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Chapter 18
The Heart
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Heart Overview• Heart anatomy • Cardiac muscle cells• Heart chambers, valves and vessels• Conducting system• EKG• Cardiac cycle• Contractile and pacemaker cells• Cardiodynamics• Cardiac disorders
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Figure 20–1
Organization of the Cardiovascular System
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Heart
• Pump of cardiovascular system• Approximate size of clenched fist• Made of cardiac muscle• Beats ~100,000 times/day • Pumps 8,000L of blood/day (how much do you
have?)• Top (base): ½ inch to left of midline• Bottom (apex): 3 inches to the left of midline• Rotated slightly so that right side faces anteriorly
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Heart
Figure 20–2a
Between 2 pleural cavities in the mediastinum
• Located directly behind sternum
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Two Circuits
• Pulmonary circuit: Carries blood to and from gas exchange surfaces of lungs– Right heart
• Systemic circuit: Carries blood to and from the body– Left heart
Blood alternates between pulmonary circuit and systemic circuit (has to go through both, then starts over again)
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Pericardium • Pericardium – a double-walled sac around the
heart composed of:– A superficial fibrous pericardium– A deep two-layer serous pericardium
• Parietal pericardium (outter) lines the internal surface of the fibrous pericardium
• Visceral pericardium (inner) or epicardium lines the surface of the heart
• They are separated by the fluid-filled pericardial cavity filled with pericardial fluid
• Protects and anchors the heart• Prevents overfilling of the heart with blood• Allows for the heart to work in a relatively
friction-free environment
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Pericardium• Pericarditis: Complication of viral
infections that causes infection of the pericardium
• Risk of cardiac tamponade
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The Heart Wall
• Epicardium:– outer layer
• Myocardium:– middle layer
• Endocardium:– inner layer
Figure 20–4
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Heart Wall• Epicardium
– Visceral pericardium, covers the heart• Myocardium = muscular wall of the heart
– Concentric layers of cardiac muscle tissue– Atrial myocardium wraps around great vessels– 2 divisions of ventricular myocardium
• Superficial ventricular muscles: surround ventricles• Deep ventricular muscles: spiral around and between
ventricles
• Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue
• Endocardium – endothelial layer (tissue type?)
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Cardiac Muscle Cells
Figure 20–5
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Characteristics of Cardiac Muscle Cells
• Small with one, central nucleus• Branching interconnections between
cells• Intercalated discs:
– interconnect cardiac muscle cells– secured by desmosomes to convey force of
contraction – linked by gap junctions to propagate action
potentials
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Cardiac Cells vs. Skeletal Fibers
Table 20-1
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Figure 20–2c
General Anatomy of the Heart• Great veins and arteries at the base• Pointed tip is apex• Surrounded by pericardial sac
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Specific Heart Anatomy
Anterior View Posterior View
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4 Chambers of the Heart
• Right atrium:– collects blood from systemic circuit
• Right ventricle:– pumps blood to pulmonary circuit
• Left atrium:– collects blood from pulmonary circuit
• Left ventricle:– pumps blood to systemic circuit
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Blood Vessels
• Arteries:– carry blood away from heart
• Veins:– carry blood to heart
• Capillaries:– networks between arteries and veins– Also called exchange vessels because only in
capillaries exchange materials (dissolved gases, nutrients, wastes) between blood and tissues
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Heart Anatomy Overview• 4 chambers (RA, RV, LA, LV)• 4 valves
– 2 at entry to ventricles (from atria)– 2 at exit from ventricles (to great vessels)– None at entry to atria
• 4 major vessels at the base– Superior vena cava (entry)– Inferior vena cava (entry)– Aorta (exit)– Pulmonary trunk (exit)4 Pulmonary veins (entry) = not major vessels
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Movie
• Heart Anatomy
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Heart dividing lines
Sulci– Grooves in the heart that divide it – contain blood vessels of cardiac muscle
• Coronary sulcus– divides atria and ventricles– Closer to base (top) than apex
• Anterior and posterior interventricular sulci– separate left and right ventricles
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Chambers of the heart• Right Atrium
– receives deoxygenated blood through vena cavae
• Left Atrium– receives oxygenated blood through
pulmonary veins• Right Ventricle
– pumps blood to lungs through the pulmonary arteries
• Left Ventricle – pumps blood into the systemic circuit through
the aorta
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Atria• Small, thin-walled• Expandable outer auricles = flaps on anterior
surface• Fill with blood passively• Separated by interatrial septum• Connected to ventricles via atrioventricular
valves• Internally covered with pectinate (comb)
muscles, ridges on anterior atrial wall and inner surfaces of right auricle
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Ventricles • Right ventricle wall is
thinner; LV develops 4-6 times more pressure than left ventricle
• Right ventricle is pouch-shaped, left ventricle is round
• Similar internally, but right ventricle has moderator band
• How do volumes compare?
