Chapter 18: The Heart and Cardiovascular System Flashcards

1
Q

Heart Size and Location:

A

o The heart is approximately the size of a fist and weighs between 8 – 10 ounces
o Location: The heart is located in the mediastinum which is the area from the sternum to the vertebral column and between the lungs in the thoracic cavity
o The Apex of the heart rests on the superior surface of diaphragm
o The Base of the heart is where the great vessels enter/exit
o Anterior to the vertebral column, posterior to the sternum (both rigid structures which allows for CPR)

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2
Q

Functions of the Cardiovascular System:

A

o Tissue cells need O2 and nutrients all the time—-also cells need to get rid of wastes
o The heart, blood vessels, and the blood work together to maintain the immediate environment of every cell. This ensures a continual supply of nutrients, and prevents waste build-up.
o HEART = THE PUMP
o HOLLOW BLOOD VESSELS = DELIVERY ROUTE
o BLOOD = MEDIUM OF EXCHANGE

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3
Q

Facts About the Cardiovascular System:

A

o The heart beats 100,000 times/day
o The heart will beat 3 billion times if you live to 80 years old
o The heart pumps about 5 liters of blood per minute (= cardiac output )
o There are 60,000 miles of blood vessels

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4
Q

Pericardium:

A

o Fibrous pericardium (the outermost layer)
o Protects, anchors, and prevents overfilling or stretching
o Consists of dense irregular connective tissue
o Serous pericardium
o Parietal layer lines and fuses with the internal surface of the fibrous pericardium
o Visceral layer (or epicardium) is on the external surface of the heart
o Pericardial cavity is the space between the parietal and the visceral layer and contains serous fluid (slippery stuff that lessens friction)

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5
Q

Pericarditis:

A

o Inflammation of the serous pericardium and is usually viral in origin, but pericarditis can follow a bacterial pneumonia.
o Can sometimes hinder the production of serous fluid, which can cause painful rubbing of the parietal and visceral layer (friction).
o Makes a “creaking” sound = pericardial friction rub.
o Characterized as pain deep to the sternum.

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6
Q

Cardiac Tamponade:

A

o Large volume of fluid accumulates in the pericardial cavity or space…..from trauma, tumor, obstruction, presence of blood (aneurysm)
o Weight of the fluid compresses the heart from the outside, this prevents the heart from contracting or relaxing
o Heart chambers are unable to completely fill with blood when heart cannot relax
o Treatment is syringe removal of fluid from space

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7
Q

Layers of the Heart Wall:

A

o Epicardium = visceral layer of the serous pericardium
o Myocardium
o Cardiac muscle fibers swirl diagonally in interlacing bundles
o Fibrous skeleton of the heart is a dense connective tissue ring that surrounds the valves of the heart, fuse, and merge with the interventricular septum (divides the two atriums and ventricles).
o Supports structure for great vessels and heart valves
o 2) It is the insertion point for cardiac muscle bundles
o 3) It is the electrical Insulator between the atria and the ventricles therefore prevents direct propagation of action potentials from the atria to the ventricles
o Endocardium = the membranous lining of chambers and valves.

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8
Q

The 4 Chambers of the Heart:

A

o Two upper atria (are seperated by the interatrial septum)
o Two lower ventricles (seperated by the interventricular septum)
o ORGANIZED INTO 2 SEPARATE PUMPS:
o Right side of heart pumps blood to lungs
o Left side of heart pumps blood to rest of body
o The two atria contract at the same time, slight pause, the two ventricles contract at the same time.

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9
Q

Atria:

The Receiving Chambers

A

o Anterior walls are ridged by pectinate muscles
o Blood enters the right atrium through 3 veins:
o Superior vena cava (blood from above the diaphragm)
o Inferior vena cava (blood from below the diaphragm)
o Coronary sinus (blood from the coronary veins of the myocardiam)
o Vessels entering left atrium:
o 2 Right and 2 left pulmonary veins (blood from the lungs that is oxygenated and goes to left atrium)

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10
Q

Ventricles:

The Discharging Chambers

A

o Walls are ridged by trabeculae carneae
o Papillary muscles project into the ventricular cavities = connects with the chordae tendinae
o Chordae tendinae chord-like ligaments that connect the papillary muscles to the tricuspid and mitral valves (AV valves) = prevents eversion (or prolapse) of AV valves into atria
o Vessel leaving the right ventricle:
o Pulmonary trunk, which becomes the R and L pulmonary arteries where deoxygenated blood goes to the lungs.
o Vessel leaving the left ventricle:
o Ascending Aorta, oxygenated blood to body tissues.

