IBHS 527 lecture 5

Card Set Information

Author:
VASUpharm14
ID:
61282
Filename:
IBHS 527 lecture 5
Updated:
2011-01-23 01:59:02
Tags:
im too cool
Folders:

Description:
Heart: Conduction & Contraction. Bryant (snow delay) ... anatomy was previous lecture .. now FUNCTION!
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user VASUpharm14 on FreezingBlue Flashcards. What would you like to do?


  1. 2 types of cardiac muscle cells
    • 1. specialized muscle cells of the conducting system
    • -controls and coordinate heartbeat
    • 2. contractile cells (muscle cells of heart)
    • -produce contractions that propel blood
  2. context: conducting system
    T/F
    cardiac muscles are similar to skeletal muscles via action potentials to create muscle contraction
    TRUE
  3. context: conducting system
    automaticity
    • ability to contract on it own without neural or hormonal stimulation (which usually is used to regulate the speed either increase or decrease)
    • this is unique property to cardiac muscle
  4. context: conducting system
    conducting system of the heart includes 3 things
    • 1. sinoatrial (SA) node
    • 2. atrioventricular (AV) node
    • 3. conducting cells:
    • -internodal pathways, AV bundle, right and left bundle branches, Purkinje fibers (stimulate directly on the ventricular cardiac muscle cells)
  5. context: conducting system
    how do conducting cells have spontaneous depolarization?
    after each repolarization the membrane drifts towards threshold and cannot maintain stable resting membrane potential (RMP)
  6. context: conducting system
    T/F
    all conducting cells can do spontaneous depolarization at the same rates
    FALSE. "different" rates
  7. context: conducting system
    rates of conducting cells (action potentials per minute)
    • 1. Sinoatrial (SA) node has fastest rate of spontaneous depolarization with 80-100 per minute
    • 2. Atrioventricular (AV) node generates 40-60 action potential per minute
    • 3. Purkinje fibers 20-40 action potential per minute
    • *the fastest rate dominates because it occurs the quickest
    • -SA node dominates usually, unless it's damaged and then AV node is next to dominate (back-up plan) ... however it's harder if it moves to Purkinje fibers
  8. context: conducting system
    5 steps in the conduction pathway
    • 1. SA node
    • 2. AV node
    • 3. AV bundle (bundle of His)
    • 4. Right and left AV bundle branches
    • 5. Purkinje fibers
  9. context: conducting system
    context: 5 steps in the conduction pathway
    SA node (start)
    • step 1
    • -located in posterior wall of right atrium
    • -contains pacemaker cells
    • -referred to as the cardiac pacemaker
    • -connected to AV by internodal pathways
    • ------
    • T = 0
    • SA node activity and atrial activation begins
  10. context: conducting system
    context: 5 steps in the conduction pathway
    AV node
    • step 2
    • -located in the floor of right atrium
    • -impulse conduction slows when passing through AV node because the atria has to contract before the ventricles to get the extra blood into the ventricles first.
    • ------
    • T = 50 msec
    • stimulus spreads across the atrial surfaces and reaches the AV node
  11. context: conducting system
    context: 5 steps in the conduction pathway
    AV bundle (bundles of His)
    • step 3
    • only electrical connection between atria and ventricles
    • ------
    • T = 150 msec
    • there is a 100-msec delay at the AV node. Atrial contraction begins
  12. context: conducting system
    context: 5 steps in the conduction pathway
    right and left AV bundle branches
    • step 4
    • -left branch is larger because it meets the need of the left ventricle which is also large
    • -both extend toward apex and fan out
    • ------
    • T = 175 msec
    • the impulse travels along the interventricular septum within the AV bundle and the bundle branches to the Purkinje fibers and, via the moderator band, to the papillary muscles of the right ventricle
  13. context: conducting system
    context: 5 steps in the conduction pathway
    Purkinje fibers
    • step 5
    • -conduct action potentials very rapidly to ventricular muscle (contractile) cells
    • ------
    • T = 225 msec
    • the impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium. Atrial contraction is complete, and ventricular contraction begins.
