CVP Flashcards

1
Q

___ is the number one cause of death, what is number two?

A

cardiovascular disease, cancer

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2
Q

CVD - major underlying cause is ___ due to (4).

A

ischemia, 1. atherosclerosis (plaquing), 2. White thrombus (platelets), 3. Red thrombus (RBC/fibrin net), 4. artery spasm

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3
Q

% occlusion before diminished blood flow?

A

70%

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4
Q

what is linked to atherogenesis?

A

high blood cholesterol

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5
Q

inflammatory mechanisms couple ___ to ___

A

dyslipidemia to artheroma formation (plaque)

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6
Q

what characterize early atherogenesis?

A

leukocyte recruitment and expression of pro-inflammatory cytokines

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7
Q

inflammatory pathways promote ___, which is responsible for (2)

A

thrombosis, MI and most strokes

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8
Q

___ can modulate ___

A

nervous system can modulate inflammation

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9
Q

Define hemostasis

A

prevention of blood loss

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10
Q

What are the four mechanisms of hemostasis?

A
  1. vascular spasm
  2. formation of a platelet plug
  3. blood coagulation
  4. fibrous tissue growth to seal
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11
Q

Hemostasis - Vascular Constriction (associated with trauma) - list the three types

A
  1. Neural reflexes
  2. local myogenic spasm
  3. local humoral factors
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12
Q

Neural reflexes - ___ induced constriction from ___

A

SNS, pain

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13
Q

Local myogenic spasm is responsible for?

A

most of the constriction

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14
Q

Local humoral factors include ___ from ___, esp. important in?

A

thromboxane A2, platelets, smaller vessels

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15
Q

___ is proportional to ___

A

degree of spasm, severity of the trauma

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16
Q

Platelets function as ___ but cannot ___

A

a whole, divide

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17
Q

Platelets contain (7)

A
  1. contractile proteins (actin, myosin)
  2. enzymes,
  3. calcium
  4. ADP and ATP
  5. Thromboxane A2
  6. serotonin
  7. growth factors
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18
Q

Platelet cell membrane contain ___ that avoid normal ___ but adhere to? They also contain ___ containing ___(aka___)

A

glycoproteins, endothelium, damaged area, phospholipids, platelet factor 3, thromboplastin (initiates clotting)

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19
Q

Platelet activation - When platelets contact damaged area they do what four things?

A
  1. swell
  2. irregular form w/ irradiating processes protruding from surface
  3. contractile proteins contract causing granule release
  4. secrete ADP, Thromboxane A2, and serotonin
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20
Q

Thromboxane A2 is a ___, meaning?

A

vasoconstrictor, constriction of smooth muscle

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21
Q

Thromboxane A2 potentiates the release of ___. Is this essential for release to occur?

A

granule contents, not essential but does accelerate process

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22
Q

Could a platelet activate with blockage of Thromboxane A2?

A

Yes, it would accelerate

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23
Q

What produces platelets?

A

bone marrow

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24
Q

Platelets are important in ___ because?

A

minute ruptures, lack of platelets associated with small hemorrhagic areas under skin and throughout internal tissues

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25
Q

Platelets have a half life of? Eliminated primarily by___ in the ___. What is a normal range?

A

8-12 days, macrophage action, spleen, 150,000 to 300,000

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26
Q

What is the role of endothelium?

A

prevents platelet aggregation (dialates)

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27
Q

What is endothelium?

A

inner lining of blood vessels

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28
Q

___ and ___ are opposites

A

Thromboxane A2 and prolactin

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29
Q

What produces PG12 (prostacyelin), which does what 3 things?

A

endothelium, 1. vasodilator, 2. stimulates platelet adenyl cyclase which suppresses release of granules, 3. limits platelet extension

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30
Q

Endothelium also produces ___, which does what?

A

factor VIII (clotting), opposes release of granule contents

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31
Q

Platelets are related to ___ synthetase

A

thromboxane, thromboxane A2

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32
Q

Endothelium is related to ___ synthetase

A

prostacyclin

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33
Q

Two roles of thromboxane A2

A
  1. vasoconstrictor

2. potentiates platelet degranulation

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34
Q

Two roles of prostacyclin

A
  1. vasodilator

2. inhibits platelet degranulation

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35
Q

(2) block (2) production by ___ which converts __ to (2)

A

Aspirin and ibuprofen block thromboxane A2 and Prostacyclin production by blocking FA cyclooxygenase, , arachidonic acid to PGG2 and PGH2

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36
Q

What does anticoagulants do? List the three ways it does this.

