CARDIOVASCULAR SYSTEM: The Heart- Chapter 20
Organization of Cardiovascular System:
Heart – the “pump”
pulmonary circuit:
systemic circuit:
Blood Vessels: conduits
Arteries
Veins
Capillaries
Blood – “transporter & exchanger”
Anatomy of the Heart
Size, Location, and Orientation of heart
•mediastinum
•size of
•apex inferior & anterior
• base:
• sits to left side from 2nd rib – 5th intercostal space
• esophagus posterior
Coverings of the Heart
Pericardium (pericardial sac): double layered sac
Surrounds & stabilizes heart
Consists of two layers:
1.) fibrous pericardium 2.) serous 1. parietal layer -
2. visceral layer or epicardium
pericardial cavity: surrounds heart
space between parietal & visceral layers
pericardial fluid:
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pericarditis:
cardiac tamponade
Heart Wall - 3 layers
1. epicardium: visceral pericardium
2. myocardium: thickest layer
Cardiac muscle
3. endocardium: endothelium
Superficial Anatomy of the Heart:
contains 4 chambers 2-atria 2-ventricles
right atrium: collects deoxygenated blood from
right ventricle: pumps deoxygenated blood to
left atrium: collects oxygenated blood from
left ventricle: pumps oxygenated blood to
atria: superior
ventricles: inferior
• contain papillary muscles and trabeculae carneae
interventricular septum
coronary sulcus: separates atria from ventricles
Cardiac Muscle: see comparison of Cardiac & Skeletal Muscle (page 686, table 20-1)
Cardiac Muscle:
•striated
•cells are smaller than skeletal muscle cells
•cardiac cells are short
•each fiber contains 1 or 2 nuclei
• many large mitochondria
•cardiac cells interconnect with dark staining junctions called intercalated discs
Cells also anchored with desmosomes
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•functional synctium
•sarcomeres have Z lines, A & I bands
•heart relies on aerobic metabolism
If deprived of oxygen can switch and work anaerobically but lactic acid increases H+ within muscle cell
which interferes with ability to move Ca++ and closes gap junctions.
Decreases ability to generate action potentials = MI
•cardiac muscle much more adaptable
•danger of inadequate blood supply
BLOOD FLOW THROUGH THE HEART:
Right Atrium receives all deoxygenated blood
from:
superior vena cava
inferior vena cava
coronary sinus:
contains foramen ovale
after birth closes: fossa ovalis
Right Ventricle
Pulmonary Trunk:
Right & Left Pulmonary Arteries
Lungs:
Pulmonary Veins (4) Right & Left
Left Atrium
Left Ventricle
Thickest myocardium
Aorta:
blood to
1. coronary arteries
2. aortic arch: 3 main arteries:
1.) brachiocephalic
2.) L common carotid
3.) L subclavian
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3. thoracic(descending)
4. abdominal aorta
Valves of the Heart (4): prevent backflow of blood
Atrioventricular (AV) Valves
•Valves located between the
•Shut to prevent blood from flowing back
•Consists of flaps of endocardium called cusps
•Flaps (cusps) anchored to papillary muscles in ventricles (myocardium) via chordae tendineae
• When the ventricles contract, the papillary muscles contract to hold the chordae tendinae which anchor
the cusps and prevents them from inverting into atria.
Right Atrioventricular Valve has 3 cusps: Tricuspid
Left Atrioventricular Valve has 2 cusps: Bicuspid or Mitral
Semilunar Valves:
•Prevent blood from flowing back
into ventricles
•Pulmonary semilunar valve
Pulmonic Valve)
•Aortic semilunar valve
(Aortic Valve)
•mechanism: flaps or cusps open and close
in response to ventricular pressure
Ventricles contract:
Ventricles relax:
Aortic sinuses: at base of aortic valve- contain blood for coronary arteries
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Coronary Blood Vessels:
Left Coronary Artery (LCA)
•Circumflex (lateral)
Right Coronary Artery (RCA): supplies
•Marginal (inferior)
•Posterior interventricular
•L.A.D. (anterior)
(left anterior descending) or
anterior interventricular
anastomoses: interconnections
(join anterior/posterior interventricular
arteries)
Great Cardiac Vein: drains
deoxygenated blood from cardiac
veins into coronary sinus
atherosclerosis: fatty deposits or
plaque – narrows blood vessel
termed Coronary Artery Disease (CAD)
(see pgs. 694)
3 general steps:
1.) Damage to endothelium (smoking, hypertension, diabetes)
2.) Inflammatory response
Inflammatory cells (WBCs, macrophages release cytokines which damage heart muscle)
C-reactive protein (CRP or hs-CRP) can be measured via blood test
3.) LDL deposited at site: narrows vessel & forms thrombus
Often first symptom is angina pectoris due to temporary ischemia
ischemia: (coronary ischemia)
infarct = dead tissue
myocardial infarction: damaged heart cells can cause ventricular fibrillation or cardiac arrest
s/s?