  14. context: conducting system
    Electrocardiogram
    • ECG or EKG
    • -recording of the electrical events in the heart (depolarization and repolarization)
  15. context: conducting system
    general parts of an ECG graph
    • 3 parts on graph:
    • 1. P wave: depolarization of atria
    • 2. QRS complex: ventricular depolarization
    • 3. T wave: ventricular repolarization
    • *don't see atria repolarization --> masked by ventricular depolarization
    • 2 measurable intervals:
    • 1. P-R interval:
    • -start of atrial depolarization (P) to start of ventricular depolarization (actually measured at start of QRS complex - but close to the R wave)
    • -if P-R interval increases to over 200 msec, this can indicate damage to conducting pathways or AV node
    • 2. Q-T interval:
    • -one complete cycle of ventricular depolarization and repolarization
    • -usually measured from end of P-R interval instead of from the bottom of the Q wave
    • -prolonged Q-T interval can indicate electrolyte disturbances, conduction problems, coronary ischemia, myocardial damage, and some drugs can cause this
  16. context: conducting system
    how are ECGs helpful?
    • diagnosing cardiac arrhythmias
    • -may indicate damage to myocardium (muscle tissue of heart), injuries to the pacemakers or conduction pathways, exposure to drugs, or abnormalities in electrolyte composition of extracellular fluids
  17. context: conducting system
    9 kinds (general) of drugs that may effect ECGs
    digoxin, antiarrhythmics classes I-IV, tricyclic antidepressants, H1 antagonists, methylxanthines, doxorubicin, lithium, catecholamines, diuretics
  18. context: conducting system
    arrhythmias (general)
    abnormal rhythm/pattern of electrical activity of the heart
  19. context: conducting system
    4 types of arrhythmias
    • 1. bradycardia
    • 2. tachycardia
    • 3. atrial fibrillation
    • 4. ventricular fibrillation
  20. context: conducting system
    context: 4 types of arrhythmias
    bradycardia
    • less than 60 BPM with exceptions to athletes who may have lower at rest
    • - caused by damage to conduction pathway or damage to SA node or damage to AV node (slower) - heart block (SA fire but AV is bad so that the atria still depolarizes of P wave but no QRST sometimes)
    • TREATMENT (general): chronic and require pacemaker rather than drugs
  21. context: conducting system
    context: 4 types of arrhythmias
    tachycardia process
    • greater than 100 BPM at rest -caused by part of conduction system being overactive or overstimulated (overacting of nervous system. ex- hyperthyroidism and thyroid hormone
    • TREATMENT (general): drugs like beta blockers and lowering heart rate.
  22. context: conducting system
    Ectopic pacemaker
    • another cause of arrhythmias (another cell on its own causing async. contraction)
    • -when a Purkinje or ventricular muscle cell depolarizes to threshold and triggers an abnormal conduction pathway or premature ventricular contraction (PVC)
  23. context: conducting system
    context: 4 types of arrhythmias
    atrial fibrillation
    • -impulses move over atrial surfaces in uncoordinated fashion (like a bag of worms - no distinct P wave and no pattern with QRST
    • -heart can still pump blood
    • -ventricles can still contract
    • -and one can live with this because it affects the atria only contribute little whereas most blood is in the ventricles
  24. context: conducting system
    context: 4 types of arrhythmias
    ventricular fibrillation
    • -impulses travel around ventricles in uncoordinated fashion
    • -premature ventricular contractions (PVCs) and ventricular tachycardia can precede/lead to fibrillation
    • -can lead to cardiac arrest (heart stops pumping blood)
    • *you can't live with this! so you would need treatment: defibrillator - shocks heart --> depolarize entire heart at once --> SA take control again --> normal rhythm
  25. context: conducting system
    anti-arrhythmics are classified by what?
