Mod 4 Physiology

  1. What is the difference in refractory period for a nerve, cardiac muscle, and skeletal muscle?
    The cardiac muscle has a longer refractory period because of the balance between K+ efflux and Ca++ influx in phase 2
  2. Steps in excitation-contraction coupling in cardiac muscle. How does the muscle relax afterwards
    • 1) depolarization
    • 2) L-type calcium channels open allowing extracellular Ca++ to enter
    • 3) exCell Ca++ open ryanodine receptors and cause the Ca++ from the SR to be released (100x more) (calcium induced calcium release)
    • 4) Ca++ change troponin and move tropomyosin off the binding sites.
    • 5) Contraction
    • 6) end of deopolarization
    • 7) L-type Ca++ channels close
    • 8) Ca ++ is taken up by SERCA pump and sarcolemma pumps
    • 9) Decrease in Ca++ causes contraction to end
  3. Difference in cardiac muscle and skeletal muscle in cell size, electrical connections, and myofilament arrangement.
    • -Cardiac muscle is smaller
    • -Less structured than skeletal
    • -can conduct faster because of gap junctions in intercalated discs
  4. Define ventricular contractility
    Strength of contraction. Related to the intrinsic cellular mechanisms that regulate the interaction between myosin and actin. Too much preload will pull the myosin too far away from the actin filaments (heart failure)
  5. What are the 5 subsystems of the heart (brief description)
    • 1) pacemaker and conduction systems: SA node (70-80), AV node(40-60, slowest conduction), internodal pathways, bachmann's, R and L bundles, purkinje fibres (fastest cond.)
    • 2) Heart muscle (myocardium): acts as a syncytium, lots of gap junctions
    • 3) Heart Valves: in theory should need six, but there are only four so that the atria don't need to create a huge negative pressure
    • 4) Coronary circulation
    • 5) autonomic innervation:
    •   -parasymp: -ve chronotropic, atria mostly
    •   -sympathetic: +ve choronotropic and ionotropic, everywhere
  6. What three things can affect rhythmicity (heart rate)
    • 1) Rate of diastolic depolarization: eg. norepinephrine increases rate of diastolic depol. (increases HR)
    • 2) Change max. diastolic potential: e.g. acetylcholine (released by neurons) decreases MDP and rate of diastol. depol. both of which decrease HR
    • 3) Change the threshold potential: e.g. quinidine increases threshold, which increases time to reach threshold, decreases HR.
  7. What do the P, T waves and QRS complex mean?
    • P-wave: depolarization of atrium
    • QRS complex: depolarization of ventricles
    • T-wave: repolarization of ventricles

