The Heart

Dr. Anderson - GCIT

The Heart -Function

• To pump blood around the body– Delivers nutrients and

O2 to cells– Enables blood to

radiate heat via convection/conduction

– Homogenizes blood

Heart Orientation

• Located in the mediastinum – the median cavity of the thorax – from the 2nd rib to the 5th intercostal space

Heart Anatomy - Pericardium

• Pericardium – double-walled sac that covers the heart

• 2 layers– Fibrous pericardium – protects the heart, anchors

to surrounding tissues (e.g. diaphragm)– Serous pericardium• Parietal Layer – lines internal surface of the fibrous

pericardium• Visceral layer (epicardium) – part of heart wall (covers

myocardium)

Pericardium

Pericarditis• Inflammation of the pericardium (usually due

to infection)• May prevent heart from beating efficiently in

severe cases (cardiac tamponade)

Heart Wall Anatomy

• Epicardium – thin covering of tissue (visceral layer of pericardium)

• Myocardium – the muscle tissue of the heart, interlace in a spiral pattern around heart– Interspersed with connective tissue (collagen) that

acts as an insulator to e- charge, limiting action potential to specific pathways

Endocardium

• Layer of squamous endothelium that lines the inside surface of the heart

• Very slick surface

• Continuous with tunica media in blood vessels

External Anatomy of the Heart

• 4 Chambers– 2 Atria (superior aspect)– 2 Ventricles (inferior aspect)

• Heart “Grooves”– Coronary sulcus – encircles the boundary between

atria and ventricles– Interventricular Sulcus – Cradles the Anterior

Interventricular artery and great cardiac vein

Heart Internal Anatomy

• Atria – Receiving chambers, separated by the inter-atrial septum

• Ventricles – Sending chambers, separated by the interventricular septum

Septum

Blood Flow Through the Heart – Right Atrium

• Receives blood from:– Superior Vena Cava –

collects blood from body above the level of the diaphragm

– Inferior Vena Cava – collects blood from body below the level of the diaphragm

– Coronary Sinus – collects blood from cardiac circulation

Right Ventricle

• Receives blood from right atrium and pumps it to lungs via the pulmonary artery (left and right branches)

Left Atrium

• Receives oxygenated blood from the lungs via the pulmonary veins, sends to left ventricle

Left Ventricle

• Receives blood from right atrium, pumps blood out to body cells via the aorta

• Most heavily muscled of the heart chambers– Why?

Coronary Circulation

• Coronary Arteries– Arise from base of aorta and encircle the heart in

the coronary sulcus

• Critical in supplying myocardium with O2, food and in removing wastes

Left Coronary Artery

• Left Coronary Artery – Branches into– Anterior

interventricular artery• Supplies

interventricular septum and ventricles

– Circumflex Artery• Supplies left atrium and

posterior wall of left ventricle

Right Coronary Artery

• Supplies right side of heart and branches into – Right marginal artery –

serves lateral right side of heart

– Posterior interventricular Artery – serves posterior ventricle walls

Cardiac Veins• Collects blood from myocardium and merge to

form the cardiac sinus (empties into right atrium)

• Great – anterior interventricular sulcus• Middle – Posterior interventricular sulcus• Small – Right inferior margin

Myocardial Infarction (MI) a.k.a.Heart Attack

• The myocardium needs a tremendous amount of resources (glucose, O2, etc.) to keep beating

• Coronary circulation can get blocked by damage or fatty deposits (plaque)

• If flow of blood is prevented long enough, the heart muscle itself can die, reducing or eliminating the heart’s ability to pump blood

Heart Valves• 4 Valves in the heart prevent backflow of

blood– Atrioventricular valves – located between atria

and ventricles– Semilunar valves – located between ventricles and

arteries

• Valves are NOT under muscular control, they only close due to the differences in pressure created during the cardiac cycle

Atrioventricular Valves

• Right AV valve – composed of three flaps of endocardium (tricuspid valve)

• Left AV valve – composed of two flaps of endocardium (mitral valve or bicuspid valve)

Semilunar Valves

• Aortic Valve – prevents blood flow back into left ventricle after contraction

• Pulmonary Valve - prevents blood flow back into right ventricle after contraction

Valve Connections• The flaps of tissue (endocardium) that make up

the AV valves are connected to the muscular walls of the heart

– Chordae tendineae – chords of connective tissue (collagen) that attach to the “ventricle-side” of the AV valves

– Papillary muscles – Connect chords to the ventricle wall and maintain chord tension

Valve Reinforcement

• The ventricles produce a tremendous amount of blood pressure

• What prevents the valves from “blowing out”?

