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adv. anatomy + physiology > m7 + 8 lecture - CV system > Flashcards

m7 + 8 lecture - CV system Flashcards

1
Q

what is hemostasis?

A

stoppage of blood flow - coagulation

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2
Q

what are the three actions produced by a tissue/vessel injury?

A

1) vascular spasm
2) platelet plug formation
3) coagulation/clotting cascade

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3
Q

what happens during vascular spasm?

A
  • damage to endothelial cells initiates release of endothelin –> stimulating vasoconstriction
    purpose: dec. blood flow + dec. blood loss
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4
Q

what happens during platelet plug formation?

A
  • adhesion begins by contact with exposed collagen fibers in damaged tissue
  • adhesion site is made bigger by release of thromboxane,
  • producing an unstable plug —> which is necessary for clotting cascade to occur
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5
Q

what happens during clotting cascade (coagulation)? (scab formation)

A

three steps: (3 min. total)
1) formation of prothrombin activator (longest)
2) formation of thrombin
3) formation of fibrin threads (shortest)

requires: a healthy liver, prod. of 13 clotting factors, vit. K, Ca++, platelet plug (PF3)

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6
Q

what is thromboxane?

A

platelets - they stick to everything, augmenting adhesion site in platelet plug formation

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7
Q

what happens during the formation of prothrombin activator (clotting cascade: 1st step)?

A

initiated by damage to the endothelium + platelet plug which releases PF3
- 10 clotting factors combine w/ PF3 + Ca to form PTA
- longest step (1-2 min.)
- causes the next step

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8
Q

what happens during the formation of thrombin (clotting cascade: 2nd step)?

A

PTA catalyzes the change from prothrombin to thrombin
- catalyzes the next step

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9
Q

what happens during the formation of fibrin fibers (clotting cascade: 3rd step)?

A

thrombin catalyzes the change from fibrinogen (soluble) to fibrin threads (insoluble)
- these fibers precipitate within the platelet plug + wound, producing a strong and stable clot
–> if visible, called a scab
–>if under skin, called a hematoma

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10
Q

what are some bleeding/clotting disorders?

A
  • hemophilia
  • Von Willdebrand’s - thrombocytopenia =low platelet #, can cause excessive bleeding (<200,000/mm3)
  • liver disease or vit k deficiency
  • DVT/embolus/blockage –> thrombus (blood clot)
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11
Q

what is the reason for clotting in an uninjured vein?

A

vein —> DVT (blood clot)
- if it breaks free = embolus (in lungs = pulmonary embolus)
- causes: dec. circulation, age, heart Dz, diabetes, post-surgical

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12
Q

what is the reason for clotting in an uninjured artery?

A

artery —> thrombus
- plaque builds up on the artery wall, damaging the inner lining and triggering the clotting process in already narrowed artery
- cause: arteriosclerosis (from cholesterol, high BP, smoking, diabetes)
- m/c in the brain (stroke) or heart (MI)

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13
Q

what are some anti-platelet medications?

A
  • plavix
  • elequis
  • brilinta
  • aspirin
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14
Q

what is a anti-prothrombin medication?

A

they are anticoagulants (blood thinners)
- coumadin (aka warfarin) - impaired by vit k

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15
Q

what is a anti-thrombin medication?

A

they are anticoagulants (blood thinners)
- heparin
- lovanox

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16
Q

what are the two classifications for anemia?

A

1) lack of RBCs
2) lack of hemoglobin

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17
Q

what are the types of anemia that have a lack of RBCs?

A

hemorrhagic anemia (2nd m/c)
- caused by a gradual blood loss
hemolytic anemia
- sepsis, splenomegaly (the spleen works harder to remove the defective red blood cells, which can cause it to enlarge and become engorged with blood)

symptoms: hypoxia, fatigue, cyanosis

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18
Q

what are the types of anemia that have a lack of hemoglobin?

A

iron deficiency anemia
- loss of iron (dark leafy greens = iron source)
pernicious anemia
- inability to process iron
- lack of b12 or lack of intrinsic factor

symptoms: hypoxia, fatigue, cyanosis

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19
Q

what is the physiology of myocardial cells?

A
  • contain striations, sarcomeres + intercalated disks (gap-junctions)
  • much like skeletal muscle in function
    cross-bridging steps
    1) cross-bridging
    2) power stroke
    3) detachment
    4) reactivation
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20
Q

where does calcium come from and its function?

