Physio - Cardio Electrophysiology Flashcards
What is the difference btw Chronotrophy, Dromotropy, Inotropy?
Chronotropy:
- Effects on the heart rate
- SA node
Dromotropy:
- Effects on AP conduction velocity
- AV node
Inotropy:
- Contractility
- Purkinje Fibers
Cardiac Action Potentials
Basics:
- SA & AV nodal cells = 1 type of AP
- slow response type AP
- lacks a stable RMP
- Atrial myocytes/ventricular myocytes/Purkinje fibers = other type of AP
- fast response type AP
- includes plateau phase + long refractry period
Explain the Action Potentials of ventricles, atria and the Purkinje system
Phase 0 = Upstroke, depolarization
-
Na+ influx (via voltage gates Na channels)
- Inside becomes more (+)
- Threshold open = -65mV
- Slope = upstroke = velocity of movement
Phase 1 = Initial repolarization
- Fast Na+ channels close
-
Outwark K+ current (via K+ channels)
- Ito = transient outward current
Phase 2 = Plateau Phase
-
Inward Ca2+ current (slow)
- mostly L-type Ca channels
- long lasting
- excitation-contraction coupling
- inward Ca2+ –> triggers release of Ca2+ from SR –> muscle contraction
-
Blocked by:
- verapamil, nifedipine, diltiazem
-
Increased by:
- catecholamines via b-adrenergic receptors (rise of cAMP)
- Outward K+ current (Ikr, I ks)
- Ca2+ in and K+ out balance each other
- creates plateau
Phase 3 = Repolarization
- Slow Ca channels close
-
Outward K+ currents (Ikr, Ik1)
- inside gets more (-)
Phase 4 = RMP
- Na+-K+ ATPase activity
- always there in excitable cells
- Na+-Ca2+ exchanger
- Ca2+ ATPase activity
- both help Ca removal from cytoplasm
- K+ current (IK1)
- Functionally similar to K+ leak channels
What are the Implications of lower dV/dT?
Lower conduction speed (dromotropy)
- size of inward current = reduced
- less current spreads to adjacent sites to depolarize
Weaker force of contraction (inotropy)
- less time for calcium inward current during phase 2
- smaller plateau
Explain the Cardiac Action Potential of Conducting Nodal Cells
Basics:
- 3 phases
- present in SA & AV node only
Phase 0 = Depolarization
- Inward Ca++
- T-type (first)
- L-type (second)
Phase 3 = Repolarization
- Outward K+ current
Phase 4 = Spontaneous Depolarization
- In SA node, no stable RMP
- Max diastolic potential = ~65mV
- Pacemaker potential
- induce by the balance of 3 varying currents:
-
if = funny current
- inward Na++ –> hyperpolarization current
- activated at -50mV or below
-
ica = inward Ca++ current
- activated at -55mV
-
ik = outward K++ current
- opposing if & ica
- diminishes throughout Phase 4
-
if = funny current
- induce by the balance of 3 varying currents:
- Activity of Na-K-ATPase, Na-Ca exchanger, Ca-ATPase
Note:
- Phase 4 determines heart beat rhythem
What are Latent Pacemakers?
Basics:
- Normal pacemaker cells = SA node
- sinus rhythm w/ auto-rhythmicity of 70bpm
When things go wrong…
-
Abnormal (latent) pacemaker cells:
- AV node (50 bpm)
- Bundle of His
- Purkinje Fibers (30 bpm)
- automaticity = suppressed by stimulating them at a higher frew than intrinsic rhythm
- Can take over if SA node is messed up
Complete heart block:
-
AV node = messed up
- Atria = SA node (70 bpm)
- Ventricles = Purkinje fibers (30 bpm)
- much slower than normal (AV node 50 bpm)
Premature Ventricular Contraction (PVC):
- Ectopic focus = faster than SA node
- abnormal pacemaker
- ie: Purkinje fibers = 140 bpm
What is the Conduction Velocity at different parts of the heart?
