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MSII Pharmacology > Unit 4 - Review of Heart Physiology > Flashcards

Unit 4 - Review of Heart Physiology Flashcards

1
Q

what are properties of excitable tissues?

A
  • membrane potential difference (Em, Vm)
  • -inside negative resting membrane potential difference
  • transmembrane electrochemical gradient
  • -combo if chemical and electrical potential differences
  • equilibrium potential (Nernst equation)
  • conductance (ionic, inverse of resistance)
  • ionic driving force (Vm - Eion) and current
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2
Q

what is the definition of conductance?

A

ability of ion to flow across cell membrane

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3
Q

what is the definition of current?

A

ionic charge carried by ion movement across membrane

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4
Q

what autonomically controls the heart?

A

GPCR (indirect ligand-gated channels)

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5
Q

what are the most important ion channels for the heart?

A 
voltage gated (by membrane voltage of cell), because they are excitable tissues
-activity dependent on membrane potential (Vm)
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6
Q

what are the major targets of cardiovascular drugs?

A
  • anti-arrhythmic

- anti-hypertensive, anti-angina

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7
Q

what are major voltage-gated ion channel types? what class of drugs do you treat these with?

A 
Na+: class I anti-arrhythmic
K+: class III anti-arrhythmic
Ca++: class IV anti-arrhythmic
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8
Q

what happens if there is faulty inactivation of voltage-gated ion channels in the heart?

A

cardiac arrythmias

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9
Q

how do the kinetics of voltage-gated ion channels differ?

A

different VG ion channels have different activation and inactivation kinetics
-do so during different phases of cardiac AP

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10
Q

explain the cardiac action potentials in “fast-response APs”, where they occur, what channels are active at each time, and whether they are inward (depolarize) or outward (hyperpolarize)

A

working myocardium: atrium, ventricle, and His-Purkinje (major active ionic current)

  • Phase 0: depolarization; Na and CaT (both depolarize)
  • Phase 1: early repolarization; To (fast and slow, hyperpolarize)
  • Phase 2: plateau; CaL (depolarize), Kur (hyperpolarize)
  • Phase 3: repolarization; Ks/r (slow and rapid, hyperpolarize)
  • Phase 4 resting (diastole); K1 (not voltage-gated, but in background, hyperpolarize)
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11
Q

explain cardiac AP in “slow response APs”

A 
pacemaker AP in sino-atrial and atrio-ventricular nodes
-Phase 0: Ca++ dependent upstroke (CaL)
-Peak: K (no phase 1 or 2)
-Phase 3: downstroke
-Phase 4: depolarization (f)
no K1 or Na
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12
Q

why are there no IK1s in the pacemaker AP?

A

IK1 suppresses pacemaker ability

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13
Q

what is the membrane voltage in pacemakers?

A

not stable

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14
Q

what are the regional cardiac APs?

A 
primary pacemaker (SAN): 60-90 bpm --> activate atria
secondary pacemaker (AVN): 40-60 bpm --> activates His-purkinje
Purkinje /tertiary pacemaker: 30 bpm --> activates ventricles
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15
Q

explain autonomic control of HR?

A

SAN > AVN > atrium > ventricle

  • sympathetic (NE, E) –> increase If,CaL –> positive chronotropy (increased slope of phase 4)
  • parasympathetic (ACh) –> increase IK,ACh, decrease If,CaL –> negative chronotrophy (suppress pacemaker, decrease slope of phase 4)
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16
Q

what is the excitation threshold for myocardial cells VS nodal cells?

A

MC: -65 mV
NC: -35 mV

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17
Q

what is the threshold potential (Vth) dependent on?

A
  • resting membrane potential (Vm)
  • -hypokalemia –> hyperpolarize –> increase threshold
  • -hyperkalemia –> depolarize –> decrease threshold
  • Na+ current availability (gNa)
  • cell size (hypertrophic heart failure)
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18
Q

how does resting membrane potential affect cardiac excitability?

A

directly, via Na+ current availability and K+ conductances

-at most negative potential, one has the most Na channels

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19
Q

what is the resting membrane potential determined by?

A

dynamic balance of inward Na+ and outward K+ ionic currents

  • this makes phase 4 constant
  • RM membrane is 20x more permeable to K+ than Na+ ions
  • thus, while it cannot be determined by Nernst equation (which only applies to one ion at a time), Vm normally follows Ek (Nernst potential for K+) with 95% accuracy
20
Q

why are both hyperkalemia and hypokalemia arrhythmogenic?

A

net effect is increased excitability (if moderate hyper)

21
Q

what occurs during hypokalemia? incidence?

A

increases threshold that should decrease excitability

  • -but low [K]o causes low IK1 –> decreased conductance
  • net effect is increased excitability
22
Q

what occurs during hyperkalemia? incidence?

A

> 5.5 - 7 mM (moderate; 8% of clinical cases)
-depolarizes Vm –> decrease threshold –> increase excitability

> 7 mM (severe)
-depolarizes Vm even more –> increases threshold (b/c INa is inactive) –> decrease excitability

23
Q

what is the functional refractory period? components?

