m7 + 8 lecture - CV system Flashcards
what is hemostasis?
stoppage of blood flow - coagulation
what are the three actions produced by a tissue/vessel injury?
1) vascular spasm
2) platelet plug formation
3) coagulation/clotting cascade
what happens during vascular spasm?
- damage to endothelial cells initiates release of endothelin –> stimulating vasoconstriction
purpose: dec. blood flow + dec. blood loss
what happens during platelet plug formation?
- 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
what happens during clotting cascade (coagulation)? (scab formation)
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)
what is thromboxane?
platelets - they stick to everything, augmenting adhesion site in platelet plug formation
what happens during the formation of prothrombin activator (clotting cascade: 1st step)?
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
what happens during the formation of thrombin (clotting cascade: 2nd step)?
PTA catalyzes the change from prothrombin to thrombin
- catalyzes the next step
what happens during the formation of fibrin fibers (clotting cascade: 3rd step)?
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
what are some bleeding/clotting disorders?
- 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)
what is the reason for clotting in an uninjured vein?
vein —> DVT (blood clot)
- if it breaks free = embolus (in lungs = pulmonary embolus)
- causes: dec. circulation, age, heart Dz, diabetes, post-surgical
what is the reason for clotting in an uninjured artery?
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)
what are some anti-platelet medications?
- plavix
- elequis
- brilinta
- aspirin
what is a anti-prothrombin medication?
they are anticoagulants (blood thinners)
- coumadin (aka warfarin) - impaired by vit k
what is a anti-thrombin medication?
they are anticoagulants (blood thinners)
- heparin
- lovanox
what are the two classifications for anemia?
1) lack of RBCs
2) lack of hemoglobin
what are the types of anemia that have a lack of RBCs?
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
what are the types of anemia that have a lack of hemoglobin?
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
what is the physiology of myocardial cells?
- 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
where does calcium come from and its function?
- from extracellular (interstitial cells - 20%)
- from intracellular (sarcoplasmic reticulum - 80%)
- calcium initiate heart muscle contraction
- calcium channel blockers slow HR
how is the heart stimulated?
- a self-initiating functional syncytium - gap junctions
- regulated by nodal system
- two contractile units: atria + ventricles
what is a functional syncytium?
a group of cells that function as a single unit while maintaining their individual cellular role
what is the nodal system? (intrinsic conduction system)
- 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
what does digoxin do to the heart?
- decrease HR
- increase contractibility
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
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)
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
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
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
what happens at the P-wave?
SA node initiates atrial depolarization then contraction
what happens at the QRS-wave?
Purkinje fibers initiate ventricular depolarization then contraction
what happens at the T wave?
ventricles repolarize (relaxation + refilling)
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
what happens at the Q-T interval?
initiated by the purkinje fibers
- all ventricular activity - depo. = contraction = ejection = repolarization = relaxation
what happens at the S-T interval?
- ejection of blood = creates circulation + pressure (BP + BF)
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
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
what can cause heart murmurs?
- genetics
- age
- infections - sepsis
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)
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
what is the CO purpose in maintaining homeostasis?
O2 supply for sufficient perfusion
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
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
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
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)
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
what helps regulate HR?
- ANS regulation
- chemoreceptors
- baroreceptors
- proprioceptors
how does the ANS regulate HR?
PSNS - cardioinhibitory - decrease HR
SNS - cardioacceletory - increase HR
what centers does the medulla oblongata contain that affect rate and systemic pressure? (ANS)
cardiac center - HR
vasomotor - vessel diameter (BP)
respiratory center - RR
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
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
what are inotropic agents?
change the force of muscular contractions (contractility)
ex.) epi, ANP, hypokalemia, CHF, age
what does age do to the heart?
- valves harden + thicken
- muscle atrophies + weakens
- muscle becomes fibrotic + stretches
- cardiac output will decrease
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
what are blood vessels are?
transportation highways
- gases are exchanged
- nutrients are delivered
- waste is removed
what do arteries do?
carry blood away from the heart (efferent)
what do veins do?
carry blood towards the heart (afferent)
what are the layers in a artery?
1) tunica externa
2) tunica media - thick
3) tunica interna
what are the layers in a vein?
1) tunica externa
2) tunica media
3) tunica interna
- large lumen ( internal lining)
what is the tunica externa? (3)
- external layer of vessel
- anchors the vessel - in larger vessels, may have own blood supply called Vasa Vasorum
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
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
what are the types of artieries ?
- elastic
- muscular
- arterioles
- capillaries
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
what are muscular arteries?
- help to distribute + redirect the blood –> branch off elastic arteries
- have large tunica media to redirect blood as needed
what are arterioles?
- located within the tissues – leading to capillary beds
- have precapillary sphincters to change local blood flow —> controlled by SNS + autoregulation processes
what are capillaries?
- smallest artery
- only have tunica intima
- form beds: multiple branchings from arterioles (nutrient + gas exchange here)
types: continuous, fenestrated, sinusoidal
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
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
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)
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
what are the two ways that fluid is gained or lost?
- colloid osmotic pressure
- capillary hydrostatic pressure
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)
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
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
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
what is blood pressure?
- pressure of the blood against the vessel walls
- generates circulation (BF)
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
what is the amount of blood circulating throughout the body?
5.25L/min
- amt. of blood circulating equals the CO in mL/min
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
what is vessel diameter?
- generates velocity of blood
— constriction = increased resistance = increased BP = increased velocity - primary variable the body uses to reg. BP + BF
what is vessel length?
- directly related to resistance
- increases greatly in obesity
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)
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)
aspects of measuring pulse?
- measured by finger pressure on artery
- carotid or radial artery
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)
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
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
what is autoregulation?
- the ability of organs to maintain a constant blood flow despite changes in blood pressure
two mechanisms: myogenic + metabolic
what is the myogenic mechanism of autoregulation?
- reflex
- maintains BP + BF during orthostatic + sympathetic changes
- seen in brain + kidneys
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
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
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
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
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
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
what are some short term localized chemicals?
- histamine (vasodilator) - results in hyperemia
- nitric oxide (vasodilator)
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
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
