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Y-HSC 111 > chapter 18 > Flashcards

chapter 18 Flashcards

1
Q

size, location, orientation of heart

A

about the size of a fist
located in the pericardial cavity and inferior mediastinum
positioned between ribs 2 to 5 oblique from midline, apex points to left hip

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2
Q

describe the three layers of the pericardium

A

superficial fibrous pericardium - outermost protective layer. tough dense C/T
Parietal Layer - lines the internal surface of the fibrous pericardium
Visceral layer - (Epicardium) separated from the parietal layer by a serous fluid filled cavity. is the outermost layer of the actual heart.

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3
Q

describe the layers of the heart wall

A

Epicardium - outermost squamous epithelium. produces serous fluid, and REDUCES FRICTION
Myocardium - thick Spiral bundles of cardiac muscle. Anchors the muscle fivers and limits the spread of action potentials. PUMPS THE BLOOD THROUGHOUT THE BODY when it contracts.
Endocardium - continuous with endothelial lining of blood vessels, innermost layer that allows a FRICTION FREE SURFACE FOR BLOOD TO FLOW EASILY

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4
Q

name the three surface grooves that carry coronary blood to the heart walls

A

atrioventricular sulcus
anterior interventricular sulcus
posterior interventricular sulcus

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5
Q

describe the atria’s of the heart

A

walls are ridged with pectinate muscles. they are the receiving chambers of the heart. receive and pump blood into the ventricles. they have auricles that increase the atrial volume. Left atrium received the pulmonary veins and the Right atrium receives the vena ceva

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6
Q

describe the ventricles

A

they are the discharging chambers and are separated by the inter ventricular septum. Thick walled with trabecular carnae form ridges in wall. Cone shaped papillary muscles anchor chordae tendonae of valves

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7
Q

compare RIGHT and LEFT ventricles

A

LEFT - receives oxygenated blood from the pulmonary veins, thicker walls (than R), pumps blood through aorta into the systemic circuit AND coronary circuit
RIGHT - receives de-oxygenated blood from the vena cava, thinner walls (than L), pumps blood through pulmonary trunk to the pulmonary circuit

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8
Q

describe the pulmonary circuit

A

short, low pressure circulation. moves blood to and from the lungs for gas exchange. starts in the right ventricle and returns into the left atrium and ventricle

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9
Q

describe the systemic circuit

A

is a long high pressure circuit that moves oxygenated blood to and from tissues for gas exchange between blood and tissue cells. starts in the left ventricle, into systemic attires and capillaries, then returns to right ventricle via veins.

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10
Q

describe the coronary circuit

A
  1. supplies blood to the heart muscle itself (myocardium). artery supply varies and contains many anastomoses (junctions) among the branches.
  2. Arteries - R and L coronary arteries, marginal, circumflex and anterior inter ventricular arteries.
  3. Veins - Small cardiac, anterior cardiac, and great cardiac veins (into the coronary sinus/right atrium)
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11
Q

Homeostatic imbalances of Coronary Circulation

A
  1. Angina Pectoris - acute thoracic pain caused by temporary blockage in blood supply to the myocardium. temporary lack of O2 weakens the cells
  2. Myocardial infarction (MI - heart attack) - prolonged coronary blockage, prolonged lack of O2, cells die. prognosis depends on extent and location of damage (severity)
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12
Q

describe the atrioventricular (AV) valves

A
  1. right TRICUSPID valve - Prevents back flow into the right atrium when the right ventricle contracts
  2. left BICUSPID valve - Prevents back flow into the left atrium when left ventricle contracts
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13
Q

what the function of the chordae tendonae

A

anchors the atrioventricular (AV) valve cusps to papillary muscles and prevents the flaps from being inverted (pushed back into) the atria during contraction

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14
Q

what is the function of the papillary muscles

A

contract just before the ventricles to take take up the slack in the chordae tendonae and prevent the valves from being pushed open backwards into the atria

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15
Q

what is the function of the semilunar (SL) valves

A

Right SL valve prevents back flow into the R ventricle when ventricle relaxes.
Left SL valve prevents back flow into the left ventricle when ventricle relaxes

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16
Q

describe the heart sounds

A

LUB-DUB. 1st sound is the closing of the AV valves (start of contraction) the 2nd sound is the closing of the SL valves (start of relaxation).