A

prevents clots from forming

  1. Chelators - tie up calcium (citrate and oxylate)
  2. heparin - complexes with antithrobin III
  3. dicumarol - inhibition of Vit K dependent factors II, VII, IX, X synthesized by hepatocytes (aka cumadin and warfarin)
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37
Q

What does lysis of clots do/mean? how?

A

dissolves clots that have already formed, plasmin from plasminogen

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38
Q

What is the inactive form of plasmin which circulates in the blood?

A

Plasminogen

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39
Q

Activators of plasminogen -

  1. Endogenous activators are found in (3)
  2. Exogenous activators include (2)
  3. which has a three hour window for ?
A
  1. tissues, plasma, and urine
  2. Streptokinase and tPA (tissue plasminogen activator)
  3. MI and stroke
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40
Q
  1. Most of the frank tissue damage associated with infarction occurs upon ___
  2. associated with the formation of ___ with ___
  3. What pressure of tissues relieved and again perfused with blood ___ are generaged
A
  1. reperfusion
  2. highly ROS with unpaired electrons “free radicals”
  3. Free radicals
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41
Q
  1. Define collateralization
  2. what two things does it do?
  3. What is the role of the SNS?
A
  1. The ability to open up alternate routes of blood flow to compensate for a blocked vessel
  2. Angiogenesis (formation of new blood vessels) and vasodilation
  3. May impede via vasoconstriction or augment via release of NPY
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42
Q
  1. Blood Coagulation is known as ___
  2. Explain extrinsic mechanism
  3. Explain intrinsic mechanism
A
  1. Thrombosis
  2. Initiated by chemical factors released by damaged tissues
  3. Requires only components in blood and trauma to blood or exposure to collagen (or foreign surface)
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43
Q

How many clotting factors are there?

A

13

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44
Q

___ synthesizes # clotting factors, list them

A

liver, 5, I, II, VII, IX, and X

45
Q

___ depresses liver formation of (4) by blocking action of ___

A

Coumarin (warfarin or cumadin), II, VII, IX, and X, Vit K

46
Q

Hemophilia -

  1. sex linked on __ chromosome, which means?
  2. % of cases - defect in factor ___
  3. % of cases - defect in factor ___
  4. severity?
A
  1. X, exclusively males (comes from mom)
  2. 85, VIII
  3. 15, IX
  4. varying, mild to severe
47
Q

Key step in clotting is the ___ which requires ___

A

conversion of fibrinogen to fibrin, thrombin

48
Q
  1. What is antiphospholipid antibody syndrome?

2. What does it cause?

A
  1. Autoimmune disorder where body makes antibodies against phospholipids in cell membranes
  2. Abnormal clots to form
49
Q

Risk Factors in Heart Disease -

1. List ten

A
  1. increasing age
  2. mal gender
  3. heredity (including race)
  4. tobacco smoke
  5. high blood cholesterol
  6. high blood pressure
  7. physical inactivity
  8. obesity/overweight
  9. diabetes mellitus
  10. high blood homocysteine
50
Q

Homocysteine -

  1. What is it?
  2. can also cause cholesterol to change into ___
  3. Can make blood more likely to ___
  4. high levels in blood (>12) can be reduced by ?
A
  1. AA in the blood that may irritate blood vessels promoting atherosclerosis
  2. oxidized LDL
  3. clot
  4. increasing intake of folic acid, B6 and B12
51
Q

Antigens in RBCs -

  1. at least # commonly occurring antigens and hundreds of rare antigens have been found on the surface of ___
  2. most of these antigens are weak and are not likely to cause ___
  3. What are the two particular antigen sets that are likely to cause blood transfusion reactions if mismatched?
A
  1. 30, RBCs
  2. a immune response when transferred from one individual to another
  3. O-A-B and Rh
52
Q