A
  • from extracellular (interstitial cells - 20%)
  • from intracellular (sarcoplasmic reticulum - 80%)
  • calcium initiate heart muscle contraction
  • calcium channel blockers slow HR
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21
Q

how is the heart stimulated?

A
  • a self-initiating functional syncytium - gap junctions
  • regulated by nodal system
  • two contractile units: atria + ventricles
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22
Q

what is a functional syncytium?

A

a group of cells that function as a single unit while maintaining their individual cellular role

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23
Q

what is the nodal system? (intrinsic conduction system)

A
  • electrical system of the heart
  • formed by autorhythmic cells (specialized cells that carry electrical signals, do not contract)
  • pacemaker potential - initiated by slow leaking Na+ channels
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24
Q

what does digoxin do to the heart?

A
  • decrease HR
  • increase contractibility
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25
Q

what are the energy requirements for the heart?

A
  • completely aerobic respiration - have more mitochondria than red muscle fibers
  • can use any nutrient for energy, prefers fatty acids
  • requires an ample supply of O2
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26
Q

why is oxygen deprivation concerning?

A

highest concern due to ischemia = decreased blood flow
- #1 cause is coronary artery disease (CAD)
- decreased blood flow generates angina pectoris (chest pain) —> minor symptoms can be treated w/nitro glycerin (vasodilator)

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27
Q

about type of atherosclerosis?

A
  • initiated by a build up of LDLs and VLDLs within the tunica media
  • stimulate macrophage activity to create plaque development
  • plaquing of arteries = leads to hardening and stenosis
  • in turn, decreasing blood flow due to increased resistance + clotting
  • leading to a MI
  • enzymes released that indicate cell death: TnT + CPK
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28
Q

structures of the nodal system: sinoatrial - SA node?

A
  • pacemaker of the heart: initiates atrial depo. —> leads to contraction that fills last 20% of ventricles
  • normally set at 100 bpm
  • slowed by PSNS: to around 60-100 bpm
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29
Q

structures of the nodal system: atrioventricular - AV node?

A
  • delays signal .1 second to allow ventricular filling
    structures:
  • bundle of His
  • bundle branches
  • purkinje fibers
    —-> initiate ventricular depo. then contraction, creating BP/BF + circulation
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30
Q

what happens at the P-wave?

A

SA node initiates atrial depolarization then contraction

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31
Q

what happens at the QRS-wave?

A

Purkinje fibers initiate ventricular depolarization then contraction

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32
Q

what happens at the T wave?

A

ventricles repolarize (relaxation + refilling)

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33
Q

what happens from the P-Q interval?

A

initiated by the SA node
- atrial depo. = contraction —> helps fill ventricles last 20%
- signal travels to purkinje fibers
- anything >.20 sec = heart block

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34
Q

what happens at the Q-T interval?

A

initiated by the purkinje fibers
- all ventricular activity - depo. = contraction = ejection = repolarization = relaxation

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35
Q

what happens at the S-T interval?

A
  • ejection of blood = creates circulation + pressure (BP + BF)
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36
Q

what are some problems w/ conduction?

A

occurs at the SA node
- arrhythmias (irregular heart beat)
ex.) fibrillation - atrial or ventricular = no circulation
—> are uncontrolled contractions

  • ectopic focus (anything outside of SA node initiating the cycle)
    —> AV node takes over at 50bpm
    —> then the bundles can work at 30 bpm
  • heart block (faulty conduction)
    —> caused by scar tissue from an MI, delays + weakens the heart
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37
Q

what is systole?

A

ventricular contraction
- depo. initiates contraction
—> AV valves close, “lub” sound
—> pressure rises + semilunar valves open
- blood flows out of the heart, causes rise in arterial BP to a systolic of 120

T-wave
- as pressure peaks, semilunar valves close, “dub” sound
- when ventricles are relaxed AV valves open

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38
Q

what can cause heart murmurs?

A
  • genetics
  • age
  • infections - sepsis
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39
Q

what is diastole?

A

relaxation of the ventricles
early part: ventricles are relaxed, AV valves open, + blood enters by gravity and venous return (after T-wave)

late part: atria contract forcing the last 20% of blood into the ventricles ( depo. causes T-wave)
- causes drop in arterial BP to diastolic of 80 (due to BF)

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40
Q

what is cardiac output?

