Anatomy and physiology of the cardiovascular system
Coronary anatomy
- RCA - RA, RV, SA node (60%), AV node (90%), inferior LV via PDA
- Right dominant 85% (PDA from RCA), left dominant 8%, co-dominant 7%
- LMCA -> LAD + LCx
- LAD - anterior wall, anterior 2/3 septum, apex. Diagonal branches
- LCx - lateral wall. Obtuse marginal branches
- Coronary flow is diastolic (LV compression abolishes systolic flow)
- Tachycardia shortens diastole -> ischaemia. Basis of rate control in angina
- Subendocardium most vulnerable (highest wall stress, end of perfusion field)
Conducting system
- SA node -> internodal -> AV node (decremental conduction, ~0.1s delay) -> His -> RBB / LBB (anterior + posterior fascicle) -> Purkinje
- Intrinsic rates: SA 60-100, AV junction 40-60, ventricle 20-40
- LAD supplies both bundle branches proximally -> bifascicular block in anterior MI = large infarct
Chamber wall thickness
- LV 8-12 mm, RV 3-5 mm
- RV tolerates volume load, fails with acute pressure load (PE)
Key numbers
- CO = HR x SV; normal 4-8 L/min, cardiac index 2.5-4 L/min/m2
- SV ~70 mL; EF = SV/EDV, normal >=55%
- MAP = DBP + 1/3 pulse pressure = CO x SVR
- Normal PCWP 6-12, RAP 0-5, PA mean <20 mmHg
- Coronary blood flow ~250 mL/min (5% of CO for 0.5% of body mass)
- Myocardial O2 extraction ~70% at rest - near-maximal, so inc demand must be met by inc flow
Determinants of stroke volume
- Preload - EDV / sarcomere length
- Frank-Starling: inc preload -> inc force (optimal sarcomere 2.2 um)
- Starling curve flattens, does not descend, in normal heart
- Afterload - wall stress
- Laplace: wall stress = (P x r) / 2h
- -> dilated ventricle has higher wall stress at the same BP -> vicious cycle
- -> hypertrophy (inc h) normalises wall stress at the cost of diastolic function
- Contractility - inotropy, independent of load
- inc by SNS (beta1 -> Gs -> cAMP -> PKA -> inc Ca entry + faster SERCA reuptake), digoxin, catecholamines
- dec by acidosis, hypoxia, beta blockade, ischaemia
Excitation-contraction coupling
- Depolarisation -> L-type Ca channel (DHPR) -> Ca-induced Ca release via RyR2 from SR
- Ca binds troponin C -> tropomyosin shifts -> actin-myosin cross-bridge
- Relaxation = active, ATP-dependent: SERCA2a pumps Ca back (inhibited by phospholamban; PKA phosphorylation relieves it), NCX extrudes
- Ischaemia -> ATP depletion -> diastolic dysfunction precedes systolic
Action potentials
| Phase | Ventricular myocyte | Ion |
|---|---|---|
| 0 | Upstroke | fast Na in |
| 1 | Notch | transient K out |
| 2 | Plateau | L-type Ca in = K out |
| 3 | Repolarisation | delayed rectifier K (IKr, IKs) out |
| 4 | Resting -90 mV | IK1 |
- SA/AV nodal cells: no phase 1-2; upstroke is Ca-dependent (slow); phase 4 spontaneous depolarisation via funny current If (HCN)
- -> ivabradine blocks If: slows rate with no inotropic effect
- -> verapamil/diltiazem and adenosine act at the AV node; lignocaine does not
- IKr (hERG) block -> QT prolongation -> torsades
Vascular control
- Endothelium: NO (shear stress, ACh) -> cGMP -> vasodilation; prostacyclin; endothelin-1 -> vasoconstriction
- Autoregulation: coronary + cerebral + renal maintain flow over wide MAP range
- Metabolic coronary vasodilation: adenosine, hypoxia, K+
Normal catheter data
| Site | Pressure (mmHg) | Sat (%) |
|---|---|---|
