Chapter 18: The Heart and Cardiovascular System Flashcards

1
Q

Function of Cardiovascular System:

A

o Tissue cells need O2 and nutrients at all hours of the day and night. Also, cells need to get rid of wastes that they generate.
o The heart, the blood vessels, and the blood work together to maintain the immediate environment of each and every cell.
o To ensure a continual supply of nutrients.
o To prevent waste build up.
o HEART = The Pump.
o HOLLOW BLOOD VESSELS = Delivery Route
o BLOOD = Medium of Exchange.

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2
Q

Characteristics of the Heart:

A

o Heart beats 100,000 times/day.
o Will beat 3 billion times if you live to 80 years old.
o Heart pumps about 5 Liters of blood/min (cardiac output).
o Over 60,000 miles of blood vessels!!!
o Heart is located in the MEDIASTINUM: area from the sternum to the vertebral column and between the lungs in the thoracic cavity.
o Size of closed fist; weighs 8 to 10 ounces.
o Lies between 2 rigid structures —makes CPR possible.
o Apex -deep to 5th intercostal space.
o Base - where the great vessels enter/exit.
o Anterior surface - deep to the sternum, ribs, and intercostal muscles.
o Inferior surface - rests on the diaphragm.

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3
Q

Pericardium:

Layers of the Heart

A
o	Fibrous pericardium
o	Dense irregular CT.
o	Protects and anchors the heart & prevents overstretching.
o	Serous pericardium:
o	Thin delicate membranes.
o	Visceral pericardium:
o	Clings to heart surface.
o	Also called the EPICARDIUM.
o	Pericardial cavity:
o	Space containing small amt. of serous fluid.
o	Parietal pericardium:
o	Fuses with fibrous pericardium.
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4
Q

Pericarditis:

A

o Inflammation of the serous pericardium—often viral in origin, but could follow a bacterial pneumonia.
o Can SOMETIMES hinder the production of the serous fluid, which can cause painful rubbing of the parietal and visceral layers.
o Makes a “creaking” sound = pericardial friction rub.
o Characterized by pain deep to the sternum.

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5
Q

Cardiac Tamponade:

A

o Large volume of fluid accumulates in the pericardial space from trauma, tumor, or rupture.
o Weight of the fluid compresses the heart from the outside—prevents the heart from contracting or relaxing normally.
o Heart chambers are unable to fill with blood when heart cannot relax.
o Treat: insert syringe into pericardial cavity and drain off the excess fluid.

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6
Q

Layers of Heart Wall:

A

o Endocardium:
o Lining of the chambers and valves.
o Myocardium:
o Cardiac muscle layer is the bulk of the heart.
o Epicardium:
o Visceral layer of serous pericardium.
o Muscle Bundles of the Myocardium: Cardia muscle fibers swirl diagonally around the heart in interlacing bundles.

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7
Q

Fibrous Skeleton of Heart:

A

o Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum.
o Support structure for heart valves.
o Insertion point for cardiac muscle bundles.
o Electrical insulator between atria and ventricles.
o Prevents direct propagation of AP’s to ventricles.

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8
Q

The 3 Types of Muscle Tissue and What They’re Derived From:

A

o Skeletal Muscle
o Cardiac Muscle
o Smooth Muscle
o All Derived from MESODERM.

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9
Q

Cardiac Muscle Histology:

A

o Intercalated discs with gap junctions and desmosomes.

o Involuntary, striated, single central nucleus/cell.

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10
Q

Histology of Myocardium:

A

o Sarcoplasmic reticulum is smaller and less organized; no terminal cisternae; smaller reserve of intracellular calcium ions 10-20% of calcium ions needed enter cardiac cells from the ECF.
o T-Tubules are less abundant (just one/sarcomere) but wider and admit more calcium ions from the EXTRAcellular fluid.
o Cardiac muscle cells have a slow onset of contraction, a prolonged contraction period, and a much longer refractory period than skeletal muscles 250 ms vs. 1-2 ms.