Heart Murmurs

• Valves do not close properly or open fully

• Incompetent Valves – valve does not close properly, leading to blood backflow (prolapse)

• Stenosis – valve narrowing – makes the heart work harder to push blood through a smaller opening

The Heart “Pacemaker”• In order to effectively pump

blood, the heart needs to contract with a rhythm – alternating contractions between atria and ventricles

• How is this accomplished?

Autorythmic Cells (Centers)

• Initiate their own contraction of the heart muscle

• Is that it?

Autorhythmic Centers

Autorhythmic Cells in the Heart

• Sinoatrial Node – (Right atrial wall)• Atrioventricular Node (just above tricuspid

valve)• Atrioventricular Bundle (Bundle of His) (superior

part of ventricular septum)• Right and left bundle branches (in ventricular

septum)• Purkinje Fibers (from ventricular septum to

heart apex and around to ventricular walls)

Rhythms

• Pacemakers (nodes) follow a hierarchy in setting the rhythm of heart depolarization

• Each node (bundle of autorhythmic cells) has its own rhythm– E.g. - Sinoatrial node drives heart rate at ~75

bpm

Arrhythmias – Irregular Heartbeat• Pacemakers follow a hierarchy in setting the

rhythm of depolarization• Each node (bundle of autorhythmic cells) has

its own rhythm• Occasionally, this hierarchy can be upset, SA

node may be damaged or malfunctioning– AV node – only 50 bpm (junctional rhythm) – AV bundle and Purkinje fibers (30 bpm)

Fibrillation – out of phase contractions

• “Squirming bag of worms”• Out of phase contractions means that there is

no coordinated movement and thus no efficient blood flow

• Can be “reset” by shocking the heart (defibrillator) to depolarize the entire heart, causing the SA node to restore rhythm

Heart Block

• Damage to the AV node prevents SA impulses from reaching ventricles

• The ventricles then beat at their intrinsic rhythm (~30 bpm)

• Pacemakers are inserted to reestablish the connection and restore functional rhythm

Extrinsic Innervation of the Heart

• Autonomic Nervous system modifies the heartbeat set by the autorhythmic cells

• Cardioacceleratory Center – regulated by sympathetic division of the autonomic nervous system

• Cardioinhibitory Center – regulated by parasympathetic division of the autonomic nervous system

Monitoring the Heart (pg 680)• Electrocardiograph (EKG) – can monitor and

record action potentials of the heart as it beats– P wave – depolarization of the pacemaker cells (the

SA node)– QRS complex – Recording of ventricular

depolarization– T wave – Ventricular repolarization– P-Q interval – time between atrial and ventricular

excitation– S-T segment – beginning of ventricular

depolarization to the end of repolarization

The QRS Wave

Heart Sounds• Lub-dub!

• First sound in the cycle is when the atrio-ventricular valves (AVs) close– Ventricular pressure higher than atrial pressure

• Second sound occurs as the semilunar valves (SLs) close– Aortic SL valve slightly before the pulmonary SL

valve

Heart Murmurs

• May be normal in older and younger people

• Can also signify a “leaky valve” – Failure to fully close = incompetent• Swishing sound is heard

– Failure to completely open = stenotic• High pitched or gurgling sound is heard

Cardiac Cycle

• Systole – contraction period– Atrial and ventricular

• Diastole – relaxation period– Atrial and ventricular

• Important to understand!

Mechanical Events of the Heart: Ventricular Filling (Step 1)

• Blood flows passively through the atria into the ventricles via the open AV valves

• Aortic and pulmonary valves are closed

• Atria contract, pushing blood into ventricles

• Ventricles are at end of diastole, and fully relaxed to receive blood from atria

Mechanical Events of the Heart: Ventricular Systole (Step 2)

• Atria relax and ventricles begin to contract

• AV valves snap shut

• Ventricular pressure rises, overcoming the pressure in the arteries and blood flows out of the heart (SL valves are forced open)

• Atria are relaxed and filling with blood

Mechanical Events of the Heart: Isovolumetric Relaxation (Step 3)

• Ventricles relax and ventricular pressure drops

• Remaining pressure in the aorta and pulmonary artery closes the SL valves

• As pressure from blood in atria increases, AV valves open, refilling the ventricles with blood

Cardiac Output

• Cardiac Output - The amount of blood moved by the heart in one minute in each ventricle

• Stroke Volume (SV)– Amount of blood pumped out by one ventricle during each contraction (~70 ml)

• Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV)

• Let’s do an experiment!

