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CV > Montemayor's DSA > Flashcards

Montemayor's DSA Flashcards

1
Q

2 types of cardiac cells

A

contractile and autorhytmic

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2
Q

contractile cells

A

perform mechanical work (99%)

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3
Q

autorhythmic cells

A

initiate action potentials (1%)

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4
Q

atuomaticity

A

Self-stimulating: Heart’s ability to initiate its own beat Cyclic depolarization of autorhythmic cells initiates electrical activity independent of neural input

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5
Q

Order and timing of electrical events

A

a. SA node
b. Inter-atrial pathway
c. AV node
d. Common AV bundle (Bundle of His)
e. R & L Bundle branches
f. Purkinje fibers

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6
Q

functional syncytium

A

Myocytes can conduct APs cell-to-cell and thus contract as a single unit: due to gap junctions (electrical synapses)

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7
Q

average beats per minute for parts of conduction system

A

SA node- 60-100 bpm
Bundle of His- 40-60 bpm
purkinje fibers- 20-40 bpm

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8
Q

Sinoatrial Node

A

Normal pacemaker of the heart. Spontaneously depolarizing SA nodal cells: origin of normal electrical impulse.
Cells in right atrium: junction between SVC and RA

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9
Q

Interatrial tracts

A 
atrial muscle conducts impulse radially from SA node through the RA.
Internodal pathway (SA node--> AV node
Anterior interatrial myocardial band (Bachmann's bundle): SA node --> left atrium.
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10
Q

Internodal pathway

A

anterior, middle, posterior

SA node–> AV node

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11
Q

Anterior interatrial myocardial band

A

Bachmann’s bundle

SA node –> left atrium

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12
Q

AV Node

A

Atrioventricular node: connects atria to ventricular conducting system
Located posteriorly on right side of interatrial septum (near ostium of the coronary sinus)

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13
Q

Bundle of His

A

Passes down right side of interventricular septum. Divides into R&L bundle branches

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14
Q

Right bundle branch

A

Direct continuation of bundle of His–> down right side of IV septum

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15
Q

Left bundle branch

A

Thicker than RBB, perforates IV septum.

Splits –> thin anterior division & thick posterior division

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16
Q

Purkinje fibers

A

Arise from RBB and Anterior & Posterior LBB
Complex network of conducting fibers spread out over subendocardial surfaces of R and L ventricles
Linearly arranged sarcomeres (like myocytes)
Typically lack T-tubule system
Largest diameter cardiac cells
Fastest conduction velocity in the heart
Rapid activation of Endocardium –> Epicardium, Apex –> Base

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17
Q

Pacemaker cells

A 
SA node, AV node, Bundle of His and Purkinje fibers
action potentials per minute: 
SA node- 70-80
AV node- 40-60
Bundle of His and Purkinje fibers- 20-40
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18
Q

what determines the pace?

A

autorhythmic cells which reach threshold first will drive the pace of the heart. If SA node is out, then AV node next at 40-60 bpm

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19
Q

What is the result of SA nodal failure?

A

bradycardia

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20
Q

how bradycardia results from SA node failure

A

SA nodal failure unmasks slower, latent pacemakers in the AV node or ventricular conduction system (escape beats or rhythms) → bradycardia
Example: Junctional rhythm (ectopic focus at the AV junction becomes pacemaker)

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21
Q

fastest conduction done by?

A

purkinje fibers (larger diamter –> decreased resistance). Bundle branches.

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22
Q

Slowest conduction by?

A

AV node: small diameter, increased resistance.
AV nodal delay: normal delay to allow time for optimal ventricular filling.
SA node
Ventricular myocytes

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23
Q

AV block or prolonged nodal delay may cause?

