1. determinant of flow in the blood vessels
    flow is equal to the change in pressure over the resistance
  2. vascular resistance
    determines how much flow occurs for a given driving pressure
  3. arterial vs. venous compliance
    arterial compliance is low (stiff walls) and stays nearly constant; venous compliance is physiologically regulated to maintain a relatively constant pressure despite volume changes
  4. vascular compliance
    transmural pressure = internal pressure - external pressure; compliance = _V/_Ptrans
  5. four main components of cardiovascular circuits
    ventricular pump; arterial distribution tree; microcirculation (arterioles & capillaries); venous return system
  6. key elements of regulation in the CV system
    central control (heart & vasculature & kidneys); local control (tissues control own blood flow); renal control (vasculature & blood volume regulation)
  7. Poiseuille's law
    used to calculate resistance in a cylindrical conduit; R is proportional to length and viscosity; R is inversely proportional to the radius raised to the 4th power
  8. control of blood flow
    in arterial system - mean arterial pressure & tissue resistance = important; resistance (in arterioles) = most important; in venous system - volume & compliance = important; compliance = regulated
  9. effects of size differences in blood vessels
    size variations in arteries & veins matter little in terms of blood flow because they are in series with high resistance arterioles; size variations in arterioles have major effects on flow
  10. pulmonary vs. systemic circuit flow
    both must have the same flow because they are circuits in series; the pulmonary circuit has 1/5 the resistance and 1/5 the pressure of the systemic circuit
  11. cardiac cycle
    late diastole (atria & ventricles relaxed); atrial systole; isometric ventricular contraction; ventricular ejection; isometric ventricular relaxation
  12. synchronization
    electrical impulses propagate rapidly from the SA node through atrial muscle to the AV node; delay in the AV node before transferrence of electrical impulses to the rapidly-conducting Purkinje fibers ensures that ventricular contraction is coordinated and occurs some time AFTER atrial contraction
  13. types of myocytes
    contractile (aka quiescent) and conductive
  14. contractile cardiac cells
    atrial & ventricular cells; cannot contract in the absence of external stimulation (as from the CNS)
  15. conductive cardiac cells
    Purkinje cells & cells of the SA and AV nodes; can contract in the absence of external stimulation (as from the CNS)
  16. differences between cardiac and skeletal muscle
    skeletal muscle depolarization is primarily caused by opening of fast sodium channels; cardiac muscle depolarization is caused by opening of fast sodium channels AND slow calcium channels -> long plateau phase; permeability of cell membrane to potassium DECREASES after onset of action potential in cardiac cells but NOT skeletal muscle cells
  17. propagation of electrical signals in the heart
    SA node -> propagation through atria -> AV node (slow - delay) -> Purkinje fibers -> fast propagation through ventricles from septum -> apex -> base
  18. phases of the ventricular action potential
    consists of 5 segments: 0 upstroke (sodium channels open -> influx of sodium); 1 notch (potassium channels open -> potassium efflux); 2 plateau (calcium channels open -> influx of calcium against electrostatic gradient; potassium efflux slows); 3 repolarization (potassium efflux against electrostatic gradient); 4 rest (potassium influx balances efflux)
  19. types of currents in a cardiac cell
    fast sodium; transient outward; L-type calcium; delayed rectifier; inward rectifier; funny
  20. fast sodium current
    very fast; quickly inactivated; opens when cell is depolarized; plays role in phase 0; allows influx of sodium
  21. transient outward current
    fast; quickly inactivated; opens when cell is depolarized; plays role in phase 1; allows efflux of potassium
  22. calcum current (L-type)
    slow; slightly inactivated; opens when cell is depolarized; plays role in phase 2; allows influx of calcium (up charge gradient but down concentration gradient)
  23. delayed rectifier current
    fast; not inactivated; opens when cell is hyperpolarized; plays role in late stage 3 and stage 4; allows efflux of potassium
  24. inward rectifier current
    very slow; not inactivated; opens when cell is depolarized; plays role in late stage 2 and stage 3; allows efflux of potassium
  25. funny current
    slow; permeable to sodium and potassium; opens when cell is hyperpolarized; present in AV node cells; play role in pacemaker function; increase in funny current decreases threshold for stimulation & thus increases heart rate
  26. mechanism of excitation-contraction coupling
    calcium enters cytoplasm during acition potential -> Ca2+ binding to ryanodine receptors on the sarcoplasmic reticulum -> SR releases Ca2+ -> Ca2+ from SR and cytoplasm bind to troponin-> contraction
