve increased afterload
- increased contractility
- increases gradient of contractility line (Ees line)
- ESPVR is shifted up and to the left
- taller, fatter box
- LV compliance curve increased contractility
- heart failure
- higher EDV, slurred contraction line, lower peak pressure, higher ESV
- Anrep effect
- an increase in afterload leads to a compensatory increase in inotropy
- lusitropy
- time taken for heart to relax
- positive (reduces time)
- negative (increases time)
- Ca overload
- reduced rate of Ca removal
- action potentials
- pacemaker
- lowest potential: -60, TP: -40, DP: 20, 150ms
- nerve cell
- RMP: -70, TP: -55, DP: 30)
- myocyte
- RMP: -90, TP: -65, DP: 30, 200ms (atrial muscles shorter)
- RMP maintained by
- Na/K pump
- differing permeability of different ions
- 100x more permeable to K than Na
- intracellular proteins (Donnan effect)
- structure
- FUNCTIONAL syncytiums of cardiac cells allow fast transmission of AP - cells are linked by intercalated disks (of which gap junctions are a part)
- ‘intercalation in space medicine is close to my heart’
- 7 phases of excitation-contraction coupling
- AP travels down T-tubules to sarcoplasmic reticulum
- depolarisation opens VG L-type Ca channels
- CALCIUM INDUCED CALCIUM RELEASE (CICR): Ca stimulates ryanodine receptors on SR, allowing Ca to flow out of SR
- Ca binds to troponin-C on actin
- Troponin C interacts with troponin I, which interacts with troponin T to move tropomyosin and expose myosin binding site on actin
- actin and myosin bind —> sarcomere shortens (2.2um at rest)
- Ca levels fall due to:
- active reuptake by SR
- timed inactivation of VG L-type Ca channels
- Na/Ca exchange pump
- routes
- from R to L atrium is through Bachmann’s bundle (anterior interatrial band)
- transmission through atrium takes 0.2ms
- Bundle of Kent between atria and ventricles in WPW
- pressure time graph
- atrial pressures
- normal
- a wave
- c wave
- triCuspid bulging from ventricular Contraction
- x descent
- v wave
- y descent
- disease
- cannon a waves
- heart block or junctional arrythmias when atria contract against closed MV/TV
- exaggerated v waves
- elevated JVP wthout waveform
- elevated with deep x and y descents
- constrictive pericarditis
- ventricular pressures
- aortic pressures
- valves
- MR
- ‘likes fast and loose!’
- faster rate reduces time for regurgitation in diastole
- low SVR reduces pressure gradient for regurgitation
- AS
- ‘likes slow and tight!'
- slower rate increases the diastolic time for coronary filling
- high SVR maintains the pressure gradient for coronary filling
- coronaries
- volumes
- heart gets 5% of CO (250mL/min), CaO2 is 200mL/L, so O2 delivery is 50mL/min, 65% is extracted, so O2 consumption is 35mL/min at rest (up to 150mL/min during exercise).
- LEFT coronary is more exposed to high pressures during systole so there is less flow then
- Gregg effect
- increased coronary blood flow splints open the ventricles and increases myocardial work
- anatomy
- LCA arises from posterior aortic sinus
- LAD
- anastomoses w. PDA
- diagonal branch
- circumflex
- RCA arises from anterior aortic sinus
- RCA supplies SAN in 60% and AVN in 90%
- NOTE: RA therefore precedes LA contraction (but LV precedes RV contraction!
- RAF: right atrium first
- LVF: left ventricle first
- Valsalva
- generation of increased intrathoracic pressure of 40mmHg
- phases
- I
- start of valsalva —> initial increase in venous return, before starting to drop. Little change in pulse.
- II
- reduced venous return due to increased intrathoracic pressure, so BP drops —> reflex tachycardia and vasoconstriction
- III
- stop valsalva —> reduced venous return as pulmonary vasculature refills —> reflex tachycardia continues
- IV
- venous return normalises —> blood pressure overshoots —> reflex bradycardia —> eventually both normalise
- ratio
- = max HR in phase II / min HR in phase IV
- >1.5 is normal
- abnormalities
- drugs
- alpha blockers
- inhibit vasoconstriction, so more pronounced tachycardia in phase II and INCREASED BP overshoot in phase IV
- beta blockers
- inhibit chronotropy, so less tachycardia in phase II and REDUCED BP overshoot in phase IV
- autonomic neuropathy
- increased BP drop without compensatory tachycardia in II
- decreased overshoot and bradycardia in IV
- CCF
- stays much the same throughout?
- increases intensity of MR murmur, decreases others
- transplant
- denervation
- resting rate 100bpm, relies on donor sinus node activity with no muscarinic inhibitory input
- no response to laryngoscopy
- drugs
- atropine
- ephedrine and metaraminol
- adenosine
- BP
- vasomotor centres
- medulla
- pressor area
- ventrolateral medulla
- ‘LP’
- depressor area
- (also remember respiratory groups)
- dorsal respiratory group
- ventral respiratory group
- influences
- hypothalamus, cerebral cortex, limbic system
- baroreceptors transmit to the nucleus tractus solitarius
- high pressure
- aortic arch
- carotid sinus
- glossopharyngeal nerve (nerve of Hering)
- higher pressures (MAP 60-180mmHg) result in increasing impulses to NTS, leading to increased inhibition of the vasomotor centres
- low pressure
- atria
- type A
- type B
- discharge during diastole
- ventricles
- pulmonary vessels
- Bainbridge reflex
- opposes baroreceptor reflex
- increased stretch increases heart rate
- Coronary arteries
- Coronary veins