Figure 20–7
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Trabeculae Carneae
• Muscular ridges on internal surface of ventricles
• Includes moderator band (in RV):– ridge contains part of conducting system– coordinates contractions of cardiac muscle
cells
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Figure 20–6a
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The Heart
Valves
Figure 20–8
Four valves, all at same level in heart
Fibrous skeleton: conective tissue
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Atrioventricular (AV) Valves • Right AV valve (tricuspid): between RA and RV • Left AV valve (bicuspid or mitral): between LA
and LV• Have 3 or 2 fibrous flaps, respectively • Permit blood flow in 1 direction: atria to
ventricles • Free edges of flaps attach via chordae
tendineae to papillary muscles of ventricle• Blood pressure closes valve cusps during
ventricular contraction– muscles tense chordae tendineae, preventing valves
from swinging into atria (opening backward)
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Atrioventricular Valve Function
Figure 18.9
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Semilunar Valves
• Pulmonary valve– between RV and pulmonary trunk
• Aortic valve– between LV and aorta
• Prevent backflow from great vessels (pulmonary trunk and aorta) into ventricles
• Have no muscular support• Both have 3 crescent-shaped cusps,
support like a tripod
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Semilunar Valve Function
Figure 18.10
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Movie
• Heart valves
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Regurgitation
• Failure of valves• Causes backflow of blood into atria• Can cause heart murmur
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Valvular Heart Disease (VHD)
• Genetic, or complication of carditis (inflammation of heart muscle)
• Rheumatic fever is a common cause• Decreases valve function to point where
adequate circulation is no longer possible
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Great Vessels - Veins
• Vena Cavae deliver systemic circulation to right atrium (oxy or deoxy?)– Superior vena cava: receives blood from
head, neck, upper limbs, and chest– Inferior vena cava: receives blood from trunk,
and viscera, lower limbs• Right and left pulmonary veins return
blood from lungs (oxy or deoxy?)
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Great Vessels - Arteries
• Aorta receives blood from LV (through which valve?) (oxy or deoxy?)– Ascending aorta curve to form aortic arch
sends off three branches and turns down to become descending aorta
• Pulmonary trunk splits into left and right pulmonary arteries to send blood from (chamber) through (valve) to lungs. (oxy or deoxy?)
