Chapter 19 - Heart

PHYL 142 Exam 2

Position of the heart int he thoracic cavity

in the center

situated between left and right lung

base of heart is at the top

apex points downward, anteriorly, to the left

The Heart wall

3 layers from deep —> superficial

• endocardium

• myocardium

• epicardium

heart is wrapped in pericardium

between pericardium & epicardium is a cavity —> pericardial cavity

epicardium & pericardium are connected —> strength and flexibiltiy

Myocardial Contractile Cells

vast majority (~99%) of the myocardium

contract to generate pressure and pump blood

Myocardial conducting cells

control & coordinate contractile cells in the cardiac cycle

generate and relay electrical action potentials

specialized cardia muscle cells, not nerves

Cardiac Muscle

need to contract as 1 unit

intercalated disc - a gap junction that connects muscle cells

numerous mitochondria power all of the cells

if electricty starts at a specific region, due to intercalated disc with gap junctions, it moves very easily

Step 1 pathway of blood in the heart

deoxygenated blood enters the heart through

• superior vena cava

• inferior vena cava

• coronary sinus

Step 2 pathway of blood in the heart

deoxygenated blood fills the right atrium

Step 2.5 pathway of blood in the heart

Deoxygenated blood passes through the tricuspid valve

step 3 pathway of blood in the heart

deoxygenate dblood passes into the right ventricle

step 3.5 pathway of blood in the heart

blood leaves the right ventricle through the pulmonary valve

step 4 pathwya of blood in the heart

deoxygenated blood exits the heart using pulmonary arteries

step 5 pathway of blood in the heart

oxygenated blood enters the heart through pulmonary veins

Step 6 pathway of blood in the heart

Oxygenated blood fills the left atrium

Step 6.5 pathway of blood in the heart

oxygenated blood passes thorugh the Bicuspid/Mitral valve

Step 7 pathway of blood in the heart

oxygenated blood passes into the left ventricle

step 7.5 pathway of blood in the heart

blood leaves the left ventricle using the aortic valve

step 8 pathway of blood in the heart

oxygenated blood exits the heart using the Aorta

Heart valves

maintain direction of blood flow

prevent blood from going backwards

thin, flexible, and strong

Atrioventricular Valves

named for being between atrium and ventricles

prevent backflow from atrium to ventricels

close when heart contracts

• papillary msucels are pulling on chordae tendineae which closes the valves

Tricuspid valve & Bicuspid/Mitral Valve

Tricuspid Valve

valve between right atrium and ventricel

Bicuspid/Mitral Valve

valve between left atrium and ventricle

Semilunar Valves

named for looking like a crescent moon

prevent backflow from vessels to ventricles

opens when heart contracts

when blood is ejected (pressure) valves open, but as soon as the blood rushes out, the valves close

Pulmonary valve & aortic valve

Pulmonary valve

valve connecting the pulmonary artery

Aortic valve

valve connecting the aorta

The Coronary Circulation

excess amount of blood is flowing into the left and right coronary arteries

Arteries of the Heart

heart’s own blood supply

Left coronary artery

• left anterior descending artery

• circumflex artery

  • left marginal artery

Right coronary artery

• posterior descending artery

• right marginal artery

Coronary veins

Great cardiac vein —> runs with the LAD

Middle cardiac vein —> runs with the PDA

small cardiac vein —> runs with the right marginal arteyr

Posterior cardiac vein —> runs with the left marginal artery

Coronary sinus

drains the veins of the heart

• drains deoxygenated blood

Epicardial fat

between heartwall and pericardial sac

insulates and cushions heart and coronary vessels

provides energy to myocardium

excess fat is assoicated iwht obesity and heart disease

Fat distribution

mostly visceral fat = more epicardial fat

msotly subcutaneous = less epicardial fat

Ischemia

↓ blood flow to tissue 

• ↓ O2 to tissue

• ↓ Nutrients to tissue

• Buildup of metabolic waste 

• Cells die

Cardiac Ischemia effects

Heart attack

Myocardial Infarction (“heart attack”)

heart is constantly beating

heart needs constant supply of O2 and nutrients

coronary arteries carry O2 and nutrients

what if a coronary artery is blocked by clots/plaque

• cardiac ischemia —> myocardial infarction

  • cardiac muscle cells die from lack of O2 and nutrients

The “widow-maker”