A

the amount of blood that is pumped thru the body in one min.
- relatively constant at rest

cardiac output = HR x Stroke Volume

41
Q

what is the CO purpose in maintaining homeostasis?

A

O2 supply for sufficient perfusion

42
Q

what is the cardiac reserve?

A
  • the ability of the heart to increase output to meet the O2 demand
    —> can be 4-5 times and up to 7 times as much
43
Q

what factors affect EDV (preload)?

A

highest volume prior to contraction
1) blood volume = hydration
- fluctuates throughout the day based on lifestyle
2) venous return
- venous valves
- muscle contractions
- deep regular breathing

other: SNS (Nor-Epi, Epi - increased EDV)
exercise - increased EDV
age - decreases EDV

44
Q

what factors affect ESV (afterload)?

A

amt. of blood left in the heart after contraction
1) hypertension (BP) - wears out heart + expands due to overexertion
causes: obesity, idiopathic = stress, salt
2) atherosclerosis - CAD, PAD –> ischemia = MI
- affects O2 delivery
3) valve disease

other: SNS (Nor-Epi, Epi - decreases ESV)
exercise - decreases ESV
age => atrophy - weakening - increases ESV

45
Q

what factors affect both EDV + ESV?

A

contractility (the strength of contraction) - increases by exercise (SNS)
- starlings law –> stretching the myocardium will enhance the force of contraction, increasing venous return, increasing ejection volume
- hyperkalemia = increased K (calcium channel blockers)

46
Q

what is the SNS action on the cardiac cells?

A

affected by Nor-Epi or Epi
- autorhythmic cells: increased RMP = increased HR
- myocardial cells: increased calcium = increased contractility

47
Q

what helps regulate HR?

A
  • ANS regulation
  • chemoreceptors
  • baroreceptors
  • proprioceptors
48
Q

how does the ANS regulate HR?

A

PSNS - cardioinhibitory - decrease HR
SNS - cardioacceletory - increase HR

49
Q

what centers does the medulla oblongata contain that affect rate and systemic pressure? (ANS)

A

cardiac center - HR
vasomotor - vessel diameter (BP)
respiratory center - RR

50
Q

what happens with each of the HR variables?

A

chemoreceptors - monitor pH, CO2, + O2
- if CO2 increases then HR increases + vasoconstriction = BP increases = increases velocity, increased RR
- if CO2 decreases then HR decreases + vasodilation = decreased BP = decreased RR

baroreceptors - sense pressure changes in vessels + maintain BP (orthostatic change)
- if BP increases then HR decreases + vasodilate = decreased BP
- if BP decreases then HR increases + vasoconstrict = increased BP (increased velocity)

proprioceptors - monitor activity

51
Q

what are chronotropic agents?

A
  • influence HR
    hormones
  • thyroxine - increase
  • cortisol - increase
  • epi - increase
    drugs
  • beta-blockers - prevents increase
  • digoxin - dec. HR, inc. contractility
  • Ca+ channel blocker - dec. HR, dec, contractility
    electrolytes
  • K (hyper- inc. HR) (hypo- dec. HR)
  • Ca
  • Na - inc. HR - hypertension
52
Q

what are inotropic agents?

A

change the force of muscular contractions (contractility)
ex.) epi, ANP, hypokalemia, CHF, age

53
Q

what does age do to the heart?

A
  • valves harden + thicken
  • muscle atrophies + weakens
  • muscle becomes fibrotic + stretches
  • cardiac output will decrease
54
Q

what does CHF do to the heart?

A
  • can happen on either side
  • leads to edema of certain areas of the body
    —> left sided: pulmonary edema
    —> right sided: systemic edema
  • causes: valve disease, atherosclerosis, smoking which leads to - CAD, lung disease
55
Q

what are blood vessels are?

A

transportation highways
- gases are exchanged
- nutrients are delivered
- waste is removed

56
Q

what do arteries do?

A

carry blood away from the heart (efferent)

57
Q

what do veins do?

A

carry blood towards the heart (afferent)

58
Q

what are the layers in a artery?

A

1) tunica externa
2) tunica media - thick
3) tunica interna

59
Q

what are the layers in a vein?