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11
Q

Metabolism of Heart Muscle:

A

o Can NOT develop a large oxygen debt—so extensive capillary supply + mitochondria take up 25% of the intracellular space of cardiac muscle cells.
o At rest, the ATP needed for cardiac muscle contraction comes from:
o 60% from oxidation of fatty acids.
o 35% from oxidation of glucose.
o 5% from other fuels such as ketones, lactic acid, and amino acids.

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12
Q

Gross Anatomy of Heart:

A

o Four Chambers:
o 2 upper atria
o 2 lower ventricles
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 Sulci: grooves on surface of heart containing coronary blood vessels and fat.
o Coronary sulcus: Encircles heart and marks the boundary between the atria and the ventricles.
o Anterior interventricular sulcus: Marks the boundary between the ventricles anteriorly.
o Posterior interventricular sulcus: Marks the boundary between the ventricles posteriorly.
o Interatrial septum partitions the 2 atria.
o Interventricular septum partitions the 2 ventricles.
o Chordae tendineae.
o Trabeculae carneae.
o Fossa ovalis is a remnant of the fetal foramen ovale.
o Ligamentum arteriosum is remnant of fetal ductus arteriosus.

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13
Q

Myocardial Thickness and Function:

A

o Thickness of myocardium varies according to the function of the chamber.
o Atria are thin-walled, and deliver blood to adjacent ventricles.
o Ventricle walls are much thicker and stronger:
o Right ventricle supplies blood to the lungs (little flow resistance).
o Left ventricle wall is the thickest to supply systemic circulation.

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14
Q

Isovolumetric Contraction:

A

o Equal volumes of blood are being pumped into the pulmonary and systemic circuits at any given moment in time.
o The output of the pulmonary circuit becomes the input of the systemic circuit.
o Important note: Although it is convenient to discuss blood flow through the heart one side at a time, in reality both atria contract at about the same time, and both ventricles contract at about the same time!

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15
Q

Atrioventricular Valves:

A

o OPEN:
o A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure.
o Occurs when ventricles are relaxed, chordae tendineae give slack, and papillary muscles are relaxed.
o CLOSE:
o A-V valves close preventing backflow of blood into atria: THIS CREATES THE FIRST HEART SOUND.
o Occurs when ventricles contract, pushing valve cusps closed, chordae tendineae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting back into the atria.

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16
Q

Semilunar Valves:

A

o SL valves open with ventricular contraction.
o Allow blood to flow into pulmonary trunk and aorta.
o SL valves close with ventricular relaxation.
o Prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the SL valves, THIS CREATES THE 2ND HEART SOUND.

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17
Q

Valve Disorders:

A
o	Etiology (can be congenital or acquired)
o	Endocarditis
o	Infection
o	Ischemia 
o	Trauma
o	Types of Valve Disorders
o	Stenosis:  valve narrowed/blocked.
o	Incompetence or Insufficiency:  valve cannot completely close.
o	Valvular regurgitation.
o	Valvular prolapse.
o	Valvular Disorder can cause murmurs.
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18
Q

Coronary Circulation:

A

o Coronary circulation = Blood supply to the heart (blood being pumped in/out of heart chambers isn’t available for the heart to USE for itself!).
o Variable from one person to next!
o Heart represents 1/200 of body weight, but requires 1/20 of the blood supply!
o Heart is a very active muscle; needs lots of O2 .
o When the heart relaxes, the high pressure of blood in the aorta pushes blood into coronary arteries .
o Many anastomoses: connections between arteries supplying blood to the same region, provide alternate routes if one artery becomes occluded (collateralization).

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19
Q

Coronary Arteries:

A

o Branch off ascending aorta above aortic semilunar valve.
o Left coronary artery (left main):
o Circumflex branch: in coronary sulcus, supplies left atrium and left ventricle.
o Left anterior descending (anterior interventricular artery): LAD supplies both ventricles anteriorly.
o Right coronary artery (RCA):
o In coronary sulcus, supplies right atrium & right ventricle.
o Marginal branches.
o Posterior interventricular artery.
o PDA supplies both ventricles posteriorly.