    classes
  26. context: conducting system
    4 classes of anti-arrhythmics (most TOP 200)
    • 1. class I: sodium channel blockers
    • 2. class II: beta-clockers
    • 3. class III: potassium channel blockers
    • 4. class IV: calcium channel blockers
  27. context: conducting system
    context: 4 classes of anti-arrythmics (most TOP 200)
    class 1
    • sodium channel blockers
    • -lidocaine (not top 200)
    • -quinidine (not top 200)
    • *when having an abnormal rhythm, slow down the depolarization rate to get to unison
  28. context: conducting system
    context: 4 classes of anti-arrythmics (most TOP 200)
    class 2
    • beta-blockers
    • -atenolol
    • -carvedilol
    • -metoprolol
    • *when having tachycardia, slow the heart rate
  29. context: conducting system
    context: 4 classes of anti-arrythmics (most TOP 200)
    class 3
    • potassium channel blockers
    • -amiodarone (can also block calcium and sodium channels)
    • *slow down repolerization --> extend refractory period so that it is hard to stimulate again -- slow down for the SA node to take over again
  30. context: conducting system
    context: 4 classes of anti-arrythmics (most TOP 200)
    class 4
    • calcium channel blockers
    • -diltiazem
    • -verapamil
    • *block/slow action potentials (AP)
  31. context: conducting system
    context: 2 types of cardiac muscle cells
    conducting system covered
    now: contractile cells
  32. context: contractile cells
    similarities between cardiac and skeletal muscle cells
    • process:
    • (1) action potential leads to appearance of Ca2+ among the myofibrils --> (2) binding of Ca2+ to troponin on thin filaments initiates contraction --> (3) actin-myosin cross-bridges form, filament slides, contraction occurs
  33. context: contractile cells
    differences between cardiac and skeletal muscles cells
    nature and duration of action potential
  34. context: contractile cells
    review of skeletal muscle action potential
    • process:
    • (1) depolarization to threshold initiates action potential [AP] --> depolarization pharse of AP due to Na+ influx --> repolarization phase of AP due to K+ efflux
    • *lasts 1-2 msec during entire AP
  35. context: contractile cells
    3 parts of cardiac muscle action potential
    • 1. rapid depolarization (still like skeletal muscle):
    • -causes Na+ entry
    • -duration is 3-5 msec
    • -ends with closure of voltage-regulated (fast) sodium channels
    • 2. plateau (MAIN DIFFERENCE):
    • -causes Ca2+ entry (K+ goes out)
    • -duration is ~175 msec
    • -ends with closure of slow calcium channels (net flux of ions is 0 because it balances with K+)
    • 3. repolarization:
    • -causes K+ loss
    • -duration is 75 msec
    • -ends with closure of slow potassium channels
    • *graph looks different and there is a longer refractory period due to plateau and longer action potential (AP) - longer contraction
  36. context: contractile cells
    comparison of skeletal vs cardiac muscle
    skeletal side
    • skeletal:
    • (1) action potential (AP) travels down T tubules --> (2) changes in membrane potential opens Na+ channels --> (3) Ca2+ released from sarcoplasmic reticulum (SR) initiates contraction --> (4) actin, myosin filaments interact
    • *AP lasts ~1-2 msec.
  37. context: contractile cells
    comparison of skeletal vs cardiac muscle
    cardiac side
    • cardiac:
    • (1) action potential (AP) travels down T tubules --> (2) changes in membrane potential opens Na+ channels (fast) and Ca2+ channels (slow - slight delay) {extracellular Ca2+ concentration affects strength (INC.) of contraction (T tubules: 5x diameter vs skeletal) which means more Ca2+ in addition to SR Ca2+} --> from out to in is Ca2+ inducing Ca2+ release from SR, initiates contraction --> actin, myosin filaments interact
    • *AP lasts ~250-300 msec (lasts longer than skeletal)

    highlight = 3 differences between skeletal vs cardiac muscle
  38. 2 differences with SA node and contractile cells action potentials (AP)
    • 1. no plateau phase (Ca2+) in SA node action potential (the calcium is responsible only for conduction and so no need for more calcium)
    • 2. Phase 4 (picture)
    • -SA node has a drifting membrane potential (prepotential or pacemaker potential)
  39. what is one cardiac cycle?