O-A-B blood types -

  1. A and B antigens on RBSs are known as ___ because they can ___
  2. __ is essentially functionless
  3. genetic locus has what three alleles?
  4. due to inheritance, people have ___ of these surface antigens on their RBCs
A
  1. agglutinogens, trigger agglutination that cause most blood transfusionreactions
  2. O
  3. IA, IB, and IO (6 possible combinations of alleles
  4. none, one or both
53
Q

Agglutinins -

  1. produced ___ arising ___
  2. No agglutinins formed against ___
  3. antibody titers peak at about # yo and then do what?
  4. Anti __ titers are 2X Anti __ in respective blood type
A
  1. after birth (2-8 months), spontaneously
  2. agglutinogens that are present on RBCs
  3. 10, decline throughout life
  4. A, B
54
Q

Hemolysis in mismatched transfusions -

  1. Is an immediate or delayed response MC?
  2. Antibodies (primarily __) cause lysis of RBCs by ?
  3. hemolysis occurs to the __ RBCs, not the ___ in case of mismatch
  4. __ is universal donor
  5. is universal recipient
  6. ___ is the most lethal effect of a transfusion reaction
A
  1. immediate is less common, delayed is MC
  2. IgM, activating the compliment system which releases proteolytic enzymes rupturing cell membrane
  3. donor’s, recipients
  4. O neg
  5. AB pos
  6. kidney failure
55
Q

Kidney Failure -

  1. toxic substances released from ___
  2. ___ shock
  3. ___ from lysed RBCs precipitates and ___
A
  1. hemolysed RBCs
  2. circulatory
  3. hemoglobin, blocks renal tubules
56
Q

Rh blood types -

  1. ___ never arise (unlike O-A-B system)
  2. # common Rh antigens (called ___)
  3. List them
  4. A person with the __ antigen does not have __ antigen and visa versa
  5. ___ antigen is MC and most ___
  6. Lacking the D antigen means?
A
  1. spontaneous agglutinins
  2. 6, Rh factor
  3. C D E c d e
  4. C, c
  5. D, antigenic (Rh +)
  6. Rh -
57
Q

Rh Blood Types -

  1. What happens when Rh+ RBCs are infused into a person who is Rh-?
  2. it is upon multiple subsequent exposure that a strong ___ typically occurs
A
  1. it will stimulate the production of anti- Rh antibodies which develop slowly and reach maximum concentrations 2-4 months later
  2. hemolysis reaction
58
Q

Erythroblastosis Fetalis -

  1. AKA ___
  2. characterized by?
  3. . causes what to happen?
  4. most cases, mother is Rh_ and father is Rh_ and the fetus is Rh_ (inherited from father)
  5. the mother develops anti Rh agglutinins from?
  6. When do symptoms start to occur?
A
  1. hemolytic disease of the newborn
  2. agglutination and hemolysis of the fetus’ RBCs by the mother’s anti Rh agglutinins
  3. agglutination of fetal blood, release Hgb which is converted by macrophages into bilirubin leading to jaundice
  4. -, +, +
  5. exposure to the fetus’ Rh+ antigen
  6. usually don’t occur with initial pregnancy and occur with 2nd (3%) or 3rd (10%) pregnancy where fetus is Rh+
59
Q

Erythroblastosis Fetalis -

  1. after birth anti Rh agglutinins from mother circulate for another ___ destroying more neonate RBCs leading to ___
  2. causes enlargement of ?
  3. Many RBCs are ___
  4. ___ may precipitate in neurons of the brain causing___
A
  1. 1-2 months, anemia
  2. neonate liver and spleen
  3. nucleated (and blastic)
  4. bilirubin, mental impairment (kernicterus)
60
Q

Prevention and Treatment of erythroblastosis Fetalis -

  1. Treatment?
  2. Prevention?
  3. What does this shot do?
A
  1. replace neonate’s blood with Rh - blood
  2. Rh immunoglobulin globulin, which is an anti-D antibody, administered to mother at 28-30 weeks of gestation
  3. interferes with the immune response to the D antigen in fetal RBCs that may cross the placenta and enter mother’s circulation
61
Q

