PT15 LEC: Cardiac Muscle Contraction / Cardiac Cycle

myocardial autorhythmic cells

- generate electrical impulses without input
- internal pacemaker
- unstable RMP

ion used by autorhythmic cells for rising phase of AP

calcium

myocardial contractile cells

contract in response to depolarization

2 characteristics of the intrinsic conduction system of the heart

rhythmicity and conduction

Rhythmicity

generate rhythmic impulses of 75beats/min. to cause rhythmical contraction of the heart muscle, & the heart beats as a coordinated unit

Conduction

impulses conducted rapidly throughout the heart in only one direction, from atria to the ventricles

pacemaker potentials

results primarily from a slow inflow of Na+ without a compensating outflow of K+

flow of pacemaker potential

- when threshold voltage is reached, voltage-gated calcium channels open
- Ca2+ influx from ECF causes depolarization
- K+ channels open and K+ leaves the cell
- electrical voltage in cytosol increasingly negative
- repolarization
- K+ channels close

differences between skeletal vs cardiac muscle contraction

- means of stimulation
- organ vs motor unit contraction
- length of absolute refractory period
- action potential

means of stimulation in cardiac vs skeletal

- Cardiac muscle cells are self-excitable & can initiate their own depolarization
- Skeletal cells must be independently stimulated

organ vs motor unit contraction in cardiac vs skeletal

- recruitment principle of skeletal muscles
- cardiac muscles contract as a single unit or not at all

length of absolute refractory period in cardiac vs skeletal

cardiac takes longer because the contraction must be sustained until ventricles are empty and blood is expelled from chambers

action potentials in cardiac vs skeletal

- AP of SM is caused by fast Na+ channels
- AP in CM is caused by fast Na+ channels and slow Ca2+ channels

unique characteristic of cardiac AP

Decreased permeability (5X) of the cardiac muscle membrane for K+ ions immediately after the onset of the AP

flow of AP in cardiac muscle cell

- voltage- gated Na+ channels open
- Na+ inflow depolarizes membrane and causes positive feedback cycle opening more Na+ channels
- Na+ channels close when cell depolarizes
- Ca2+ entering thru slow Ca2+ prolongs depolarization (PLATEAU)
- slight K+ leakage causing plateau to fall
- Ca2+ channels close and Ca2+ goes out of the cell
- K+ channels open and rapid outflow of K+ returns RMP

excitation-contraction coupling in cardiac muscles

- AP passes over sarcolemma
- spreads along T tubules
- T tubule AP spreads to SR tubules
- release of Ca2+ from SR into sarcoplasm
- Ca2+ diffuses into myofibrils
- chemical rxns that promote sliding filament mechanism
- contraction

structural differences of cardiac and skeletal SR & T Tubules

- less developed SR of cardiac
- T tubules of cardiac muscle have greater diameter (5X)

rigor complex

formed when the chemical energy derived from ATP hydrolysis has been expended/used to perform mechanical work

strength of cardiac muscle contraction depends on

- concentration of Ca2+ in ECF
- quantity of Ca2+ ions in T tubules

metabolism of cardiac muscle cells

depends almost exclusively on aerobic respiration to make ATP

main fuel source of cardiac muscle at rest

fatty acids

cardiac cycle

refers to all events of one complete heartbeat, associated with blood flow through the heart during one complete contraction & relaxation of all four heart chambers

systole

contraction

diastole

relaxation

principles of blood pressure & blood flow

- blood flowing thru heart is controlled by pressure changes
- blood flows along pressure gradient
- pressure & resistance govern fluid flow
- pressure changes govern the operation of heart valves and entry & expulsion of blood

pressure

impels fluid to move

resistance

opposes flow of fluid

Sphygmomanometer

used to measure blood pressure

Boyle's law

Given a constant temperature, pressure is inversely proportional to the volume of a container (greater volume = lower pressure)

principles of pressure & flow related to heart

- Ventricles relax as it expands = internal pressure within ventricles fall
- Blood flows into ventricles from atria through open AV valve
- AV valve closes
- Ventricles contract = internal pressure increase
- SL valves open
- Blood flows into arteries leaving the heart

phases of cardiac cyle

- ventricular filling or atrial diastole
- atrial systole
- isovolumetric contraction phase
- ventricular systole
- isovolumetric relaxation phase

Atrial Diastole / Ventricular filling

- Ventricles expands as they relaxed, the pressure in the heart is low as blood enters atria & passively flows into ventricles from the pulmonary & systemic circulation
- SL valves closed and AV valves open

atrial systole

Ventricles remain in diastole & as the atria contract, atrial systole occurs forcing blood remaining in their chambers into the ventricles to complete ventricular filling

isovolumetric contraction phase

- atrial systole end & ventricular systole begins
- ventricles contract simultaneously and AV valves close

ventricular systole

- ventricular ejection phase
- SL valves open and blood rushes into pulmonary artery & aorta
- atria relaxed & atrial chambers are passively filling w/ blood

isovolumetric relaxation

- ventricles relax
- blood flows back from arteries and force SL valves to close

dicrotic notch

- brief rise in aortic pressure caused by brief backflow of blood rebounding off the SL valves
- occurs during isovolumetric relaxation phase

heart sounds

distinct sounds heard during each cardiac cycle

lubb (S1)

AV valves close; beginning of systole

dupp (S2)

SL valves close; beginning of ventricular diastole

pause

quiescent period; period of diastole for both atrium and ventricles

S3

heard in children and adolescents but rare in adults >30

triple rhythm or gallop

abnormal 3rd heart sound in adults with CHF or cardiomegaly

heart murmurs

abnormal or unusual heart sounds

incompetent heart valve

valve does not close tightly; swishing sound

valvular stenosis

narrowed heart valves