Ch 17 - Part B Flashcards
defects in intrinsic conduction system may cause:
arrhythmias, fibrillation
Arrhythmias
irregular heart rhythms; uncoordinated atrial and ventricular contractions
Fibrillation
rapid, irregular contractions; heart becomes useless for pumping blood, causing circulation to cease
ectopic focus
an abnormal pacemaker that takes over pacing; caused by defective SA node
Extrasystole (premature contraction)
ectopic focus of small region of heart that triggers impulse before SA node can, causing delay in next impulse; can be from excessive caffeine or nicotine
heart block
caused y defective AV node; few impulses or no impulses reach ventricles which is too slow to maintain adequate circulation
heart block treatment
artificial pacemaker, which recouples atria and ventricles
Heartbeat is modified via…
cardiac centers in medulla oblongata
cardioacceleratory center
sends signals thorugh sympathetic trunk to increase both rate and force
cardioinhibitory center
parasympathetic signals via vagus nerve to decrese rate
contractile muscle fibers
make up bulk of heart muscle are are responsible for pumping action
How are contractile muscle fibers different from skeletal muscle?
in skeletal muscle contraction, cardiac muscle action potentials have plateau
electrocardiograph
can detect electrical current generated by heart
electrocardiogarm (ECG or EKG)
a graphic reccording of electrical activity; composite of all action potential at a given time, not a tracing of a single one
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
systole
period of heart contraction
diastole
period of heart relaxation
cardiac cycle
blood flow through heart during one complete heartbeat
One Cardiac cycle
atrial systole and diastole are followed by ventricular systole and diastole
Isovolumetric contraction
split-second period when ventricles are completely closed, volume remains constant, ventricles continure to contract
Isovolumetric relaxation: early diastole
following ventricular repolarization (T wave), ventricles relax
End systolic volume (ESV)
volume of blood remaining in each ventricle after systole
dicrotic notch
closure of aortic valve raises aortic pressure as backflow rebounds off closed valve cusps
Quiescent period
total heart relaxation that lasts about 0.4 seconds
First heart sound
closing of AV valves at the beginning of ventricular systole
second heart sound
closing of SL valves at the beginning of ventricular diastole
heart murmurs
abnormal heart sounds heard when blood hits obstructions
incompetent valve
fails to close completely, allowing backflow of blood; causes swishing sound as blood regurgitates backward from ventricle into atria
stenotic valve
fails to open completely, restricting blood flow through valve; causes high-pitched sound or clocking as blood is forced through narrow valve
cardiac output
amount of blood pumped out by each ventricle in 1 minute; equals heart rate times stroke volume
stroke volume
volume of blood pumped out by one ventricle with each beat
cardiac reserve
difference between resting and maximal CO
Three main factors that affect SV
preload, contractility, afterload
preload
degree to which cardiac muscle cells are stretched just before they contract
venous return
amount of blood returning to heart; most important factor in preload
Contractility
contractile strength at given muscle length
negative intropic agens
decrease contractility; acidosis, increased extracellular K+, calcium channel blockers
positive inotropic agents
increase contractility; thyroxine, glucagon, epinoephrine
afterload
pressure that ventricles must overcome to eject blood
Atrial (Bainbridge) reflex
sympathetic reflex initiated by increased venous return, hence increased atrial filling
Hormones heart regulation
epinephrine from adrenal medulla increases heart rate and contractility; thyroxine increases heart rate which enhances effects of norepinephrine and epinephrine
Ions heart regulation
intra and extracellular ion concentrations (CA2+ & K+) must be maintained for normal heart function
Hypocalcemia
depresses heart
Hypercalcemia
increases HR and contractility
Hyperkalemia
alters electrical activity, which can lead to heart block and cardiac arrest
Hypokalemia
results in feeble heartbeat; arrhythmias
Tachycardia
abnormally fast heart rate (>100 bpm)
Bradycardia
heart rate slower than 60 bpm
Congestive heart failure (CHF)
progressive condition; CO is so low that blood circulation is inadequate to meet tissue needs
Coronary atherosclerosis
clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells
multiple myocardial infarcts
heart becomes weak as contractile cells are replaced with scar tissue
Dilated cardimyopathy (DCM)
ventricles stretch and become flabby, and myocardium deteriorates
pulmonary congestion
left-sided failure; blood backs up in lungs
peripheral congestion
right-sided failture; blood pools in body organs, causing edema