Heart Muscle -

  1. Atrial and ventricular are ___ grouped in ___
  2. # ___ located nuclei
  3. Contains (3) specialized excitatory and conductive muscle fibers
  4. Which contract ___ and have ___ fibrils
A
  1. striated enlongated, irregular anatamosing columns
  2. 1-2 centrally
  3. SA node, AV node, Purkinje fibers
  4. weakly, few
62
Q

Syncytial nature of cardiac muscle -

  1. syncytium = ___
  2. due to ?
  3. What are intercalated discs?
  4. they are the presence of ___
A
  1. many acting as one
  2. presence of intercalated discs
  3. low resistance pathways connecting cardiac cells end to end
  4. gap junctions
63
Q

Actions Potentials in cardiac muscle -

  1. duration of AP is from ___
  2. What are three channels?
  3. Na+ sharp ___ at onset of ___
  4. Ca++ ___ during the ___
  5. K+ ___ during the ___
A
  1. .2-.3 sec
  2. fast Na+, flow Ca++/Na+, K+
  3. increase, depolarization
  4. increased, plateau
  5. increased, resting polarized state
64
Q

Membrane physiology -

  1. in excitable tissue an AP is ___
  2. Na+ increases at onset of ___, decreases during ___
  3. Ca++ increases at onset of ___, decreases during ___
  4. K+ decreases at onset of ___, increases during ___
A
  1. a pulse like change in membrane permeability
  2. depolarization, repolarization
  3. depolarization, repolarization
  4. depolarization, repolarization
65
Q

Slow vs Fast cardiac cell -

  1. related to the channels that?
  2. typical cardiac muscle have both ___ channels that open during depolarization
  3. specialized excitatory cells like the ___ only __ Ca++/Na+ channels are operational during depolarization ___depolarization time
  4. ___ blocks ___ channels selectively changing a fast response into a slow response
A
  1. open during depolarization
  2. fast Na+ channels and slow Ca++/Na+ channels
  3. SA node, slow, increasing
  4. tetradotoxin, fast Na+
66
Q

Passive ion movement across cell -

  1. What are three considerations we need to think about?
  2. in ion channels are open, an ion will seek its ___
  3. concentration gradient favoring ion movement in one direction is offset by ___
A
  1. concentration gradient (high to low), electrical gradient (opposite charge attract, like charge repel), and membrane permeability (dependant on ion channels open or closed)
  2. Nernst equilibrium potential
  3. electrical gradient
67
Q

Resting membrane potential (Er) -

  1. during the Er in cardiac muscle, __ and __ are closed while ___ channels are open
  2. therefore K+ ions are ___, and when they reach their Nernst equilibrium postential ___ occurs
A
  1. fast Na+ and slow Ca++/Na+, K+

2. free to move, a stable Er is maintained

68
Q

Na+K+ ATPase (pump) -

  1. this pump with is ___ dependent operates to pump Na+ ___ and K+ ___ the cardiac cell at a ration of ___
  2. as pumping occurs, there is a net loss of ___ from the interior each cycle, helping the interior of the cell remain ___
  3. the protein pump utilized energy from ___
  4. __ binds to and __ this pump
A
  1. energy, out, into, 3:2
  2. one + charge, negative
  3. ATP
  4. digitalis, inhibits
69
Q

Ca++ exchange protein -

  1. in the cardiac cell membrane is a protein that exchanges ___ from the interior in return for ___ that is allowed to enter the cell
  2. the function of the exchange protein is tied to the ___
  3. if the Na+/K+ pump is inhibited, function of this exchange protein is ?
A
  1. Ca++, Na+
  2. Na+/K+ pump
  3. reduced and more Ca++ is allowed to accumulate in the cardiac cell increasing contractile strength
70
Q

Refractory Period -

  • Absolute*
    1. unable to?
    2. occurs during the ___
  • Relative*
    1. requires ___
    2. occurss during ___
  1. In a slow response cardiac muscle cell the relative refractory period is __ and the refractory period is about % longer
  2. in AV node and bundle this serves to?
A
  1. re-stimulate cardiac cell
  2. plateau
  3. a supra-normal stimulus
  4. repolarization
  5. prolonged, 25%
  6. protect the ventricles form supra-ventricular arrhythmias
71
Q