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20
Q

Coronary Veins:

A

o Collects wastes from cardiac muscle.
o Drains into a large sinus on posterior surface of heart called the coronary sinus.
o Coronary sinus empties into right atrium.

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21
Q

Cardiovascular Disease

Vs.

Coronary Artery Disease

A

o CVD = cardiovascular dz (big umbrella category)
o Includes:
o HTN = hypertension.
o CVA = stroke.
o CHF = congestive heart failure (HF).
o CAD = coronary artery dz.
o MI = myocardial infarction.
o Congenital heart dz.
o CVD = #1 killer in US since 1900.
o 71 million US adults have some form of CVD.
o CAD = coronary artery dz.
o Heart muscle receiving insufficient blood supply = ischemia
o Narrowing of vessels. Causes: 1. Artery spasm 2. Clot in artery 3. Atherosclerosis
o Atherosclerosis–smooth muscle & fatty deposits in walls of arteries

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22
Q

Risk Factors for Coronary Artery Disease:

A
o	High blood pressure = hypertension = HTN
o	Smoking
o	Dyslipidemia (abnormal fat levels in blood)
o	Diabetes Mellitus (DM)
o	Obesity
o	Sedentary lifestyle
o	Low daily fruit & vegetable intake
o	ETOH (alcohol) overconsumption
o	Stress or Type “A” personality
o	Increased CRP (C-reactive protein)
o	Family history
o	Male Gender
o	Increasing Age
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23
Q

Plasma Lipids and Heart Disease:

A

o One risk factor for developing heart disease is dyslipidemia = abnormal blood fat (lipid) levels.
o Blood lipids include:
o Cholesterol.
o Triglycerides.
o Fatty acids.
o Most lipids are transported on lipoproteins:
o HDLs (high-density lipoproteins) remove excess cholesterol from circulation.
o LDLs (low-density lipoproteins) are associated with the formation of fatty plaques if excessive.
o VLDLs (very low-density lipoproteins) can contribute to increased fatty plaque formation.

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24
Q

Desirable Adult Levels of Blood Lipids:

A

o TC (total cholesterol) under 200 mg/dL.
o LDL under 130 mg/dL (controversial!).
o HDL over 40 mg/dL (>45 mg/dL in females).
o Triglycerides (TG) under 150 mg/dL.
o Therapies to reduce blood cholesterol level include:
o Exercise.
o Diet.
o Meds (statin meds blocking cholesterol synthesis; meds blocking cholesterol absorption).

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25
Q

Important Characteristics of Cholesterol:

A

o Sources of cholesterol in the body
o Food (eggs, dairy, organ meats, meat).
o Synthesized by the liver & intestinal cells.
o Cholesterol is TOO IMPORTANT in body to rely only on food intake!
o Structural part of most cell membranes!
o Precursor to Vitamin D.
o Precursor to all steroid hormones.
• Cortisol, aldosterone, sex hormones.
o Used to make bile (to digest dietary fat).

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26
Q

Treatments for Coronary Artery Disease:

A

o Percutaneous Transluminal Coronary Angioplasty or PCI (percutaneous coronary intervention).
o Balloon procedures.
o Stents: Maintain patency in coronary arteries.
o CABG = Coronary Artery Bypass Graft.
o Single vessel vs. double vs. triple vessel.
o 2008 NEJM article:
o DEATH RATE after one year:
o CABG: 3.5% Stent: 4.3%
o Need for additional surgery at one year:
o CABG: 6.0% Stent: 14.0%
o Strokes (from emboli) at one year:
o CABG: 2.0% Stent: almost 0%
o Recovery time from initial intervention:
o CABG: 4-6 weeks Stent: 3 to 4 days

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27
Q

Conduction System of Heart:

A

o Autorhythmic Cells: modified cardiac muscle cells!
o Cells fire spontaneously, act as pacemaker and form conduction system for the heart
o SA node
o Cluster of cells in superior wall of right atrium.
o Begins heart activity that spreads to both atria.
o Excitation spreads to AV node…very fast (1 meter/s).
o AV node
o Located in the inferior atrial septum
o Impulse slows to 0.05 m/s and impulse is DELAYED by100 ms (0.1 second), then transmits signal to AV Bundle of His.
o AV bundle of His
o The connection between atria and ventricles
o Divides into right and left bundle branches called purkinje fibers.
o PURKINJE FIBERS, large diameter fibers that conduct signals quickly up to 4 m/s!!

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28
Q

Electrical Sequence of Events for Heart (5 Steps):

A

o 1. Depolarization of autorhythmic pacemaker cells and generation of an AP.
o 2. AP’s spread through entire myocardium via gap junctions along conduction system pathway.
o 3. AP’s stimulate depolarization of cardiac muscle cells to threshold.
o 4. Depolarization then contraction
o 5. Repolarization of cardiac cells.

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29
Q

Autorhythmic Pacemaker Cells:

A

o Do not have a stable resting membrane potential then starts out at –60 mV and drifts up spontaneously to threshold at –40 mV.
o Threshold opens voltage gated fast calcium ion channels, explosive entry of Ca2+ from ECF leads to further depolarization.
o Unlike cardiac MUSCLE cells, the movement of CALCIUM IONS into the pacemaker cells is responsible for the threshold depolarizing phase of the AP.

30
Q

Calcium Channel blockers:

A

o Meds that block voltage gated calcium ion channels, e.g., Verapamil.
o Used for tachycardia and some types of arrhythmias…slow the development of AP’s in the pacemaker cells.
o Also decrease the amount of work performed by the heart because less calcium enters the cardiac MUSCLE cells to activate the contractile process.

31
Q

Rhythm of Conduction System:

A

o SA node fires spontaneously 90-100 times per minute…each depolarization = one AP = 1 heartbeat.
o AV node fires at 40-60 times per minute.
o If both nodes are suppressed, fibers in ventricles by themselves fire only 20-40 times per minute.
o Artificial pacemaker needed if pace is too slow.
o Extra beats forming at other sites are called ectopic pacemakers:
o Caffeine and nicotine increase activity.
o Lyte imbalances, hypoxia, toxic reactions to drugs.
o Tachycardia: >100 beats/minute.
o Bradycardia:

32
Q

Timing of Atrial and Ventricular Excitation:

A

o SA node sets the pace since it is the fastest—pace can be modified by ANS or hormones.
o In 50 msec, excitation spreads through both atria and down to AV node.
o 100 msec delay at AV node due to smaller diameter fibers– allows atria to fully contract–filling ventricles before ventricles contract.
o In 50 msec, the excitation spreads through both ventricles simultaneously.

33
Q

Sequence of Events in Muscle Contraction:

A

o 1) Depolarization leads to positive ions rush into cell.
o 2) Reversal of membrane potential to threshold with generation of AP.
o 3) AP travels down T-tubules leads to sarcoplasmic reticulum releases stored calcium ions leads to increase in calcium ions in cytoplasm
o 4) Sliding filament hypothesis with shortening of sarcomere = muscle contraction.
o 5) Repolarization leads to calcium ions pumped back into SR leads to relaxation of muscle.

34
Q

Cardiac Muscle Contraction Phases:

A

o Depolarization:
o Cardiac cell resting membrane potential is -90mv.
o Excitation spreads through gap junctions.
o Fast Na+ channels open for rapid depolarization.
o Plateau phase:
o 250 msec (only 1msec in neuron)
o slow Ca+2 channels open, let Ca +2 enter from outside cell and from storage in sarcoplasmic reticulum, while few K+ channels open.
o Ca +2 binds to troponin to allow for actin-myosin cross-bridge formation and tension development.
o Repolarization:
o Ca+2 channels close and K+ channels open & -90mv is restored as potassium leaves the cell.
o Refractory period:
o Very long so heart can fill.