Left anterior descending artery blockage is the deadliest coronary occlusion

LAD heart supply

supplies most of the left ventricle

supplies most of the interventricular septum

Ventricular Remodeling

loss of cardiomyocytes

• remaining cardiomyocytes thicken

fibroblast secrete collagen (fibrosis)

colalgen fbers patch areas where the infarct occured

new fibrotic scar does not contract

Myocardial Infarction symptoms

chest pain

dizziness, nausea, vomitting

jaw/neck/back pain

pain in arm or shoulder

shortness of breath

Referred pain

pain at a site different from where it is actually happening

common in myocardial infarctions

Sex diffenec in MI risks

higher lifetime risk in males

males develop MIs earlier

Sex difference in MI symptoms

chest pain/discomfort common in females and males

however, femlaes are more likely to experinece

• shortness of breath

• vomiting/nausea

• back or jaw pain

MI treatments

cardiac muscle regenerates, but very slowly

depends on severity and time since MI

drugs and medications: anticoagulants, betablockers

Angioplasty & stents

Coronary Artery Bypass Graft

Coronary Artery Bypass Graft (CABG)

uses blood vessels from elsewhere to deliver blood around blockages

routes oxygenated blood from aorta or major arteries

delivers blood downstream of blockage

Percutaneous Coronary Intervention (PCI)

angioplasty - uses inflatable balloons to widen blocked areas

frequently used to ufold synthetic/metal meshes (stents) to hold vessels open

Cardiac cycle

how the heart contracts and pumps blood

conduction system

what coordinates and drives cardiac muscle contraction

systole

“squeeze”

contraction

contraction —> ↑ pressure → ejection

Diastole

“downtime and dilate”

relaxation

relaxation —> ↓ pressure → filling

Cardiac Cycle steps

1. Atrial systole

2. Isovolumetric Ventricular Contraction

3. Ventricular Ejection

4. Isovolumetric Ventricular Relaxation

5. Ventricular Filling

Atrial Systole

atrium are trying to squeeze the last bit of blood into the ventricel

arrows are showing the atria contracting

the AV valves are open, most of the blood is already in the ventricles, only a sall amount are still in the atria

Atria: systole

Ventricels: diastole

AV valves: open

Semilunar valves: closed

Isovolumetric Ventricular Contraction

identified by two facets, the actual ventricels are contracting but have not got to the point of volume to actually eject out the blood

Ventricles cause AV valves to close, but no blood movement yet

Atria: diastole

Ventricles: systole

AV valves: closed

Semilunar valves: closed

Ventricular Ejection

All of the blood is ejected out, the blood pusehs itsway through the semilunar vlaves going to the pulmonary artery and aortic arch

ventricles are still in systole

Atria: diastole

Ventricles: systole

AV valves: closed

Semiluar valves: open

Isovolumetric Ventricular Relaxation

all the blood has been ejected out the ventricels, going to the body

blood is moved back into the heart —> all chambers have to be relaxed

4 vlaves are closed, blood starts to fill the atrium, but no blood in the ventricles

Atria: diastole

Ventricles: diastole

AV valves: closeed

Semilunar valves: closed

Ventricular Filling

AV valves open adn start to fill with blood

Atria are not yet squeezing

not a lot of blood in ventricles yet compared to Step 1

Atria: diastole

Ventricles: diastole

AV valves: open

Semilunar valves: closed

Electrical Conduction system

prepotential : slow influx of Na+ from a leakage channel

• once threshold is reached, voltage gated channels open

depolarization : rapid influx of Ca2+ cuases massive depolarization

repolarization: K+ channels open cuasing K+ to leave causing sharp repolarization

