Download The Heart

The Heart
Dr. Rob Anderson
Rowan University
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
http://www.youtube.com/watch?v=U4A_1Igh_2w
• 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
http://www.youtube.com/watch?v=UAs6SDI7HZw
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 atrioventricular 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
Heart Diastole (1st part of cardiac
cycle)
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 to start the
next cycle
Heart Systole (2nd part of cardiac
cycle)
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.
Stroke Volume Factors
• 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
• 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
Autonomic Control of Heart Rate
• Negative Chronotropic Factors are under
parasympathetic control
– K+ channels are opened via acetylcholine
(neurotransmitter) release, which hyperpolarizes
sarcolemma
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
Heart Attack
(Myocardial Infarction)
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