Cardiology Exam 2

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Cardiology Exam 2
2010-09-04 20:24:19
Cardiology medical svetik

cardio review
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  1. Edema mechanisms:
    Inflammatory: ↑ vascular permeability

    • Non-inflammatory: ↑ hydrostatic pressure and/or ↓ plasma
    • oncotic pressure
  2. Active hyperemia
    • (↑ inflow to capillary beds → exercise,
    • redness/warmth of inflammation, blushing)
  3. Passive hyperemia
    • aka congestion;
    • ↓ outflow from capillary beds (ie, impaired venous return) → obstruction, congestive heart failure
  4. Congestive Heart Failure (CHF)
    edema, organomegaly, chronic congestion from ↑ pressure in systemic capillaries caused by anything that impedes blood thru right heart (like pulmonary stenosis)
  5. Left-sided CHF:
    • dyspnea (SOB)
    • orthopnea (difficulty breathing),
    • hemoptysis (spitting up blood from resp tract)

    • → all due to pulmonary edema from ↑ pressure
    • in pulmonary capillaries caused by anything that impedes blood through left heart (like aortic stenosis, systemic HTN)
  6. Hypoperfusion (aka shock):
    • syncope, coma, tissue necrosis, etc.
    • from ↓ flow in systemic capillaries caused by low pressure or volume –
    • MI, fib, hemorrhage, etc.
  7. Hypoxemia:
    weakness, cyanosis, drowsiness from ↓ flow in pulmonary capillaries caused by R→L shunt heart malformations, pulmonary HTN, lung diseases
  8. HTN & Circulatory Dysfunction
    • ↑ resistance seen in HTN causes ↓ blood to flow while an increased pressure is needed to overcome the increased resistancethus in pulmonary HTN:
    • the ↑ resistance seen in HTN causes ↓ blood flow thru lungs
    • → less blood oxygenized & thus the hypoxemiaexplains why we get right-sided hypertrophy as a result since more force is needed (and thus the higher pressure seen) to overcome the increased resistancethus in systemic HTN:
    • the ↑ resistance seen in HTN causes ↓ blood flow thru body, leading to left-sided CHFsystemic HTN (→ left-sided CHF) vs. pulmonary HTN ( → hypoxemia & right-sided CHF)
  9. hematoma:
    • a hemorrhage that forms a mass of blood in an organ/space“Hemo-”: blood
    • in a body cavity (ex: hemothorax is a hemorrhage that fills the
    • thoracic cavity)
    • Hemorrhages along skin surface: petechiae (tiny, pinpoint) vs. purpura
    • (larger, palpable) vs. ecchymoses (largest, black and blue
    • areas)diapedesis: the escape of individual RBCs out of a vessel
  10. Hemostasis:
    Hemostasis: protective mechanism at the site where blood was leaking out of vessel primary: attachment, aggregation, and then activation of platelets to form hemostatic plugsecondary: tissue factor combines with platelet factors to activate coagulation cascade → fibrin
  11. Thrombosis
    → an extension of hemostasis
  12. Virchow’s triad:
    damaged vascular endothelium, increased coagulability of blood, alterations to normal blood flow
  13. Virchow’s triad:
    • stasis (→ venous thrombus) vs. turbulence (→ arterial thrombus)
    • thrombus (within the cardiovascular system) vs. blood clot (outside cardiovascular system)
    • exception → post-mortem clots: small blood clots that are found within vessel but not attached to the vessel walls and no internal structure
  14. Thrombi
    • arterial (usually occlusive; defined Lines of Zahn – alternating layers of platelets & red cells) vs. venous thrombi (defined valve markings) → blood clots lack such an internal organization
    • mural thrombi: those attached to heart chambers, valves, & aortaHigh risk in those with atrial fibrillation → loss of true atrial contraction (just twitches uncoordinatedly) → atrium becomes a more static blood chamber allowing for the development of mural thrombi which can cause a stroke
  15. Embolus:
    any material (fragments of thrombi, atherosclerotic plaque, bone marrow, gas, fat droplets, etc.) that is carried in bloodstream that can block a vesselpulmonary artery: most common site for emboli to become lodged → right-sided CHF“Economy Class Syndrome”: the very easy formation of venous thrombi due to static blood flow in leg since workers are always sitting down behind a computer all day
  16. Hypoxia
    (reduced oxygen availability → injures tissues less since they can still produce energy from glycolysis)
  17. Ischemia
    (reduced blood flow → injures tissues more since less delivery of substrates/removal of metabolites for glycolysis)
  18. infarct
    • localized area of ischemic necrosis due to loss of blood supply → 2 types:
    • anemic (appear as pale, artery to organ is completely blocked and organ has no other means to get blood) vs.
    • hemorrhagic (appear as red, artery is blocked but organ has another means to get blood)
  19. Control of Microcirculation (Hogan)
    Arterial System (regulation of resistance) vs. Venous System (regulation of compliance)
  20. precapillary resistance
    (anti-motion function → muscle contraction here leads to ↑ resistance to slow blood flow thru capillary)
  21. venous compliance
    (pro-motion function → muscle contraction here leads to ↑ wall stiffness that creates the pressure to quicken blood flow back to heart)
  22. Smooth muscle → thick filament regulation (ie, regulation of the phosphorylation of myosin to control muscle contraction)
    • Ca enters cell (either from SR or extracellular fluid) and binds to calmodulin (CaM)
    • Ca-CaM complex activates MLCK which phosphorylates the myosin heads, increasing it’s ATPase activity and thus exposes binding site to allow crosslinking to occur and muscle to contract
    • cAMP-kinase & cGMP kinase regulates MLCK by phosphorylating it to deactivate it so it cannot form the Ca-CaM-MLCK complex which activates contraction
  23. Regulation of Vascular Smooth Muscle
    • Depolarization (via vessel wall stretching) → influx of Na which ↑ influx of Ca via the VGCC → vasocontriction
    • Hyperpolarization (via adenosine or endothelial hyperpolarizing factor (EDHF) released from endothelial cells) → outflux of K which ↓ influx of Ca via the VGCC → muscle relaxation
  24. NE:
    binds to α1 receptors to activate IP3 which causes ↑ Ca release from SR → vasoconstriction
  25. Endothelin
    (most powerful veno-/vasoconstrictor in the body; released from endothelial cells): binds to ETa receptors then activates IP3 just like NE → vasoconstriction
  26. PGI2 / Epinephrine (on β2 receptors)