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11
Q

Pathway of Blood Through the Heart:

A

o The heart is two side-by-side pumps:
o Right side is the pump for the pulmonary circuit. Vessels that carry blood to and from the lungs.
o Left side is the pump for the systemic circuit. Vessels that carry the blood to all body tissues.
o Equal volumes of blood are pumped through the pulmonary and systemic circuits
o Pulmonary circuit is a short, low-pressure circulation.
o Systemic circuit blood encounters much resistance in the long pathways.
o Anatomy of the ventricles reflects these differences = myocardial walls of the left ventricle is thicker.

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12
Q

Process of Blood Circulating Through the Body:

A

o 1) Right atrium, tricuspid valve, right ventricle
o 2) Right ventricle, pulmonary semilunar valve, pulmonary trunk, pulmonary arteries (deoxy blood), lungs.
o 3) Lungs, pulmonary veins (oxy blood), left atrium.
o 4) Left atrium, mitral valve or bicuspid valve, left ventricle.
o 5) Left ventricle, aortic semilunar valve, aorta.
o 6) Aorta, systemic circulation.

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13
Q

Coronary Circulation:

A

o The functional blood supply to the heart muscle itself.
o Heart needs lots of oxygen.
o When the heart relaxes, the high pressure of the blood in the aorta pushes blood into the coronary arteries (openings just above the aortic semilunar valve).
o Arterial supply varies considerably and contains many anastomoses (or junctions) among branches in case one artery becomes occluded (referred to as collateralization).
o Collateral routes provide additional routes for blood delivery.
o Arteries
o Right coronary artery = in coronary sulcus and supplies right atrium/ventricle
o Coronary sulcus = groove between the atria and ventricles where arteries and veins are located.
o Right marginal artery = supplies right ventricle
o Posterior interventricular artery = supplies both ventricles posteriorly
o Left coronary artery =
o Circumflex artery (in coronary sulcus) = supplies left atrium/ventricle
o Anterior interventricular arteries or LAD (in anterior interventricular sulcus) = supplies right and left ventricles.

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14
Q

Coronary Veins:

A

o Coronary veins collects wastes from the cardiac muscle.
o Small cardiac vein (right anterior).
o Anterior cardiac vein (right anterior).
o Great cardiac vein (in the coronary sulcus and feeds into the coronary sinus).
o Coronary sinus dumps venous blood from the heart muscle into the right atrium.

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15
Q

Homeostatic Imbalances:

A

o Angina pectoris
o Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium
o Cells are weakened
o Myocardial infarction (heart attack)
o Prolonged coronary blockage with ischemia
o Areas of cell death are repaired with noncontractile scar tissue

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16
Q

Heart Valves:

A

o Heart Valves ensure unidirectional blood flow through the heart.
o Atrioventricular (AV) valves: Prevent backflow into the atria when ventricles contract:
o 1) Tricuspid valve (between R atrium and R ventricle.
o 2) Mitral (or Biscupid) valve (between L atrium and L ventricle).
o Chordae tendineae: anchor AV valve cusps to papillary muscles which prevents the tricuspid and mitral valves from inverting into the atria when the ventricles contract.
o Semilunar (SL) valves: 3 cup-like leaflets shaped like a half moon. They prevent the backflow into the ventricles when the ventricles relax.
o Aortic semilunar valve (junction of left ventricle and aorta)
o Pulmonary semilunar valve (junction of the right ventricle and pulmonary trunk)

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17
Q

Conduction System of the Heart:

A
o	Autorhythmic Cells: These pacer cells are noncontractile excitable cardiac fibers (1% of fibers) that fire spontaneously and act as the pacemaker and form the conduction system of the heart and activate the myocardium = autorhythmicity
o	SA (sinoatrial) node (pacemaker): A cluster of cells in the superior wall of the right atrium. Begins heart activity that spreads to both atria and continues to spread to the AV node (very fast = 1m/sec)
o	AV (atrial ventricular) node. Located on the inferior right atrial septum
o	Impulse slows and delayed (to .05 m/sec), then the signal is sent to AV Bundle of His.
o	AV bundle of His is the point of connection of the atria and ventricles, it divides into the right and left bundle branches.
o	Bundle branches are two separate (R / L) pathways in the interventricular septum that carry the impulses toward the apex of the heart and activates the myocardium of both ventricles
o	Bundle Branches have Purkinje Fibers (depolarize) cardiac muscle in ventricles) that are large in diameter which allows for fast conduction (4 m/sec)
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18
Q