  8. Describe, in detail, the two main components of a cardiac cycle
    • A) Ventricular Systole
    •   1)Isovolumetric vent. contraction
    •   2) Rapid ejection phase
    •     i)rapid ejection phase
    •     ii)reduced ejection phase
    • B) Ventricular Diastole
    •   1)Isovolumetric ventricular relaxation
    •   2)Ventricular Filling
    •     i)Rapid filling phase
    •     ii)reduced filling phase
  9. Name 3 accessory (abnormal) tracts of conduction in the heart
    • 1) James' Fibres: Fibres from atrial internodal pathway that bypass AV node and go straight to I/V septum. Can cause premature excitation of ventricles. Can cause tachycardia (faster than normal HR)
    • 2) Mahaim Fibres: any direct connection between AV node, AV bundle, or bundle branches into ventricles. Can also cause premature ventricular contraction
    • 3) Bundle of Kent: direct connection between atrium and ventricle. Can cause fibrillation or tachycardia
  10. Why is the P-wave wider than the QRS complex??
    Because the signal moves slower in the atrial myocytes compared to the purkinje fibres in the ventricles
  11. How does hyperkalemia (hi K+) cause a wider QRS complex
    Interferes with the proper operation of the fast voltage-gated sodium channels.
  12. How is pressure generated in the CV system?
    • Force of contraction of the heart (contractility)
    • Vascular tone
  13. Normally, what is preload determined by?
    • 1) ventricular compliance
    • 2) venous return
    • 3) Length-tension relationship
    • 4) HR (to a lesser degree)
  14. For a given EDP, what happens to the EDV if you have: 1) ventricular dilation; 2) ventricular hypertrophy
    • 1) increase EDV
    • 2) decrease EDV
  15. What is preload?
    Think about it as the amount of blood in the heart before systole (essentially end diastolic volume)
  16. What is afterload?
    ventricular wall stress developed during systole. Essentially aortic pressure. the load which the heart must overcome in order to eject blood.
  17. How can you decrease afterload?
    • 1) diuretic: decreases blood volume (pee it out)
    • 2) Calcium Channel blockers: decreases the force of contraction. The effect in the smooth muscle of arteries is most pronounced (vasodilation)
    • 3) ACE inhibitor.
  18. What is contractility?
    property of contractile myocytes that account for strength of contraction. Related to the intrinsic mechanisms that regulate the interaction between myosin and actin. Usually independent of preload and afterload (except for preload in a failing heart)
  19. How can you change contractility?
    • sympathetic stimulation (norepinephrine)(increases)
    • epinephrine (increases) 
    • Parasympathetic (ACh) (decreases)
    • myocardial ischemia
  20. How does increased HR increase contractiliy?
    bowditch effect: basically there isnt time to restore ionic concentrations, so there is an accumulation of Ca++ in the cytostolic space.
  21. What happens when you increase contractility?
    • increase Vmax
    • increase ejection velocity
    • increase stroke volume
    • reduce ESV
    • reduce ESP
  22. What are the 6 factors that affect blood flow?
    • Velocity
    • Pressure
    • Viscosity 
    • resistance 
    • flow pattern
    • hematocrit (relates to viscosity)
  23. What are 5 ways that you can increase CVP?
    • -Decreased CO: (blood backing up)
    • -Increase total blood volume: e.g. renal failure
    • -standing to supine position: (blood goes from leg to thorax)
    • -aterial dilation: (more blood from arterial side to venous side)
    • -force expiration: compressing your thorax (and vena cava)-muscle contraction: skeletal muscles move blood
  24. What can cause edema?
    • 1) Increase permeability of capillary
    • 2) decrease plasma concentration in blood (lower oncotic pressure)
    • 3) elevation of venous pressure (increase hydrostatic in venules)
    • 4) blockage of the lymphatic system
  25. What are the three levels of autonomic neural control in CV?
    • 1) higher centres such as cortex: emotional stress
    • 2) Hypothalamus: modulates medullary neuronal activity
    • 3) medulla: afferent fibres from receptorsenter at nuclear tractus solitarius. inhibits sympathetic, excites parasympathetic
  26. What does the vagus nerve release and what effect does it have?
    • Releases ACh which:
    • -decreases chronotropy (HR)
    • -decreases ionotropy (contractility)
    • -decreases dromotropy (conduction velocity)
    • -dilates the coronary arteries
  27. What effect does the sympathetic nervous system have on the CV system?
    Heart: increases dromotropy, chronotropy, ionotropy. 

    Vasculaure: vasoconstriction (constricts both the resistance (arterioles) and capacitance (veins) vessels. Transient vasoconstriction of coronary arteries, followed by steady state vasodilation.
  28. What happens when there is an increase in BP (regarding baroreceptors)
    • 1) firing rate of baroreceptors increases
    • 2) Signal goes to NTS
    • 3) causes inhibitory effect on symp. stimulatory effect on parasymp.
    • 4)results in a decrease in HR and BP
  29. Describe the Bainbridge reflex
    • 1) increase in venous return increases firing rate of stretch receptors in heart
    • 2) goes to NTS
    • 3) medulla increases sympathetic innervation to the SA node, speeding up the heart
  30. What are the 4 major factors of CV humoral control?
    • 1) Catecholamines (epinephrine and norepinephrine)
    • 2) Renin-angiotensin-aldosterone system (increase arterial pressure)
    • 3) ANP (decrease arterial pressure)
    • 4) vasopressin (increase arterial pressure)
  31. what do the alpha, beta 1, and beta 2 receptor modulate?
    • alpha: vasoconstriction 
    • beta1: vasoconstriction, increases force of contraction, increases chronotropy, increases dromotropy
    • beta1:vasodilation
  32. How does epinephrine increase BP (3 ways)?
    • vasoconstriction (alpha receptors)
    • increased force of contraction (beta1 in the ventricle)
    • increases heart rate (beta 1)
  33. What is the difference between norepi and epi?
    • norepi: strong beta1 and alpha agonist, weak beta 2
    • epi: strong agonist for all three, strongest for beta2
  34. What are the three functions of the lymphatic system?
    • 1) fluid resorption: about 3L a day are returned to venous circulation this way
    • 2) fat absorption: through lymph vessels called lacteals in the small intestine
    • 3) defence: lots of macrophages, only at the lymph nodes
  35. What types of substrates are normally used for myocardial metabolism?
    • Heart will generally use what is available, but at rest:
    • 1) fatty acids (60%)
    • 2) carbohydrates (35%)
    • 3) amino acids and ketones (5%)
  36. Name 4 types of impulse and conduction alteration
    • 1) overdrive supression
    • 2) escape rhythm
    • 3) Heart blocks
    • 4) re-entry loop
Card Set
Mod 4 Physiology
Mod 4 Physiology