SA Node -

  1. ___ of the heart
  2. ___ nature
  3. list 6 reasons why
A
  1. normal pacemaker
  2. self excitatory
  3. less neg Er, leaky membrane to Na+/Ca++, only slow Ca++/Na+ cennels operational, spontaneously depolarizes at fastest rate (overdrive suppression), contracts feebly, and lacks stability and plateau
72
Q

Overdrive Supprestion -

  1. if you drive a self excitatoyr cell at a rate faster that its own inherent rate, you will ___
  2. mechanism may be due to?
  3. cells of the (2) system are under overdrive suppression by the ___
A
  1. suppress the cell’s own automaticity
  2. increased activity of Na+/K+ pump creating more negative Er
  3. AV node and purkinje, SA node
73
Q

AV node -

  1. delays ___
  2. this allows the atria to?
  3. ___ conduction velocity due to ___
  4. in absence of SA node, AV node may act as apcemaker but at a ___ rate
A
  1. the wave of depolarization from entering the ventricle
  2. contract slightly ahead of the ventricles (.1 sec delay)
  3. slow, smaller diameter fibers
  4. slower
74
Q

Effect of HR on systole/diastole -

  1. as HR ___ cycle length (CL) ___
  2. at a resting heart rate systole __ diastole
  3. both the duration of systole and diastole ___, but ___ shortens to a greater extent (at a high HR the ventricle may not fill adequately)
  4. HR of 75 BPM = CL ___, S ___, D ___
  5. HR of 150 BPM = CL ___, S___, D___
  6. during systole perfusion of the myocardium is restricted by?
A
  1. increases, decreases

2.

75
Q

Cardiac Cycle -

  • Systole*
    1. ___ beat
    2. contraction or relaxation
    3. inflow or outflow?
  • Diastole*
    1. ___ beat
    2. contraction or relaxation
    3. Rapid ___
A
  1. during
  2. contraction
  3. ejection
  4. b/w
  5. relaxation
  6. inflow (70-75%)
76
Q
Ventricular Volumes - 
Define
1. EDV
2. ESV
3. Stroke Volume
4. Ejection fraction, what is normal?
A
  1. end diastolic volume - volume in ventricles at the end of filling
  2. end systolic volume - volume in ventricles at the end of ejection
  3. (EDV-ESV) - volume ejected by ventricles
  4. % of EDV ejected ( SV/EDV X 100%), 50-60%
77
Q

Terms - define

  1. Preload
  2. afterload
A
  1. stretch on the wall prior to contraction (proportional to the EDV)
  2. the changing resistance 9impedance) that the heart has to pump against as blood is ejected, changing aortic BP during ejection of blood from the left ventricle
78
Q

Atrial Pressure Waves -

  1. What are the 3 waves?
  2. define A wave
  3. C wave
  4. V wave
A
  1. A, C, V waves
  2. associated with atrial contaction
  3. associated with ventricular contraction (bulging of AV valves and tuggin on atrial muscle)
  4. associated with atrial filling
79
Q

Function of Valves -

  1. Open with a ___
  2. example: when ___ pressure > the ___ pressure the ___ is open
  3. close with ___
  4. example: when ___ pressure > __ pressure the ___valve is closed
A
  1. forward pressure gradient
  2. LV, aortic, aortic valve
  3. backward pressure gradient
  4. aortic, LV, aortic
80
Q

Heart Valves -

  1. What are the two types of valves?
  2. What are the two AV valves?
  3. Explain
  4. what are the two semilunar valves?
  5. explain
A
  1. AV and semilunar valves
  2. mitral and tricuspid
  3. thin and filmy, chorda tendineae act as check lines to prevent prolapse, papillary muscles increase tension on chorda tendineae
  4. aortic and pulmonic
  5. stronger construction
81
Q

Valvular dysfunction -

  1. what is it called when a valve does not open fully?
  2. what is it called when a valve does not close fully?
  3. what is it called when a valve creates vibrational noise?
A
  1. stenotic
  2. insufficient/regurgitant/leaky
  3. murmurs
82
Q

