heart ii Flashcards
Sequence of excitiation
Cardiac pacemaker cells pass imipulses in order across heart in 220 ms
Sinoatrial node atrioventricular node atrioventricular bundle right and left bundle branches Subendocardial conducting network (Purkinje fibers)
Sinoatrial node
- pacemaker of heart in right atrial wall
- depolarizes fater than rest of myocardium
- 75 impulses/minute = sinus rhythm
- Inherent rate = 100/min, but PNS slows it down
- Impulse spreads to atria and to AV node
Atrioventricular node
- in inferior interatrial septum
- Delays impulses by 0.1 s because fibers are small and have fewer gap junctions –> allows atrial contraction to finish b4 ventricular contraction
- inherent rate of 40-50/min, but SA node speeds it up
Atrioventricular bundle
- Bundle of His
- in superior interventricular septum
- only electrical connection between atria and ventricles
- atria and ventricles not connected via gap junctions
Right and left bundle branches
- two pathways in interventricular septum
- carry impulses toward apex of heart
Subendocardial conducting network
- Purkinje fibers
- complete pathway thru interventricular septum into apex and ventricular walls
- more elaborate on left
- AV bundle and Purkinje fibers depolarize at 30/min w/o AV node
- Ventricular contraction immediately follows from apex toward atria
Arrhythmias
irregular heart rhythms
-uncoordinated atrial and ventricular contraction
Fibrillation
- rapid, irregular contractions
- if in ventricles, can’t pump blood and circulation ceases and brain dies
- fixed with defibrillation
What can a defective SA node cause?
Ectopic foucs: abnormal pacemaker –> AV node takes over and sets junctional rhythm (40-60/min)
Extrasystole: premature contraction –> ectopic focus sets high rate –> can be from too much caffeine or nicotine
Results of defective AV node
Heart block: few (partial) or no (total) impulses reach ventricles –> ventricles beat at intrinsic rate which is too slow for life
Treated with artificial pacemaker
ECG/ EKC
electrocardiograms
P wave = atrial depolarization
QRS complex = ventricular depolarization and atrial repolarization
T wave = ventricular repolarization
Cardiac cycle
Bloodflow thru heart during one complete heartbeat: atrial systole/diastole followed by ventricular systole/diastole
Systole = contraction Diastole = relaxation
caused by pressure and blood volume changes
Phases of the cardiac cycle
- Ventricular filling
- Ventricular systole
- Isovolumetric relaxation
Ventricular filling
- happens during mid to late diastole
- AV valves are open and pressure is low
- Ventricle filling = 80% of blood passively flows to ventricles
- atrial systole occurs, delivering the remaining 20%
-End diastolic volume = volume of blood in each ventricle at the end of ventricular diastole
Ventricular systole
- atria relax and ventricles begin contraction
- rising ventricular pressure and closing of AV valves
- Isovolumetric contraction phase (all valves are closed)
- Ventricular ejection phase= ventricular pressure exceeds pressure in large arteries forcing SL valves open
End systolic volume = volume of blood in ventricle after systole
Isovolumetric relaxation
- early diastole
- ventricles relax and atria are relaxed/filling
- Backflow of blood in aorta and pulmonary trunk closes SL valves (dicrotic notch = brief ries in aortic pressure)
- ventricles are totally closed off
- When atrial pressure exceeds that of ventricles, AV valves open and cycle begins again
Hear sounds
lub dup:
- Av valves close (start of systole)
- SL valves close (start of diastole)
* pause = heart relaxation
Murmurs = abnormal heart sounds
- stenosis: valve doesn’t open right
- regurgitation: valve doesn’t close right
Cardiac output
volume of blood pumped by each ventricle in a minute
CO= heart rate x stroke volume CO = (beats/min) x (volume of each beat)
Normal = 5.25 L/min at rest
Max CO is 4-5x resting CO
Athletes CO can be 35 L/min
Cardiac reserve
dif between resting and max CO
Regulation of stroke volume
SV = end diastolic volume - end systolic volume
EDV affected by length of ventricular diastole and venous pressure
ESV affected by arterial BP and force of ventricular contraction
3 main factors affecting SV
Preload
Contractility
Afterload
Preload
- degree of stretch of cardiac muscle cells before they contract
- “Frank-Starling law of heart”)
- there’s a length-tension relationship
- at rest, cardiac muscle cells are shorter than optimal length
- VENOUS RETURN is most imp factor in stretching cardiac muscle (increased by slow heartbeat and exercise)
Contractility
- contractile strength at given muscle length independant of muscle stretch and EDV
- Increased by sympathetic stimulation (more Ca influx –> more cross bridges) and positive ionotropic agents
- Decreased by negative ionotropic agents
positive vs negative ionotropic agents
Pos: thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca
Neg: acidosis, increased extracellular K, calcium channel blockers
Afterload
- pressure ventricles must overcome to eject blood
- hypertension increases afterload resulting in increased ESV and reduced SV
What regulates heart rate
positive and negative chronotropic factors
SNS: releases NE which makes pacemaker fire more rapidly and increases contractility (binds to beta1-andrenergic receptors) (lowers EDV bc of decreased fill time)
PNS: Acetylcholine hyperpolarizes pacemaker cells by opening K channels–> slower HR, but little effect on contractility
vagal tone
Heart at rest with PNS as dominant influence
Extrinsic innervation of the heart
Heartbeat modified by ANS via cardiac centers in medulla oblongata
- sympatheric increases rate and force
- Parasympathetic decreases rate
- Cardioacceleratory center = sympathetic –> affects SA, AV nodes, heart muscle, and coronary arteries
- Cardioinhibitory center = parasympathetic and inhibits SA/AV nodes via vagus nerves
Atrial (brainbridge) reflex
- sympathetic reflex initiated by increased venous return –> increased atrial filliing
- stretch of atrial walls stimulates SA node to increase HR
- also stimulates atrial stretch receptors, activating sympathetic reflexes
Chemical regulation of heart rate
Hormones
- epinephrine from adrenal medulla increases heart rate and contractility
- thyroxine increases heart rate and enhances NE and Epinephrine
Intra and extra- cellular ion concentrations (CA and K) must be maintained for normal heart function
Hypocalcemia
Hypercalcemia
Hyperkalemia
Hypokalemia
- depresses heart
- increases heart rate and contractility
- alters elec activity–> heart block and cardiac arrest
- feeble heartbeat and arrhythmias
Random factors that influence heart rate
Age: fetus has fast HR
Gender: females have faster HR
Exercise: increases HR
Body temp: increases HR with temp
Tachycardia
abnormally fast heart rate (>100/min)
-if persistent, may lead to fibrillation
Bradycardia
heart rate slower than 60/min
- may result in inadequate blood circulation in nonathletes
- desireable, though, in endurance athletes