note: dying cardiac cells rupture and release proteins in to blood
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Cardiac Physiology:
Heartbeat: single contraction of the heart
Heart contracts in series: first the atria (together) then ventricles (together)
Two types of cells: 1.) Autorhythmic cells: excitable cells
EKG show their activity
2.) Contractile cells: 99% of cardiac muscle cells
Conduction System of the Heart – Autorhythmic or pacemaker cells
Found in SA & AV nodes, Intermodal Pathways, AV bundle (bundle of His), Bundle Branches &
Purkinje Fibers
●very excitable – depolarize on their
own
● have unstable resting potential &
slowly drift toward threshold (termed
pacemaker potential)
● connected via gap junctions
● rely on Ca2+ influx at threshold
rather than Na+
Sequence of Excitation:
Cells in SA node depolarize fastest and set HR – known as pacemaker cells
Form action potentials at 80-100 per minute
SA node is innervated by parasympathetic nervous system
1.) SA NODE: pacemaker
•located in the wall of
• causes sinus rhythm
• sets HR at 60 - 80 bpm
(parasympathetic dominant)
receives info from vagus &
cardiac nerves which act as
brakes & accelerator
Impulse spreads via gap junctions
& Internodal pathways to
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2.) AV NODE
•impulse delayed
3.) Bundle of His or Atrioventricular Bundle
4.) Right & Left Bundle Branches
5.) Purkinje Fibers:
myocardium
Papillary muscles
ECG or EKG: Electrocardiogram – will be discussed in lab
Cardiac Contractile Cells:
Receive action potential from conducting system cells
Action potential necessary to allow Ca2+ to enter myocardial cells from SR
(depolarization travels down T tubules to SR to release Ca2+ into sarcoplasm)
(Remember need Ca++ to bind to troponin to weaken the T-T complex also need Ca++ for plateau
phase of muscle contraction)
However Cardiac Muscle:
RMP = -90mv, threshold -75mv & Na gates close at- +30mv
Cardiac muscle more dependant on blood Ca2+
EC Ca2+ also triggers release of Ca2+ from SR
at threshold voltage-regulated Na+ channels open – Na+ enters
depolarization also opens slow Ca2+ channels for plateau stage
Importance of the plateau stage:
Repolarization – K+ channels open and K+ rush out of cell
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Fundamental Differences between Skeletal & Cardiac Muscle:
1.) All or None Law:
2.) Means of Stimulation:
Autorhythmicity:
3.) Length of the absolute refractory period:
Cardiac Physiology
Cardiac Cycle: “mechanical follows electrical”
All mechanical events that occur during one heartbeat.
(.7 to .8 seconds)
both atria contract/relax together:
push blood into ventricles
both ventricles contract/relax together
push blood into pulmonary trunk & aorta
Key Terms:
Systole:
Diastole:
Blood follows pressure gradients
Note pressures are higher on left side of heart but volume of blood is the same on both sides.
Atrial systole:
Occurs after atria depolarize
Atria contract
Atrial pressure > ventricular pressure
Blood flows through AV valves into ventricles
ventricular filling:
EDV: end-diastolic volume
Ventricular Systole:
Occurs after ventricles depolarize
ventricular pressure rises which closes the AV valves (1st heart sound)
Isovolumetric contraction: (all 4 valves are closed) – ventricle contracts which increases pressure
when ventricular pressure reaches aprx. 80 mmHg opens aortic valve
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Ventricular ejection:
SV: stroke volume:
ESV (end-systolic volume):
EDV – ESV = SV
Ventricular Diastole: begins after ventricles repolarize
Ventricles relax & ventricular pressure decreases
Backflow of blood closes semilunar valves (2nd heart sound)
Dicrotic notch:
Isovolumetric relaxation: all 4 valves are closed and
isovolumetric relaxation phase important because?
when pressure in ventricles drops to below atria pressure, cycle starts all over again.
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Cardiodynamics:
CO (Q) – amount of blood pumped by heart per minute
CO (Q) = HR x SV
CO = 72 bpm x 70 ml/beat = 5L/min
EDV - ESV = SV
120 ml - 50 ml=
• ejection fraction: SV/EDV (normally 60%)
• cardiac reserve:
Factors Affecting Heart Rate
Autonomic Innervation
cardiac centers located in
cardioacceleratory center
cardioinhibitory center
• Sympathetic stimulation: via cardiac nerve
NE binds to β1 receptors opens Na+ & Ca++ channels
increases rate of depolarization & shortens repolarization
• Parasympathetic stimulation: via vagus nerves
ACh binds to muscarinic receptors to open K+ channels to slow depolarization
also extends repolarization time
Cardiac Reflexes: visceral sensory fibers from vagus nerve and cardiac plexus carry baroreceptor and
chemoreceptor information to cardiac centers.
