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Chapter 20: The Cardiovascular System THE HEART

Chapter 20: The Cardiovascular System

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Chapter 20: The Cardiovascular System. THE HEART. Heart Anatomy. Location diaphragm, mediastinum, 2/3 left of midline Orientation Apex- points anterior, inferior, left Base- directed posterior, superior, right Vessels Superior and Inferior Vena Cava - PowerPoint PPT Presentation

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Page 1: Chapter 20: The Cardiovascular System

Chapter 20: The Cardiovascular

System

THE HEART

Page 2: Chapter 20: The Cardiovascular System
Page 3: Chapter 20: The Cardiovascular System

Heart Anatomy Location

diaphragm, mediastinum, 2/3 left of midline Orientation

Apex- points anterior, inferior, left Base- directed posterior, superior, right

Vessels Superior and Inferior Vena Cava Pulmonary trunk pulmonary arteries(lungs) Pulmonary veins Aorta

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Page 5: Chapter 20: The Cardiovascular System
Page 6: Chapter 20: The Cardiovascular System

Pericardium- figure 20.2 Membrane that surrounds & protects Confines to position in mediastinum 2 main parts:

Fibrous pericardium- superficial, anchor Tough, inelastic, dense irregular CT Baglike, open end attached to vessels Prevents overstretching of heart

Serous pericardium- thinner, delicate Forms double layer (pericardial fluid in pericardial cavity -

reduces friction, allows movement): Parietal layer- fused to fibrous Visceral layer- inner = EPICARDIUM- adheres tightly to heart

surface

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Layers of the heart wall Epicardium- thin, transparent, outer

Visceral layer of serous pericardium Smooth slippery outside of heart

Myocardium- middle Cardiac muscle- striated but involuntary Bulk of heart Pumping action

Endocardium- inner Thin endothelium over CT Smooth lining of chambers and valves Continuous with b.v.

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Heart Anatomy fig 20.3-6 Heart chambers = 4

2 Atria Right- receives blood from vena cavae Left- receives blood from pulmonary veins

2 Ventricles Right- pumps deoxygenated blood to lungs Left- pumps oxygenated blood to systemic circ

Myocardium much thicker than right ventricle

Heart valves = 4 Atrioventricular valves = tricuspid & bicuspid Semilunar valves = aortic and pulmonary

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Valve function When AV valve open:

Cusps project into ventricle Ventricle relaxed papillary muscle relaxed chordae

tendineae slack Blood: pressure atria pressure ventricle

Ventricle contracts, pressure cusps up, close Papillary muscles contract chordae tendineae tighten

SL valves open when pressure in ventricles exceeds pressure in arteries As ventricles relax blood moves back toward heart SL

valves close

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Terms Auricles – on anterior surface of atria

Increases capacity of each atrium so each can hold a greater volume of blood

Coronary sulcus – separation between atria and ventricles

Systole – contraction Diastole – relaxation Tachycardia – high heart rate, > 100bpm Bradycardia – low heart rate, 50 bpm

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Pulmonary and systemic circuits

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Coronary circulation (1)

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Coronary circulation (2) Coronary – “crown,” encircles heart

contracts, little blood flows coronary artery but as relaxes, aorta pushes blood thru coronary arteries

Anastomoses – area where 2 or more arteries supply the same region Provide alternate routes for blood to reach a

particular organ or tissue Myocardium contains Provides detours if main route is obstructed

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Problems… Myocardial ischemia – partial obstruction of blood

flow in coronary arteries blood flow to myocardium hypoxia may weaken cells w/out killing them Silent = episodes without pain, dangerous in that no

forewarning to attack Angina pectoris – “strangled chest”

Severe pain usually accompanies myocardial ischemia Tightness or squeezing sensation Can occur during exertion when requires more O2 Pain referred to neck, chin, left arm

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Myocardial infarction (MI) Heart attack Complete obstruction of blood flow to coronary

artery Infarction = death of tissue area due to

interrupted blood supply Tissue distal to obstruction dies, replaced by non-

contractile scar tissue loses strength May also disrupt conduction system and cause sudden

death – ventricular fibrillation – rapid uncoordinated twitching that disrupts regular rhythm

treatment: injection of clot dissolver, plus heparin, coronary angioplasty or coronary artery bypass

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Properties of cardiac muscle cells Shorter than skeletal Branching Central nucleus, sometimes binucleate Intercalated discs- thickenings of

sarcolemma, contain: Desmosomes- hold fibers together Gap junctions- for AP conduction