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Pulmonary Circuit
• To RA from superior and inferior vena cavae
• RA through open tricuspid valve to RV• Conus arteriosus (superior right ventricle)
through pulmonary valve to pulmonary trunk
• Pulmonary trunk divides into left and right pulmonary arteries, to right and left lungs, respectively
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Systemic Circuit
• Blood returns from lungs to left atrium through 2 left and 2 right pulmonary veins
• Left atrium to left ventricle through mitral valve
• Left ventricle through aortic SL valve into ascending aorta
• Ascending aorta turns (aortic arch) and becomes descending aorta
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Complete Pathway of Blood Through the Heart and Lungs
• Right atrium tricuspid valve right ventricle pulmonary semilunar valve pulmonary arteries lungs pulmonary veins left atrium bicuspid valve left ventricle aortic semilunar valve aorta systemic circulation vena cavae repeat
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Foramen Ovale
• Before birth, is an opening through interatrial septum
• Connects the 2 atria• Seals off at birth, forming fossa ovalis
• Why connect the two atria?• PFO – can cause problems in adulthood
but usually only with strenuous exercise or high altitude
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Aortic Sinuses
• Dilations at the base of ascending aorta • Prevent aortic semilunar valve cusps from
sticking to aorta when open• Origin points of right and left coronary
arteries
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Internal Heart Dividing Lines
Septa• Interatrial septum:
– separates atria • Interventricular septum:
– separates ventricles
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Coronary Circulation
Figure 18.7a
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Coronary Circulation
• Coronary arteries– Left and right– Originate at aortic sinuses– Elastic rebound forces blood through coronary
arteries only between contractions• Cardiac veins
– return blood to coronary sinus, opens into right atrium
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Coronary Arteries
• Right Coronary Artery. Supplies blood to:– right atrium, portions of both ventricles, cells of
sinoatrial (SA) and atrioventricular (AV) nodes – Branches include
• marginal arteries (surface of right ventricle)• posterior interventricular artery
• Left Coronary Artery. Supplies blood to:– left ventricle, left atrium, interventricular septum– Main branches:
• circumflex artery • anterior interventricular artery
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Arterial Anastomoses
• Interconnect anterior and posterior interventricular arteries
• Stabilize blood supply to cardiac muscle by providing collateral circulation
• e.g. RCA meets with the circumflex artery (which is a branch of the LCA)
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2 Types of Cardiac Muscle Cells
• Contractile cells:– account for 99% of heart tissue– activated by change in the membrane
potential (just like skeletal muscle cells)– produce contractions, generate force
• Conducting system: – initiate and distribute electical activity – consists of nodes and internodal pathways– controls and coordinates heartbeat
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Action Potentials in Skeletal and Cardiac Muscle
Figure 20–15
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Cardiac activity – contractile cells
• Resting Potentials – Ventricular cells -90 mV. Threshold = -75mV– Atrial cells: -80 mV
• Signal to depolarize comes from:– Conducting system– Adjacent myocytes (via gap junctions)
• Threshold is usually reached in the latter manner in a portion of membrane near intercalated discs
• Then…
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Cardiac Action Potential1. Rapid depolarization:
– voltage-regulated sodium channels (fast channels) open
2. Plateau:– At ~+30mV sodium channels close and inactivate,
but no net loss of positive ions occurs because…– voltage-regulated calcium channels (slow
channels) open and calcium ion entry roughly balances Na+ ion loss
– Holds membrane at 0 mV plateau for ~175msec3. Repolarization:
– slow calcium channels close– slow potassium channels open– rapid repolarization restores resting potential
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The Refractory Periods
• Absolute refractory period:– long – cardiac muscle cells cannot respond
• Relative refractory period:– short– response depends on degree of stimulus
• Length of cardiac action potential in ventricular cell is 250–300 msecs– 30 times longer than skeletal muscle fiber– long refractory period prevents summation and tetany
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Calcium and Contraction
• Contraction of a cardiac muscle cell is produced by an increase in calcium ion concentration around myofibrils
20% of calcium ions required for a contraction enter cell membrane through slow channels during plateau phase
This extracellular Ca2+ triggers release of calcium ion reserves from sarcoplasmic reticulum (80%)
This is why heart is so sensitive to blood calcium
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Pacemaker potentials
• At special site in the heart, cells have unstable resting potential
• These pacemaker cells depolarize spontaneously to initiate heartbeat = automaticity
• The SA and AV nodes have the greatest concentrations of autorhythmic cells
• Spontaneous electrical activity caused by special channels:– Na+ channels slowly open, allowing Na+ in– K + channels close– Ca2+ channels open to start, sustain AP
• No fast Na + channels at all!
