CV - Electrical Activity of the Heart Flashcards
Describe the phases of an action potential in the body:
Phase 0 - Upstroke :
- rapid Na⁺ influx through voltage-gated Na⁺ channels
- membrane potential rises to +30 mV
- rapid depolarisation
Phase 1 - Initial Repolarisation:
- voltage activated
K channels (ITO) open
- K+ move out
- opening of Na+ and closure of Ca 2+ channels
Phase 2 Plateau Phase:
- balance between Ca²⁺ influx (via L-type Ca²⁺ channels) and K⁺ efflux (via delayed rectifier K⁺ channels, IKs and IKr).
- little activity through hERG
- Only Kv7.1 channels act to oppose Na and Ca
dependent depol
Phase 3 Repolarisation:
- dominated by K⁺ efflux as Ca²⁺ channels close
- Kv7.1 Hyperpol Process
- continues to hyperpol.
- Kir2.1-2.3 passes current.
- Na and Ca channels close.
- HERG channels activate due to voltage gated channels.
Phase 4 Return to RMP/ Resting:
- IK1 reestablished, RMP restored
- KIR remain active
Describe how voltage and current changes differ in different structures in the heart, relate this to the function of each structure
Sinoatrial node:
- slow depolarisation due to funny current (I_f): slow Na⁺ influx and reduced K⁺ efflux
- lacks fast Na⁺ channels; relies on Ca²⁺ influx for depolarisation
- generates rhythmic pacemaker activity
Atria:
- rapid depolarisation via fast Na⁺ channels
- shorter action potential compared to ventricles
- extra K+ current making it shorter
AV Node:
- slower conduction due to smaller cell size and fewer gap junctions
- prevents rapid ventricular activation, allowing time for atrial contraction
Ventricles:
- Prolonged plateau phase (Phase 2) due to Ca²⁺ influx, ensuring effective contraction
His-Purkinje System:
- fastest conduction (2–4 m/s) due to abundant gap junctions and Na⁺ channels.
- rapid spread ensures synchronised ventricular contraction
Explain how the pacemaker responds to acetylcholine and adrenaline
Acetylcholine - Parasympathetic Effect:
- acts on M2 muscarinic receptors in the SA node
- increases K⁺ efflux via GIRK channels, hyperpolarizing the membrane
- decreases funny current (I_f) and Ca²⁺ influx, slowing depolarisation
- Result: Reduced heart rate and negative chronotropy
Adrenaline - Sympathetic Effect:
- acts on β1-adrenergic receptors in the SA node
- increases If current and Ca²⁺ influx → Faster depolarization rate.
- enhances L-type Ca²⁺ channel activity → More robust action potentials
- Result: Increased heart rate (positive chronotropy) and force of contraction (positive inotropy)
Describe the events of the ECG trace:
P Wave:
- atrial depolarisation
- electrical activity originates from SA node and spreads through the atria
- ECG observation is positive deflection as the atrial depolarisation vector moves toward the positive electrode
PR Interval:
- conduction through the atria, atrioventricular (AV) node, His bundle, bundle branches, and Purkinje fibres
- reflects delay in AV node to allow ventricular filling
QRS Complex:
Q wave - initial downward deflection due to septal depolarisation
R wave - positive deflection from depolarisation of the ventricular free walls
S wave - downward deflection as depolarisation progresses upward through the base of the ventricles
ST segment - Plateau phase of ventricular action potentials (isoelectric period)
T Wave:
- ventricular repolarisation
- progresses from epicardium to the endocardium (reverse direction of depo)
- positive deflection in most leads of ECG
Describe the directionality of signals in different leads
Standard limb leads:
- Measure electrical activity in the frontal plane.
- Lead II is the most aligned with the heart’s normal electrical axis (~60°), showing the largest positive deflections
- Lead I measures activity horizontally (0° axis), with prominent P waves and R waves
Augmented Limb Leads (aVR, aVL, aVF):
- provide additional views in the frontal plane.
- aVR: Typically shows negative deflections as it views the heart from the right atrium, opposite the overall depolarisation vector
- aVL and aVF: Show variable deflections depending on the heart’s axis
Precordial (Chest) Leads (V1–V6):
- Measure electrical activity in the horizontal plane.
- V1–V2: Positioned over the right ventricle, often show small R waves and deep S waves due to depolarization moving away.
- V3–V4: Over the interventricular septum and apex, show a transition zone with balanced R and S waves.
- V5–V6: Positioned over the left ventricle, show large R waves due to alignment with the main depolarization vector.
Describe the intracellular voltage and current changes associated with excitation of the ventricle:
0 - Upstroke:
- Fast Na+ channels open , inward Na movement (INa)
- rapid depolarisation
- short lived
- Ca2+ channels start to activate
1 - Early repolarisation:
- Voltage activated K channels (ITO) open
- K moving out (short lived) + closure of Na channels and opening of Ca2+ channels
2 - Plateau:
- small number of Na channels remain open (depolarisation)
- Ca channels remain relatively open (depol)
- Little activity through hERG + IK1 switches off (no repol)
- Only Kv7.1 channels act to oppose Na and Ca dependent depol
3 - Late repolarisation:
- IKr and IKs dominate, driving K⁺ efflux → repolarization
- Ca²⁺ channels close
- hERG channels activate
4 - Resting:
- Na⁺/K⁺ ATPase, Na⁺/Ca²⁺ exchanger restore ionic balance
- IK1 maintains RMP
Relate events on the ECG to electrical activity within the heart, explaining directionality of signals in different leads:
Lead I (RA to LA): Leftward depolarization.
Lead II (RA to LL): Downward-rightward depolarization (largest signal).
Lead III (LA to LL): Downward-leftward depolarization.
aVR (RA): Opposite to Lead II, inverted QRS and T wave.
aVL (LA): Leftward depolarization.
aVF (LL): Downward depolarization.
Precordial Leads (V1-V6): Transition from rightward depolarization (V1, V2) to leftward depolarization (V5, V6).
Integrate electrical events of the ECG with contractile events and the cardiac cycle
P wave - atrial depolarisation, atrial contraction + late diastole
QRS Complex - ventricular depolarisation, ventricular contraction begins, isovolumetric contraction
ST segment - Ventricles fully depolarised, maximal ventricular contraction and ejection phase
T wave - ventricular repolarisation, ventricular relaxation and isovolumetric relaxation
Describe the Nernst equation:
Used to calculate equilibrium potential (Eion) for an ion
Describe the Goldman Hodgkin Equilibrium Equation:
Describes resting membrane potential (Vm) considering multiple ions
Describe the Ventricular AP and underlying currents:
Phase 0 (Depolarization): INa (Fast Na⁺ influx).
Phase 1 (Early Repolarization): Ito (Transient outward K⁺).
Phase 2 (Plateau): ICa-L (Ca²⁺ influx), IK (K⁺ efflux balance).
Phase 3 (Repolarization): IKr, IKs (Delayed rectifier K⁺).
Phase 4 (Resting Potential): IK1 (Inward rectifier K⁺).
Differences from Pacemaker Cells:
Ventricular myocytes have a stable RMP (-90 mV).
No funny current (If), unlike SA node pacemaker cells.
Depolarization initiated by adjacent myocyte, not autonomously.
Describe the re-entry of signals:
A pathological loop of electrical activity within the heart, causing arrhythmias
Requirements for re-entry:
- Unidirectional block (damaged or refractory tissue).
- Slow conduction in one limb of circuit
- Excitable tissue to allow reactivation