| RA | 3 (mean) | 73 (SVC 70, IVC 75) |
| RV | 30/5 | 73 |
| PA | 25/10 | 73 |
| PCWP | 6-12 | - |
| LA | 6 (mean) | 95 |
| LV | 100/5 | 95 |
| Aorta | 100/60 | 95 |
- Step-up in saturation between chambers = left-to-right shunt
- RA step-up -> ASD / anomalous pulmonary venous drainage
- RV step-up -> VSD
- PA step-up -> PDA
- Qp:Qs >1.5 = haemodynamically significant shunt
JVP waveform
- a - atrial contraction (absent in AF)
- c - tricuspid closure bulging into atrium
- x descent - atrial relaxation
- v - atrial filling against closed TV during ventricular systole
- y descent - atrial emptying as TV opens
| Abnormality | Meaning |
|---|---|
| Giant a | TS, PS, pulmonary HTN (a wave vs a closed-ish valve) |
| Cannon a | Atrium contracts against closed TV - complete heart block, VT, junctional rhythm |
| Giant v / CV | Tricuspid regurgitation |
| Steep x+y, Kussmaul | Constrictive pericarditis |
| Absent y | Tamponade |
Heart sounds
- S1 - MV+TV closure; loud in MS, soft in severe MR/long PR
- S2 - AV+PV closure; physiological splitting widens on inspiration
- Wide fixed split - ASD
- Wide split - RBBB, PS
- Reversed (paradoxical) split - LBBB, severe AS, RV pacing
- S3 - rapid early filling; normal <40yr, otherwise volume overload / HF
- S4 - atrial contraction into stiff ventricle; never in AF
Receptor physiology you titrate against
Physiology you titrate against
- Beta1 -> inc HR, contractility, AV conduction, renin
- Beta2 -> vasodilation, bronchodilation
- Alpha1 -> vasoconstriction
- M2 (vagal) -> dec SA rate, dec AV conduction (atropine reverses)
- Baroreceptor reflex (carotid sinus, aortic arch) - inc BP -> inc vagal, dec SNS
- Carotid sinus massage exploits this - transient AV block unmasks atrial activity
Pressure-volume loop
- Width = stroke volume; area = stroke work
- ESPVR slope = contractility (load-independent)
- inc afterload -> loop taller and narrower -> dec SV
- inc preload -> loop wider
- MR: no isovolumic contraction phase (leak from the start)
Anatomical remnants and relations
- Fetal-to-adult remnants - ductus arteriosus -> ligamentum arteriosum; foramen ovale -> fossa ovalis (PFO in 25%); umbilical vein -> ligamentum teres
- Aortic arch branches - brachiocephalic, left common carotid, left subclavian
- Left recurrent laryngeal loops under arch -> hoarseness in aortic aneurysm/dilated LA (Ortner)
- Pericardium - fibrous + serous; normally 15-50 mL fluid; phrenic nerve runs in it
- Coronary sinus drains into RA - the CRT LV lead route
- Bachmann bundle - interatrial conduction; disease -> P mitrale, AF
Ageing cardiovascular system
- inc arterial stiffness -> isolated systolic hypertension, wide pulse pressure
- LV wall thickening + dec compliance -> diastolic dysfunction, inc reliance on atrial kick
- -> AF is poorly tolerated in the elderly
- dec SA node cells (~10% remain by 75) -> sick sinus
- dec beta-adrenergic responsiveness -> blunted HR response to stress and to beta agonists
- dec maximal HR ~ (220 - age)
Common exam traps
- Coronary perfusion is diastolic - AS + tachycardia = subendocardial ischaemia with normal coronaries
- RV infarct is preload-dependent - nitrates cause profound hypotension
- A normal EF does not mean normal cardiac function - look at filling pressures
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