Chapter 19

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Chapter 19
Cardiovascular
System: Heart
Cardiac Anatomy 1
• Pericardial sac:
3 layers – fibrous, parietal, and visceral
endothelium (pericardium) surrounds the heart;
visceral & parietal endothelium form pericardial
cavity (potential space) which contains serous
fluid
• Location:
Thorax (mediastinum), left of midline with apex
antero-inferior and base postero-superior; the
right ventricle rests on the superior border of
the diaphragm. The heart sits between the right
& left lung.
Cardiac Anatomy 2
• Four chambered pump:
Atria (right and left) - superior to and smaller
than the ventricles. On the outer surface they are
separated from the ventricles by a groove (coronary
sulcus).
Ventricles (right and left) - On the outer surface
anteriorly & posteriorly, they are separated from
each other by a sulcus (anterior and posterior
interventricular sulcus, respectively).
Fig. 19.6
Cardiac Anatomy 3
• Anterior external view
Great vessels arise superiorly (from rt to lt)
1) superior vena cava to the rt. atrium
2) ascending aorta from the left ventricle (giving
rise to coronary arteries which travel along coronary
sulcus); branches to form systemic circulation
3) pulmonary trunk from the right ventricle
(giving rise to pulmonary arteries); branches to
form pulmonary circulation.
4) inferior vena cava to the rt. atrium from
inferior aspect.
Cardiac Anatomy 4
Branches from Aorta to supply the heart muscle.
• Right coronary artery:
travels along the rt. coronary sulcus. It branches
to rt. marginal artery (runs along the inferior
surface of rt. ventricle)
• Left coronary artery:
branches to circumflex art. (travels posteriorly in
coronary sulcus) and LAD(Left Anterior
Descending)/Anterior Interventricular art. (traveling
inferiorly within the anterior interventricular
sulcus)
Cardiac Anatomy 5
• Coronary arts.:
supply the very active muscles of the heart wall.
They are functional end arteries (anastomoses are
ineffective in supply needs).
• Cardiac veins :
(great, middle & small) run alongside LAD,
posterior interventricular & marginal arts
respectively. drain into the coronary sinus (posterior
surface) which drains into right atrium.
Fig. 19.13
Cardiac Function 1
• Two pump structure: left (A) and right (B) sides
A) systemic – circulates oxygenated to body’s
cells; removes metabolic wastes from the cells.
B) pulmonary – circulates deoxygenated blood
to lungs for oxygenation and removal of CO2.
Each pump has a receiving chamber, atrium, and
a pumping chamber, ventricle.
• Perfusion:
the delivery of blood (ml) to tissues (gm) per
unit time (min.): ml/gm/min.
Requires a healthy heart and blood vessels for
adequate perfusion for healthy tissues and body.
Fig. 19.3
Cardiac Function 2
Cardiac Anatomy 6
• Interior view
Cardiac muscle wall structure: (outer to inner)
epicardium, myocardium, and endocardium
Epicardium – visceral layer of pericardium. It is
simple squamous epithelium with underlying layer
of adipose connective tissue.
Myocardium – muscular layer of the wall of the
heart; thickest layer; contraction of the myocardium
forces the blood through the circulatory system.
Endocardium – inner lining; simple squamous
epithelium; covers the surface of heart valves and is
continuous with blood vessel endothelium.
Fig. 19.8
Cardiac Anatomy 7
Ventricular walls are thicker than atrial walls.
Left ventricle is thicker than rt. ventricle. Septae
separate the atria and ventricles, respectively.
• Rt. atrium: pectinate muscles; fossa ovalis; tricuspid
valve (rt. AV valve) opens to Rt. Ventricle; coronary
sinus
• Rt. ventricle: papillary muscles; chordae tendineae
pulmonary semilunar valve; trabeculae carneae
• Lt. atrium: pectinate muscles; bicuspid valve (Lt.
AV/Mitral valve) opens to Lt. Ventricle
• Lt. ventricle: papillary muscles; chordae tendineae
aortic semilunar valve; trabeculae carneae;
Cardiac Anatomy 8
Cardiac Valves
Heart valves 1
• Heart Valves
two categories of valves ensure one-way flow of
blood through the heart.
AV valves – permits flow from atria to ventricles;
right AV is tricuspid valve (3 leaflets); left AV is
bicuspid/Mitral valve (2 leaflets).
Semilunar valves – permits flow from left & right
ventricles to aorta and pulmonary trunk,
respectively. Each valve contains 3 ‘half moonshaped’ leaflets.
Heart valves are flexible & made of fibrous
connective tissue covered by endothelial lining.