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Pacemaker cells
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Figure 20–11
The Cardiac Cycle
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The Heartbeat
• A single contraction of the heart• Lasts about 370msec (cf. neurons?)• The entire heart contracts in series:
– first the atria– then the ventricles
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The Cardiac Cycle
• Period from the start of one heartbeat to the start of the next
• Includes:– 370msec for heart contraction– A ~400msec delay
• Begins with action potential at SA node• Transmitted through conducting system• Produces action potentials in cardiac
muscle cells (contractile cells) force
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The Conducting System
• A system of specialized cardiac muscle cells that initiates and distributes electrical impulses that stimulate contraction
• Cells display automaticity: contract automatically (without need for any external stimulation from nerves or other muscles
• SA and AV nodes are the pacesetters
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Figure 20–12
The Conducting System
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Sinoatrial (SA) Node
• In posterior wall of right atrium• Contains pacemaker cells • Connected to AV node by internodal
pathways• Begins atrial activation (Step 1)
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Atrioventricular (AV) Node
• In floor of right atrium• Receives impulse from SA node @
50msec (Step 2)• Takes ~100msec for impulse to travel
through the AV node, delays impulse (Step 3)
• Atrial contraction begins (@150 msec)• Delay limits maximum HR to ~230bpm
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Pacemaker potential• An unstable resting potential of conducting
cells in SA and AV node that gradually depolarizes toward threshold
• SA node depolarizes faster (80-100 APs/min) than AV node (40-60 per minute) and so SA fires first, establishing heart rate (hence we call these the pacemaker cells)
• Why is your resting heart rate not 80 -100bpm?
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Conducting Cells
• Interconnect SA and AV nodes • Distribute stimulus through myocardium• In the atrium, called internodal pathways• In the ventricles: AV bundle and bundle
branches
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The AV Bundle (bundle of His)
• Only electrical connection between A and V• Travels in the septum• Carries impulse to left and right bundle
branches, which conduct to Purkinje fibers at 175 msec (Step 4), and to the moderator band, which conducts to papillary muscles
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The Purkinje Fibers
• Distribute impulse through ventricles (Step 5) to contractile cells
• Trigger ventricular contraction to begin (@ 225msec) after atrial contraction is completed
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Figure 20–13
Impulse Conduction through the Heart
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Abnormal Pacemaker Function
• Bradycardia:– abnormally slow heart rate
• Tachycardia:– abnormally fast heart rate
• Ectopic Pacemaker– Abnormal cells generate high rate of action
potentials– Bypass conducting system– Disrupt ventricular contractions
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SA node generates impulse;atrial excitation begins
Impulse delayedat AV node
Impulse passes toheart apex; ventricular
excitation begins
Ventricular excitationcomplete
SA node AV node Purkinjefibers
Bundlebranches
Figure 18.17
Heart Excitation Related to ECG
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Electrocardiogram (ECG)
• Electrical events in the cardiac cycle can be recorded at the surface of the body using an electrocardiogram (ECG)
• Abnormal patterns diagnose cardiac arrhythmias, (abnormal patterns of cardiac electrical activity) due to damage or disease
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Figure 20–14b
ECG
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Features of an ECG
• P wave:– SA node and atria depolarize (begin
contraction ~25msec after P wave starts)• QRS complex:
– ventricles depolarize (begin contracting just after R peak)
• T wave:– ventricles repolarize
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Time Intervals
• P–R interval:– from start of atrial depolarization to start of
QRS complex• Q–T interval:
– from ventricular depolarization to ventricular repolarization
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EKG problems
• Large QRS – caused by hypertrophy• Small QRS – reduced heart muscle mass• Small T – low energy reserves, ischemia• Long P-R interval – damage to conducting
pathways• Long Q-T interval – conduction problems,
myocardial damage, ischemia, congenital defect