A

ventricular bradycardia
Result in distal pacemaker sites generating the ventricular rhythm
Secondary pacemaker sites have a lower intrinsic rate than the SA node
(e.g., Purkinje fibers ~ 20 – 40 bpm: very slow)

24
Q

Normal order of ventricular depolarization

A

Step 1: AV node–> bundle branches
Step 2: IV septum depolarizes L–>R
Step 3: anteroseptal region depolarizes –> apex
Step 4: myocardium depolarizes from endocardium –> epicardium
Step 5: depolarization spreads from apex –> base via purkinje fibers
Step 6: ventricles are fully depolarized

repolarization occurs in the opposite order, and more slowly than depolarization phase

25
Q

significance of order of events in ventricular depolarization

A

Early contraction of the IV septum:
Rigid anchor point for ventricular contraction

Early contraction of the papillary muscles:
Prevents prolapse of atrioventricular (AV) valves during ventricular systole

Final depolarization from apex to base:
Allows efficient emptying of ventricles into aorta and pulmonary trunk at the base

26
Q

describe cardiac muscle

A

sarcomeres: z line to z line
striated- filaments (thick myosin and thin actin, troponin, tropomyosin)
mononucleated
intercalated disks: gap junctions (low resistance)
many mitochondria
t tubules & SR- calcium stores in ECF and SR
Calcium regulation of contraction: binds troponin
relatively slow speed of contraction

27
Q

Biomarkers of myocardial injury

A

troponin (cTnT, cTnI)- commonly used iomarker for cardiac damage.
CK-MB- creatine kinase isoform specific to cardiac muscle.

28
Q

Electrical syncytium of the heart

A

If one cardiac cell depolarizes, all will eventually depolarize via:

Gap junctions electrical connection (low resistance) allowing AP propagation cell-to-cell
Normally, cardiac APs are conducted via the conduction system to the ventricles and then spread cell-to-cell
Cell-to-cell conduction of APs is by ventricular myocytes is much slower than via Purkinje fibers

29
Q

clinical correlate of ventricular depolarization that spreads only cell-to-cell via Gap Junctions:

A

slower than following the normal pathway of the conduction system. This slower process of spreading a depolarizing current through the ventricles results in the widening of the QRS complex on an ECG
Examples of arrhythmias where a widened QRS complex is commonly seen: Premature Ventricular Conductions (PVCs)
Ventricular Tachycardia

Atria and ventricles EACH form a functional syncytium–> contract as separate units

30
Q

All-or-None Law for the Heart:

A

Normally, either all cardiac cells contract or none do
There is NO variation in force production via motor unit recruitment as in skeletal muscle
Due to functional syncytium

31
Q

sources of calcium for cardiac contraction

A

Influx of extracellular Ca2+ is required for additional Ca2+ release from the SR (This is different from skeletal muscle)

2 Sources of Ca2+ in for Cardiac Contraction
Ca2+ influx from ECF via voltage-gated L-type Ca2+ channels (DHPR) during long plateau phase (phase 2) of cardiac m. AP

  1. Ca2+-induced (Ca2+-dependent) Ca2+ release from the SR via Ca2+- release channels (RYR)
    Release of Ca2+ from the SR also required
    Amount of Ca2+ from the ECF alone is too small to promote actin-myosin binding
    Ca2+ influx from the ECF triggers Ca2+ release from the SR
32
Q

Relaxation (diastole): removal of calcium by 3 pumps

A

Removal of Ca2+ to the ECF
1. 3Na+- 1Ca2+ antiporter [sarcolemma]
Ca2+ removal against large gradient
[Na+] higher in ECF, Na+ gradient powers Ca2+ removal
2. Ca2+ pump [sarcolemma]
ATP used to extrude Ca2+ from cell against gradient

Sequestering Ca2+ into the SR
3. SR Ca2+ pump (SERCA); Regulated by phospholamban
(β-adrenergic mediation of phosphorylation increases SERCA activity)

33
Q

No Tetanus in Cardiac Muscle

A

Cardiac tetanus would be fatal because a sustained contraction would inhibit effective pumping of blood

Long AP in cardiac muscle results in a long refractory period
(Primarily due to L-type Ca2+ channels and slow, delayed K+ channel opening)
Thus, relaxation of myocytes occurs prior to complete repolarization of AP such that ‘twitches’ cannot be summed like they can in skeletal muscle

34
Q

Resting membrane potential of cardiac cells

A

Pacemaker cells
No true RMP
“Maximum Diastolic Potential”
Spontaneous slow depolarization phase (phase 4)

