CH 18 - Heart

layers of the heart

1. Pericardium
- fibrous pericardium
- parietal layer of serous pericardium
2. Epicardium
= visceral layer of serous pericardium
3. myocardium
4. endocardium
= simple squamous epithelium

pericardial cavity

- space within the space of the thoracic cavity
- space between parietal layer of serous pericardium and epicardium
- contains pericardial fluid

what is the heart lined by

lined by pericardium within the pericardial cavity

visceral pericardium

covers outer surface of heart

parietal pericardium

liners inner surface of pericardial sac

myocardium

- responsible for the pumping action of the heart
- made of cardiac muscles

cardiac muscle

- cells are joined end to end by intercalated discs
- one centrally located nucleus
- striated

special features of cardiac muscles

- desmosomes = physically join cells
- gap junctions
- many mitochondria
- lack terminal cisterns = no triads
- T tubules are wider and fewer

gap junctions function

- form channels to allow the flow of ions and spread of action potentials between cells
- allow electrical impulses to spread quickly and the heart contracts as a whole

arteries

- leaving the heart
- not always red

aorta - arteries

systemic circulation vessels

pulmonary trunk/arteries

- pulmonary (lung) circulation
- appear blue

veins

- returning to the heart
- not always blue

inferior vena cava - veins

drains the lower body

superior vena cava - veins

drains the upper body

pulmonary veins

- carries oxygenated blood to the heart
- appear red

what separates the right & left atrium and ventricle

atrium = interatrial septum
ventricle = interventricular septum

right & left atria (singular = atrium)

- collecting chambers
- receive venous blood

right & left ventricles

- pumping chambers
- eject atrial blood

tricuspid valve

- atrioventricular valve
- between right atrium and right ventricle

bicuspid valve

= Mitral valve
- atrioventricular valve
- between the left atrium and left ventricle

pulmonary valve

- semilunar valve
- between the right ventricle and the pulmonary trunk

aortic valve

- semilunar valve
- between the left ventricle and the aorta

how does heart valve open and close

open and close in response to changes in pressure between heart chambers and the flow of blood

function of heart valves

1. allow the forward flow of blood when open
2. prevent the backflow of blood when closed

what does the pressure changes depend on

1. the filling of blood
2. heart contraction

AV valve cusps

anchored to papillary muscles of the myocardium by the chordae tendinea

what happens to the AV valve cusps when the heart is relaxed

AV valves are open and blood flows into the ventricles

what happens to the AV valve cusps when the heart contracts

- blood is pumped out of the ventricles
- the AV valves close to prevent the backflow of blood into the atria (blood pushes upwards)
- papillary muscles contract and the chordae tendinea pull on the valves
- pulling on the chordae tendinea prevents the inversion of valve cusps into the atria

What is happening when the semilunar valves are closed and the AV valves are open

semilunar valves prevent blood that has entered the arteries from flowing back into the ventricles during ventricular relaxation

what is happening when the semilunar are open and the AV valves are closed

during ventricular contraction, the AV valves remain closed to prevent blood flow backward into the atria

which valves are open and closed during ventricular contraction

Av valve = closed
Semilunar valve = open

pathway of blood flow

R Atria→ R Ventricle → pulmonary artery → lungs
Lungs → pulmonary vein → L Atria → L Ventricle →aortic valve
Aortic Valve → Aortic Arch & Coronary arteries → circulation
Arterial circulation capillaries → veins
Veins → SVC & IVC & coronary sinus → R atria

cardiac cycle

- all events associated with one heart beat
- both atria contract while the ventricles relax (vice versa)

diastole

relaxation of the heart

systole

Contraction of the heart

relaxation period of cardiac cycle

- begins at the end of the cardiac cycle
- repolarization of ventricular muscle fibers
- all four chambers are in diastole (relaxed)
- atria fill with blood from vena cava
- when atrial pressure > ventricular pressure AV valves open and ventricles start filling
- 75% of ventricular filling occurs before the atria contract
- resting cardiac cycle = 0.8 seconds

atrial systole

- occurs just after the AV valves open
- firing of the SA node results in atrial depolarization = contraction
- AV valves are opened and semilunar valves are closed
- the last 25% of atrial blood enters the ventricles

ventricular systole

- as ventricular contraction occurs, blood is forced against the AV valves, forcing them shut (AV valves are one way)
- when ventricular pressure > aortic or pulmonary trunk pressure → semilunar valves open and blood is ejected
- ejection of blood continues until the relaxation phase begins again