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The Cardiac Cycle
• The period between the start of one heartbeat and the beginning of the next
• Includes both contraction and relaxation• Each chamber undergoes:
– systole (contraction) pressure rises– diastole (relaxation) pressure falls
• Blood flows from high to low pressure, controlled by timing of contractions and directed by one-way valves
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Phases of the Cardiac Cycle
1. Atrial systole2. Atrial diastole3. Ventricular systole 4. Ventricular diastole
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Figure 20–16
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Cardiac Cycle and Heart Rate
• At 75 beats per minute, each cardiac cycle lasts about 800 msecs
• When heart rate increases all phases of cardiac cycle shorten, but particularly ventricular diastole (less time spent resting)
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Figure 20–17
Pressure and Volume in the Cardiac Cycle
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8 Steps in the Cardiac CycleBegin: all relaxed, ventricles 70% filled1. Atrial systole begins
– atrial contraction begins– rising pressure forces open right and left AV valves– no venous flow into atria but little backflow either
2. Atria eject blood into ventricles:– filling ventricles (topping them off)
3. Atrial systole ends (100msec): – ventricles contain maximum volume = end-diastolic
volume (EDV) which is normally about 130ml
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8 Steps in the Cardiac Cycle4. Ventricular systole begins:
– AV valves close as Pvent quickly exceeds Patria
– pressure in ventricles continues to rise– All valves closed: isovolumetric ventricular
contraction5. Ventricular ejection:
– When pressure in ventricles exceeds arterial pressure in great vessels, semilunar valves forced open
– blood flows into pulmonary and aortic trunks (isotonic contraction)
– Stroke volume (SV) = 80ml. Percent of end-diastolic volume that is ejected = ejection fraction around 60%
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8 Steps in the Cardiac Cycle6. Ventricular pressure falls near end of systole:
– backflow from vessel trunks closes semilunar valves– ventricles contain end-systolic volume (ESV), about
40% of end-diastolic volume or 50ml– Aortic elastic recoil causes dicrotic notch (double
beat). ESV = 50ml or 40%7. Ventricular diastole (starts at 370msec):
– ventricular pressure is still higher than atrial pressure– all heart valves are closed– ventricles relax (isovolumetric relaxation)– Lasts for remaining 430msec of cycle plus 100msec
of the next cycle
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8 Steps in the Cardiac Cycle
8. Falling ventricular pressure drops below atrial pressure:
– forces AV valves open– passive atrial filling (continuous during atrial
diastole)– passive ventricular filling (to 70% full)– cardiac cycle ends
• Repeat
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Movie
• Cardiac cycle• Note that:
– AV valves close early (step 3), open late (step 8)
– SL valves open and close in between (step 5 open, step 6 closed)
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Heart Failure
• Lack of adequate blood flow to peripheral tissues and organs due to inadequate cardiovascular output (usually due to ventricular damage)
• Atrial damage can be inconsequential, or problematic depending on what is damaged.
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Auscultation - Heart Sounds• “lub-dup”• S1: loud sounds produced by AV valves closing,
signifies beginning of systole• S2: loud sounds produced by semilunar valves
closing at the beginning of ventricular diastole
• Sounds are actually produced by blood changing flow patterns
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Aerobic Energy of Heart
• From mitochondrial breakdown of fatty acids and glucose (lots of mitochondria in cardiac myocytes)
• Oxygen from circulating hemoglobin• Cardiac muscles store oxygen in
myoglobin
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Important Cardiodynamics Terms
• End-diastolic volume (EDV)– Max filling after atrial systole (usually about
130ml)• End-systolic volume (ESV)
– Residual volume after ventricular systole (usually about 50ml)
• Stroke volume (SV): SV = EDV - ESV– Volume (ml) of blood ejected per beat
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Figure 20–19
Stroke Volume
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Important Cardiodynamics Terms
• Ejection fraction:– the percentage of EDV represented by SV
• Cardiac output (CO):– the volume pumped by each ventricle in 1
minute (equals how much blood gets to the tissues every minute)
– CO = HR (in bpm) x SV• What is CO for a HR of 80bpm and a SV
of 80ml/beat?