Heart valves 2
Myocardium 1
•
•
•
•
•
•
Cardiac muscle anatomy
Relatively short, branched, striated muscle cells
sarcolemma (plasma membrane) forms T-tubules to
SR (sarcoplasmic reticulum)
Endomysium: areolar connective tissue surrounds
muscle fiber; supports cellular structure
sarcomere : Z disc to Z disc; unit of muscle structure
intercalated discs (gap junctions, desmosomes)
mechanical & electrical link between cells
T-tubules: invaginations of sarcolemma, overlying Zdiscs; one ‘t-tubule /sarcomere; extends to SR.
Fig. 19.11
Heart pathology 1
• Coronary arteries: atherosclerosis, coronary muscle
spasm causes:
Angina pectoris: workload exceeds blood supply
Myocardial Infarction: cellular death due to
sudden, complete occlusion; myocardial tissue
replaced by nonfunctional scar tissue;
• Valvular disorders: murmurs: heard on ascultation;
back flow of blood;
insufficiency
stenosis (Streptococcal infections)
Fig. 19.14
Fibrous Skeleton
• Dense irregular connective tissue
structural & mechanical support of heart
anchor for heart muscle attachment; fibrous
rings anchor heart valves; forms septa
electrical insulation of conduction system
action potentials do not leak from atria to
ventricles or vice versa; independent contraction
• Cardiac muscle
arranged in spiral bundles causing inward
compression of heart chambers; ventricular
contraction starts at the apex moving superiorly
Cardiac function 1
• Perfusion: delivery of blood per tissue per time
ml/ min/gm.
Exchange of gases, nutrients and wastes take
place at level of the capillary network.
• Circulation:
a) arteries – blood away from the heart
b) veins – blood towards the heart
c) capillaries – joins arterioles to venules;
exchange of nutrients, gases, wastes
• Cardiac cycle: systole & diastole (contract/relax)
Cardiac output: HR x SV = CO
Heart rate x Stroke volume
Cardiac function 2
• Conduction system:
regulates heart pumping action:
rate (chronotropic) and/or force (inotropic)
SA (sinoatrial) node: pacemaker
AV node, AV bundle, Purkinje fibers (larger);
ANS
Cardioaccelaratory Center: Sympathetic (T1-5)
Cardioinhbitory Center: Parasympathetic (Vagus
n.:CN X); Vagal tone
Atrial reflex (Bainbridge reflex) stretch of atrial
wall stimulates sympathetic response; protection
from overfilling.
Cardiac function 3
• SA Node: generates action potential
RMP: - 60mV; (Na+/K+) pumps; (Na+) leak
channels; (K+) leak channels.
(Ca2+) pumps: > conc. Ca2+ extracellular.
*Na+ channels: slow voltage-gated
Ca2+channels: fast voltage-gated
K+ channels: voltage-gated
Threshold: -40mV;
Pacemaker potential: RMP (-) Threshold (20mV)
*autorhythmic; self regulating;
Cycle: 0.8 secs; SA nodal rhythm: ~100/min
Vagal tone: parasympathetic (ANS): 75beats/min
Heart pathology 2
• Conduction:
Ectopic pacemaker – focus other than SA node;
SA node inherent rhythm of ~100/min; AV node
rhythm of ~45/min; Cardiac muscle cells: 20-40/min
Arrhythmias
Flutter: regular atrial contractions 200-400/min;
Fibrillation: irregularly irregular rate; chaotic
disturbances in heart rate; atrial or ventricular;
atrial bombardment causes ventricular irregularity.
V. fibrillation- twitching/fibrillary movement
replaces regular contractions; incompatible with life
(cardiac arrest) treated with defibrillation.
Heart pathology 3
• PVC: single/bundles; initiated in AV node or
ventricular conduction; caused by stress/stimulants.
Usually not problematic if they don’t occur in large
numbers.
• Heart block – AV block
1st degree: delayed ventricular depolarization
2nd degree: some atrial AP’s are blocked
3rd degree: no SA nodal AP’s reach AV node; life
threatening requiring medical intervention.
Bradycardia: less than 60beats/min, resting HR
Tachycardia: 100+ beats/min. resting HR.
Cardiac Muscle 1
• Electrical Events
Depolarization of sarcolemma
RMP: -90mV
stimulated by action potential in SA/AV node,
fast voltage gated Na+ channels open;
sarcoplasm become relatively positive;
K+ channels open, initiating repolarization;
simultaneously, slow voltage-gated Ca2+channels open
prolonging depolarization (*plateau).
Ca2+channels close, K+ channels remain open,
the sarcolemma repolarizes.
*Refractory period is extended preventing tetany.
Cardiac muscle 2
Cardiac muscle 3
• Muscle contraction (mechanical events)
Ca2+ enters sarcoplasm (on depolarization)
Ca2+ binds troponin initiating crossbridge cycling.
Sarcomeres shorten as thin filaments slide past
thick filaments (reference slide #41), cardiac muscle
contracts (systole).
