Cardiovascular Physiology Part A Flashcards
Heart
- Dual pump with valves
2. muscle cells connected by gap junctions
Conduction System
- non-contractile cardiac muscle cells
- initiate and distribute impulses through heart
- produce APs spontaneously (no stimulus) BUT at different rates
Parts of Conduction System
- Sinoatrial (SA) node
- Atrioventricular (AV) node
- Bundle of His (AV) bundle
- Purkinje Fibers
Sinoatrial node
- where is it?
- rate
- In RA
- rate= 100 APs/min
- produces APs faster than other areas. Therefore, is the pacemaker
Atrioventricular node
- where is it?
- rate
- In RA
2. rate= 50 APs/min
Bundle of His
- where is it?
- rate
- Originate at AV node
- ONLY route for electrical activity to go from atria to ventricles + bundle branches
- 30 APs/min
Purkinje Fibers
- where is it?
- rate
- terminal fibers- stimulate contraction of ventricular myocardium
- 30 APs/min
Damaged Conduction System
-what is an artificial pacemaker?
- next fastest part becomes pacemaker
ex) damaged SA, AV node takes over (atria may not contract + ventricles contract at AV speed= 50 beats/mon - Artificial pacemakers- stimulate if SA or AV nodes damaged
APs of SA & AV nodes
- cells= non-contractile autorythmic cardiac muscle cells
- threshold = -40mV
- NO RMP
APs of SA & AV nodes:
Phases of Pacemaker Activity
- Pacemaker Potential
- AP Depolarization
- AP Repolarization
- Na+ channels open at -60mV
APs of SA & AV nodes:
Pacemaker potential
- Low K+ permeability (K+ voltage gates closed)
2. Slow inward leak of Na+ (Na+ voltage gates open) which cause slow depot. to threshold (-40mV)
APs of SA & AV nodes:
AP Depolarization
- at threshold -> AP
- Ca2+ voltage gates open and move in
- Na+ voltage gates close at threshold- not involved in AP
- Ca2+ voltage gates close at peak
APs of SA & AV nodes:
AP Repolarization
- K+ voltage gates open at peak, K+ out
2. K+ gates close below threshold
APs of SA & AV nodes:
Na+ channels open at ____
-60mV
Starts pacemaker potential again (continuous cycle)
APs in Ventricular Myocardium
- cells= contractile
- purkinje fiber AP -> ventricular myocardial AP (spread cell to cell by gap junction)
- RMP= -90mV
APs in Ventricular Myocardium:
Phases
- Depolarization
- Plateau
- Repolarization
APs in Ventricular Myocardium:
Depolarization
- Na+ voltage gates open (fast) = same gate as neutron, skeletal muscle
- MP to +30mV
APs in Ventricular Myocardium:
Plateau
- Na+ channels close and inactivate (slight drop in MP)
2. Ca2+ slow voltage gates are open (Ca2+ IN maintains depol.)
APs in Ventricular Myocardium:
Repolarization
- Ca2+ channels close
2. K+ voltage gated channels open (increased K+ OUT -> MP decrease to RMP
APs in Ventricular Myocardium:
Absolute Refractory Period
Long- Na+ channels inactivated until MP is close to -70mV
APs in Ventricular Myocardium:
Excitation-Contraction Coupling in Myocardial Cells
- open voltage-gated Ca2+ channels of AP = small ⇑ cytosolic Ca2+ (from ECF) ⇒ not enough to trigger contraction BUT…
- opens chemically-gated Ca2+ channels on SR ⇒ ⇑⇑ cytosolic Ca2+ ⇒ binds to troponin, etc, etc ⇒ leads to contraction
- Contraction
- sliding filaments
- begins a few msec after AP begins
- duration of AP =~250 msec and duration of twitch = ~ 300 msec
- ∴ contraction almost over when AP ends
- Result = NO summation ∴ NO tetanus - get alternation of contraction/relaxation