35
Q

Electrocardiogram (ECG Or EKG):

A

o EKG = a composite of all action potentials of all active cardiac cells. Can be detected at body surface and recorded by positioning electrodes at 6 positions on chest and 4 positions on the limbs, can evaluate different areas of heart.
o Allows for Evaluation of Abnormal heart rate, abnormal heart rhythms, abnormal conduction pathways, hypertrophy or atrophy of portions of the heart, and approximate location of damaged cardiac muscles.

36
Q

The 3 Deflection Waves of an EKG:

A

o P wave: Atrial depolarization.
o QRS complex: Ventricular depolarization, hides atrial repolarization.
o T wave: Ventricular repolarization.

37
Q

EKG Interval:

ST Segment

A

o Represents time when depolarized ventricular muscle cells are in the plateau phase and contracting.
o Elevated above baseline in an acute MI.
o Depressed below baseline with ischemia to heart muscle.

38
Q

Abnormal Deflection Waves and Meanings:

A

o Enlarged P wave: Enlargement of atrium.
o Missing P wave: SA node damage.
o Enlarged Q wave: MI.
o Missing QRS complex: Heart block.
o Enlarged R wave: Enlargement of ventricles.
o Abnormal ST segment: Elevated with MI.
o Flatter T wave: Insufficient oxygen to heart muscle.
o Elevated T wave: Hyperkalemia.

39
Q

Cardiac Cycle:

A
o	Single cardiac cycle = all the events associated with one heart beat:
o	Pressure changes.
o	Blood volume changes.
o	Heart sounds.
o	Arbitrarily look at 3 phases in the cardiac cycle:
o	Ventricular diastole (relaxation)
o	Atrial systole (Contraction). 
o	Ventricular systole (Contraction).
40
Q

Systole:

A

Contraction Phase

41
Q

Diastole:

A

Relaxation Phase

42
Q

Isovolumetric:

A

Volume of blood in the ventricles remains the same

43
Q

Ventricular Ejection:

A

Ventricles contract and force blood through the semilunar valves.

44
Q

Stroke Volume:

A

Actual Amount (Volume) of blood ejected per beat from each ventricle

45
Q

Important Concepts Pertaining to the Heart:

A

o Blood flow through the heart 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 ventricular 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.” (i.e., direction of bl. flow).
o Closing of heart valves creates a turbulence that results in typical heart sounds (lubb, dupp)

46
Q

End Diastolic Volume (EDV):

A

o Volume in Ventricle at end of Diastole. Usually about 130 mL.

47
Q

End Systolic Volume (ESV):

A

o Volume in ventricle at end of systole, about 60 mL.

48
Q

Stroke Volume (SV):

A

o The volume ejected per beat from each ventricle. About 70 mL.
o SV= EDV – ESV

49
Q

Ejection Fraction:

A

o Stroke Volume (SV) Divided by End Diastolic Volume (EDV) multiplied by 100.
o Normally 50-70 percent.

50
Q

Ventricular Diastole:

A

o Ventricle starts out with 60 mL of blood in it (ESV)
o Blood starts returning to the atria…the AV valves will open when enough blood accumulates in the atria for atrial pressure to be greater than ventricular pressure.
o This adds another 45 mL or so to the ventricles.

51
Q

Atrial Systole (Contraction):

A

o SA node depolarizes and APs spread thru atria.

o Both atria contract at the same time; about 25 mL is pushed into each ventricle.

52
Q

Ventricular Systole:

A

o AV node fires and causes depolarization of the ventricles.
o Ventricles START to contract. This closes the AV valves to prevent backflow of blood into the atria.
o Now all 4 valves are closed.
o Ventricles continue to contract until the pressure in the ventricles is greater than the pressure in the aorta/pulmonary trunk.
o Semilunar valves will now open then blood flows out.