A

minimum time duration after an AP for threshold stimulus to produce full response again

  • divided into effective (absolute) and relative RP
  • ERP: no AP may be elicited no matter how strong
  • RRP: higher than normal stimulus will elicit AP with reduced amplitude and duration
24
Q

what are the major determinants of conduction velocity?

A
  • rate of phase 0 depolarization
  • threshold potential (less negative Vth = slower conduction; more ICa, less INa)
  • resting membrane potential (more negative Vth = faster conduction; more INa)
  • gap junction conductance (2nd most important)
  • -intercellular connectivity/conductance
  • -site of cell-to-cell AP transfer
25
Q

what does electric current require to complete circuit?

A

extracellular, internal, and gap junction resistances in closed loop circuit

26
Q

where is an AP recorded?

A

between two adjacent cells

-delay = 100-200 us

27
Q

explain the cardiac conduction sequence

A

complete w/in 1/4 of a second with every heartbeat

  • AV node delay is critical to ensure atrial contraction finishes before ventricular contraction begins
  • slow AV node conduction and recovery from refractoriness protects ventricles from supraventricular arrythmias –> essential life-saving function of AVN
28
Q

what are the conduction velocities of:

  • atria
  • AV node
  • His-BB
  • Purkinje fibers
  • ventricles
A 
atria: 0.5 m/s
AVN: 0.05 m/s
His-BB: 2 m/s
PF: 4 m/s
vent: 0.5 ms

(fastest) PF > His-BB > atria/vent > AVN (slowest)

29
Q

what happens if you block Ca,L?

A

blocked phase 2 = no cardiac contraction

30
Q

what is active tension dependent on?

A
  • AP duration (decrease together)

- sarcomere length (increase together)

31
Q

what is AP duration dependent on?

A

frequency

32
Q

explain excitation-contraction coupling for contraction

A
  1. Ca++ ions enter thru Ca,L channel
  2. Ca++ ions activate ryanodine receptor (CARC, RyR2)
  3. CaRC releases sarcoplasmic Ca++ into cytosol, initiates contraction
    - CICR (Ca++-induced Ca++ release) involved
33
Q

explain excitation-contraction coupling for relaxation

A

cytosolic Ca++ is reduced back to resting levels by SERCA (SR Ca++ ATPase) and NCX (sarcolemmal Na+/Ca++ exchanger)

34
Q

what does increasing preload do to myocardial contractility?

A

increase together (w/in limits)

  • stretching heart muscle increases sarcomere length and actin-myosin X-bridge sites –> increased active tension upon muscle contraction
  • sarcomere length > 2.2 microns reduces crossbridge overlap
35
Q

what does the Frank-Starling curve tell you about inotropy?

A

positive inotropy: SV increases as ventricular EDV increases

  • occurs in exercise and at rest normally
  • increased Ca,L and SERCA
  • increased Ca++ sensitivity of contractile filaments

negative inotropy: SV decreases as VEDV increases

  • occurs in heart failure and cardiogenic shock
  • decreased Ca,L and SERCA
  • decreased Ca++ sensitivity of contractile filaments
36
Q

what does systolic dysfunction cause? chronically?

A

abnormal reduction in SV

  • increased afterload
  • decreased contractility

chronically:

  • volume overload (mitral/aortic valve insufficiency; PDA, ASD, VSD)
  • DCM (congenital or cardiotoxic)
37
Q

what does diastolic dysfunction cause? chronically?

A

decreased ventricular compliance

  • increased P/V relationship
  • decreased Frank-Starling mechanism

chronically:

  • pressure overload (HTN, aortic stenosis –> increased afterload)
  • HCM (congenital or obstructive)
  • RCM (increased filling pressure, reduced compliance, reduced ventricular volume)
38
Q

what does the P wave represent?

A

atrial activation (phase 0)

39
Q

what does the Q wave represent?

A

His, bundle branch, septum activation (phase 0)

40
Q

what does the R wave represent?

A

ventricular (left) activation (phase 0)

41
Q

what does the S wave represent?

A

late ventricular (right) activation (phase 0 in QRS, phase 2 in ST)

42
Q

what does the T wave represent?

A 
ventricular repolarization (direction is opposite of activation)
-phase 2 in ST, phase 3 alone
43
Q

what does the PR interval represent?

A

measure of AVN conduction

44
Q

what does the QT interval represent?

A

ventricular AP duration

45
Q

what does the U wave represent?

A

Purkinje repolarization

  • hypokalemia (prolonged QT)
  • hyperkalemia (decreased QT, sharper T wave)
46
Q

what does the J wave represent?

A

occurs during ST segment

  • hypothermia, hypocalcemia (decreased QT interval)
  • hypercalcemia (increased QT interval)
47
Q

what does the ST elevation represent? depression?

A

elevation: transmural infarct, coronary vasospasm (Prinzmetal)
depression: subendocardial ischemia, exertional (stable) angina

MSII Pharmacology (43 decks)

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