Cardiac Muscle, Conduction, Cycle

Myogenic

self-initiated by cardiac muscle

cardiomyocyte

cardiac muscle cell

intercalated disc

A complex of fascia adherens, gap junctions, and desmosomes that join two cardiac muscle cells end to end

In cardiac muscle, the sarcoplasmic reticulum

features footlike sacs associated with the T tubules.

T tubules allow

calcium ions from the extracellular fluid to enter during cell excitation, which is crucial for muscle contraction

cardiomyocytes are joined end to end by

Intercalated discs

Intercalated discs function is

interdigitating folds, which increase the surface area for cell contact, enhancing mechanical and electrical connectivity.

Three distinctive features of intercalated discs

interdigitating folds - increase surface area intercellular contact

mechanical junctions - Fascia adherens and desmosomes tightly join

electrical junctions - gap junctions allow ion flow, electrically stimulate neighbor cell to contract in unison

Fibrosis

scarring, only way cardiac muscle can repair

Cardiac muscle depends on

aerobic respiration and to make ATP

Mitral and aortic valves are closed when pulmonary and tricuspid are open

pulmonary and tricuspid are open

cardiac conduction system

internal pacemaker and nervelike conduction pathways through myocardium, it generates electrical signals

Cardiac conduction system generates electrical signals in following order

SA node - in right atrium, initiates heartbeat and rate

AV node - near AV valve, acts as electrical gateway to ventricles

AV bundle - path signals leave AV node, branches into left and right bundle

The subendocardial or Purkinje fibers, - ensuring that signals reach cardiomyocytes of ventricles, more network in left than right

after limits reached cardiomyocytes continue the transmission through gap junctions

sinus rhythm

normal heartbeat triggered by SA node

Any spontaneous firing other than SA node is called

Ectopic focus

A slower heartbeat of 40 to 50 beats per minute is known as

Nodal ryhthm governed by the AV node when the SA node is impaired.

If neither SA or AV node is working

ectopic foci can fire at 20-40 bpm, which is insufficient for brain blood flow, pacemaker needed

Why does SA nodes fire spontaneously at regular intervals?

It lacks a stable resting membrane potential. Starting around -60 mV, the membrane potential gradually depolarizes because slow inflow of Na

pacemaker potential

gradual depolarization in the SA node cells

When the potential reaches -40 mV, calcium channels open, leading to depolarization and triggering a heartbeat.

When an SA node fires

it excites other components, serving as pacemaker, fires at .08 sec creating 75 BPM

Firing of SA nodes excites arterial cardiomyocytes and stimulates

two atria to contract simultaneously, signal reaches AV node

The signal in AV node is slower because

its thinner and fewer gap junctions

Av node has

slower conduction speed of electrical impulses and gives delay time for ventricles to fill with blood before contraction.

Ventricular contraction would not be synchronized and pumping of ventricles would be compromised if

ventricular myocardium was only route for conduction

SA Node Threshold

Threshold = −40 mV

Cardiocytes have stable resting potential

-90 MV depolarize when stimulated

In cardiac muscle calcium keeps cells depolarized atleast

250 ms longer than compared to 1 to 2 ms in skeletal muscle refractory period
– Prevents summation and tetanus

Calcium drives

muscle contraction

EKG or ECG

electrodes placed on skin to detect electrical currents of heart

P wave is produced when

signal from SA node spreads through Atria and depolarizes

Atrial systole begins 100 ms after SA signal

QRS complex

produced when signal from AV spreads representing the depolarization of the ventricles. Greatest electrical current

Complex shape of spike due to different thickness and
shape of the two ventricles

ST segment

ventricular systole
– Plateau in myocardial action potential

T wave

– Ventricular repolarization and relaxation

Arrhythmia

any deviation from regular Sa node rhythm

Ventricular fibrillation is a severe

arrhythmia where chaotic electrical signals causes uncoordinated heart contractions

caused by electrical signals reaching different regions at
widely different times

Heart Block

No QRS follows P wave due to failure of signal in ventricles, bundle brach block, damage to AV node causes TOTAL HEART BLOCK

Atrial flutter/fibrillation

Atria fail to stimulate ventricles, ectopic foci in atria

Atria beat 200 to 400 times per minute

Premature ventricular contractions (

stimulus, stress, lack of sleep. Inverted QRS

cardiac cycle

rhythmic sequence of heartbeats

Cardiac Cycle Phases

atrial systole, ventricular systole, and diastole.