53
Q

Summary of Ventricular Pressures:

A

o Ejection of blood from the LEFT ventricle occurs when left ventricular pressure exceeds aortic pressure (80 mm Hg). Pressure continues to go up in the left ventricle to about 120 mm Hg during ventricular systole.
o Ejection of blood from the RIGHT ventricle occurs when right ventricular pressure exceeds pressure in the pulmonary trunk (about 20 mm Hg). Pressure continues to go up to about 25 to 30 mm Hg. It is a LOW PRESSURE system.

54
Q

Auscultation:

A

o S1: 1st Heart Sound, created by the closing of the AV Valves.
o S2: 2nd Heart Sound, created by the closing of the SL Valves.
o S3: Caused by blood flowing in a turbulent fashion into the ventricles.
o S4: Caused by blood turbulence during atrial systole.

55
Q

Heart Murmurs:

A

o Abnormal heart sounds that are heard before, between, or after normal heart sounds.
o Can be clicking, rushing, or gurgling noises.
o Heart murmurs are common in children because their heart walls are thin and literally transmit the sound of blood rushing into the chambers easily.
o Murmurs can also indicate valve disorders.

56
Q

Cardiac Output (CO):

A
o	The amount of blood pushed into either the aorta or pulmonary trunk by a ventricle EACH MINUTE!!!!
o	CO= HR x SV
o	Mild exercise:
o	HR may increase to 100 bpm
o	SV may increase to 100 mL/beat
o	Intense exercise
o	HR may increase to 165 bpm
o	SV may increase to 127 mL/beat
57
Q

Cardiac Reserve:

A

o The difference between a person’s MAXIMUM CO and his CO at REST.
o Average cardiac reserve is 4 to 5 times resting CO.

58
Q

Regulation of Heart Rate:

A
o	Normal HR = 60 to 80 beats/minute.
o	(120 bpm is normal for infants!)
o	Tachycardia:  HR greater than 100 bpm.
o	Exercise, fever, anxiety, meds, heart dz.
o	Bradycardia:  HR less than 60 bpm. 
o	Hypothermia, dive reflex, endurance-trained athletes.
o	Regulated by ANS.
o	MEDULLA OBLONGATA contains several cardiovascular centers:
o	Cardioaccelerator center:
o	Increases sympathetic N.S.
o	Increases HR
o	Cardioinhibitory center
o	Increases parasympathetic N.S.
o	Decreases HR.
59
Q

Regulatory Input Coming into Medulla Oblongata:

A

o MEDULLA OBLONGATA gets information from: Cerebral cortex, HYPOTHALAMUS, Limbic system, Baroreceptors in the periphery, Chemoreceptors in the periphery, Proprioceptors from joints, muscles, tendons

60
Q

Positive Chronotrophic Agents:

A

o Positive chronotropic agents are things that INCREASE HEART RATE.
o Sympathetic nervous system activity:
o Increase in NE on B-1 receptors of SA node
o Causes adrenal medulla to release the HORMONES Ep and NE, which bind to same B-1 receptors on SA node.
o Stimulation of B-1 receptors of SA node increases heart rate!
o Sympathomimetic meds (e.g., pseudofed).
o Stimulant chemicals:
o Methylxanthines (caffeine, theobromine).
o Nicotine (stimulates secretion of catecholamines).
o Select hormones (e.g., thyroid hormone).
o Lyte imbalances (e.g., moderate hypercalcemia).
o Misc. factors (fever, stress, exercise, etc.

61
Q

Brainbridge Reflex:

A

o This is a reflex of the sympathetic N.S.
o Increase venous return to the heart, leads to increased atrial filling, leads to increased stretch of atria, leads to stretch stimulating SA node, leads to stretch reflexively and increases sympathetic activity.

