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
3 phases of the cardiac cycle (following left side, start with total relaxation)
1) Ventricular Filling; mid-to-late diastole:
- pressure is low; 80% of blood flows from atria through open AV valves into ventricles from atria (SL waves closed)
- atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle (end diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole)
- depolarization spreads to ventricles (QRS wave)
- atria finish contracting and return to diastole while ventricles begin systole
2) Isovolumetric Contraction:
- atria relax, ventricles begin to contract
- rising ventricular pressure causes closing of AV valves
- isovolumetric contraction phase is split-second period when ventricles are closed (all valves closed), volume stays constant, ventricles continue to contract
- when ventricle pressure exceeds pressure in large arteries, SL valves are forced opened (pressure in aorta reaches about 120 mm Hg)
3) Isovolumetric Relaxation; Early Diastole:
- following ventricular repolarization (T wave), ventricles relax
- end systolic volume (ESV): volume of blood remaining in each ventricle after systole
- ventricular pressure drops causing backflow of blood through aorta and pulmonary trunk that triggers closing of SL valves
- ventricles are closed chambers momentarily (referred to as isovolumetric relaxation phase)
- dicrotic notch: closure of aortic valve raises aortic pressure as backflow rebounds off closed valve cusps
- atria continues to fill during ventricular systole and when atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again
- heart beats around 75x/min
- cardiac cycle lasts about .8 sec (atrial systole lasts about .1 sec, ventricular systole lasts about.3 sec, quiescent period: total heart relaxation that lasts about .4 sec)
Heart Sounds
- 2 sounds (lub-dup) associated with closing of heart valves
- first sound is closing of AV valves at beginning of ventricular systole
- second sound is closing of semilunar (SL) valves at beginning of ventricular diastole
- pause between lub-dups shows heart relaxation
- mitral valve closes before tricupspid, and aortic closes before pulmonary valve
- differences allow auscultation of each valve when stethoscope is placed in 4 different regions
(CLINICAL) Heart Murmurs
they are abnormal heart sounds heard when blood hits obstruction
- usually indicate valve problems
- incompetent (or insufficent) valve: fails to close completely, allow backflow of blood (causes swish sound as blood reguritates backward from ventricle into atria)
- senotic valve: fails to open, restricts blood flow through valve (cause high-pitch sound or clicking as blood is forced through narrow valves)
Regulation of Pumping
- cardiac output (CO): amount of blood pumped out by each ventricle in 1 min
- equals heart rate (HR) times stroke volume (SV)
- stroke volume: volume of blood pumped out by one ventricle with each beat (correlated with force of contraction)
- At rest:
CO(ml/min)=HR (75 beats/min) x SV (70 ml/beat) = 5.25 L/min - maximal CO is 4-5 times resting in nonathletic people (20-25l L/m)
- maximal CO can reach 35 L/m in trained athletes
- cardiac reserve: difference between resting and maximal CO
- CO changes (increase/decrease) if either or both SV or HR is changed
- CO is affected by factors leading to:
- regulation of stroke volume
- regulation of heart rates
Regulation of stroke volume
- math: EDV - ESV = SV
- EDV is affected by length of ventricular diastole and venous pressure (about 120 ml/beat)
- ESV is affected by arterial BP and force of ventricular contraction (about 50 ml/beat)
- normal is 120 ml - 50 ml = 70 ml/beat
- 3 factors that affect SV:
1) Preload: degree of stretch of heart muscle
- preload: degree to which cardiac muscle cells are stretched just before they contract
- changes in preload cause changes in SV ( affects EDV & Frank-Starling law of the heart: relationship between preload and SV)
- cardiac muscle exhibits a length-tension relationship (at rest, cardiac muscle cells are shorter than normal, leads to increase in contractile force)
- venous return: amount of blood returning to heart ( slow heartbeat and excersise increase venous return & increased venous return distends (stretches) ventricles and increases contraction force