Pressure changes govern

operation of heart valves, entry of blood and expulsion

Cardiac cycle is

one complete contraction and relaxation of all
four chambers of the heart

Atrial systole occurs while

ventricles are in diastole relaxed

Atrial diastole occurs while

ventricles in systole

Quiescent period

all four chambers relaxed at same time

how is heart sound lub produced

It's caused by the closure of the tricuspid and mitral valves, which separate the atria from the ventricles, turbulence and movement in blood contribute

how is dub sound produced?

closure of semilunar valves, softer sound, turbulance movement of blood

valve disorders

Heart murmur -

Valvular insufficiency - Mitral valve prolapse

Valvular stenosis - cusps are stiffened

Interchamber Disorders

ASD - atrial septal defect
VSD - abnormal opening between ventricles
can happen in newborns if dont close, gaps should close or blood can intermix, O2 rich and poor

Foramen Ovale

in fetal development connects right and left atria, problem if doesnt close

should become fosa ovalis

during systole the heart has how many ml in it?

around 60ml, never fully empty

during diastole how many ml are in heart?

120 ml

cardiac output

the amount ejected by ventricle in 1 minute

Cardiac output =

heart rate x stroke volume

RBC leaving the left ventricle will arrive back

in about 1 minute

Vigorous exercise increases

cardiac output up to 35L/min

Pulse

surge of pressure produced by each heart beat

Tachycardia

resting heart rate above 100 bpm

Bradycardia

heart rate of less than 60 bpm

Positive chronotropic agents

factors that raise the heart rate

Negative chronotropic agents

factors that lower heart rate

Stroke Volume

The other factor in cardiac output, besides heart rate, is
stroke volume (SV

Frank–Starling law of the heart:

Stroke volume is proportional to venous return,more stretch harder contract

Three variables govern stroke volume

Preload
Contractility
Afterload

Preload

the amount of tension in ventricular myocardium immediately before it begins to contract

stretch before the squeeze

Exercise increases

venous return and stretches myocardium

Contractility

refers to how hard the myocardium contracts for a given preload

Afterload

the blood pressure in the aorta and
pulmonary trunk immediately distal to the semilunar
valves

Opposes the opening of these valves
– Limits stroke volume

Ductus arteriosus in fetus becomes

ligamentum arteriosum

Blood flow to heart during ventricular contraction is

slowed

during angina attack

Myocardium shifts to anaerobic fermentation, producing lactic
acid and thus stimulating pain

Myocardial infarction

Interruption of blood supply to the heart  death of cardiac
cells within minutes

half of deaths in US

Coronary Veins drains directly into

right atrium and right
ventricle—by way of the thebesian veins

Cardiac Muscle does not

fatigue and is involuntary

Heart is Adaptable to organic fuel

Fatty acids (60%); glucose (35%); ketones, lactic acid, and amino
acids (5%

Phases of the Cardiac Cycle

Ventricular filling
• Isovolumetric contraction
• Ventricular ejection
• Isovolumetric relaxation

Ventricular filling

Begins when the ventricular pressure exceeds arterial
pressure

T wave occurs late in this phase

Pressure peaks in left ventricle at about 120 mm

55% of what ventricle holds gets

ejected

Isovolumetric contraction

Ventricles depolarize and begin to contract, all valves close, first heart sound occurs

Ventricular ejection

Begins when the ventricular pressure exceeds arterial
pressure

T wave occurs late in this phase

If left ventricle pumps less blood than the right, the
blood pressure

backs up into the lungs and causes
pulmonary edema

If the right ventricle pumps less blood than
the left

pressure backs up in the systemic circulation and causes systemic
edema

Ectopic foci

spontaneous firing, hypoxia, electrolyte
imbalance, or caffeine, nicotine, and other drug

If SA node is damaged The AV will beat

40-50bpm

voltage gated sodium and calcium open causing depolarization, K channels open and leave cell to cause

repolarization

Arrhythmia

any abnormal cardiac rate or rhythm

Cardiac centers in

medulla receive input and integrate it in
the “decision” to speed or slow the heart

Baroreceptors

Pressure sensors in aorta and internal carotid arteries

Chemoreceptors

In aortic arch, carotid arteries, and medulla oblongata
– Sensitive to blood pH
– Acidosis  raise heart rate