Jeeves
Cardiac Physiology
Cardiac Action Potential
Conduction System
Contents
Cardiac Cycle
Ventricular Pressure Volume Loop
Starling’s Curve
Types of ion channels
Ion
Action
Sodium
Fast
Rapid depolarisation, phase 0
Slow
Funny current
Potassium
Inward Rectifier
Maintain RMP
Transient Outward
Phase 1 non-pacing AP
Delayed Rectifier
Phase 3 repolarisation
Calcium
L-type
Slow, longer lasting current –
many phases
T-type
Transient current for phase 4
pacing cells
Resting Membrane
Potential
• -90mV in cardiac cells
• Concentration/Electrical gradient maintained
passively and actively
Cardiac
Myocytes
Refractory Periods
1
0
4
2
3
4
Pacemaker
Cells
Conduction
System
Clinical Case - Palpitations
40M
12 hour history of palpitations following a heavy night of drinking
Now associated with shortness of breath, no chest pain
Fit and well
NKDA
Supraventricular Tachycardia
Narrow complex tachycardia 140-280 BPM
Above Bundle of His
Symptoms:
Rapid, regular palpitations
Presyncope, syncope
Chest pain (NB b/g IHD)
Dyspnoea
Anxiety
Rarely poluria (ANP)
Often tolerated, can self resolve
Supraventricular Tachycardia
Narrow complex tachycardia
Above Bundle of His
atrial/irregular atrial/regular atrioventricular
Causes
Paroxysmal
Exertion
Caffeine, alcohol
B-agonists
Sympathomimetics
(M>F)
Management
-
Vagal maneuvers
Adenosine
Calcium-channel blockers, beta blockers, amiodarone
DCCV rarely or if compromised
Catheter ablation if recurrent
Conduction sites and their arrhythmias
B
C
The Cardiac
Cycle
A
D
Ventricular Pressure/Volume Loop
Preload and Afterload
Frank-Starling Law
Clinical Case
70M presents with SOBOE, worsening over 3 months. Now walking 10
paces, limited by fatigue, swollen ankles.
Sleeping propped up 4 pillows
BG: IHD, T2DM, ^chol, HTN, ex smoker 40 pack years.
O/e raised JVP, displaced apex beat, coarse crackles bilaterally, reduced
air entry bibasally, pitting oedema to mid thigh
Heart Failure
Impaired systolic and/or diastolic failure
(ie pump failure)
Affects both preload and afterload
Reduced forward flow (reduced perfusion pressure), leading to back
pressure (oedema)
Accumulation in both lungs and tissue
Neurohormonal sequalae (RAAS, ADH, sympathetic activation)
Cardiovascular changes
Cardiac
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Decreased stroke volume & cardiac output
Increased end-diastolic pressure
Ventricular dilation or hypertrophy
Impaired filling (diastolic dysfunction)
Reduced ejection fraction (systolic dysfunction)
Vascular
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Increased systemic vascular resistance
Decresed aterial pressure
Impaired arterial pressure
Impaired organ perfusion
Decreased venous compliance
Increased venous pressure
Increased blood volume
Causes
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Myocardial infarction
Coronary artery disease
Chronic hypertension
Valve disease
Idiopathic cardiomyopathy
Viral or bacterial cardiomyopathy
Myocarditis
Pericarditis
Arrhythmias
Congenital heart disease
Diabetes
Thyroid disease
Pregnancy
Septic shock
Clinical Scenario
72F (70kg) presents with fall, # L humerus, for ORIF on trauma list
Nil other injuries
BG: CCF, HTN (160/90), T2DM, IHD (2x stents), LVEF 35%, cannot find echo report.
Resp: clear chest, good expansion
CVS: 170/90, HR 90 irregular, wwp, displaced apex beat
Neuro: GCS 15, in pain, moving all limbs CN intact
Renal: creat 65, UO 60-100ml/hr
How would you anaesthetise this patient?
What are your anaesthetic considerations and concerns?
What are your physiological goals/parameters
What would you consent this patient for?
Questions
Cardiac Cycle
The Myocardial Cell
Tissue
- Contractile
- Rhythm and conduction
Arranged as syncytium
- Atria
- Ventricles
Coordinated conduction across gap junctions
- Nernst Equation
- Goldman Constant Field Equation
Ventricular Pressure Volume Loop
Myocytes vs Pacemaker Action Potentials
• Compare shapes of Aps 4 phases
• Channels involved
• Na, K, Ca,