Prepotential

gradual slow increase in membrane potential towards threshold

pacemaker cells use prepotential to reach their threshold by themselves

Autorhythmicity

pacemaker cells can trigger their own action potentials

Contractile cell potentials

triggered by pacemaker cell action potential

influx of Na+ cuases voltage gated ion channesl to open

Na+ channel closes and slow Ca2+ channel opens

Slow Ca2+ channesl close cuasing repolarization, then K channels close

• causes a refractory period: cannot contract a second time to prevent hyper contraction

Electrocardiogram

measures electricity coursing through the heart

reads from bottom to top

most view lead 2 - runs between right arm and left leg

P wave

depolarization of the atriums

atrial systole

QRS complex

depolarization of the ventricles

repolarization of the atrium also happens at this point

Ventricular systole

T wave

repolarization of the ventricels

ventricular diastole

normal resting heart rate range

60-100 BPM

tachycardia

heart rate above 100 BPM

Bradycardia

heartrate below 60 BPM

Reading EKGs

can give detailed information on conductive system and heart functioning

depending of lead amount you can pinpoint cardiac injury

basic reading is important to understand heart rate and rhythmic patterning

Heart Rate from EKG tracing

Large box = 0.2 sec

Small box = 0.04 sec

Measure the amount of time per heartbeat from top to top

Normal Sinus Rhythm

normal human heart rhythm with normal EKG tracings

Sinus Rhythm

normal depolarization of the Sinus (SA) node and atria

Atrial Fibrillation

more waves between QRS complexes

atrium is contracting erractically

results in higher chance of stroke due to blood pooling and clotting in atrium

Ventricular Tachycardia

abnormal and frequent QRS waves

heart rate increases starting with ventricels

results in less blood filling ventricles and less blood being pumped out leading to weakness and lightheadedness

Ventricular Fibrillation

electrical current is entirely abnormal

ventricels contract erratically and frequently leading to no functionality

results in no blood being pumped out (cardiac arrest) and has symptoms similar to myocardial infarction

Cardiac Arrest

sudden stop in heart function

deadly; surviavl depends on the scale of second/minutes

golden time: 90 minutes to intervention

Defibrillation

Automated External Defibrillator (AED)

delivers ~3000 volt charges

depolarizes entire heart

• stops arrhythmia

• allows SA node to restore rhythm

ineffective on hearts that are completly stopped

Cardiac Output

a measurement of the effectiveness of the heart

often this is measured by determining the volume of blood pumped out by a single ventricle in a minute

measured in volume/time (mL/min)

Calculating Cardiac Output

multiply your heart rate and stroke volume together

CO = HR x SV

Stroke volume

volume of blood pumped out in a single stroke of a ventricel

SV = EDV - ESV

End-diastolic volume (EDV)

volume of blood in the ventricles before ventricular systole

aslo defined as volume of blood in ventricles after atrial systole

aslo called preload

End-systolic volume (ESV)

volume of blood in ventricels after ventricular systole

Ejection Fraction

(blood pumped out in a beat / chamber volume when fully filled) %

EF = SV/EDV x 100%

Venous Return

amount of blood returnign to the heart at the right atrium

Preload

amount of blood in the ventricels before systole

Ex. as the balloon fills with water it expands, the more it fills the heavier it gets so more strength is needed ot hold it

• higher SV is needed to move larger voluems of blood

higher preload causes the body to increase stroke volume

much like more strength is used when weights are heavier

Afterload

force required to push blood into the vessels during systole

arteries naturally resist the flow of blood going into the vessels

if the arteries are clogged, it is harder to pump blood into them

clogged arteries lead to higher blood pressure

if more force is required then less blood moves thorugh vessels

higher = lower stroke volume (decreases stroke volume)

Contracility

inotropic agents - factors that affects stroke volume by changing strength of contraction

• positive inotrpic agents - increase force of contraction

• negative inotropic agents - decrease force of contraction

higher prelaod caused by body to increase stroke volume

stronger afterload decreases stroke volume

increasing contractility increases stroke volume by ejecting more blood