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Adjusting CO to Conditions
• Cardiac output:– Can be adjusted by changes in heart rate or
stroke volume• Stroke volume can be increased 2x:
– adjusted by changing EDV or ESV• Heart rate can be increased 2.5:
– adjusted by autonomic nervous system or hormones (How?)
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Factors Affecting Stroke Volume• Changes in EDV or ESV
– Slow heartbeat and exercise increase venous return to the heart, increasing SV
– Blood loss and extremely rapid heartbeat decrease SV• EDV affected by:
– filling time (duration of ventricular diastole)– rate of venous return (rate of blood flow during ventricular
diastole)• ESV affected by:
– Preload: degree of ventricular stretching during diastole due to amount of blood (increased by greater venous return)
– Contractility: force produced during contraction, at a given preload
– Afterload: tension the ventricle must produce to open the semilunar valve and eject blood to the great vessels
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Preload and Afterload
Figure 18.21
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EDV and Stroke Volume
• At rest:– EDV is low– myocardium stretches little (low preload)– stroke volume is low, ESV is high (lots left)
• With exercise:– EDV increases (increased venous return)– myocardium stretches more – stroke volume increases, ESV decreases
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The Frank–Starling Principle
• Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
• As EDV increases, stroke volume increases (and vice versa)
• Basically, if there is a lot of blood in the ventricles (increased venous return), stretching causes them to pump more blood out. More in more out
• Keeps the two sides of the heart in balance
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ESV and Stroke Volume• Contractility Is affected by:
– Sympathetic activation• NE released by postganglionic fibers of cardiac nerves• E and NE released by adrenal medullae• cause ventricles to contract with more force• increases ejection fraction and decreases ESV
– Parasympathetic activity • acetylcholine released by vagus nerves reduces force of
cardiac contractions– Hormones– Drugs mimic hormone actions:
• stimulate or block beta 1 receptors (beta-blockers)• affect calcium ions e.g., calcium channel blockers (negative
inotropic effects) decrease contractility
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ESV and Stroke Volume
• Afterload – As afterload increases, takes longer before
SL valves open and thus less blood will be ejected: ESV increases and stroke volume decreases
– Increased by any factor that restricts arterial blood flow (like atherosclerosis)
– Extremely high afterload can cause heart failure
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Heart Rate Control Factors
1. Autonomic nervous system: sympathetic and parasympathetic
Note: we just saw how the autonomic NS can affect contractility, which affects stroke volume
2. Circulating hormones (thyroxine, E and NE in blood all increase HR)
3. Venous return and stretch receptors
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Figure 20–21 (Navigator)
Autonomic NS Innervation
• Heart is stimulated by the sympathetic cardioacceleratory center
• Heart is inhibited by the parasympathetic cardioinhibitory center
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Autonomic Innervation
• Vagus nerves (X) carry parasympathetic preganglionic fibers to small ganglia in cardiac plexus SA and AV nodes
• Sympathetic postganglionic fibers cardiac plexus SA and AV nodes
• Autonomic tone: – dual innervation maintains resting tone by
releasing ACh and NE (which dominates?)– fine adjustments meet needs of other systems
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Cardiac reflexes
• Cardiac centers in medulla monitor:– baroreceptors (blood pressure)– chemoreceptors (arterial oxygen and carbon
dioxide levels)• Cardiac centers adjust cardiac activity via
sympathetic (NE increases HR) and parasympathetic (ACh decreases HR) activity
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Atrial (Bainbridge) Reflex
• Sympathetic reflex initiated in response to increased venous return (remember that increased venous return also caused increased stroke volume, called?)
• Stretch receptors in right atrium trigger increase in heart rate through increased sympathetic activity to “pump out the excess” blood and decrease venous pressure
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Autonomic NS Regulation of Pacemaker Cells in SA, AV Nodes
• Membrane potential of pacemaker cells is less negative than other cardiac cells (-60mv)
• Sympathetic and parasympathetic stimulation are both greatest at SA node (heart rate)
• Rate of spontaneous depolarization depends on: resting membrane potential (where you start)– ACh (para NS) opens K+ channels. Result?– NE binds to Beta adrenergic receptors, opens
sodium-calcium ion channels. Result?