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17
Q

what is a heart murmur

A

abnormal heart sounds most often indicative of valve problems

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18
Q

describe imbalances in valve function

A

leaky valves - produce murmurs, turbulence in flow

stenosis - narrowing of valves (stiffening), impedes flow

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19
Q

describe the anatomy of muscle cells

A

striated, short, fat, branched, uninucleate and interconnected by intercalated discs. Connective tissue matrix, T-Tubules but less numerous (no Triads). Many mitochondria, irregular sarcomeres.
Intercalated discs or junctions between cells (desmosomes and gap junctions)
HEART MUSCLE BEHAVES AS A FUNCTIONAL SYNCYTIUM, it contracts as a single unit

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20
Q

how is cardiac muscle different than skeletal muscle

A

1% of cells are auto excitable (pacemakers), the rest are contractile (PUMP), it has an all or nothing contraction, and long refractory period which enables the pumping motion to take place

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21
Q

describe what the pacemaker cells do

A
  1. specialized cardiac cell that initiates and distributes impulses.
  2. auto-rhythmic cells have an unstable resting potential (pacemaker potential) that continually depolarizes
  3. has a resting potential of -60mv
  4. slow depolarization to threshold potential due to open slow sodium channels
  5. fast Calcium gates open when 40mv is reached and calcium rushes in
  6. membrane depolarizes further and generates action potential
  7. Calcium gates shut, Potassium opens, K leaves the cell and depolarization occurs
  8. Action potential is transmitted to the rest of the myocardium via intrinsic conduction system
  9. heart contracts: first the atria, then the ventricles
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22
Q

key points to the intrinsic conduction system

A
  1. coordinates heart activity
  2. causes the heart to beat faster
  3. Order of auto rhythmic cells.
    A) Sinoatrial Node (pacemaker) generates the sinus rhythm (75x/min) and depolarizes.
    B) intermodal pathway to Atrioventricular (AV) node (smaller fibers, fewer gap junctions, delayed impulse 0.1 sec)
    C) AV Bundle (Bundle of HIS) electrically connects atria and ventricles then branches into L and R pathways on the septum towards the apex.
    D) purkinje fibers complete the pathway into the apex and ventricular walls. AV bundle and Purkinje fibers depolarize only 30 times/minute in absence of AV node
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23
Q

describe the sequence of stimulation and contraction

A

SA node develops pacemaker potential, transmits to walls of atria, atria begin to contract, impulse delayed 0.1sec at AV node (atria complete contraction), impulse transmits from AV node to walls of ventricles, ventricles contract, produces the NORMAL SINUS RHYTHM.

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24
Q

What is an arrhythmia

A

irregular hert rhythm

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25
Q

what is fibrillation

A

rapid, irregular contractions. (useless for pumping blood)

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26
Q

defective SA node may result in…

A

ectopic focus (abnormal pacemaker takes over) causes a junctional rhythm if AV node takes over

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27
Q

defective AV node may result in…

A

partial to total heart block. impulses don’t reach ventricles and beat at different rate than atrias

28
Q

what can coffee or nicotine do to the heart

A

PVC - premature ventricular contraction (extra contractions)

29
Q

describe the contraction of contractile cells

A
  1. stimulus (action potential) from pacemaker cells
  2. A) Na+ gates open, rush in, positive feedback = depolarization. B) Fast Calcium gates open, calcium enters, triggers the Ca gates to open in the sarcoplasmic reticulum.
  3. Na+ gates shut, SR releases Calcium into cell
  4. Calcium binds to troponin
  5. crossbridges form, myofiliment slide, etc. = Contraction
  6. slow calcium gates stay open, which prolongs contraction, causing the depolarization plateau
  7. Potassium gates open, moves out = repolarization
  8. long absolute refractory period, prevents tetany (stay contracted), and ensures rhythmic pumping
30
Q

