anatomy ch 18 Flashcards

1
Q

cardiovascular system - blood circulation

A
  • delivers to tissues
    • fresh nutrients
    • hormones
    • electrolytes
  • removes from tissues
    • metabolic wastes
      • nitrogenous wastes
      • carbon dioxide
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2
Q

anatomy of the heart

A
  • heart is in the mediastinum
  • size of a fist
  • weighs less than 1lb
  • 2/3 of mass lies left of body midline
  • broad base points to right shoulder
  • narrow apex points to left hip
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3
Q

point of maximal intensity (PMI)

A
  • where apex contacts chest wall
    • between 5th and 6th rib on left side
  • heat beats felt strongest here
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4
Q

heart coverings - pericardium

A
  • double walled sac that encloses the heart

- two layers: fibrous and serous

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5
Q

fibrous pericardium

A
  • loose, superficial layer
  • tough
    • dense irregular connective tissue
  • functions:
    • protect
    • anchor
    • prevent overfilling
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6
Q

serous pericardium

A
  • two layers:
    • parietal (outer)
    • visceral (inner) AKA epicardium
  • pericardial cavity
    • fluid filled space in between
  • function: reduces friction
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7
Q

heart defect - pericarditis

A
  • inflammation of the pericardium
  • roughens serous membrane surfaces
  • heart rubs against pericardium as it beats
    • creaking sound
    • deep pain over sternum
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8
Q

heart defect - cardiac tamponade

A
  • caused by severe or prolonged pericarditis
  • large amount of fluid accumulates in
    pericardial cavity
  • heart is compressed - interferes w/
    beating
  • cardiocentesis
    -drains fluid with catheter
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9
Q

layers of heart wall - epicardium

A
  • most superficial
  • same as the visceral layer of the serous
    pericardium
  • infiltrated by fat with aging
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10
Q

layers of the heart - myocardium

A
  • middle layer of heart wall
    • most of heart mass
    • thickness varies with different part
  • made mostly of cardiac muscle cells
    • layer that contracts
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11
Q

layers of the heart - endocardium

A
  • inner layer
    • lines chambers and valves
    • continuous with lining of blood vessels
  • glistening white smooth endothelium
  • reduces friction between blood and heart
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12
Q

circulation of blood: veins

A
  • veins carry blood into heart
  • deoxygenated(blue) when returning from
    systemic circulatory system
    -superior vena cava
    -inferior vena cava
    -coronary sinus
  • oxygenated (red) when returning from
    lungs
    - 4 pulmonary veins
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13
Q

circulation of blood - arteries

A
  • carry blood into body
  • deoxyginated(blue) when leaving for lungs
    - pulmonary arteries
  • oxygenated (red) when leaving for
    systemic circulatory system
    -aorta
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14
Q

pulmonary pump

A
  • right side of heart

- pumps deoxygenated blood to lungs

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15
Q

systemic pump

A
  • left side of heart

- pumps oxygenated blood to body

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16
Q

ventricular contraction

A
  • ejects blood into pulmonary and
    systemic circuits
  • equal amount of blood goes into each
  • systemic circuit is longer
    -has more resistance to blood flow
    -myocardium of left ventricle is thickest
    - must push harder to get blood out
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17
Q

blood flow

A
  • four valves keep blood flow unidirectional
  • thin flaps of connective tissue
  • closed valves block blood flow
  • open valves allow blood to pass through
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18
Q

atrioventricular (AV) valves

A
  • connect atria to ventricles
  • open when bp in atria<bp in ventricles
  • close when ventricles contract
    • prevents backflow into the atria
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19
Q

two AV valves

A
  • tricuspid valve - right AV valve between
    right atrium and ventricle. 3 flaps
  • bicuspid valve (mitral)- left AV valve
    between left atrium and ventricle. 2 flaps
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20
Q

chordae tendineae (heart strings)

A
  • collagen cords connecting AV valves to
    ventricular wall at papillary muscle
  • ventricular contraction tugs on cords.
    Holds valve flaps closed against high
    intraventricular pressure
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21
Q

semilunar (SL) valves

A
  • made of 3 flaps of tissue
  • located between ventricles and arteries
  • open when ventricles contract
  • close when ventricles relax
    • blood flows backward filling cusps
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22
Q

two SL valves

A
  • aortic SL valve - on left between aorta
    and left ventricle
  • Pulmonary SL valve - on right between
    pulmonary trunk and right ventricle
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23
Q

heart defect - incompetent valves

A
  • do not close all the way; leaky
  • causes backflow; heart re-pumps same
    blood
  • danger of inadequate blood flow to tissues
  • diagnose by abnormal heart sounds
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24
Q

replacement of incompetent valves

A
  • mechanical valves
    -made from metal
    -last a long time
    -patient needs blood thinners
  • biosynthetic valves
    -made from treated tissue
    -cadavers, pig valves, cow
    pericardium
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25
Q

heart defect - mitral valve prolapse

A
  • chordae tendineae don’t hold mitral valve
    in place during contraction. Bulges into
    left atrium
  • can lead to:
    -incompetent valve
    -irregular heatbeat
    -pain and shortness of breath
  • fairly common; 1% population. 7% autopsy
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26
Q