  27. mechanism of excitation-contraction relaxation
    calcium is released from troponin; phosphorylation of PLB up-regulates the activity of SERCA on the SR; calcium is taken up into the SR by SERCA; excess cytoplasmic calcium is exchanged with sodium at the cell membrane by the Na-Ca ATPase pump
  28. mechanism of cardiac muscle contraction
    calcium binds troponin C -> conformation change of troponin complex -> release of tropomyosin from active sites of actin -> binding of myosin head to actin -> power stroke using energy from ATP
  29. sympathetic regulation of cardiac function
    sympathetic fibers innervate nodal regions & conduction system & atrial & ventricular myocytes; increase in inotropy (contractility) mediated by NE and beta-adrenergic receptors; beta-adrenergic receptor binding also phosphorylates phospholambin -> increased lusitropy (allows faster calcium release -> faster relaxation)
  30. parasympathetic regulation of cardiac function
    parasympathetic fibers innervate SAN (right vagus nerve) and AVN (left vagus nerve) and atria (sparse in ventricles); cholinergic fibers release ACh; muscarinic (G-protein coupled) receptors activated
  31. mechanisms of altering cardiac muscle contraction strength
    alteration of size of calcium transient (through inotropic/lusotropic agents); Frank-Starling mechanism; myofilament sensitizers; frequency of stimulation
  32. Frank-Starling mechanism
    increased stretching of the sarcomere -> increased pressure -> increased cardiac output
  33. force frequency relationship
    in healthy hearts - strength of contraction increases as heart rate increases
  34. contractility
    force with which the heart ejects blood; increased contractility increases the stroke volume
  35. relationship between CO and MAP and TPR
    cardiac output is approximately equivalent to mean arterial pressure divided by total peripheral resistance
  36. pulse pressure
    equal to systolic pressure minus diastolic pressure
  37. preload
    the pressure stretching the ventricles of the heart just prior to ejection; increased preload increases the stroke volume (according to the Frank-Starling mechanism)
  38. afterload
    equivalent to the pressure in the aorta leading from the ventricle; corresponds to the peak in systolic pressure in the left ventricle; corresponds to the arterial pressure against which the ventricle must contract; increasing the afterload decreases the stroke volume
  39. stroke volume
    equal to end diastolic volume - end systolic volume
  40. mean arterial pressure
    approximately equal to the end diastolic pressure plus 1/3 of the pulse pressure
  41. total peripheral pressure
    equivalent to the mean pressure in arteries AND veins
  42. factors affecting central venous pressure
    blood volume; venous compliance; cardiac performance
  43. ECG leads
    lead I = left arm (positive) - right arm (negative); lead II = left leg (positive) - right arm (negative); lead III = left leg (positive) - left arm (negative)
  44. effects of ventricular hypertrophy on ECG output
    axis deviation (L ventricle -> L axis deviation; R ventricle -> R axis deviation)
  45. effects of bundle brach blockage on ECG output
    axis deviation (L bundle branch block -> L axis deviation; R bundle branch block -> R axis deviation); inversion of T wave
  46. mean electrical axis
    refers to the overall direction of the heart's depolarizing wavefront; can be calculated from information from 2 leads
  47. premature ventricular contraction
    PVC occurs when ventricular contraction is initiated by ventricles instead of the SA node; produce large abnormal QRS waves on ECG followed by skipped beats
  48. first & second & third-degree AV block
    first-degree block results in prolonged P-R interval; second-degree block results in skipped ventricular beats; third-degree block results in spontaneous ventricular establishment of signal -> dissociation of P from QRS-T
  49. Starling forces
    delta P = hydrostatic pressure (tends to be outward & drive filtration); delta pi = colloid oncotic pressure (tends to be inward & drive absorption)
  50. types of capillaries
    continuous; fenestrated; discontinuous
  51. capillary filtration coefficient
    Kf; involved in the Starling equation to determine net filtration; describes the permeability of the capillary
  52. effects of venous pressure on net filtration
    increased venous pressure increases the net filtration rate
  53. structural features of the lymphatic system
    valves to prevent backflow & generate negative interstitial pressure; smooth muscle; body movements -> compression of lymphatics
  54. edema
    excess interstitial fluid; results from excess filtration or inadequate reabsorption
  55. interstitial fluid vs. plasma
    have almost the same composition in most of the body b/c of capillary leakiness; exception = CNS (due to blood-brain barrier)
Card Set
Introduction to the cardiovascular system