importance of oxygen for homeostatic imbalances

A
  1. heart depends on aerobic respiration, lack of oxygen has a serious consequences
  2. Ischemia - blockage of coronary artery leads to deficient oxygen supply to myocardium
  3. Angina pectoris - temporary blockage of oxygen flow to the heart. causes pain in chest
  4. heart attack - results from prolonged blockage of O supply so that the myocardial cells die. Outcome depends on the extent of damage to tissue
  5. FUEL - the cardiac muscle is very adaptable and can use glucose, fatty acids, lactic acid (whatever is available) as long as OXYGEN is there as it it the limiting factor for heart function
31
Q

what is an electrocardiogram (ECG)

A

its a composite of all the action potentials generated by nodal and contractile cells at a given time

32
Q

describe the 3 deflection waves

A
  1. P wave = depolarization of the Atria.
  2. QRS complex = depolarization of the ventricles
  3. T wave = repolarization of ventricles
  4. repolarization of atria is masked by the ventricle depolarization (QRS complex)
33
Q

what is a cardiac cycle

A

all events associated with blood flow through the heart during one complete heart beat. Systole (contraction) and diastole (relaxation)

34
Q

describe the phases of the cardiac cycle

A
  1. ventricular filling, blood flows into ventricles. 70% passively, 30% by atrial systole. END DIASTOLIC VOLUME - the blood in each ventricle at end of ventricular diastole.
  2. ventricular systole, atria relax, ventricles begin to contract, isovolumetric phase (all valves close), then ejection phase where SL valves open, leaving END SYSTOLIC VOLUME - the blood remaining in each ventricle at end of ventricular systole.
35
Q

what is isovolumetric relaxation

A

occurs early in diastole. the ventricles relax and bloodflow in aorta and pulmonary trunk closes the semilunar (SL) valve and causes dicrotic notch, or brief rise in aortic pressure.

36
Q

describe the Quiescent period

A

Both atria and ventricles are relaxed. It last about 0.4 sec

37
Q

describe the length of cardiac cycle

A 
about 0.8 sec. and 75 bpm
-atrial systole 0.1sec
-ventricular systole 0.3 sec
-quiescent period 0.4sec
TOTATL length = 0.8sec
38
Q

define cardiac output

A 
Volume of blood pumped by each ventricle in one minute
Cardiac Output (CO) = Heart Rate (HR - beats per minute) X Stroke Volume (SV - volume of blood pumped out by each beat)
CO = HR x SV (in ml/minutes)
39
Q

what affects cardiac output

A

increase/decrease of SV or HR will result in increase/decrease of CO

40
Q

describe stroke volume

A

EDV - ESV = SV
end diastole volume (max volume in ventricle prior to contraction) MINUS volume left in the ventricles at the end of systole contraction EQUALS stroke volume in ml/beat

41
Q

what are the three main factors affecting stroke volume (SV)

A

PRELOAD, CONTRACTILITY, AFTERLOAD
Preload - stretch of cardiac muscle before it contracts. EDV is increased by slow heart beat / exercise. whereas EDV is decreased by a very rapid HR and decreased blood volume.
Contractility - caused by more calcium ions from SR and extracellular fluid increases force of contraction. (+) inotropic agents increase contraction, (-) inotropic agents decrease contraction.
Afterload - pressure that must be overcome for ventricles to eject blood. back pressure makes it more difficult for ventricles to empty (caused by hypertension)

42
Q

what affects cardiac output

A

increase/decrease of SV or HR will result in increase/decrease of CO

43
Q

describe stroke volume

A

EDV - ESV = SV
end diastole volume (max volume in ventricle prior to contraction) MINUS volume left in the ventricles at the end of systole contraction EQUALS stroke volume in ml/beat

44
Q

what are the three main factors affecting stroke volume (SV)

A

PRELOAD, CONTRACTILITY, AFTERLOAD

45
Q

describe the preload stage of stroke volume (SV)

A
  1. stretch of cardiac muscle before contraction
  2. Frank Starling law of the heart - the more the heart muscles is stretched, the harder it will contract.
  3. EDV is increased by slow heart beat rate and exercise. And increase venous return.
  4. EDV is decreased by a very rapid heart rate and decreased blood volume (blood loss and dehydration)
46
Q

describe the contractility stage of stroke volume (SV)