Stroke Volume Regulation• Stroke volume is the difference in the volume left

in a ventricle at diastole (end diastolic volume or EDV) minus the blood left in a ventricle at the end of systole (end systolic volume or ESV)

• SV = EDV – ESV

• Can be affected by preload, contractility and afterload

Stroke Volume Factors• Preload – the degree to which cardiac muscle

cells are stretched just before they contract– Determined by • Maximum # of active cross-bridge attachments

between actin and myosin• The force of contraction is maximal

• In the heart this is determined by venous return – the amount of blood extending the ventricles prior to contraction.

• Because cardiac muscle is normally shorter than optimal length, stretching cells can produce a huge increase in contractive force

• Increases in ventricular volume = increase in stroke volume

• Increase in ventricular volume caused by – Exercise– Resting

• Decrease caused by – Hemorrhage– Tachycardia

Stroke Volume Factors

Stroke Volume Factors• Contractility - the contractile strength of a

muscle at a certain length– Contractility is increased by greater Ca2+ influx into

the cytoplasm from extracellular fluid and sarcoplasmic reticulum (SR)

• Increased contractility results in a lower end systolic volume (ESV)– Contractility can be increased by• Sympathetic stimulation• Norepinephrine release (hormones!)

Stroke Volume Factors

• Afterload - The arterial pressure that must be overcome for the ventricles to eject blood

• Pressure required by the heart ventricles to “open the door” of the aortic and pulmonary (semilunar) valves due to blood pressure– Pressure in aorta is about 10x the pressure in the pulmonary

artery

• Usually only a problem in people with hypertension (reduction in stroke volume)

Heart Rate Regulation• Heart rate (and thus cardiac output) is

relatively constant in healthy individuals, but can be affected by:

• Factors that increase HR and CO are positive chronotropic factors, while those that decrease are negative chronotropic factors

Autonomic Control of Heart Rate

• Positive Chronotropic factors are under sympathetic control– Norepinephrine is released– Norepinephrine binds to cardiac cell membrane

receptors (see pathway on pg. 685)– Ca2+ enters (and is removed) more rapidly into

cytoplasm to facilitate increased in heart rate

• Negative Chronotropic Factors are under parasympathetic control – K+ channels are opened via acetylcholine

(neurotransmitter) release, which hyperpolarizes sarcolemma

Autonomic Control of Heart Rate

Simultaneous Autonomic Influence• The heart is constantly under BOTH sympathetic and

parasympathetic influence, however, the parasympathetic influence (via the vagal nerve) is dominant under normal conditions

• If the vagal nerve is cut, HR immediately increases 25bpm (to ~ 100 bpm)

• However, stimulation of one arm of the autonomic nervous system depresses the other– E.g. Bainbridge reflex (increased atrial volume = increased

heart rate)

Chemical Regulation of HR

• Hormones – Epinephrine– Thyroxine– Hormones that regulate K+, Ca+ or Na+

Other factors that affect HR

• Age– Prenatal heartrate ~ 140-170 bpm

• Exercise• Fever

Fast and Slow HR

• Tachycardia – abnormally fast HR• Caused by– Drugs– Heat stress– Emotional Stress

• Bradycardia – Lower HR– Physically fit people have hypertrophy of the

ventricles– May lead to clotting and edema in sedentary people

CO Problems• Important to maintain balance between

arterial flow and venous return

• Congestive heart failure (CHF) – blood pumping is not sufficient to meet the demands of the body

Reasons for Heart Failure• Coronary Atherosclerosis– Fatty buildup (plaque) in coronary arteries that limits

flow of blood to the myocardium

• Chronic High blood Pressure– Leads to gradual weakening of the left ventricle

• Damage from Heart Attacks (Myocardial Infarction)

• Dilated Cardiomyopathy– Heart becomes overstretched – CO is impaired

Right vs. Left Ventricle Failure

• The heart has to maintain an even flow between right and left ventricles

• Right ventricle failure = pulmonary congestion– Lungs become over engorged with blood resulting

in pulmonary edema• Left ventricle failure = peripheral congestion– Blood stagnates in body organs resulting in blood

pooling and swelling

Heart Developmental Defects

• Ventricular Septal Defect - “hole in the heart”– During development, the hole in the interventricular

septum does not close, resulting in mixing of high and low O2 blood

• Coarctation “constriction” of the aorta – narrowing causes heart to work harder

• Tetrology of Fallot – – Multiple defects