    Histamine → all activate cAMP kinase which deactivates MLCK by phosphorylating it → muscle relaxation
  27. ACh
    • (on muscarinic receptors)
    • When acting directly on vascular smooth muscle cell → inhibits cAMP to cause vasoconstriction
    • But! when it binds to endothelial cells, it causes NO to be released which activates cGMP kinase which deactivates MLCK by phosphorylating it → muscle relaxation
  28. Multi unit
    large vessels → “federal” neurogenic control
  29. Single unit
    small vessels → “local” myogenic and metabolic control
  30. Neurogenic Control of Vascular Smooth Muscle
    • adrenergic (α receptors → NE → vaso/venocontraction) vs.
    • cholinergic (muscarinic receptors → ACh → “anticipatory vasodilation” – useful before you’re about to run a sprint)
  31. Adrenergic Constrictor System:
    • venomotor tone (sympathetic response causes ↑ stiffness in veins which brings blood back to heart quicker)
    • vs. vasomotor tone (sympathetic response causes ↑ precapillary
    • resistance)
    • Parasympathetic: cholinergic (muscarinic receptors → ACh → vaso-relaxation)
    • Pcap = [(Rpost/Rpre)• Pa + Pv] / [1 + (Rpost/Rpre)]
    • Shows that regulation of precapillary resistance controls both flow & mean capillary pressure
  32. Local Control
    Myogenic Control
    • ↑ lateral pressure (aka “inflation pressure”) of the vessel → vessel wall stretching →
    • ↑ tension & vasoconstriction
    • thus ↓ vessel radius & ↑ resistance, ultimately leading to a ↓ pressuredefensive mechanism against over-inflation of the vessel
  33. CCP (critical closing pressure):
    point at which vessel collapses (despite the fact that pressure does not equal zero)
  34. Metabolic Control →
    • “circulation is the slave to metabolism”
    • Nearly all by-products of metabolism released from cells have a vasodilator ability to them, which ↓ resistance in arterioles & thus ↑ flow ie, ↑ metabolism → ↑ blood flow (active hyperemia)
  35. reactive hyperemia:
    • the spike in blood flow from the build up of metabolites when a vessel is occluded
    • the longer the vessel is occluded, the larger the spike in blood flow due to the longer amount of time the metabolites had to build upeach tissue has arterioles that have a max dilation & max constriction → steady state establishes a resting blood flow demand based on normal pressure in that tissue
    • thus, the greater the slope of the Q vs. ∆P curve, the higher the metabolism is in that tissue
  36. flow reserve:
    allows for ↑ flow whenever needed (such as during an ↑ in metabolism) → becomes a problem in a disease like coronary artery disease when that reserve is compromised
  37. Local Response to Pressure Change
    • every tissue has an autoregulation range that is able to maintain the resting demand of blood flow despite ∆s of pressure
    • if under-perfusion, the buildup of metabolites will cause vasodilation that brings the ∆P vs. Q curve back to resting demand
    • if over-perfusion, the ↑ in pressure creates an unneeded ↑ in flow since metabolism hasn’t changed
    • the ↑ flow washes out the metabolites to cause vasoconstriction to bring the ∆P vs. Q curve back to resting demand
  38. Tissue Volume Recruitment
    • Whenever the sympathetic response is stimulated, there is first a sharp drop in tissue volume (“intravascular recruitment” – the blood within the vessels of the tissue is dumped into central circulation)
    • And then a more gradual drop in tissue volume (“extravascular recruitment” – the blood sitting within the ISF is brought into the central circulation)
    • Following the sympathetic stimulation, there is a rapid filling of blood back into the vessels of the tissue from the reactive hyperemia and then a gradual increase for the rehydration of the ISF