A
  1. increase in force of contraction independent of muscle stretch and EDV
  2. caused by more Ca++ from S/R and extracellular fluid
  3. Positive INOTROPIC agents increase contractility (sympathetic nervous system release of norepinephrine)
  4. Negative INOTROPIC agent decrease contractility (calcium channels blocked, acidosis)
47
Q

describe the afterload stage of stroke volume (SV)

A
  1. pressure must be overcome for ventricles to eject blood
  2. back pressure in vascular system makes it harder for ventricles to empty
  3. caused by hypertension (high BP increases after load, resulting in increase ESV & decrease SV = decreased CO
48
Q

what do chronotropic factors do to the heart rate

A

positive will increase the heart rate

negative will decrease the heart rate

49
Q

How is the heart beat rate modified

A

through autonomic nervous system regulation located in the medulla oblongata.

  • Cardioacceleratory centre innervates SA and AV nodes through sympathetic neurone
  • Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves
50
Q

describe the sympathetic nervous system

A

activated by emotional or physical stressors “fight or flight”
-mediated by norephinephrine stimulates the SA node

51
Q

describe the parasympathetic nervous system

A

mediated by acetylcholine and inhibits the SA node
at rest, heart rate = 75bpm
vagus nerve carries fibers to the heart. if vagus nerves were cut heart rate would increase by 25 bpm

52
Q

what are the baroreceptors (atrial bainbridge reflex)

A

stretching of atrial walls stimulates the SA node and also stimulates sympathetic reflexes.

53
Q

what hormones regulate heart rate

A
  • Epinephrine from adrenal medulla increases heart rate and contractibility.
  • Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine
54
Q

What intra- and extracellular ion concentrations must be maintained for normal heart function

A

Calcium, potassium and sodium ions

55
Q

what is hypercalcemia

A

increased Ca++ levels that increases heart rate

56
Q

what is hypocalcemia

A

decreased Ca++ levels that decreases heart rate

57
Q

what is hyperkalemia

A

increased K+ levels that leads to heart block and arrest

58
Q

what is hypokalemia

A

decreased K+ levels that leads to a feeble heart rate

59
Q

hypernatremia

A

increased Na+ to water ratio causing decreased heart rate (dehydration)

60
Q

what factors influence heart rate

A

Age
Gender
Exercise
Body temperature

61
Q

describe tachycardia

A

abnormally fast heart rate (>100bpm).
may lead to fibrillation.
decreases venous return which leads to decreased cardio output

62
Q

describe bradycardia

A

abnormally slow hear rate (<60bpm)
inadequate blood circulation
may be a desirable result of endurance training

63
Q

describe congestive heart failure (CHF)

A

progressive condition where the cardiac output is so low that blood circulation is inadequate to meet tissue needs
caused by:
-coronary atherosclerosis (blockage of arteries with fat)
-persistent high BP (weakens the heart)
-multiple myocardial infarcts (contractile cells replaced with scar tissue. myocardial cells die)

64
Q

describe dilated cardiomyopathy (DCM)

A

“flabby ventricles” ventricles enlarge but lose ability to contract. Caused by alcohol, cocaine, inflammation after infection

65
Q

describe LEFT and RIGHT sided heart failure

A

LEFT - causes pulmonary congestion and blood accumulates around lungs. Fluid leaks into lungs
RIGHT - causes systemic congestion (edema) and blood accumulates at extremities. Fluid leaks into interstitial spaces in tissues

66
Q

name some age related changes affecting the heart

A
  1. Sclerosis and thickening of valve flaps causing them not to close tightly, back flow occurs
  2. decline in cardiac reserve - heart has less ability to stress
  3. fibrosis of cardiac muscle - muscle replaced by scar tissue and can’t pump as effectively
  4. Atherosclerosis - artery blockage - diet probably major cause leads to hypertensive heart disease and occlusion of coronary arteries. (decreased Oxygen supply to affected parts.

Y-HSC 111 (9 decks)

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