Heart Murmur Considerations - Timing

  1. Systolic: aortic and pulmonary __, mitral and tricuspid ___
  2. Diastolic: aortic and pulmonary ___, mitral and tricuspid ___
  3. both?
A
  1. stenosis, insufficiency
  2. insufficiency, stenosis
  3. patent ductus arteriosis and combined valvular defect
83
Q

Law of Laplace -

  1. wall tension = ___
  2. at a given operating pressure as ventricular radius __, developed wall tension ___
  3. increased tension leads to?
  4. two ventricles operating at the same __ but with different ___, the larger chamber will have to?
  5. How does this law explain how capillaries can withstand high intravascular pressure?
A
  1. (pressure)(radius)/2
  2. increases, increasess
  3. increased force of ventricular contraction
  4. pressure, chamber radii, generate more wall tension, consuming more energy and oxygen
  5. small radius = small wall tension
84
Q

Terminology - define

  1. Chronotropic
  2. Dromotropic
  3. inotropic
A
  1. (+ increases HR and - decreases HR), anthing that affects HR
  2. anything that affects conduction velocity
  3. anything that affects strength of contraction (ex. caffeine would be a + chronotropic agent)
85
Q

Control of Heart Pumping -

  1. ___ properties of cardiac muscle cells
  2. Explain Frank- Starling Law of the Heart
A
  1. intrinsic
  2. within physiologic limits the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins (heterometric and homeometric autoregulation, direct stretch on the SA node)
86
Q

Mechanism of Frank-Starling -

  1. increased venous return causes?
  2. explain
A
  1. increased stretch of cardiac muscle fibers
  2. increase cross bridge formation, increased calcium influx (both increases force of contraction), increased stretch on SA node (increases HR)
87
Q

Heterometric autoregulation -

  1. within limits as cardiac fibers are stretched the ___ is increased
  2. ___ is removed
  3. more Ca++ influx into cell associated with the ___
A
  1. force of contraction
  2. more cross bridge formation as actin overlap
  3. increased stretch
88
Q

Homeometric autoregulation -

  1. it is the ability to?
  2. list the 3 parts that induce
  3. Explain flow induced
  4. explain pressure induced
  5. explain rate induced
A
  1. increase strength of contraction independent of a length change
  2. flow, pressure, and rate
  3. increase stroke volume maintained as EDV decreases
  4. increase in aortic BP (afterload) will + force of contraction
  5. increased HR will + force
    treppe”
89
Q

Direct stretch on SA node -

1. stretch on SA node will ___

A
  1. increase Ca++ and/or Na+ permeability which will increase HR
90
Q

Extrinsic Influences -

1. Iist four

A
  1. ANS
  2. Hormonal influences
  3. ionic influences
  4. temp influences
91
Q

Control of Heart by ANS -

  1. explain Sympathetic innervation
  2. explain parasympathetic innervation
A
  1. increases HR, strength of contraction, and conduction velocity
  2. decreases HR, strength of contraction, and conduction velocity
92
Q

Interaction of ANS -

  1. SNS effects on the heart are blocked using ___ which blocks ___
  2. Parasympathetic effects blocked using ___ which blocks ___
  3. Explain
  4. What can be concluded?
A
  1. propranolol (beta blocker), beta receptors
  2. atropine, muscarinic receptors
  3. HR will increase, strength of contraction decreases
  4. perfectly off setting each other
93
Q

Interation of ANS -
1. From the previous results it can be concluded that under resting conditions: Parasympathetic NS exerts a dominate ___ influence on ___, and sympathetic NS exerts a dominate ___ influence on ___

A
  1. inhib on HR, stim on strength of contraction
94
Q

Direct vs indirect SNS influence -

  1. direct innervation of cardiac cells accounts for ___ of the SNS effect
  2. indirect effects would be due to ?
A
  1. most ( NE acting on B-1 receptors (85%))
  2. circulating catacholamines (epinephrine and NE) released primarily from the adrenal medulla (blood borne) which would find their way to the cardiac B-1 receptors (15%))
95
Q

SNS balance side to side -

  1. What happens with stimulation of Left stellate ganglion?
  2. What happens with stimulation of right stellate ganglion?
A
  1. decreased ventricular fibrillation threshold, prolongation of QT interval
  2. increased ventricular fibrillatin threshold
96
Q