Coronary circulation

A
  • heart requires a large amount of fresh
    blood. without it cardiac tissue dies
  • coronary arteries supply the heart with
    blood
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27
Q

coronary arteries

A
  • main two leaving the aorta:
    -left and right coronary arteries
  • deliver blood when the heart is relaxed.
    -squeezed shut by contraction of
    myocardium
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28
Q

cardiac veins

A
  • collect blood and return it to heart
  • great, middle and small
    -drain blood into coronary sinus
  • coronary sinus - drains directly into the
    right atrium
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29
Q

heart defect - angina pectoris

A
  • thoracid pain
  • brief loss of blood to myocardium
  • causes:
    -stress induces spasms of coronary
    arteries
    -physical activity
  • cardiac muscle cells weaken but don’t die
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30
Q

heart defect - myocardial infarction (MI)

A
  • heat attack
  • caused by prolonged coronary blockage
    -blood clots or plaque
  • cardiac muscle cells die
    -replaced by connective tissue
    -if too much death, heart won’t beat
  • dead cells fall apart releasing proteins
    that can be tested for CPK & troponin
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31
Q

Cardiac cycle

A
  • events that occur in a single heartbeat
  • systole - contract
  • diastole - relax
  • atria and ventricles contract and relax at
    different times in cardiac cycle
  • when heart is in systole, ventricles are
    contracting
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32
Q

systole

A
  • contraction increases intraventricular
    pressure
    -SL valves open, blood flows into
    arteries
  • atria are relaxed (atrial diastole) when
    ventricle contracts
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33
Q

diastole

A
  • period of ventricular relaxation
  • blood flows through AV valves into
    ventricles
    -lasts longer than systole
    -early and mid-late diastole
    -atria are in systole during part of diastole
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34
Q

overview of steps cadiac cycle

A
  1. ventricular filling during mid-late diastole
  2. ventricular systole - two stages
  3. isovolumetric relaxation during early
    diastole
35
Q

Step 1 - ventricular filling

A
  • occurs in mid-late diastole
  • ventricles are relaxed - pressure is low
  • SL valves are closed
  • AV valves are open
    -80% of blood passively flows into
    ventricles
  • ends with atrial contraction
    -remaining 20% of blood forced into
    ventricles
36
Q

step 2 - ventricular systole

A
  • occurs during systole
  • atria relax and ventricles begin contracting
    • increases pressure inside ventricles
    • closes AV valves
  • 2 phases of ventricular systole
    • isovolumetric contraction
    • ventricular ejection
37
Q

isovolumetric contraction

A
  • AV valves close before SL valves open
    • all valves close for a split second
  • ventricles are at fullest point
    • EDV - end diastolic volume
38
Q

ventricular ejection

A
  • pressure in ventricles exceeds pressure
    in large arteries
  • SL valves open - pressure > 120mmHG
  • Atria begin filling
39
Q

step 3 - isovolumetric relaxation

A
  • occurs during early diastole
  • ventricles relax
    -pressure decrease causes SL valves
    to close
    -when aortic SL valve closes pressure
    in aorta rises - dicrotic notch
  • AV valves still closed
  • ventricles are at their emptiest
    -ESV - end systolic volume
40
Q

stroke volume (SV)

A
  • the total amount of blood ejected from
    one ventricle in one cardiac cycle
  • EDV-ESV = SV
  • equal amounts of blood leave right and
    left ventricles
41
Q

heart defect - asystole

A
  • period when heart fails to contract
    • neither atria nor ventricles contract
  • no electrical signals from cardiac muscle
    • flatline
42
Q

cardiac tissue characteristics

A
  • cardiac tissue has two cell types
  • cardiac muscle cells - actually contract
  • pacemaker cells
    • look same but don’t contract
    • located along conduction pathways
    • control timing of contraction
43
Q

characteristics of cardiac muscle cells

A
  • short, fat, may be branched
  • one or two nuclei
  • striated - sarcomeres of actin and myosin
  • physically connected at intercalated discs
    -gap junctions - allow current to pass
    from cell to cell
    -desmosomes - keep tissue from
    tearing during contraction
  • contain over 10x more mitochondria than
    skeletal muscle
  • quickly die without oxygen
    -ischemia
    -1-3 hours
44
Q