Mitochondria large & numerous Like skeletal- arrangement of proteins

SR smaller less intracellular Ca2+ T-tubules wider but less abundant

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Functional syncytium stimulation of individual muscle cell results

in contraction of all muscle cells due to gap junctions in intercalated discs

an application of the all-or-none principle If stimulus in cardiac muscle is great enough to

initiate contraction of a single cell, the entire muscular syncytium will undergo contraction

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Contraction physiology 1% of cardiac fibers become autorhythmic

during embryonic development Pacemaker function- set rhythm of electrical

excitation Conduction system- network of specialized

fibers provide path for excitation to progress thru heart

Ensuring coordinated contraction of chambers Both atria contract at same time Both ventricles contract at same time

Cardiac AP goes thru following sequence…

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Contraction physiology (2) Pathway of stimulation

1. Sinoatrial (SA) node- cells do not have a stable resting membrane potential

depolarized spontaneously = pacemaker potential 2. Atrioventricular (AV) node 3. Bundle of His 4. Bundle branches 5. Purkinje fibers 6. Ventricular cells- contraction pushes blood

up to SL valves

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Cardiac Action Potentials, 20.11 Depolarization: Na+ gates open= fast channels

Rapid depolarization because they open fast Plateau: opening of slow Ca2+ channels in the

sarcolemma More Ca2+ outside cell cytosol also causing Ca2+

to pour out of SR Ca2+ contraction K+ channels opening but Ca2+ balances it remains

depolarized for about 0.25 sec (in skeletal muscle 0.001 sec, no plateau phase)

Repolarization: K+ outflow restores resting m.p. Ca2+ channels also are closing

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Cardiac Action Potentials (2) Positive inotropic agents contractility

(substances promote inflow of Ca2+ channels strength contractions NE and Epinephrine modify

Timing strength of contraction Do NOT establish a rhythm

Digitalis interstitial Ca2+

Negative inotropic agents contractility Ach released by Parasymp NS slows SA node pacing

from 100 to about 75 AP/minute Also: anoxia, acidosis, some anesthetics, K+, Ca2+

channel blockers

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Long refractory pd- cardiac muscle Refractory pd- time interval during which

second contraction cannot be triggered In cardiac- longer than contraction pd

Another contraction cannot happen until relaxation is happening

Tetanus cannot occur If tetanus occurred blood flow would cease

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Arrhythmias Irregular rhythm due to conduction defect Causes:

Caffeine, nicotine, alcohol, other drugs, anxiety, hyperthyroidism, K+ deficiency, & some heart disease

Examples: Heart block – AP slowed or blocked (3 types)

1st °= AP slow thru AV, 2nd °= some AP not thru AV node, 3rd ° = no AP thru AV node

Atrial flutter – rapid atrial contractions Atrial fibrillation – asynchronous cont- atrial fibers Ventricular fibrillation– async cont ventricular fibers* Premature ventricular contraction – ectopic area of high

excitation abnormal AP (before SA node intends)

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Cardiac excitation and the ECG

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Electrocardiogram (ECG) P wave – atrial depolarization atrial

contraction ventricular filling QRS complex – ventricular depolarization

ventricular contraction SL valves open blood ejection Rt ventriclepulmonary trunk pul arteries

lungs Left ventricle aorta systemic circulation

T wave – ventricular repolarization

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Heart sounds

A. Normal

First sound – lubb – closure of AV valves

Second sound – dupp – closure of SL valves

B. Abnormal sounds (murmurs) 1. stenosis – failure of valve to open 2. insufficiency – failure of valve to close

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The Cardiac Cycle Ventricular filling

AV open, SL closed Isovolumetric contraction

AV closed, SL closed Ventricular ejection

AV closed, SL open Isovolumetric relaxation

AV closed, SL closed Ventricular filling

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Regulation of Cardiac Output Cardiac output = stroke volume x heart rateCO = SV x HR Stroke volume = ml/ beat

EDV - ESV Heart rate = beats/ min

Cardiac output = L/ min rest = 5.25 L/min (70 mL/beat x 75 bpm)exercise = 19.5 L/min (130mL/beat x 150bpm)

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Regulation of stroke volume 1. Effect of preload = Frank-Starling Law

of the Heart > preload > force of contraction

rubberband

2. Effect of afterload Pressure rqrd for ejection of blood

3. Effect of contractility-each individual fiber Positive inotropic agents- eg. norepinephrine Negative inotropic agents - eg. propranolol

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Regulation of Heart Rate 1. Normal rate = vagal tone 2. Regulation

1. Autonomic Nervous system 2. Chemical

a. Hormones b. Ions

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