62
Q

Negative Chronotrophic Agents:

A

o Negative chronotropic agents are things that DECREASE HEART RATE
o Parasympathetic nervous system activity:
o Increased vagal output to the heart results in the release of ACh onto muscarinic receptors of the SA Node.
o Opens ligand-gated channels that hyperpolarize the SA node cell membranes.
o Maximum vagal output can lower heart rate to 20 beats/minute!
o Inhibitory meds:
o Beta blockers.
o Calcium channel blockers.
o Parasympathomimetics.
o Lyte imbalances (e.g., hypocalcemia).
o Cold temperatures (e.g., hypothermia).
o Misc. factors (e.g., hypoxia, dive reflex, endurance-trained athletes).

63
Q

Factors Influencing Stroke Volume:

A

o PRELOAD: Amount of blood returning to the atria.
o CONTRACTILITY: The force of contraction at a given preload.
o AFTERLOAD: Resistance to the forward flow of blood, “back pressure” from aorta or pulmonary trunk.

64
Q

Preload:

A

o Frank Starling Law of the Heart
o The more the ventricles are stretched, the greater the force of contraction or the greater the EDV, the greater the force of contraction of that ventricle.
o Increased preload means Increased S! (direct relationship)
o Ways to Increase Preload:
o Increase venous return to atria and to ventricles:
• Exercise.
• Sympathetic stimulation.
• Volume overload.
• Water retention (SIADH).
• Pregnancy.
o Increase duration of ventricular diastole
• The longer the heart relaxes, the longer the filling time.

65
Q

Contractility:

A

o Contractility refers to the STRENGTH or FORCE of contraction at a given preload.
o The greater the contractility, the greater the stroke volume (direct relationship).
o Positive inotropic agents increase contractility.
o Negative inotropic agents decrease contractility.

66
Q

Positive Inotropic Agents:

A

o These agents increase the force of contraction of cardiac muscle cells.
o These agents promote the flow of calcium ions INTO the myocyte during contraction.
o Examples of positive inotropic agents:
o Hormones (NE, Ep, thyroid hm, glucagon).
o Meds (digitalis, dopamine).
o Moderate hypercalcemia.

67
Q

Negative Inotropic Agents:

A

o These agents decrease the force of contraction of cardiac muscle cells in a variety of ways.
o Examples of negative inotropic agents:
o Medications: Some Anesthetics.
o Myocardial ischemia (hypoxia) & acidosis
o Hypocalcemia
o Parasympathetic stimulation has very little (if any) effect!!!

68
Q

Afterload:

A

o Afterload is the resistance to the forward flow of blood.
o If afterload INCREASES, then stroke volume DECREASES (negative relationship).
o Things that Increase Afterload:
o Coarctation of aorta or restrictive atherosclerosis.
o High blood pressure in the aorta will decrease SV from left ventricle.
o High blood pressure in pulmonary circulation will decrease SV from right ventricle.
o Right ventricular failure due to obstructed pulmonary circulation is called COR PULMONALE.

69
Q

Congestive Heart Failure (HF):

A

o HF is the FAILURE of either ventricle to pump blood OUT of the ventricle.
o Various causes:
o Ischemic heart disease.
o Heart weakened by MI, HTN, or valvular disorders.
o Congenital defects.
o Dilated Cardiomyopathy (DCM): Ventricles become over-stretched and flabby.
o Causes of DCM: Drug toxicity, Alcohol, Cocaine, Excess catecholamines, Hyperthyroidism, Infection with inflammation of heart (pathogens).

70
Q

Left-Sided Heart Failure:

A

o Left ventricle fails to eject adequate amounts of blood.
o Leads to pulmonary edema.
o Symptoms: SOB, crackles in lungs.

71
Q

Right-Sided Heart Failure:

A

o Right ventricle fails to eject adequate amounts of blood.

o Leads to: Systemic edema, hepatomegaly, and ascites, and distension of external jugular veins.

72
Q

Treatment of Heart Failure:

A

o Must treat the cause!
o Treat any infection
o Surgery for new valves, reconstruction of ventricles, stents/bypass surgery, even new heart transplant!
o Typical meds:
o Diuretics to decrease edema (decreases preload)
o Reduce afterload with meds that decrease BP.
o Increase contractility with meds that increase the force of contraction of the heart (e.g., digitalis).