Anatomy of the Intrinsic Conduction System Showing the Sequence of Electrical Excitation:

A

o 1) The Sinoatrial (SA) node (pacemaker) generates impulses.
o 2) The impulses pause (0.1s) at the atrioventricular (AV) node.
o 3) The atrioventricular (AV) bundle connects the atria to the ventricles.
o 4) The bundle branches conduct impulses through the interventricular septum.
o 5) The Purkinje fibers depolarize the contractile cells of both ventricles.

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19
Q

Electrical Activation (Aps) of Pacemaker Cells:

A

o Pacemaker cells have unstable resting potentials (pacemaker potentials) due to slow opening of Na+ channels. Resting potential starts out at -60mV and gradually drifts up spontaneously to threshold at -40mV.
o At threshold, Ca2+ channels open. This Ca2+ influx from extracellular fluid produces the rising phase of the action potential = depolarization.
o Repolarization results from closing of Ca2+ channels and the opening of voltage-gated K+ channels = cell cytoplasm becomes more negative once again

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20
Q

Electrical Sequence of Events:

Pacemaker Cells

A

o 1) Depolarization of autorhythmic pacemaker cells generates an action potential
o 2) Action potentials of pacemaker cells stimulate depolarization of cardiac muscle cells to threshold.
o 3) Action potentials of pacemaker cells spread through the entire myocardium via gap junctions (intercalated discs) along the conduction system pathway (very fast conduction).
o Depolarization: contraction of muscle cells.
o Repolarization: relaxation of muscle cells.

21
Q

Rhythm of the Conduction System:

A

o SA node fires spontaneously 90 – 100 times per minute…each depolarization = one AP = 1 H. Beat.
o AV node fires 40 – 60 times per minute.
o If both SA node and AV nodes are suppressed, cardiac muscle fibers in the ventricles themselves fire only 20-40 times per minute = will require artificial pacemaker.
o Extra beats can form at other sites called ectopic pacemakers = caused by caffeine, nicotine, drugs.

22
Q

Timing of Atrial and Ventricular Excitation:

A

o SA node sets the pace since it is the fastestà but can be modified by the ANS or hormones
o In 50 msec, excitation spreads to both atria and down to the AV node
o A 100 msec delay at the AV node occurs due to the smaller diameter fibers that are there. This allows atria to fully contract filling the ventricles before the ventricles contract.
o In 50 msec, excitation spreads through both ventricles simultaneously (Purkinje cells = fast transmission).

23
Q

Cardiac Muscle Contraction:

A

o Depolarization is caused by the opening of voltage-gated fast Na+ channels and Na+ rushes into the sarcoplasm.
o Stimulated by the action potentials of the pacer cells.
o AP’s spread quickly to other cardiac muscle cells due to gap junctions (no neurotransmitters, ions flow between cardiac fibers which causes rapid depolarization.
o Membrane potential reaching threshold (–90 mV) which results in the generation of an action potential (to +30 mV).
o The action potential travels down the T tubules causing the SR (not well developed) to release Ca2+
o Depolarization wave also opens slow Ca2+ channels on the sarcolemma, Ca++ enters from the extracellular fluid.
o Ca2+ surge prolongs the depolarization phase or (plateau phase).
o Ca2+ influx from extracellular fluid triggers opening of more Ca2+-sensitive channels in the sarcoplasm reticulum, which liberates bursts of Ca2+
o Actin-myosin cross-bridging occurs as Ca2+ binds to troponin and sliding of the filaments begins.
o Duration of the action potential and the contractile phase is much longer in cardiac muscle than in skeletal muscle due to the slow influx of Ca++ from extracellular fluids.
o Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channel until the resting membrane potential is reached (-90 mV).
o Refractory period is very long so the heart can fill.

24
Q

Homeostatic Imbalances:

A

o Defects in the intrinsic conduction system may result in arrhythmias: irregular heart rhythms
o Tachycardia: > 100 beats/minute
o Bradycardia:

25
Q

Extrinsic Innervation of the Heart:

A

o Heartbeat is modified by the ANS.
o Cardiac centers are located in the medulla oblongata.
o Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons.
o Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves.