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Autonomic Pacemaker
Regulation
Figure 20–22
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KEY CONCEPT• Cardiac output:
– the amount of blood pumped by the left ventricle each minute
– adjusted by the ANS in response to:• circulating hormones• changes in blood volume • alterations in venous return
• Most healthy people can increase cardiac output by 300–500% = cardiac reserve
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Summary
• Heart anatomy • Cardiac muscle cells• Heart chambers, valves and vessels• Conducting system• EKG• Cardiac cycle• Contractile and pacemaker cells• Cardiodynamics
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Heart Failure
• Inadequate cardiac output to meet demand• Due to left ventricular insufficiency• If LV not pumping enough, blood backs up in the
pulmonary circulation. Elevated pressures cause increased loss of plasma to interstitial fluid of lungs = CHF (congestive heart failure). If severe, can cause pulmonary edema (fluid fills air spaces)
• Treatment? Digoxin – positive inotrope to increase contraction force. Blood pressure reducers: diuretics, vasodilators, spirinolactone (ald antagonist)
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Cardiomyopathy
• Cardiac muscle degeneration and fibrosis• Can lead to heat failure• Hypertrophic cardiomyopathy ; thickened
left ventricular walls
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Heart Block
• Damage to conduction pathways• Often show abnormal ECG• Escape
– when condicting pathways damaged, ventricles can “escape” control of SA or AV node usually by autorhythmicity of Purkinje fibers. Ventricles continue to beat but only at 40-50bpm (which the intrinsic rate of the Purkinje fibers)
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Tachycardias
• Atrial fibrillation: – atrial depolarization occurs so fast that the
atrium appears to quiver. Ventricles cannot follow this rate
• Not usually life threatening because of escape
• Ventricular arrhythmias– Ventricular tachycardia (V-tach)– Ventricular fibrilation (V-fib) = cardiac arrest
• No rhythm. Defibrillator can restore by unifying cell activity
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Cardiac technologies• Pacemakers: treat chronic bradycardia due to
conduction deficits, etc.• External defibrillators (clear!): can rescue from
cardiac arrest• Implantable defibrillators: for people with chronic
heart conditions (often congenital)• LVAD: Left ventricular assist device
– Implantable pump in parallel with the left ventricle for those with LV insufficiency
– Boosts cardiac output by allowing some blood to bypass the left ventricle and enter the aorta at sufficient pressure
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Examining the heart
• Coronary angiogram: catheter is threaded up through femoral artery into aortic sinus. Dye released that can be seen on a series of high speed X-rays
• Echocardiogram: heart ultrasound
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Ionic imbalances
• Potassium – Hyperkalemia – decreases K+ gradient,
inhibits repolarization– Hypokalemia- increases K+ gradient, causes
hyperpolarization of resting membranes• Calcium
– Hypercalcemia: cardiac muscle cells become very excitable
– Hypocalcemia
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Coronary artery disease• Can cause coronary ischemia (reduced blood
flow) to heart• Atherosclerosis: plaques caused by fatty
deposits in vessels cause narrowing of artery• Angina pectoris: pain associated with heart
ischemia• Treatments:
– Vasodilators (nitroglycerin)– Beta blockers (propanolol)– Calcium channel blockers– Balloon angiplasty with stents– recently shown to be
no better at preventing death from a second heart attack than drugs alone
– Coronary artery bypass – leg vein grafts
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MIs• Myocardial infarction – blockage in coronary
circulation causes cells to die• Most due to CAD, usually thromboses• Blood tests for markers of anerobic metabolism,
like lactate dehydrogenase, can indicate a heat attack
• About 25% die before receiving any medical attention
• About 50% die within the first year• Women have fewer MIs but their mortality rate is
higher. Recent evidence indicates that men and women have different kinds of CAD