SA node/Artial muscle = ~1 m/sec
AV node = ~0.01 - 0.05 m/sec (SLOWEST)
Bundle of His = ~2 m/sec
Purkinje fibers = ~ 4 m/sec (FASTEST)
What are the different Excitability and Refractory Periods?
Absolute refractory period (ARP)
- time second AP absolutely cannot be initiated
- In ventricle 0.25-0.3 sec, in atrium 0.15 sec
Effective refractory period (ERP)
- time normally no AP occurs
- slightly longer than absolute refractory period
Relative refractory period (RRP)
- time second AP is inhibited, but not impossible
- In ventricle 0.05 sec, in atrium 0.03 sec
Supranormal period (SNP)
- time where s_lightly smaller than normal stimulus elicits response_
- Typically, the amplitude of the new AP is reduced
Vulnernable period
- Time during serious arrythmias are likely if a stimulus occurs
- late ERP & SNP
Explain the Autonomic Control of the Heart
Sympathetic:
- Preganglia:
- Spinal cord
- lower 1-2 cervical to upper 5-6 thoracic segments
- C6-7 - T1-6
- Efferent nerve:
- paravertebral chains
- Postganglia:
- in the stellate & middle cervical ganglia
- Effector organs:
- SA node, AV node, Atrial/Ventricular myocardial cells, blood vessels
Parasympathetic:
- Preganglia:
- dorsal motor nucleus of vagus
- nucleus ambiguus in medulla oblongata
- Efferent nerve:
- Vagus nerves
- Postganglia:
- epicardial surface
- walls of heart near SA node & AV node
- Effector organs:
- SA/AV nodes & only few blood vessels
Autonomic Receptors of the Cardiovascular System
Sympathetic:
- NE = beta1 = Heart
- NE = alpha1 + beta2 = skeletal muscle
Parasympathetic:
- Ach = M2 = Heart
- Ach = M3 = skeletal muscle
- indirect vasodilation due to NO
What are the Autonomic Control Centers?
Hypothalamus, Thalamus, Cerebral cortex
- Cardiac response to:
- environmental temp changes
- exercise
- excitement, anxiety, and other emotional states
Sympathetic - Medulla Oblongata:
- Rostral Ventrolateral nucleus (RVL)
- Distinct accelerator & augmentor cells
- Provide tonic excitatory activity to heart & blood vessels
Parasympathetic - Medulla Oblongata:
- Nucleus vagus & Nucleus ambiguus
- triggered by reflexes & respiratory center
Effect of Parasympathetic on the Heart
Basics:
- Muscarinic acetylcholine receptors (M2 type)
- slows down HR
- Blocked by atropine
- Beat by beat control
Effects:
-
(-) chronotropic effects on SA node
- Effects Phase 4
- Increase in K+ permeability (Ik-ach)
- Decrease in Na+ permeability (If)
- Effects Phase 4
-
(-) dromotropic effects on AV conduction velocity
- Effects Phase 0
- decrease in Ica
- increase in Ik-ach
- Effects Phase 0
- Only minor inotropic effects on myocardial cell
- mainly on atria
- Some fibers end on sympathetic fibers
- downregulate their activity
Note:
- Effects appear & disappear quickly due to high efficiency of acetylcholinesterase
What is the Effect of Sympathetic on the Heart?
Basics:
- beta1-adrenergic receptors
- (+) Agonist: Isoproterenol
- speed up HR
- (-) Antagonist: Beta blockers e.g. propranolol
- slow down HR
Effects:
- NE has (+) chronotropic effects
- Effects Phase 4
- Increase in Na+ permeability (If)
- Enhances ventricular contractility
- Enhances “atrial kick”
- NE has (+) dromotropic & inotropy
- Increase in Ica
Note:
- Effect of stimulation decays slowly
- does NOT allow beat by beat regulation