Voltage gated Ca2+ channels close,
reuptake of Ca2+ from sarcoplasm by SR, and release
of Ca2+ from troponin causes cardiac muscle
relaxation (diastole).
Cardiac muscle contraction
Electrocardiogram
• EKG/ECG:
reflect electrical changes in myocardium
P wave – depolarization of atria
QRS complex – depolarization of ventricles;
atrial repolarization is masked by ventricular activity
T wave - repolarization of ventricles.
P, QRS, and T wave sequence indicate one heart
cycle
Fig. 19.20
Cardiac Cycle 1
• One cycle includes:
the start of one heart beat to the next; it is the
contraction and relaxation of the two sets of heart
chambers (atria & ventricles) & includes five
phases:
atrial systole, early ventricular systole, late
ventricular systole, early ventricular diastole, late
ventricular diastole (ref. slide # 46 for details).
Systole is the contraction of a heart chamber.
Diastole is the relaxation of a heart chamber.
Cardiac Cycle 2
• Ventricular contraction and relaxation along with
the pressure changes within the heart chambers are
the primary cause of unidirectional blood flow and
valve function preventing back flow.
Cardiac output 1
• The amount of blood pumped in one minute by
either the left or right ventricle.
It is determined by heart rate and stroke volume
and expressed in liters/minute:
HR x SV = CO (L/min)
75beats/min x 70ml = 5250 ml/mi
Exertion demands require an increase in CO (both
HR & SV increase).
Cardiac Reserve: an increase in CO beyond the
heart’s resting level. May increase to four fold (20L)
in a healthy individual; to seven fold (35L) in an
athlete.
Cardiac output 2
• CO is influenced by variables which affect either HR
or SV or both (chronotropic or ionotropic,
respectively).
• Chronotropic influences: affect SA/AV node
ANS – Positive chronotropic agents cause an
increase in HR include: sympathetic pathways and
hormonal stimulants.
Norepinephrine, Epinephrine bind β1 receptors
releasing Ca2+ to nodal cells, increasing AP rate.
Thyroid hormone increases # of β1 receptors,
increasing response to sympathetic stimulation.
Caffeine, nicotine & cocaine increase HR.
Cardiac output 3
• Chronotropic influences:
Negative chronotropic agents: cause a decrease
in HR include: parasympathetic pathways and β
blockers.
Acetylcholine binds voltage-gated K+ channels
releasing K+ from the nodal cells, hyperpolarizing
nodal cells and delaying threshold, slowing HR. β
blockers stop NE & Epi binding and block nodal cells
from reaching threshold, decreasing action
potentials and slowing HR. β blockers are generally
used to treat high blood pressure (HBP).
Cardiac output 4
• Stroke volume influences
(SV is the amount of blood pumped each heart
beat)
venous return, ionotropic agents, and afterload
Venous return determines EDV : the amount of
blood in the ventricle prior to contraction. This
determines the preload: the stretch on the cardiac
wall due to filling capacity prior to contraction.
• Frank Starling law: increasing venous return,
increases preload, resulting in a more forceful
contraction, due to increased overlap of thick & thin
filaments, increasing crossbridging. A more forceful
contraction increases SV.
Cardiac output 5
• Stroke volume influences
Decrease in venous return, decreases preload,
decreasing overlap & crossbridging. The force of
contraction is thereby decreased, decreasing SV.
Venous return is influenced by: 1) an increase or
decrease in venous pressure; 2) an increase or
decrease in filling time.
• Ionotropic agents: increase/decrease the force of
contraction (positive/negative respectively). This is
due to the concentration of Ca2+ in the sarcoplasm.
Ca2+ forms the crossbridging by binding troponin.
Cardiac output 6
• Ionotropic agents:
Positive ionotropic agents – increase the [Ca2+]
in the sarcoplasm, include: sympathetic axon
release of NE, adrenal medulla release of NE & Epi.,
thyroid hormone, digitalis.
Negative ionotropic agents - decrease the [Ca2+]
in the sarcoplasm, include: electrolyte imbalances increases of K+ and H+, Ca2+; channel blockers
(Nifedipine/Procardia) used to treat HBP.
• Afterload: arterial resistance to ventricular ejection;
increases with aging as the arterial lumen size
decreases.
The pericardial cavity is located between the
a) fibrous pericardium and the parietal layer of
the serous pericardium.
b) parietal and visceral layers of the serous
pericardium.
c) visceral layer of the serous pericardium and
the epicardium.
d) myocardium and the visceral layer of the
serous pericardium.
During the recycling of components following
the normal destruction of erythrocytes, globin
is broken down, and its components are:
a) used to synthesize new proteins.
b) stored as iron in the liver.
c) eliminated from the body in the bile.
d) removed in the urine.
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