ANHS308 Ex. Phys. Chapter 4 The heart moving O2 and Blood

Heart pumps this oxygenated blood from

lungs to exercising muscles

In 490 BC greek messenger Pheidippides ran 26 miles and delivered a message about the war and he

collapsed and died

Congenital defects increase

risk of sudden death

most common cause of sudden death is

hypertrophic (enlargement) cardiomyopathy (disease of heart muscle)

Pericardium

encases the heart

The heart has four chambers

left and right atrium, left and right ventricle

the septum separates the left and right side of the heart preventing

blood from mixing between 2 sides

Atrioventricular valve (AV)

ensures forward blood flow

Tricuspid valve right side has

three flaps

Bicuspid valve (left side)

has two flaps

As blood in atria pushes down on valves, valves open downward.

Blood flows into ventricles

When ventricles contract, pressure increases.

Blood pushes against valves forcing them closed.

Upper and lower chambers

alternately contract and relax

each round of contraction and relaxation is called a

cardiac cycle

diastole

relaxed state of ventricles

systole

contraction of ventricles

Mechanical Events of Cardiac Cycle

1. both atria and ventricles are relaxed, venous blood is passing through atria and filling ventricles passively

2. Atria contract to finish filling ventricles

3. ventricles begin contraction forcing AV valves closed while ventricular pressure is still insufficient to force open semilunar valves

4. rising ventricular pressure forces open semilunar valves, ejecting blood

5. Ventricles relax while blood in the aorta and pulmonary artery flows backward forcing semilunar valves shut

regular bp

less than 120/ less than 80

elevated bp

120-129/less than 80

stage 1 hypertensive

130-139/80-89

stage 2 hypertensive

140 or greater/ 90 or greater

isovolumetric contraction

ventricular volumes remain constant for a brief period; the heart is contracting but no change in volume

if it is an effective pump than contraction of all fibers must be

contracted in a synchronized rhythm

Action Potential in Cardiac Fibers Phase 0: Depolarization:

Na+ channels open allowing influx of Na depolarizes to 20 mV

Action Potential in Cardiac Fibers Phase 1: Initial Repolarization:

closure of Na channels and opening of K channels. efflux of K quickly repolarizes membrane potential

Action Potential in Cardiac Fibers Phase 2: Plateau:

occurs when the slow Ca channels open and fast K channels close, influx of Ca and efflux of K counterbalance so there is little change

Action Potential in Cardiac Fibers Phase 3: Rapid repolarization:

Ca channels close although slow K channels remain open

Action Potential in Cardiac Fibers Phase 4: Resting Membrane Potential:

occurs when all the ion channels have closed and membrane potential returns to -90 mV

Autorhythmic cells

pacemaker of the heart, control the heart rate

Heart cells are capable of depolarizing spontaneously because of

specialized leaky Na channels that allow slow influx of Na

what catecholamines are responsible for speeding of heart rate during exercise

epinephrine and norepinephrine

depolarization begins at

SA node (pacemaker)

Path

SA node, AV node (vent. filling), AV Bundle, Bundle Fibers, Purnje Fibers

when depolarization reaches av node it

delays to allow ventricular filling

cardiac muscle fibers are in what arrangement

spiral arrangement

the arrangement of the conduction pathway and spiral muscle fibers allow

blood to travel upward to top of ventricles where aorta and pulmonary artery are located

autonomic nerves control

heart rate by influencing rate of depolarization

Vagus nerves release

acetylcholine causing channels to leak K

sympathetic neurons release norepinephrine

causes increased Na and CA leakage

EKG or ECG allows us to see

electrical activity in the heart

what are the three major waves an electrocardiogram

P wave indicates depolarization of atria, QRS complex is a recording of ventricular depolarization, T wave reflects repolarization of ventricles

Normal resting rate

normal: 60-80 bpm athletes: 40 bpm

heart is mostly branching cardiac muscle

myocardium

intercalated disks

connect cardiac fibers made of desmosomes

plasma membrane surrounds

each cardiac fiber

In cardiac fibers influx of Ca opens ryanodine receptors this results in

cytosolic Ca concentration calcium induced calcium release

Ca Influx must be returned to maintain homeostasis

Sarco-endoplasmic reticulum Ca-ATPase (SERCA) halts Ca signal and allows relaxation, requires 1 atp, returning 2 CA

Cardiac Output (Q)

rate at which blood is pumped from the heart

equation for cardiac output

Q= HR x Stroke Volume SV

Stroke volume SV

volume of blood ejected from heart during contraction

Stroke volume equation

SV=End diastolic volume (EDV) - End systolic volume (ESV)

End diastolic volume (EDV)

volume of blood in ventricles at end of diastole

End systolic Volume (ESV)

volume of blood remaining at end of systole

ejection fraction

percent of blood ejected from ventricles during exercise Ef+ SV/EDV x 100

Frank Starling law

stroke volume must match venous return, stroke volume will always adjust to venous return

strength of graded contractions are influenced by

ventricular cardiac fiber stretch, cardiac fiber length, influx of Ca

liver and kidneys receive

cardiac output filters it