    from the start of one heartbeat to the beginning of the next
  40. 2 divisions of the cardiac cycle
    • 1. atrial systole and diastole
    • 2. ventricular systole and diastole
    • *systole = contraction
    • *diastole = relaxation
  41. T/F
    blood will move from an area of lower pressure to an area of higher pressure
    FALSE. from "higher" to "lower"
  42. T/F
    the left side of the heart deal with higher pressures
    TRUE. has to deal with systemic circulation
  43. T/F
    left and right ventricles contract and eject blood at different times
    FALSE. "same" time (it's different between atria and ventricles)
  44. cardiac cycle diagram
    • start = atrial systole
    • isotonic - moving and changing muscle length
    • 2 phases of ventricular systole
    • 2 phases of ventricular diastole (early and late)
    • ventricles fill passively in step f
  45. heart sounds
    • stethoscope --> listen for normal/abnormal heart sound
    • S1: closing of AV valves = "Lubb"
    • S2: closing of semilunar valves = "Dubb"
    • S3 and S4 = not often audible in healthy adults
    • -S3: blood flowing into ventricles
    • -S4: atrial contraction
    • heart murmur: AV valve regurgitation (rushing, gurgling sound)
  46. 2 cardiac disorders/diseases
    • 1. myocardial infarction (MI)
    • 2. congestive heart failure (CHF)
  47. context: 2 cardiac disorders/diseases
    myocardial infarction (MI)
    • when a region of the coronary circulation is blocked and cardiac muscle cells die from lack of oxygen
    • -caused (often): by coronary artery disease (CAD)
    • *approximately every minute an American dies from a coronary event (MI is just one of them)
  48. infarct
    region of damaged nonfunctional tissue
  49. T/F
    cardiac muscle can be replaced by the body
    FALSE. they "cannot" be replaced unlike skeletal satellite cells
  50. 2 ways to detect or determine myocardial infarction
    • 1. diagnostic blood tests
    • -lactate dehydrogenase (LDH), creatine phosphokinase specific to cardiac muscle (CK-MB), cardiac troponin I, cardiac troponin T
    • *if you have MI, those cells that die then go to the bloodstream and release these enzymes and proteins --> they are not normally found in the bloodstream = damage occurred
    • 2. ECG findings
    • -elevated/longer than normal S-T segment
    • -enlargement of T waves
  51. 3 treatments for myocardial infarction
    • 1. vasodilators
    • 2. anticoagulants
    • 3. fibrinolytics
    • *depends on the cause
  52. 10 risk factors for myocardial infarction
    • 1. smoking
    • 2. high blood pressure (BP)
    • 3. high blood cholesterol levels
    • 4. high LDLs
    • 5. diabetes: it's own risk factor - INC. mortality
    • 6. male gender (below 70 yrs) - although risk of MI is lower in females under 70 (with hormone levels), mortality rate is higher if you have one
    • 7. severe emotional stress
    • 8. obesity
    • 9. genetic predisposition
    • 10. sedentary lifestyle
  53. context: 2 cardiac disorders/diseases
    congestive heart failure (CHF)
    • -inability for heart to function
    • condition in which heart is unable to eject the volume of blood delivered to it; decreased cardiac output (amount of blood pumped per minute ~5L)
  54. process of congestive heart failure
    • 1. heart becomes engorged with blood
    • 2. increased pressure, blood backs up into pulmonary or systemic circulation
    • 3. typically due to cardiac muscle damage
    • 4. initially compensates for the damage
    • 5. eventually becomes decompensated (dHF)
  55. 4 disease/disorders that lead to congestive heart failure (CHF)
    • 1. coronary artery disease (CAD)
    • 2. myocardial infarction
    • 3. hypertension
    • 4. valve disease
  56. 2 stages of congestive heart failure (CHF)
    • 1. compensated CHF
    • 2. decompensated CHF
  57. context: 2 stages of congestive heart failure (CHF)
    compensated CHF
    • -cardiac hypertrophy (heart enlarges and increases in muscle size to increase contraction and not increase in numbers because cardiac muscle cells can't regenerate)