26
Q

Electrocardiography:

A

o Electrocardiogram (ECG or EKG) : A composite of all the action potentials generated by all active cardiac cells. Can be detected at the body surface and recorded by positioning electrodes at 6 positions on the chest and 4 positions on the limbs.
o Three waves
o P wave = SA node depolarizes the atria. Do not see a wave for atrial repolarization.
o QRS complex = ventricular depolarization.
o T wave = ventricular repolarization.
o Allows for the evaluation of: Abnormal heart rate, Abnormal heart rhythms, Abnormal conduction pathways, Hypertrophy or atrophy of portions of the heart, Approximate location of damaged cardiac muscle.

27
Q

6 Steps of Heart Rhythm Breakdown:

A

o 1) Atrial depolarization, intiated by the SA node, causes the P wave.
o 2) With atrial depolarization complete, the impulse is delayed at the AV node.
o 3) Ventricular depolarization begins at apex, causing the QRS complex, atrial repolarization occurs.
o 4) Ventricular depolarization is complete.
o 5) Ventricular repolarization begins at apex, causing the T wave.
o 6) Ventricular repolarization is complete.

28
Q

The 4 Types of Heart Rhythms:

A

o Normal Sinus Rhythm
o Junctional Rhythm: The SA node is nonfunctional, P waves are absent, and heart is paced by AV node at 40-60 beat/min.
o Second-Degree Heart Block: Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1.
o Ventricular Fibrillation: These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

29
Q

Heart Sounds:

A

o Two sounds (lub-dup) associated with closing of heart valves.
o First sound occurs as AV valves close and signifies beginning of ventricular systole (contraction).
o Second sound occurs when SL valves close at the beginning of ventricular diastole (relaxation).
o Heart murmurs: abnormal heart sounds most often indicative of valve problems.

30
Q

Where Valve Sounds are Heard:

A

o Aortic Valve: Sounds heard in 2nd intercostal space at right sternal margin.
o Pulmonary Valve: Sounds heard in 2nd intercostal space at left sternal margin.
o Mitral Valve: Sounds heard over heart apex in line with middle of clavicle.
o Tricuspid Valve: Sounds typically heard in right sternal margin of 5th intercostal space.

31
Q

Mechanical Events:

The Cardiac Cycle

A

o Single Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat, Pressure changes, Blood volume changes, Heart sounds.
o 3 phases in the cardiac cycle:
o 1) Atrial systole (contraction)
o 2) Ventricular systole (contraction)
o 3) Relaxation period (or quiescent period)

32
Q

Systole:

A

Contraction Phase.

33
Q

Diastole:

A

Relaxation Stage.

34
Q

Isovolumetric:

A

Volume of blood in both ventricles remains the same.
o Isovolumetric contraction = systole of ventricles
o Isovolumetric relaxation = diastole of ventricles

35
Q

Ventricular Ejection:

A

Ventricles contract and force blood through the semilunar valves (pulmonary / aortic).

36
Q

Stroke Volume:

A

Actual amount (volume) of blood ejected per heart beat from each ventricle.

37
Q

Important Concepts About the Heart:

A

o Blood flows through the heart and is controlled entirely by pressure changes, blood flows down pressure gradients through any available opening.
o As a chamber of the heart contracts (atrial systole or ventricle systole) blood pressure within that chamber increases.
o Heart valves (and associated structures such as the chordae tendineae) determine which openings are “open” and “available” to create the direction of blood flow.
o Closing of the heart valves creates a turbulence that results in typical heart sounds (lubb, dupp).
o Lub = AV (tricuspid, mitral) valves closing.
o Dup = Semilunar (aortic, pulmonary) valves closing.

38
Q

One Cardiac Cycle:

A

o At 75 beats / min, one cardiac cycle requires 0.8 sec
o One cardiac cycle is defined as systole (contraction) and diastole (relaxation) of both atria, plus the systole and diastole of both ventricles = one heart beat
o End diastolic volume (EDV) = amount ventricles are filled, volume in ventricle at the end of diastole à app. 130 ml.
o End systolic volume (ESV) = ventricles eject blood, volume remaining in ventricle at end of systole is app. 60 ml.
o Stroke volume (SV) = the amount of blood actually ejected, the volume ejected per beat from each ventricle is app. 70 ml.
o SV = EDV minus ESV.

