Heart Part II: Exam 2 Flashcards
Electrical Events of the Heart
The heart depolarizes and contracts without nervous system stimulation, but the rhythm can be altered by the autonomic nervous system
Coordinated heartbeat is a function of:
- presence of gap junctions
- intrinsic cardiac conduction system
- network of noncontractile (autorythmic) cells
- initiate and distribute impulses to coordinate depolarization and contraction of heart
Action Potential Initiation by pacemaker cells:
- cardiac pacemaker cells have unstable resting membrane potentials called pacemaker potentials or prepotentials
- 3 parts of action potential
1) pacemaker potential: K+ channels are closed, slow Na+ channels are open, causing the inside to become more positive
2) depolarization: Ca2+ channels are open (around -40 mV), allowing influx of Ca2+, leading to rising phase of action potential
3) Repolarization: K+ channels open, allowing efflux of K+, causing the cell to become more negative
Sequence of excitation
- cardiac pacemaker cells pass impulses, across heart in about .22 seconds
(in the following order)
1) sinoatrial node
2) atrioventricular node
3) atrioventricular bundle
4) right and left bundle branches
5) subendocardial conducting network (Purkinje fibers)
Sinoatrial node (SOE)
- pacemaker of heart in right atrial wall
- depolarizes faster than rest of myocardium
- generates impulses about 75x/min (sinus rhythm)
- rate of 100x/min tempered by extrinsic factors
- impulse spreads across atria, and to AV node
Atrioventricular (AV) Node (SOE)
- in inferior interatrial septum
- delays impulses about .1 second
- because fibers are smaller in diameter, have fewer gap junctions
- allows atrial contraction prior to ventricular contraction
- rate of 50x/min in absence of SA node input
Atrioventricular (AV) Bundle (SOE)
(bundle of His)
- in superior interventricular septum
- only electrical connection between atria and ventricles
- atria and ventricles not connected by gap junctions
Right & Left Bundle Branches (SOE)
- 2 pathways in interventricular septum
- carry impulses toward apex of heart
Subendocardial Conducting Network (Purkinje Fibers) (SOE)
- complete pathway through interventricular septum into apex and ventricular walls
- more elaborate on left side of heart
- AV bundle and subendocardial conducting network depolarize 30x/min in absence of AV node input
- ventricular contraction immediately follows from apex toward atria
- process from initiation at SA node to complete contraction takes about .22 sec
(CLINICAL) A defective SA node can cause ectopic focus: an abnormal pacemaker that takes over pacing
- if AV node takes over, it sets junctional rhythm at 40-60 beats/min
- extrasystole (premature contraction): ectopic focus of small region of heart that triggers impulse before SA node can, causing delay in next impulse
- heart has longer time to fill, so next contraction is felt as larger volumes of blood being pushed out
- can be from too much caffeine or nicotine
- to reach ventricles, impulse must pass through AV node
(CLINICAL) Defects in intrinsic conduction system may cause:
- arrhythmia: irregular heart rhythms
- uncoordinated atrial and ventricular contractions
- fibrillation: rapid, irregular contractions
- heart stops pumping blood, causing circulation to stop, may result in brain death
- treatment: a defibrillation interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations
(CLINICAL) If AV node is defective, may cause heart block
- few impulses (partial block) or no impulse (total block) reach ventricles
- ventricles beat at their own intrinsic rate
- too slow to maintain adequate circulation
- treatment: artificial pacemaker, which recouples atria and ventricles
Heartbeat modified by autonomic nervous system by cardiac centers in medulla oblongata
- cardioacceleratory center: sends signals through the sympathetic trunk to increase rate and force
- stimulates SA and AV nodes, heart muscles, and cornonary arteries
- cardioinhibitory center: parasympathetic signals by vagus nerve to decrease rate
- inhibit SA and AV nodes by vagus nerves
Action potentials of contractile cardiac muscle cells:
- contractile musle fibers make up bulk of heart and responsible for pumping actions
- different from skeletal muscle contraction; cardiac muscle action potentials have plateau
Steps involved in action potential:
1) depolarization opens fast voltage-gated Na+ channels; Na+ enters cell - positive feedback influx of Na+ cause rising phase of AP (-90 mV to +30mV)
2) slow Ca2+ channels opened due to Na+ depolarization - at +30mV, Na+ channels close, but slow Ca2+ channels stay open, prolonging depolarization
- seen as plateau
3) after about 200 ms, slow Ca2+ channels close, and voltage-gated K+ channels open - rapid efflux of K+ repolarizes cell to RMP
- Ca2+ is pumped back into SR and out of cell into extracellular space
- different from skeletal muscle contraction; cardiac muscle action potentials have plateau
Difference between contractile muscle fiber and skeletal muscle fiber contractions
- AP in skeletal lasts 1-2 ms; cardiac lasts 200 ms
- contraction in skeletal lasts 15-100 ms; cardiac contraction lasts over 200 ms
Benefit of longer action potential and contraction
- sustained contraction ensures efficient ejection of blood
- longer refractory period prevents tetanic contractions
Electrocardiography
- electrocardiograph: can detect electrical currents generated by the heart
- electrocardiogram (ECG or EKG): graphic recording of electrical activity
- composite of all action potentials at given time, not tracing a single AP
- electrodes are placed at various points on body to measure voltage differences
- 12 lead ECG is most typical
Main Features of Electrocardiography
- P wave: depolarization of SA node and atria
- QRS complex: ventricular depolarization and atrial repolarization
- T wave: ventricular repolarization
- P-R interval: beginning of atrial excitation to beginning of ventricular excitation
- S-T segment: entire ventricular myocardium depolarized
- Q-T interval: beginning of ventricular depolarization through ventricular repolarization
(CLINICAL) Changes in patterns or timing of ECG may reveal a diseased or damaged heart, or problems with heart conduction system
Problems that can be detected:
- enlarged R waves may indicated enlarged ventricles
- elevated or depressed S-T segment indicates cardiac ischemia
- prolonged Q-T interval reveals a repolarization abnormally that increases risk of ventricular arrhythmias
Normal & Abnormal ECG Tracings: Normal sinus rhythm
normal ECG trace
Normal & Abnormal ECG Tracings: Junctional rhythm
the SA node is nonfunctional; as result:
- P waves are absent
- the AV node paces the heart at 40-60 beats per min
Normal & Abnormal ECG Tracings: Second degree heart block
the AV node fails to conduct some SA node impulses
- as a result, there are more P waves than QRS waves
Normal & Abnormal ECG Tracings: Ventricular fibrillation
electrical activity is disorganized. action potentials occur randomly throughout the ventricles
- results in chaotic, grossly abnormal ECG deflections
- seen in acute heart attack and after and electrical shock
Mechanical events of the heart
- systole: period of heart contraction
- diastole: period of heart relaxation
- cardiac cycle: blood flow through heart during one complete heartbeat
- atrial systole and diastole are followed by ventricular systole and diastole
- cycle represents series of pressure and blood volume changes
- mechanical events follow electrical events seen as ECG