cardiac electrophysiology

A
  • resting membrane potential is -90mV
  • established by outward movement of K+
    ions
    -K+ leak channels are always open
45
Q

cardiac electrophysiology - depolarization

A
  • voltage-gated Na+ channels open
    • faster than in skeletal muscle
    • Na+ rapidly flows into cell
  • Sarcolemma depolarizes at +30mV
46
Q

depolarization triggers contraction

A
- at +30mV voltage-gated slow calcium 
   channels open
      -calcium enters the cell
      -causes contraction
      -plateau on graph
47
Q

repolarization

A
  • voltage-gated K+ channels open and K+
    leaves the cell
    -membrane potential returns to -90mV
48
Q

refractory period

A
  • time when cell cannot depolarize again
  • longer in cardiac muscle than skeletal
  • prevents tetany
    • cramps, spasms, tremors
49
Q

characteristics of pacemaker cells

A
  • do not contract
  • spontaneously produce action potentials
    -autorhythmic
  • gap junctions spread the depolarizing
    current to cardiac muscle cells
    -causing contraction
  • located throughout heart along special
    conduction pathways
50
Q

pacemaker electrophysiology

A
  • hovers around -60mV
  • due to closing of K+ channels and
    opening of slow Na+ channels
    -cell slowly becomes positive
  • in most excitable cells resting membrane
    potential is constant
    -K+ leak channels always open
51
Q

pacemaker electrophysiology

A
  • threshold is -40mV
  • At -40mV voltage-gated calcium
    channels open
    -causes action potential - depolarize
    to 0mV
    -unique to pacemakers - usually Na+
    influx causes action potential
    -triggers action potential in contractile
    cells
52
Q

pacemaker electrophysiology- repolarization

A
  • voltage-gated K+ channels open

- same as in other muscle cells

53
Q

conduction pathways

A
  • run throughout myocardium
  • made of pacemaker cells
  • connected to cardiac muscle cells by
    gap junctions
  • act as wires carrying the message to
    contract
54
Q

sinoatrial (SA) node

A
  • initiates heart beat
  • small mass of pacemaker cells in the
    right atrial wall
    -inferior to the superior vena cava
  • generates about 75 impulses per minute
    -faster than any other heart cell
  • true pacemaker of the heart
    -where every beat begins
55
Q

bachmann’s bundle

A
  • connects right and left atria
  • depolarization wave is quickly sent to left
    atrium, keeping atria in synch
  • depolarization of SA node causes both
    atria to contract at the same time
  • no gap junctions between atrial and
    ventricular myocardium
    -ventricles do not contract
56
Q

internodal pathways

A
  • connect SA to AV node
  • depolarization wave travels quickly to the
    atrioventricluar node
    -located in the interatrial septum
    -near the tricuspid valve
57
Q

AV node - delays depolarization

A
  • delays depolarization by 100ms
    -smaller diameter
    -fewer gap junctions = bottleneck
  • enough time for atria to finish contraction
    before ventricles start
  • generates 50 impulses per minute
    -can run the heart if SA node is
    damaged
58
Q

atrioventricular bundle

A
  • connects AV node to ventricles
  • AKA bundle of His
  • only electrical connection between the
    atria and the ventricles
  • splits into the right and left bundle
    branches
  • bundles continue on to form Purkinje fibers
59
Q

perkinje fibers

A
- depolarize the contractile cells of the 
   ventricles
- AKA subendocardial conducting network
- also innervate papillary muscles
     -anchor chordae tendineae
- ventricles contract from the apex
     - push blood superiorly
     - b/c of anatomy of pathway
- 220 ms from SA node to systole
60
Q

ion imbalances - hypercalcemia

A

-too much calcium
-causes prolonged and spastic heart
contractions

61
Q

ion imbalances - hypocalcemia

A
  • low calcium levels

- reduces the force of each heartbeat

62
Q

ion imbalances - hyperkalemia

A

-high potassium levels
-speeds up membrane repolarization
disrupting heart rhythm