    • -heart attempts to maintain cardiac output for short term
    • -increased sympathetic nervous system output
    • -release of adrenal hormones (epi/norepinephrine)
    • -clinically asymptomatic
  58. context: 2 stages of congestive heart failure (CHF)
    decompensated CHF
    • after compensated stage
    • -dilation and thinning of ventricular wall (chambers in heart enlarges)
    • -heart can't maintain cardiac output
    • -decreased blood flow to organs
    • -venous congestion (backup of flow to heart)
    • -clinical symptoms observed
  59. ventricular chamber example of congestive heart failure (CHF)
  60. 2 types of congestive heart failure
    • 1. right heart failure
    • 2. left heart failure
  61. context: 2 types of congestive heart failure
    right heart failure and symptoms
    • right ventricular dilation
    • DEC. cardiac output
    • INC. pressure in venous circulation (more blood back up in veins)
    • systemic edema:
    • -swelling of ankles and feet
    • -distension of veins in neck
    • *often caused by left heart failure
  62. context: 2 types of congestive heart failure
    left heart failure and symptoms
    • left ventricular dilation
    • DEC. cardiac output
    • INC. pressure in pulmonary circulation (inc. back up in pulmonary)
    • pulmonary edema
    • breathlessness
    • acidosis (due to accumulation of CO2 and not enough O2)
    • *often caused by cardiac tissue damage
  63. T/F
    people can have both left and right heart failure (CHF)
    TRUE
  64. Decreasing cardiac output due to compensation with congestive heart failure (CHF) causes what?
    • *making matters worse ...
    • process:
    • DEC. in renal/kidneys/body blood flow --> renin-angiotensin-aldosterone system (RAAS) stimulated --> angiotensin II --> (1) INC. blood pressure (BP) to increase blood flow while heart is already having hard time, (2) production of aldosterone --> aldosterone causes INC. Na+ and H2O retention to increase blood volume to increase blood pressure which is worse for heart
  65. 5 types of treatments for congestive heart failure (CHF)
    • 1. positively inotropic drugs
    • 2. Beta-adrenergic receptor antagonists
    • 3. diuretics
    • 4. vasodilators
    • 5. aldosterone receptor antagonists
  66. context: 5 types of treatments for congestive heart failure (CHF)
    2 positively inotropic drugs
    • 1. Digitalis glycosides: Digoxin (top 200 - inhibit Na+/K+ ATPase --> INC. [Na+] --> INC. Ca2+ influx --> INC. fiber shortening = INC. strength of contraction)
    • -INC. Ca2+ in cardiac muscle cells (INC. strength of contractility)
    • -INC. cardiac output
    • 2. adrenergic Beta-receptor agonists: dobutamine
    • -acute
    • -INC. contractility
    • -INC. heart rate
  67. context: 5 types of treatments for congestive heart failure (CHF)
    2 beta-adrenergic receptor antagonists
    • beta-blockers block effects of sympathetic nervous system
    • -chronic
    • top 200:
    • 1. carvedilol (Coreg)
    • 2. metoprolol (Toprol XL)
  68. context: 5 types of treatments for congestive heart failure (CHF)
    2 diuretics
    • DEC. fluid volume
    • DEC. edema
    • top 200:
    • 1. loop diuretics: furosemide (most efficacious - larger extent in DEC. edema)
    • 2. Thiazide diuretics: hydrochlorothiazide
  69. context: 5 types of treatments for congestive heart failure (CHF)
    2 vasodilators
    • 1. ACE inhibitors:
    • top 200:
    • -Enalapril
    • -Lisinopril
    • *inhibits conversion of angiotensin I to angiotensin II (active form)
    • 2. angiotensin receptor antagonists/blockers (ARBs)
    • -Valsartan (DIOVAN; top 200)
    • *blocks angiotensin II receptors
  70. context: 5 types of treatments for congestive heart failure (CHF)
    aldosterone receptor antagonists
    • top 200:
    • spironolactone
    • *act to INC. Na+ excretion (INC. water excretion) - like a diuretic

What would you like to do?

Home > Flashcards > Print Preview