Chapter 20 - The Heart

Location and Size of Heart Located in thoracic

cavity in mediastinum

About same size as closed fist base is the wider

anterior portion apex is tip or point

Pericardium: Heart Covering

Fibrous Pericardium Rests on and is

attached to diaphragm

Tough, inelastic sac of fibrous connective tissue

Continuous with blood vessels entering, leaving heart at base

Protects, anchors heart, prevents overstretching

Parietal (Outer) Serous Pericardium

Thin layer adhered to inside of fibrous pericardium

Secretes serous (watery) lubricating fluid

Pericardial Cavity Contains pericardial

(serous) fluid lubricates surface of

parietal and visceral serous pericardium

decreases friction

Visceral (Inner) Serous Pericardium

Adheres to Heart Forms epicardium Secretes watery

(serous) lubricating fluid

Pericardium

Pericarditisinflammation of pericardiumpainful, rubbing of tissuescan damage myocardium

Cardiac tamponadea buildup of pericardial fluid bleeding into pericardial cavitymay result in cardiac failure

Homeostatic Imbalances

Heart wall - Three layers Epicardium (outer)

visceral layer of pericardium

thin, transparent smooth, slippery

Myocardium (middle) - cardiac muscle

Endocardium (inner) endothelium over

connective tissue smooth lining for inside of

heart, valves continuous w/

endothelium of vessels

Chambers of the Heart

External landmarks coronary sulcus

separates atria/ventricles

anterior/posterior interventricular sulcus separates right/left ventricles

Internally - 4 compartments R/L atrium w/

auricles R/L ventricles

Interatrial septum separates atria

Interventricular septum separates ventricles

Ventricular thickness varies depending on function

Right – pumps to lungs (pulmonary circulation) Left – pumps to the body (systemic circulation)

Valves of the Heart Function to prevent

backflow of blood into/through heart

Open, close in response to changes in pressure in heart

Four valves

Valve Structure

Dense connective tissue covered by endocardium

AV valves chordae

tendineae - thin fibrous cords

connect valves to papillary muscles

Valve Function

Opening and closing a passive process when pressure low,

valves open, flow occurs

with ventricular contraction, pressure increases

papillary muscles contract, prevent valves from pushing back into atria

Separate atria, ventricles tricuspid valve -

right bicuspid (mitral)

valve - left

Atrioventricular (AV) valves

In arteries that exit heart to prevent blood from re-entering heart pulmonary semilunar

valves aortic semilunar valves

Pathologies incompetent – do not

close stenosis – stiff and do

not close

Semilunar valves

Blood Flow Through Heart Right atrium (RA) -

receives deoxygenated blood from three sources superior vena cava

(SVC) inferior vena cava

(IVC) coronary sinus

Right ventricle (RV) receives blood from RA pumps to lungs

Pulmonary trunk - from RV branches into pulmonary arteries (PA)

Pulmonary arteries from heart to lungs for

gas exchange right and left branches for

each lung blood gives up CO2 and

picks up O2 Pulmonary veins (PV) -

oxygenated blood from lungs to heart

Pulmonary Circulation

Left atria receives blood from

PV pumps to left ventricle

Left ventricle (LV) sends blood to body

via ascending aorta aortic arch

curls over heart three branches off of it

that feed superior portion of body

thoracic aorta abdominal aorta

Myocardial Blood Supply Myocardium has own

blood supply coronary vessels diffusion into tissue

impossible due to thickness

much overlap of vessels and anastomoses (art-art connections)

Heart can survive on 10-15% of normal arterial blood flow

Arteries left coronary artery divides

into anterior interventricular artery and circumflex arteries

anterior interventricular artery supplies walls of both ventricles and septum

circumflex supplies LV and LA

right coronary artery small branches to RA, divides into posterior interventricular and marginal artery

posterior interventricular supplies walls of both ventricles

marginal branch supplies RV

Coronary veins blood into muscle then

drains into coronary sinus

supplied by great cardiac vein (drains anterior of heart) and middle cardiac vein (drains posterior)

Coronary Circulation Pathologies

Faulty coronary circulation due to: blood clots fatty atherosclerotic

plaques smooth muscle

spasms in coronary arteries

Problems ischemia hypoxia

Pathologies (cont.)Angina pectoris - "strangled chest"

pain w/ myocardial ischemia - referred pain!tight/squeezing sensation in chestlabored breathing, weakness, dizziness,

perspiration, foreboding

often during exertion - climbing stairs, etc

silent myocardial ischemia

Pathologies (cont.) Myocardial infarction

(MI) - heart attack thrombus/embolus in

coronary artery tissue distal to

blockage dies if survival, muscle

replaced by scar tissue

Long term results size of infarct, position pumping efficiency? conduction efficiency,

heart rhythm

Pathologies (cont.)