63
Q

ion imbalances - hypernatremia

A
  • blood Na+ concentration is too high
  • prevents the entry of calcium into the
    myocardium
  • heart beats feebly
64
Q

heart defect - arrhythmia

A
  • uncoordinated atrial and ventricular
    contraction
    -often the ventricles contract too soon
    and do not properly fill with blood
    -types of arrhythmia:
    -paroxysmal atrial tachycardia (PAT)
    -bursts of atrial contractions
    -ventricular tachycardia (V-tac)
    -rapid, uncoordinated ventricular
    contractions
65
Q

heart defect - fibrillation

A
  • rapid and irregular contraction of cardiac
    muscle
    -tachycardia can lead to fibrillation
  • a defibrillator can be used to depolarize
    the heart
    -restarts entire electrical system
66
Q

heart defect - ectopic focus

A
- inappropriate region of the heart controls 
   rhythm
      -can appear in atria or ventricles
- caused by:
       -ischemic damage to conduction 
         pathways
       -stimulants
       -fever
- can lead to arrhythmias and fibrillation
67
Q

heart defect - heart block

A
  • damage to AV node or AV bundle
    -drugs or disease
  • first degree
    -depolarization is delayed for too long
  • second degree
    -only some of the impulses are
    transmitted
  • third degree
    -no action potential pass to the
    ventricles - AKA complete heart block
68
Q

cardiac output (CO)

A
- the amount of blood pumped out by each 
   ventricle in 1 minute
- cardiac output = heart rate x stroke 
   volume. CO=HR x SV
- stroke volume = end diastolic - end 
    diastolic volume. SV= EDV-ESV
69
Q

heart rate

A
  • how often the heart contracts
  • average is about 75 beats per minute
  • chronotropic effectors change the speed
    of heart, positive or negative
70
Q

positive chronotropic factors increase heart rate

A
- activation of the sympathetic nervous 
   system
        -epi/norepinephrine
- T3/T4
- heat
71
Q

tachycardia (hurry heart)

A
  • abnormally fast heart beat
    - greater than 100 bpm
  • caused by:
    • fever
    • stess
    • drugs
    • heart disease
  • can lead to fibrillation
72
Q

negative chronotropic factors decrease heart rate

A
  • activation of the parasympathetic nervous
    system, via vagus nerve
  • cold
73
Q

bradycardia

A
  • abnormally slow heart rate
    -less than 60 bpm
  • caused by:
    -hypothermia
    -drugs; heroin THC
    -parasympathetic nervous system
    activation
74
Q

cardiac output - stroke volume

A
  • SV=EDV-ESV
  • three factors affects a hearts SV
    • degree of stretch of the heart muscle
      = preload
      -backpressure exerted by arterial blood
      vessels = afterload
      -force of contraction = contractility
75
Q

preload - degree of stretch

A
  • more stretch = larger EDV
    -larger EDV = larger SV
  • frank-starling law:
    -heart will pump any amount of blood
    delivered to it in a single stroke
  • increasing venous return increases
    stretch
    -which increases force of contraction
76
Q

afterload - back pressure from arterial blood vessels

A
  • vascular resistance to cardiac emptying
    during systole
    -must be overcome to force blood out
    of heart
  • if a person has a high diastolic bp
    -heart must contract with greater
    force to pump the same amount of
    blood; heart works harder
77
Q

contractility - force of contraction

A
  • a measure of how much force is
    generated by each cardiac cell
  • inotropic effectors change contractility
    -positive inotropic effectors - increase
    force
    -negative inotropic effectors - decrease
    force
78
Q

positive inotropic effectors

A
  • activation of sympathetic nervous system
  • glucagon
  • TH
  • epi/norepinephrine
  • digitalis
    -given when heart not pumping enough
    blood - congestive heart failure
79
Q

negative inotropic effectors

A
  • acidosis - excessive H+
  • high extracellular K+
  • calcium channel blockers
    • decrease time of contraction
80
Q

heart defect - heart palpatations

A
  • increased force of contraction causes a
    noticeable heartbeat
  • most are not life threatening -
    symptomatic of mild arrhythmias
81
Q

heart defect - congestive heart failure

A
  • weak or damaged myocardium
    -heart can not maintain adequate blood
    flow
  • causes:
    -multiple myocardial infarctions
    -hypertension
    -coronary atherosclerosis
  • two types:
    • pulmonary
      -peripheral
82
Q

pulmonary congestion

A
  • left side of heart fails
    • right side still pumping away into lungs
  • blood is trapped in pulmonary circuit
    • causes pulmonary edema
    • interferes with gas exchange in lungs
83
Q

peripheral congestion (Cor pulmonale)

A
  • right side of heart fails
  • blood accumulates in systemic circulation
  • caused by high bp in pulmonary arteries
    • acute cases due to embolism
    • chronic cases due to lung damage
      • usually caused by smoking
84
Q

heart defect - fibrosis

A
- dead contractile cells are replaced with 
   non-contractile scar tissue
- interferes with
     -contraction
     - electrical conduction