2) Contractility
- contractile strength at given muslce length (independent of muscle stretch and EDV)
- increased contractility lowers ESV, caused by:
- sympathetic epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations
- positive intropic agents increase contractility (thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+)
- decreased by negative intropic agents (acidosis (excess H+), increased extracellular K+, calcium channel blockers)
3) Afterload: back pressure exerted by arterial blood
- afterload: pressure that ventricles overcome to eject blood
- back pressure from arterial blood pushing on SL valves is major pressure (aortic pressure is around 80 mm Hg; pulmonary trunk is around 10 mm Hg)
- hypertension increases afterload, results in increased ESV and reduced SV
Regulation of Heart Rate
- if SV decreases as a result of decreased blood volume of weakened heart, CO can be maintained by increasing HR and contractility
- positive chronotropic factors increase heart rate
- negative chronotropic factors decrease heart rate
- heart rate can be regulated by:
- autonomic nervous system
- chemicals
- other factors
Autonomic nervous system regulation of heart rate
- sympathetic nervous system can be activated by emotional or physical stressors
- norepinephrine is released and binds to B1-adrenergic receptors on heart, causing:
- pacemaker to fire more rapidly, increasing HR (EDV decrease because of decreased fill time)
- increased contractility (ESV decrease because of increased volume of ejected blood)
- because EDV and ESV decrease, SC remains unchanged
- parasympathetic nervous system opposes sympathetic effects
- acetylcholine hyperpolarizes pacemaker cells by opening K+ channels, which slows HR
- little to no effect on contractility
- heart at rest exhibits vagal tone
- parasympathetic is dominant influence on heart rate
- decrease rate about 25 beats/min
- cutting vagal nerve leads to HR of about 100
- when sympatheic is activated, parasympatheic is inhibited, vice-versa
- atrial (brainbridge) reflex: sympathetic reflex inhibited by increased venous return, hence increased atrial filling
- atrial walls are stretched with increased volume
- stimulates SA node, increased HR
- stimulates atrial stretch receptors that activate sympathetic reflexes
Chemical Regulation of Heart
- Hormones
- epinephrine from adrenal medulla increases HR and contractility
- thyroxine increases HR, enhances effects of norepinehrine and epinephrine
- Ions
- intra- and extracellular ion concentrations (Ca2+ & K+) must be maintained for normal heart function
- imbalances are very dangerous to heart
Other Factors that Influence Heart Rate
- Age
- fetus fastest HR; declines with age
- Gender
- females have faster HR than males
- Exercise
- increases HR
- trained athletes can have slower HR
- Body Temp
- HR increase with increased body temp
(CLINICAL) Tachycardia
it is abnormally fast heart rate (>100 beats/min)
- if persistent, may lead to fibrillation
(CLINICAL) Bradycardia
it is heart rate slower than 60 beats/min
- may result in grossly inadequate blood circulation in nonathletes
- may be desirable result of endurance training
(CLINICAL) Congestive Heart Failure (CHF)
- progressive condition, CO is so slow that blood circulation is inadequate to meet tissue needs
- reflects weakened myocardium caused by:
- coronary atherosclerosis: clogged arteries caused by fat buildup, impairs oxygen delivery to cardiac cells (heart becomes hypoxic, contracts ineffectively)
- persistent high blood pressure: aortic pressure >90 mmHg causes myocardium to exert more force
- chronic increased ESV causes myocardium hypertrophy and weakness
- multiple myocardial infaracts: heart becomes weak as contractile cells are replaced with scar tissue
- dilated cardiomyopathy (DCM): ventricles stretch and become flabby, myocardium deteriorates (drug toxicity or chronic inflammation can play a role)
- either side of heart can be affected:
- left side failure in pulomonay congestion (blood backs up in lungs)
- right side failure results in periphreal congestion (blood pools in body organs, causing edema)
- failure of either side weakens other side
- leads to decompensated, very weakened heart
- treatment: removal of fluid, drugs to reduce afterload and increase contractility