Unilateral denervation -

  1. sympathetic denervation is antiarrhythmic, but also antifibrillatory… and effect exquisitely important for?
  2. left cardiac sympathtic devervation increases ___ activity
A
  1. any condiction with a high risk for ventricular fibrillation and sudden cardiac death
  2. vagal
97
Q

Cardioacclerator reflex -

  1. stretch on right atrial wall will?
  2. AKA ___
  3. helps prevent?
A
  1. simulate stretch receptors which in turn send signals to MO stimulating SNS outflow to heart
  2. bainbrige reflex
  3. damning of blood in the heart and central veins
98
Q

Neurocardiogenic syncope -

  1. Benzold Jarisch reflex (___), stimulation of sensory ending mainy in the ___ that reflex via the ___ to the CNS
  2. reflex effects results in (2)
  3. reflex in stimulated by (2)
A
  1. Baroreceptors in ventricles, ventricles, CN X
  2. hypotension and bradycardia
  3. occlusion of circumflex artery (inferior wall infarct) and increase in LVP and LV volume (aortic stenosis)
99
Q

Major Hormonal Influences -

  1. ___ hormones
  2. explain
A
  1. thyroid

2. stim both inotropic and chronotropic, also causes and increase in CO by increasing BMR

100
Q

Ionic Influences -

  1. What is the effect of elevated K+?
  2. Effect of elevated Ca++?
A
  1. dilation and flaccidity of cardiac muscle at concentrations 2-3 times normal
  2. spastic contraction
101
Q

Effect of body temperature -

  1. Explain elevated body temp
  2. explain decreased body temp
A
  1. HR increases about 10 beats for every degree F elevation in body temp, contractile strength will increase temporarily but prolonged fever can decrease contractile strength due to exhaustion of meabolic systems
  2. decreased HR and strength
102
Q

Energy substrate for cardiac cells -

1. heart is versatile and can use many different energy substrates, List 6

A
  1. FA 70% preferred
  2. Glucose
  3. Glycerol
  4. Lactate
  5. Pyruvate
  6. AA
103
Q

Relationship of Evergy to work -

  1. 75% of energy the heart utilizes is converted to ___
  2. the remaining 25% is utilized as work which is broken down into (2)
A
  1. heat

2. pressurization of blood (99%) and acceleration of blood (1%)

104
Q

Work output of the heart -

  1. pressurization of the blood (___): explain
  2. acceleration of blood to its ejection velocity (___) : explain
A
  1. potential energy, moving blood from low pressure to high pressure (volume pressure work or external work)
  2. kinetic energy, out the aortic and pulmonic valves normally accounts for less that 1% of the work component (can increase to 50% with valvular stenosis)
105
Q

EKG -

  1. What does it mearsure?
  2. what is lead?
  3. what is axis of lead?
  4. what is transition line?
A
  1. potential difference across the surface of the myocardium with respect to time
  2. pair of electrodes
  3. line connecting leads
  4. line perpendicular to axis of lead
106
Q

Rate -

  1. paper speed?
  2. normal rate ranges usually b/w?
  3. tachycardia
  4. bradycardia
A
  1. 25mm/sec, 1 mm = .04sec
  2. 60-80 BPM
  3. greater than 100
  4. less than 50
107
Q

Intervals -

  1. __ interval (includes ___)
  2. should be about ___
  3. greater than ___ = ___
  4. less than __ = ___
A
  1. PR, AV nodal delay
  2. .16 sec
  3. .2 sec = 1st degree AV block
  4. .1 sec = inadequate delay - possible accessory conduction pathway from atria to ventricle
108
Q

Electrocardiography -

  1. P wave
  2. QRS complex
  3. T wave
  4. ___ is also part of the QRS complex
A
  1. atrial depolarization
  2. ventricular depolarization
  3. ventricular repolarization
  4. atrial repolarization
109
Q

Leads -

  1. what are they?
    • electrode is ___, - electrode is ___
  2. the direction of the deflection (+ or -) is based on?
  3. routine EKG consists of # leads
A
  1. a pair of recording electrodes
  2. active, reference
  3. what the acctive electrode sees relative to the reference electrode
  4. 12 (6 frontal plane and 6 chest/horizontal)