m7 + 8 lecture - CV system Flashcards
1
Q
what is hemostasis?
A
stoppage of blood flow - coagulation
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
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
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
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)
6
Q
what is thromboxane?
A
platelets - they stick to everything, augmenting adhesion site in platelet plug formation
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
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
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
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)
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
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)
13
Q
what are some anti-platelet medications?
A
- plavix
- elequis
- brilinta
- aspirin
14
Q
what is a anti-prothrombin medication?
A
they are anticoagulants (blood thinners)
- coumadin (aka warfarin) - impaired by vit k
15
Q
what is a anti-thrombin medication?
A
they are anticoagulants (blood thinners)
- heparin
- lovanox
16
Q
what are the two classifications for anemia?
A
1) lack of RBCs
2) lack of hemoglobin
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
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
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
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
21
Q
how is the heart stimulated?
A
- a self-initiating functional syncytium - gap junctions
- regulated by nodal system
- two contractile units: atria + ventricles
22
Q
what is a functional syncytium?
A
a group of cells that function as a single unit while maintaining their individual cellular role
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
24
Q
what does digoxin do to the heart?
A
- decrease HR
- increase contractibility
25
what are the energy requirements for the heart?
- 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
26
why is oxygen deprivation concerning?
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)
27
about type of atherosclerosis?
- 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
28
structures of the nodal system: sinoatrial - SA node?
- 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
29
structures of the nodal system: atrioventricular - AV node?
- 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
30
what happens at the P-wave?
SA node initiates atrial depolarization then contraction
31
what happens at the QRS-wave?
Purkinje fibers initiate ventricular depolarization then contraction
32
what happens at the T wave?
ventricles repolarize (relaxation + refilling)
33
what happens from the P-Q interval?
initiated by the SA node
- atrial depo. = contraction ---> helps fill ventricles last 20%
- signal travels to purkinje fibers
- anything >.20 sec = heart block
34
what happens at the Q-T interval?
initiated by the purkinje fibers
- all ventricular activity - depo. = contraction = ejection = repolarization = relaxation
35
what happens at the S-T interval?
- ejection of blood = creates circulation + pressure (BP + BF)
36
what are some problems w/ conduction?
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
37
what is systole?
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
38
what can cause heart murmurs?
- genetics
- age
- infections - sepsis
39
what is diastole?
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)
40
what is cardiac output?
the amount of blood that is pumped thru the body in one min.
- relatively constant at rest
cardiac output = HR x Stroke Volume
41
what is the CO purpose in maintaining homeostasis?
O2 supply for sufficient perfusion
42
what is the cardiac reserve?
- 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
what factors affect EDV (preload)?
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
what factors affect ESV (afterload)?
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
what factors affect both EDV + ESV?
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
what is the SNS action on the cardiac cells?
affected by Nor-Epi or Epi
- autorhythmic cells: increased RMP = increased HR
- myocardial cells: increased calcium = increased contractility
47
what helps regulate HR?
- ANS regulation
- chemoreceptors
- baroreceptors
- proprioceptors
48
how does the ANS regulate HR?
PSNS - cardioinhibitory - decrease HR
SNS - cardioacceletory - increase HR
49
what centers does the medulla oblongata contain that affect rate and systemic pressure? (ANS)
cardiac center - HR
vasomotor - vessel diameter (BP)
respiratory center - RR
50
what happens with each of the HR variables?
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
what are chronotropic agents?
- 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
what are inotropic agents?
change the force of muscular contractions (contractility)
ex.) epi, ANP, hypokalemia, CHF, age
53
what does age do to the heart?
- valves harden + thicken
- muscle atrophies + weakens
- muscle becomes fibrotic + stretches
- cardiac output will decrease
54
what does CHF do to the heart?
- 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
what are blood vessels are?
transportation highways
- gases are exchanged
- nutrients are delivered
- waste is removed
56
what do arteries do?
carry blood away from the heart (efferent)
57
what do veins do?
carry blood towards the heart (afferent)
58
what are the layers in a artery?
1) tunica externa
2) tunica media - thick
3) tunica interna
59
what are the layers in a vein?
1) tunica externa
2) tunica media
3) tunica interna
- large lumen ( internal lining)
60
what is the tunica externa? (3)
- external layer of vessel
- anchors the vessel - in larger vessels, may have own blood supply called Vasa Vasorum
61
what is the tunica media? (2)
- 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
what is the tunica interna? (1)
- thin layer made of endothelium --> protects blood from friction
- this is the only layer in the smallest vessels - capillaries
63
what are the types of artieries ?
- elastic
- muscular
- arterioles
- capillaries
64
what are elastic arteries?
- 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
what are muscular arteries?
- help to distribute + redirect the blood --> branch off elastic arteries
- have large tunica media to redirect blood as needed
66
what are arterioles?
- located within the tissues -- leading to capillary beds
- have precapillary sphincters to change local blood flow ---> controlled by SNS + autoregulation processes
67
what are capillaries?
- smallest artery
- only have tunica intima
- form beds: multiple branchings from arterioles (nutrient + gas exchange here)
types: continuous, fenestrated, sinusoidal
68
what are continuous capillaries?
- 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
what are fenestrated capillaries?
- 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
what are sinusoidal capillaries?
- 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
what is capillary exchange?
- 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
what are the two ways that fluid is gained or lost?
- colloid osmotic pressure
- capillary hydrostatic pressure
73
what is colloid osmotic pressure?
- 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
what is capillary hydrostatic pressure?
- 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
what are venuoles?
- 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
what are veins?
- 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
what is blood pressure?
- pressure of the blood against the vessel walls
- generates circulation (BF)
78
what is BP generated by?
primary factor - bc H2O
1) blood volume
short-term + change quickly
2) peripheral resistance - vessel diameter
3) cardiac output = HR
79
what is the amount of blood circulating throughout the body?
5.25L/min
- amt. of blood circulating equals the CO in mL/min
80
what is peripheral resistance?
- 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
what is vessel diameter?
- generates velocity of blood
--- constriction = increased resistance = increased BP = increased velocity
- primary variable the body uses to reg. BP + BF
82
what is vessel length?
- directly related to resistance
- increases greatly in obesity
83
what is viscosity?
- 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
aspects of measuring BP?
- 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
aspects of measuring pulse?
- measured by finger pressure on artery
- carotid or radial artery
86
what is pulse pressure?
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
what is Mean Arterial Pressure (MAP)?
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
what is venous return?
- 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
what is autoregulation?
- the ability of organs to maintain a constant blood flow despite changes in blood pressure
two mechanisms: myogenic + metabolic
90
what is the myogenic mechanism of autoregulation?
- reflex
- maintains BP + BF during orthostatic + sympathetic changes
- seen in brain + kidneys
91
what is the metabolic mechanism of autoregulation?
- 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
how is BP maintained (short-term)?
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
what receptors do the autonomic medullary centers use?
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
how is BP maintained (long-term)?
- 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
what is RAAS?
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
what are other hormonal factors?
atrial natriuretic peptide (ANP) - diuretic
- prod. by the atria when elevated pressure exists
- antagonistic to aldosterone - reduces BP + BV
vasopressen (ADH) - vasoconstrictor
97
what are some short term localized chemicals?
- histamine (vasodilator) - results in hyperemia
- nitric oxide (vasodilator)
98
what is circulatory shock?
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
what are the types of circulatory shock?
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