Baroreceptors & chemoreceptors are located in the
baroreceptors monitor
chemoreceptors monitor
(are excited by?)
CO (Q) directly affects BP: controlling HR controls CO which controls BP
Baroreceptor Response:
If BP increased, baroreceptors detect
stretch and send impulse to the
center. The center responds by sending impulse through the
nerves, which release the neurotransmitter
at the SA node which
to HR which
CO (Q) which then
BP.
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And if BP decreased?
baroreceptors detect
stretch and send impulse to the
center. The center responds by sending impulse through the
nerves, which release the neurotransmitter
at the SA node which
to HR which
CO (Q) which then
BP.
Autonomic Tone
• Heart exhibits vagal tone: parasympathetic stimulation dominant
Atrial Reflex (Bainbridge reflex):
• occurs when increased venous return stretches right atrium
2. Chemical Regulation
•Hormones: Which hormones increase HR?
•Ions
-hyper and hypo-natremia: Na+ competes with Ca++
Increased Na+ results in decreased Ca++ uptake into cell
-hyper and hypo-kalemia: K+ necessary for repolarization of heart
Remember: resting cell – more K+ within cell and K+ follows diffusion gradient to leave
If too much K+ leaves =
If K+ doesn’t leave cell can’t repolarize
Hyperkalemia: increased K+ in IF & blood
Hypokalemia: decreased K+ in IF & blood
-hyper and hypo-calcemia
Hypercalcemia: increases Ca++ uptake into cell = stronger contraction
3. Other Factors: gender, age, caffeine, nicotine
Factors Affecting Stroke Volume
SV = EDV - ESV
EDV:
•the critical factor for controlling SV is EDV which is dependent on filling time and venous return.
filling time is based on length of ventricular diastole – higher HR = decreased time
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venous return – changes in response to blood volume, peripheral circulation, gravity, skeletal muscle
activity, cardiac output
Preload: degree of stretch in during ventricular diastole
cardiac muscle cells resting length is shorter than optimal so stretching muscle causes stronger
contraction (within limits)
preload is directly proportional to EDV
Frank -Starling Principle of the Heart
•the factor that stretches cardiac muscle is venous return (amount of blood) and EDV (distending the
ventricle)
•increasing EDV = increased SV – within limits:
Cardiac muscle isn’t very elastic – can stretch it out
•contractility = increase in contractile strength independent of EDV
usually ions, drugs or hormones
positive inotropic action –
usually stimulate Ca++ entry into cardiac muscle cells
negative inotropic action
-may block Ca++ uptake or suppress cardiac metabolism
Positive inotropic effect: NE, Epi, T4, dopamine, digitalis
Negative inotropic effect: ACh, Beta-blockers (propranolol/inderal, metoprolol), Ca++ channel blockers
(nifedipine/procardia or verapamil)
ESV
Afterload:
amount of tension that must be produced by ventricle to force open semilunar valve to eject blood.
higher afterload = longer isovolumetric contraction – shorter ventricular ejection and larger
ESV
afterload increases = decreased SV
afterload increased by anything that restricts blood flow through arterial system
vasoconstriction, blockage in vessel
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Additional Clinical Information
1. Heart Sounds "lub-dup"
1st sound due to the closing of the
2nd sound due to the closing of the
2. Heart Murmurs: valvular heart disease (VHD)
1.) Valvular Regurgitation:
MVP: mitral valve prolapse
require prophylactic antibiotics
2.) Valvular Stenosis:
3. Congestive Heart Failure (CHF)
Chronic disease – heart loses ability to adequately pump blood
Caused by:
 Coronary atherosclerosis
 Persistent high blood pressure (increased afterload)
 Multiple myocardial infarcts
Blood can back up into lungs: pulmonary hypertension may lead to pulmonary edema
Right side of heart weakened blood backs up into systemic circulation
Tx:
Drugs to lower HR (β blockers)
Drugs to lower BP (diuretics, ACE inhibitors) (↓afterload)
4. CAD – coronary artery disease (page 694):
balloon angioplasty:
CABG: coronary artery bypass graft
5. Angina pectoris:
Nitroglycerin (Nitrostat)
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6. MI (page 702)
MI : Myocardial Infarction
cardiac muscle cells die from lack of O2
damaged cells rely more on anaerobic metabolism & accumulate enzymes for it
when cell is damaged, cell membrane deteriorates and enzymes released to blood
lactate dehydrogenase (LDH), creatine phosphokinase (CPK or CK), CK-MB, and troponin
Tx – limit size of infarct, improve circulation, give O2, reduce workload of heart,
decrease abnormal clotting
clot-busters help dissolve clot if given quickly (aspirin, t-PA, streptokinase)
What are the 10 factors that increase risk of heart attack? (page 702)
Read the information on page 702.
7. Cardiomyopathy
Abnormal cardiac muscle cells (mutated gene)
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