A

1) tunica externa
2) tunica media
3) tunica interna

  • large lumen ( internal lining)
60
Q

what is the tunica externa? (3)

A
  • external layer of vessel
  • anchors the vessel - in larger vessels, may have own blood supply called Vasa Vasorum
61
Q

what is the tunica media? (2)

A
  • mainly smooth muscle
  • thicker in the arteries to control BF (ANS)
  • has layer of elastic tissue ( external elastic lumina) - this is the layer affected by atherosclerosis
62
Q

what is the tunica interna? (1)

A
  • thin layer made of endothelium –> protects blood from friction
  • this is the only layer in the smallest vessels - capillaries
63
Q

what are the types of artieries ?

A
  • elastic
  • muscular
  • arterioles
  • capillaries
64
Q

what are elastic arteries?

A
  • receive the blood as it rushes out of the heart
  • large elastic lamina to expand + withstand the force of blood (loss of elasticity causes rise in BP)
    ex.) aorta
65
Q

what are muscular arteries?

A
  • help to distribute + redirect the blood –> branch off elastic arteries
  • have large tunica media to redirect blood as needed
66
Q

what are arterioles?

A
  • located within the tissues – leading to capillary beds
  • have precapillary sphincters to change local blood flow —> controlled by SNS + autoregulation processes
67
Q

what are capillaries?

A
  • smallest artery
  • only have tunica intima
  • form beds: multiple branchings from arterioles (nutrient + gas exchange here)
    types: continuous, fenestrated, sinusoidal
68
Q

what are continuous capillaries?

A
  • m/c type
  • function: small clefts allow passage of materials
  • location: skin, all muscles, most connective tissues + CNS
  • form blood brain barrier w/ astrocytes
69
Q

what are fenestrated capillaries?

A
  • formed w/ narrowed windows (aka fenestrations) –> allows rapid filtration/absorption to take place
  • very porous type is found in endocrine glands, small intestine, + kidneys
70
Q

what are sinusoidal capillaries?

A
  • extremely porous w/ large intracellular clefts
  • location in special organs: liver, bone marrow, spleen, lymph nodes
  • endothelium is discontinuous + need to be held together by Kupffer cells (macrophages)
71
Q

what is capillary exchange?

A
  • changes as fluid travels from proximal to distal capillary ends
  • nutrients + gases are exchanged based on concentration gradients (simple diffusion)
    —> from high to low con.
  • O2 + CO2 are exchanged due to concentrations which are measured in mmHg
  • waste moves into capillary at venuole end along w/ water movement
72
Q

what are the two ways that fluid is gained or lost?

A
  • colloid osmotic pressure
  • capillary hydrostatic pressure
73
Q

what is colloid osmotic pressure?

A
  • pulls fluid from the vessel (like a sponge)
  • generated by con. of albumin + Na
  • if Na increases, fluid is pulled into the capillary = increases BP
  • if albumin increases, BP increases
  • if albumin decreases, BP decreases (dev. edema/ascites)
74
Q

what is capillary hydrostatic pressure?

A
  • this pressure pushes fluid away or out of vessel
  • equals capillary blood pressure
  • capillaries lose avg. 2mL of fluid per min.
    —> lost fluid will cause edema if not recycled by lymphatics
75
Q

what are venuoles?

A
  • attach to the capillaries + begin carrying the blood to the heart
  • they remain very porous like a capillary, + allow fluid + WBCs to move in and out
76
Q

what are veins?

A
  • thin walled – less tunica media
  • one-way valves to help promote venous return to the heart (formed from tunica interna)
    — varicose veins, venous sinuses
77
Q

what is blood pressure?

A
  • pressure of the blood against the vessel walls
  • generates circulation (BF)
78
Q

what is BP generated by?

A

primary factor - bc H2O
1) blood volume
short-term + change quickly
2) peripheral resistance - vessel diameter
3) cardiac output = HR

79
Q

what is the amount of blood circulating throughout the body?

A

5.25L/min
- amt. of blood circulating equals the CO in mL/min

80
Q

what is peripheral resistance?

A
  • back pressure the heart has to overcome - necessary for systemic flow
  • too much = bad
    three factors contributing to resistance:
    1) vessel diameter
    2) vessel length
    3) viscosity
81
Q

what is vessel diameter?

A
  • generates velocity of blood
    — constriction = increased resistance = increased BP = increased velocity
  • primary variable the body uses to reg. BP + BF
82
Q

what is vessel length?

A
  • directly related to resistance
  • increases greatly in obesity
83
Q

what is viscosity?

A
  • thickness of blood
  • directly related to resistance
  • polycythemia - a blood disorder occurring when there are too many red blood cells (causes it to thicken)
84
Q

aspects of measuring BP?