why is the myocardium of the left ventricle thicker than that of the right ventricle

left ventricle pumps blood into the systemic circulation, which requires higher pressure to deliver blood throughout the body

coronary blood vessels

coronary circulation supplies blood to the myocardium muscles of heart

coronary arteries

- 2 originate at base if ascending aorta
- each gives rise to 2 branches =
- nourish the heart tissue, just like any other tissue, resulting in coronary venous blood being formed

conduction system of the heart

- action potentials generated by the SA node spread to the rest of the heart via an electrical conduction system (pacemaker potential)
- cardiac muscle cells are stimulated to contract as the action potential travels through this system

pacemaker cells description

- specialized cardiomyocyte cells (<1% of heart) that spontaneously and rhythmically generate action potentials that result in cardiac muscle contraction
- Unlike nerves in that they are discrete cardiomyocytes and don't have dendrites/axons.
- Unlike cardiac muscle cells in that they do not contract
- specialized myocytes (muscle cells)

what do the pacemaker cells form

- Sinoatrial (SA) Node
- Atrioventricular (AV) Node
- Bundle of His (aka AV bundle)
- R & L bundle branches
- Purkinje fibers

SA node

- located in the Right atrium
- Natural pacemaker of the heart
- parasympathetic: the cranial vagus nerve directly innervates the SA node
- Sympathetic: cardioaccelerator nerve
- AP spread to both atria simultaneously → atrial systole

steps to how pacemaker potential occur

1. pacemaker cells have voltage-gated Ca2+ (T-type) and voltage-gated Na+ (slow-acting) channels that slowly open causing depolarization to threshold
2. the resulting AP spreads throughout both atria via gap junctions = the atria contract
3. AP reaches the AV node and travels along the AV bundle to the right and left bundle branches within the interventricular septum → conducts the AP towards the apex (bottom of the heart)
4. The left and right bundle branches propagate the AP on the outer wall of the left and right ventricles
5. purkinje fibers distribute the AP upward and more deeply into the ventricular myocardium → the ventricles contract (systole) and blood is pushed upwards

where is the AV node located

in the floor/interatrial septum of the right atrium

Electrocardiogram (ECG or EKG)

a recording of electrical currents detected at the body surface resulting from the propagation of action potentials throughout the heart

what does ECG detect

- Arrhythmias/abnormality in a conducting pathway
- the cause of chest pain
- the location of heart damage (based on lack of electrical activity)
- if the heart is enlarged (electrical signal will be exaggerated)
- electrolyte imbalances (especially K+ and Ca2+)

P wave - ECG wave

atrial depolarization

QRS complex - ECG wave

ventricular depolarization

T wave - ECG wave

ventricular repolarization

flat portion between the P wave and QRS complex - ECG wave

atria are contracting and delay at AV node

when does atrial & ventricular contraction start on the ECG wave

atrial contraction = midway through the P wave
Ventricular contraction = midway through the QRS complex

excitation of cardiac muscles that overlap with skeletal muscles

- an excitatory wave excites the muscle sarcolemma (Na influx causing depolarization)
- Sarcolemma AP excites the SR to release calcium into the muscle fibres.
- Still have actin, myosin, troponin, creatine kinase, etc.

excitation of cardiac muscles - exceptions

- Resting membrane potential is -90 (not -70 as before)
- The arrival on an AP from a NEIGHBOURING cell (e.g. pacemaker, other cardiac cell) depolarizes the cardiac muscle cell to threshold, thanks to gap junctions
- Ca+2 AND Na+ influx is responsible for depolarization
- Voltage gated Ca+2 channels which cause an INFLUX of calcium in addition to the Na+ channels during the plateau phase
- SR release of Ca
- coordinate contraction to occur in the repolarization phase.

cardiac muscle AP - depolarization

- voltage-gated 'fast acting' Na+ channels open
- channels open rapidly allowing the influx of Na+ down its electrochemical gradient

cardiac muscle AP - plateau phase

- Like before, at full repolarization, Na+ channels close
- At +30mV and start of repolarization, TWO things happen at once:

1. Voltage gated Ca+2 channels open
- Ca2+ enters the cell, following its concentration gradient

2. Voltage gated K+ channels open
- cause repolarization
- efflux of K+ down its electrochemical gradient
- K+ outflow balances Ca2+ inflow
- membrane potential ~ 0 to +20 mV

cardiac muscle AP - Ca influx

- Ca influx is simultaneous with cardiac muscle contraction
- Ca2+ influx stimulates the release of Ca2+ from the SR into the sarcoplasm
- increased [Ca2+] stimulates muscle contraction

cardiac muscle AP - repolarization phase

- Ca2+ channels close
- More voltage-gated K+ channels open (like before)
- RMP is restored (-90mV) → NA/K ATPase pump

refractory period vs contraction period - cardiac muscle AP

refractory period is longer than the contraction period

what is Cardiac Output

- amount of blood pumped out by each ventricle in 1 minute
- determines the delivery of oxygen and nutrients to peripheral tissues for aerobic metabolism
- the right ventricle must pump the same volume as the left

cardiac output

Increased cardiac demand (e.g. exercise, stress) requires more blood to feed tissues. You increase cardiac output to meet the demand

CO = HEART RATE X STROKE VOLUME

- The amount of blood ejected/min from the LV = Cardiac Output (CO)
- If you have high HR, you will pump out more blood → incr CO
- If you have extra volume of blood in your LV, you will pump out more blood = stroke volume → increased CO

Summary: you can increase your CO by increasing your HR OR your stroke volume OR both!

how is cardiac output modified by SA node

1. autonomic nervous system (principle mechanism)
2. hormones (e.g. adrenaline/noradrenaline, thyroid hormone)
3. body temperature changes
- When body temperature is high, your HR increases because it has to pump the blood "farther" to facilitate vasodilation & sweating
4. emotions (fear, rage, anxiety)
- Part of the sympathetic nervous system

baroreceptors

detect changes in blood pressure in two locations
- Aortic arch & carotid arteries

chemoreceptors

detect chemical changes in the blood (pH, O2 and CO2 levels) in two different locations (aortic & carotid bodies)

proprioceptors

detect changes of limb and muscle position

limbic system

monitors emotions and anticipation of activity

hypothalamus

monitors body temperature

ANS regulation of heart rate

- The brain controls heart rate through dedicated nerves which receive and send messages
- Brain receives messages via nerves from baroreceptors in the arteries which measure the strength the blood is leaving the heart & carotids and the stretch of the heart
- In response, the brain sends a nervous message to the heart pacemakers.

Sympathetic: If the heart is not pumping blood out strongly enough, the message will tell the pacemaker to beat faster.
Parasympathetic : If the heart is pumping out blood too strongly (or there's too much blood in the heart), then the brain tells the pacemaker to slow down.

- Because the brain is the control center, neural activity can sometimes trick the outgoing motor message to the heart (e.g. heart races when hearing a sudden noise)

Stroke volume

- the volume of blood ejected from each ventricle in a single heart beat

SV = End diastolic volume - End systolic volume

- THE VENTRICLE DOES NOT COMPLETELY EMPTY with each beat! It only ejects about 65% of its volume!

End diastolic volume

how full the ventricles are when they start to contract

End systolic volume

how much blood remains in the ventricle after contraction

what influences Stroke volume

1. preload
2. afterload
3. myocardial contractility

preload

how much the ventricles "stretch" when the blood volume fills during ventricular diastole ie - BEFORE ventricular systole starts

afterload

the pressure the ventricles must overcome to eject the blood during ventricular systole
1. the resistance of semilunar valves opening
2. peripheral blood pressure (measure by diastolic bp),

myocardial contractility

the pumping power of the ventricles, based on ventricular contraction
- Contractility depends on the myocardium's ability to contract:
1. the amount of contractile proteins in muscle cells
2. levels in intracellular Ca2+
3. availability of ATP

lub-dup

- sound of heart valves closing
- first sound occurs as the AV valves close
- mitral/bicuspid valve close slightly before the tricuspid valve

what is happening when ventricular pressure rise

filling of blood in the ventricles

isovolumetric contraction

- Occurs at the beginning of systole

- AV & SL valves are closed

- Ventricular pressure increases rapidly as the ventricles contract, but no blood is ejected because the semilunar valves are still closed

isovolumetric relaxation

- Occurs at the beginning of diastole

- AV & SL valves are closed

- Ventricular pressure decreases rapidly as the ventricles relax, but no blood flows into the ventricles because the AV valves are still closed