Treatment clot-dissolving agents angioplasty

Reperfusion damage re-establishing blood flow may damage tissue

oxygen free radicals - electrically charged molecules w/ unpaired electron

radicals attack proteins (enzymes), neurotransmitters, nucleic acids, plasma membranes

further damage to previously undamaged tissue or already damaged tissue

Myocardium (Cardiac Muscle)

Cells are involuntary, striated, branched Fibers connected to others by intercalated discs

gap junctions allow AP's to pass from fiber to fiber desmosomes

“spot welds” prevent cardiac fibers from separating

Intercalated Discs

Normal Action Potential

Cardiac Muscle Action Potential

Long absolute refractory period

Pacemaker potentials Leaky membranes Spontaneously

depolarize

Conduction System and Pacemakers

Autorhythmic cells cardiac cells repeatedly fire

spontaneous action potentials

autorhythmic cells: the conduction system

pacemakers SA node

origin of cardiac excitation fires 60-100/min

AV node conduction system

AV bundle of His R and L bundle branches Purkinje fibers

Conduction System and Pacemakers

Arrhythmias irregular rhythm abnormal atrial and ventricular contractions

Fibrillation rapid, out of phase contractions squirming bag of worms

Ectopic pacemakers (ectopic focus) abnormal pacemaker controlling the heart SA node damage, caffeine, nicotine, electrolyte

imbalances, hypoxia, toxic reactions to drugs Heart block

AV node damage - severity determines outcome

may slow conduction or block it

Conduction System and Pacemakers

SA node damage (MI)AV node can run things (40-50 bts/min)if AV node out AV bundle, bundle

branch/conduction fibers fire at 20-40 bts/min

Artificial pacemakers - can be activity dependent

Atrial,Ventricular Excitation Timing

SA node to AV node - small delayabout 0.05 sec from SA to AV, 0.1 sec to

get through AV node conduction slowsallows atria time to finish contraction and

better fill the ventricles

once to AV bundle, conduction rapid to rest of ventricle

Extrinsic Control of Heart Rate Basic rhythm of heart set

by pacemaker system Central control from

medulla sympathetic input parasympathetic input

Electrocardiogram Electrical activity

of the heart P wave QRS complex T wave

Cardiac Cycle

Connection between electrical and mechanical events

Systole Diastole Isovolumetric

contraction Isovolumetric

relaxation

Quiz!!!!! 1. Superior vena

cava 2. Right atrium 3. Tricuspid valve 4. Right ventricle 5. Papillary muscle 6. Aorta (aortic

arch) 7. Pulmonary trunk 8. Left atrium 9. Bicuspid valve 10. Interventricular

septum

Cardiac OutputAmount of blood pumped by each

ventricle in 1 minuteCO = HR x SV

HRheart rate70 bts/min

SVstroke volume70 ml/min

CO 5 L/min (70 bts x 70 ml)

Regulation of Stroke VolumeSV = EDV – ESV

EDV End Diastolic Volumevolume of blood in the heart after it fills

(following diastole)120 ml

ESVEnd Systolic Volumevolume of blood in the heart after contraction

(after systole)50 ml

each beat ejects about 60% of blood in ventricle

Most important factors in regulating SV: preload, contractility and afterload

Preload degree of stretch of cardiac muscle cells before

contraction determined by EDV

Contractility increase in contractile strength separate from

stretch and EDV determined by changes in Ca++ availability

Afterload pressure that must be overcome for ventricles

to eject blood from heart determined by TPR

Preload Muscle mechanics

length-tension relationship? fiber length determines # of cross bridges cross bridge # determines force

increase/decrease fiber length increase/decrease force generation

Cardiac muscle how is cardiac fiber length

determined/regulated? fiber length determined by filling of heart – EDV factors that effect EDV (anything that effects

blood return to heart) increase/decrease filling increase/decrease SV

Preload – Frank-Starling Law of the Heart length tension relationship of heart length = EDV tension = SV

ContractilityIncrease in contractile strength

separate from stretch and EDVDo not change fiber length but

increase contraction force?what determines force?how can we change this if we don’t

change length?

Increase the number of cross bridges by increasing amount of Ca++ inside the cell – positive inotrope

Sympathetic nervous system opens channels to allow Ca++ to enter the cell

Increase force of contraction without changing fiber length

AfterloadFlow = P/RIf blood pressure is high (TPR),

difficult for heart to eject bloodMore blood remains in ventricle with

each beatHeart has to work harder to eject

blood, change the length/tension of the heart

Regulation of Heart Rate Intrinsic regulators

pacemakers Bainbridge effect

increase in EDV increases HR filling stretches SA node increasing depolarization and

HR

Extrinsic regulators autonomic nervous system

sympathetic parasympathetic

hormones – epinephrine, thyroxine ions – Na+, K+, Ca++

body temperature age gender exercise