A
  • normally on left arm
  • BP sounds - sounds of korotkoff (turbulence from blood rushing through artery)
  • hypotension (BP less than 90 systolic)
  • hypertension (BP over 120/80)
85
Q

aspects of measuring pulse?

A
  • measured by finger pressure on artery
  • carotid or radial artery
86
Q

what is pulse pressure?

A

PP = systolic - diastolic
- necessary to determine MAP
- seen in the larger arteries which receive the rush of blood from the heart
- palpated to determine: rigor (strength), rate (HR), regularity ( rhythm)

87
Q

what is Mean Arterial Pressure (MAP)?

A

MAP = diastolic pressure + 1/3 pulse pressure
- the force moving blood forward in the arteries
— should be greater than 60 to maintain good perfusion to organs
— below 50 = hypoxia

88
Q

what is venous return?

A
  • pressure is lowest in veins >10 mmHg, but they contain the most blood volume (60%)

venous return is helped by:
- valves
- muscular pump - skeletal muscles squeeze the veins, increase venous return
- respiratory pump - deep breathing increases intra-thoracic + intra-abdominal pressure
— both increase CO by affecting SV

89
Q

what is autoregulation?

A
  • the ability of organs to maintain a constant blood flow despite changes in blood pressure
    two mechanisms: myogenic + metabolic
90
Q

what is the myogenic mechanism of autoregulation?

A
  • reflex
  • maintains BP + BF during orthostatic + sympathetic changes
  • seen in brain + kidneys
91
Q

what is the metabolic mechanism of autoregulation?

A
  • will cause a dilation of the arterioles to increase BF in a local area
  • due to a need for O2 + waste (CO2)
  • seen in active muscles + areas of healing
92
Q

how is BP maintained (short-term)?

A

autonomic medullary centers
- vasomotor center (sympathetic)
—> establishes tone of arterioles (will dilate or constrict to vary diameter + affect systemic flow
- cardiac center = HR
—> modifies HR to maintain BP
- respiratory center - VRG = RR

93
Q

what receptors do the autonomic medullary centers use?

A

baroreceptors: stimulated by BP changes or stretch of blood vessel walls
- location: carotid sinus + aortic arch

chemoreceptors: measures chemicals like CO2 in the blood (CO2 inc. = O2 dec. = pH dec.)
- CO2 increase = RR, HR, BP increase
- CO2 decrease = RR, HR, BP decrease

94
Q

how is BP maintained (long-term)?

A
  • done thru maintaining blood volume
  • in hypothalamus
    1) stimulates desire to drink (thirst)
    2) releases ADH to reduce urine loss
    (ADH - targets collecting duct, inc. H2O retention, dec. urine loss
95
Q

what is RAAS?

A

renin-angiotensin aldosterone system
- BP drops and renin is released by JG apparatus of kidney
- renin targets the liver to release angiotensin
- ACE (angiotensin converting enzyme) converts angiotensin to angiotensin II at the lungs
angiotensin II stimulates:
1) systemic vasoconstriction = increases BP
2) increases release of ADH - targets collecting duct, increased H2O retention = decreased urine loss
3) the release of aldosterone - targets renal tubules to increase Na + H2O reabsorption

96
Q

what are other hormonal factors?

A

atrial natriuretic peptide (ANP) - diuretic
- prod. by the atria when elevated pressure exists
- antagonistic to aldosterone - reduces BP + BV
vasopressen (ADH) - vasoconstrictor

97
Q

what are some short term localized chemicals?

A
  • histamine (vasodilator) - results in hyperemia
  • nitric oxide (vasodilator)
98
Q

what is circulatory shock?

A

homeostatic feedback mechanism
- sympathetic reaction to maintain circulation
- causes widespread vasoconstriction to prevent drop in BP at vital organs
— pushes blood to organs - lose color (paleness)
— rapid RR
— may see positional syncope w/ hemorrhaging
— disorientation/confusion
— rapid pulse (weak/ thready in late stages)
not designed for long term use

99
Q

what are the types of circulatory shock?

A

1) hypovolemic shock - m/c
- loss of blood volume
causes: traumatic injury, severe dehydration
2) cardiogenic shock
- CHF, MI
3) vascular shock
- severe vasodilation as in anaphylactic shock (allergies) - head trauma

adv. anatomy + physiology (18 decks)

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