39
Q

Phases of the Cardiac Cycle:

Phase 1

A

o Ventricular filling:
o 1) AV valves are open.
o 2) 80% of blood passively flows into ventricles.
o 3) Atrial systole occurs, delivering the remaining 20%.
o 4) End diastolic volume (EDV): total volume of blood in each ventricle at the end of ventricular diastole (relaxation of ventricles).

40
Q

Phases of the Cardiac Cycle:

Phase 2

A

o Ventricular systole (contraction)
o 1) Atria relax and ventricles begin to contract
o 2) Rising ventricular pressure results in closing of AV valves
o 3) Isovolumetric contraction phase (all valves are closed) = ventricles are “reving up”!!!
o 4) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open
o 5) End systolic volume (ESV): volume of blood remaining in each ventricle = 60 ml

41
Q

Phases of the Cardiac Cycle:

Phase 3

A

o Isovolumetric relaxation occurs in early diastole
o 1) Ventricles relax
o 2) Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure).

42
Q

Cardiac Output:

A

o Cardiac output = volume of blood (SV) pumped by each ventricle in one minute
o CO = heart rate (HR) x stroke volume (SV)
o HR = number of beats per minute
o SV = volume of blood pumped out by a ventricle with each beat
o At rest:
o CO (ml/min) = HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min.
o Maximal CO is 4–5 times the resting CO in nonathletic people = 21 – 26 L/min.
o Maximal CO may reach 35 L/min in trained athletes.
o Cardiac reserve: difference between resting and maximal CO.

43
Q

Regulation of Stroke Volume:

A

o Afterload = resistance to the forward flow of blood from left ventricle (The greater the afterload or resistance, the less the amount of blood ejected from the ventricles. The less the afterload or resistance, the greater the amount of blood will be ejected from the ventricles).
o Preload = the amount of stretching of cardiac cells before ejection of blood from ventricles (the greater amount of blood in the ventricles after diastole, the greater of preload).
o Hypertension increases afterload, resulting in increased ESV (more blood left in ventricles) and reduced SV (less blood ejected).

44
Q

Regulation of Heart Rate:

A

o Positive chronotropic factors are those factors that increase heart rate =
o Sympathetic nervous system (affects SA node)
o Epinephrine released by adrenal medulla
o Caffeine, sympathomimetic drugs (stimulants)
o Negative chronotropic factors are those factors that decrease heart rate=Parasympathetic nervous system.
o Parasympathomimetic drugs = beta blockers (decrease the effects of epinephrine and nor-epinephrine) & calcium blockers.

45
Q

Autonomic Nervous System Regulation:

A

o Sympathetic nervous system is activated by emotional or physical stressors
o Epinephrine/Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility) which causes increase in heart rate, contractility, BP, and hence stroke volume.
o Epinephrine/Norepinephrine targets Beta-1 Adrenergic receptor sites on the heart.
o Drugs called beta-blockers block adrenergic beta-1 receptor sites (hence, decrease BP, arrythymias, congestive heart failure, migraines, panic attacks) = Inderal, lopressor, coreg. These are sympatholytic drugs (counter the effects of epinephrine/ norepinephrine).
o Parasympathetic nervous system opposes sympathetic effects.
o Acetylcholine from the vagus (CN X)hyperpolarizes pacemaker cells by opening K+ channels = cardiac sarcoplasm becomes more negative.
o The heart at rest exhibits vagal tone (parasympathetic).

46
Q

Chemical Regulation of Heart Rate:

A

o Hormones:
o Epinephrine from adrenal medulla enhances heart rate and contractility
o Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine.
o Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function.

47
Q

Congestive Heart Failure:

A

o Progressive condition where the Cardiac Output (CO) of left ventricle is so low that blood circulation is inadequate to meet tissue needs
o Caused by:
o Coronary atherosclerosis
o Persistent high blood pressure
o Multiple myocardial infarcts
o Dilated cardiomyopathy (DCM) = hearts becomes weakened and enlarged and cannot pump blood effectively.

48
Q

Developmental Aspects of the Heart:

A

o Fetal heart structures that bypass pulmonary circulation
o Foramen ovale connects the two atria, becomes the fossa ovalis.
o Ductus arteriosus connects the pulmonary trunk and the aorta, becomes the ligamentum arteriosum.

49
Q

Age-Related Changes Affecting the Heart:

A

o Sclerosis and thickening of valve flaps.
o Decline in cardiac reserve.
o Fibrosis of cardiac muscle (MI).
o Atherosclerosis (fatty plaque formation).