Non-pacemaker cells
True resting potential (~ - 80 to - 90 mV) (phase 4)

35
Q

Ion distribution

A

Membrane potential: Determined by ion concentration gradients and conductance (membrane permeability)

Time-dependent changes in membrane permeability and ion conductance result in depolarization and repolarization

Primary ions: Ca2+, K+ and Na+

36
Q

K+ contribution to RMP

A

Resting cell membrane is relatively permeable to K+ (Much more permeable vs. Na+ and Ca2+)
Conductance to K+ (gK) is ~ 100x > conductance to Na+ (gNa)

37
Q

Na+ contribution to the RMP

A

RMP: Because gNa is so small in the resting cell, changes in ECF [Na+] do not significantly affect resting membrane potential (Vm)

38
Q

General properties of cardiac action potentials

A

Initiation time, shape, & duration of APs are distinct for cardiac cells of varied function within different cardiac regions
AP propagation requires careful timing to synchronize ventricular contraction to optimize ejection of blood

39
Q

Main types of cardiac action potentials

A

Characterized by rate of depolarizing upstroke (phase 0)
1. Slow response:
SA & AV nodes
2. Fast response: Atrial, ventricular myocytes & Purkinje fibers

40
Q

Fast response action potentials

A 
Fast depolarizing upstroke  (phase 0)
Early, partial repolarization (phase 1)
Plateau (phase 2)
Final repolarization (phase 3)
Resting potential (phase 4)
41
Q

slow response action potentials

A

Slow depolarizing upstroke (phase 0)
Absent: early repolarization (phase 1)
Absent: Plateau is less prolonged or absent (phase 2)
Repolarization (phase 3)
No true resting potential (phase 4)

42
Q

compare fast vs slow AP

A

Resting membrane potential (phase 4):
More negative in fast- response APs vs. slow response (no true)

Threshold potential:
Slow-response threshold potential: ~ −40 mV
Fast-response threshold potential: ~ −70 mV

Greater slope of upstroke (phase 0), AP amplitude, and extent of overshoot in fast-response vs. slow response

Conduction velocities:
Slow-response (SA & AV nodes)

43
Q

major time-dependent & voltage-gated currents of cardiac APs

A

Na+ current (INa):
Primarily responsible for the rapid depolarizing phase in atrial m., ventricular m., and Purkinje fibers
Ca2+ current (ICa):
Responsible for the “rapid” depolarizing phase in SA node and AV node
Primarily responsible for plateau phase of fast-response APs
Triggers contraction in all contractile cardiomyocytes
K+ current (IK):
Responsible for the repolarizing phase in all cardiomyocytes
Pacemaker (“funny”) current (If):
Responsible, in part, for pacemaker activity (slow depolarization phase) in SA and AV nodal cells and sometimes Purkinje fibers
Funny channel = non-specific cation channel; primarily Na+ current

44
Q

Phase O

A

Upstroke
Slow: if upstroke is only due to ICa
Fast: if upstroke is due to both INa and Ica

45
Q

Phase 1

A

Early, rapid (partial) repolarization

Activation of minor K+ current (Ito = transient outward) Inactivation of INa or ICa (likely T-type Ca2+ channels)

46
Q

Phase 2

A

Plateau phase
Continued influx of Ca2+ countered by small K+ current (Small, remaining Na+ current possible and a minor membrane current due to the Na-Ca exchanger)

47
Q

Phase 3

A

Final Repolarization

IK in all cells

48
Q

Phase 4

A

Electrical diastolic phase
Changes in IK, ICa, and If produce pacemaker activity in SA and AV nodal cells
Atrial and ventricular muscle have no time-dependent currents during phase 4

49
Q

parts that use many voltage-gated sodium channels and a large Na current

A

ventricular m., atrial m., and purkinje fibers

50
Q

Voltage-gated sodium channels

A

Closed at negative resting potentials
Rapidly activate when membrane depolarizes to threshold
Na+ influx mainly responsible for rapid upstroke of AP (phase 0)
Inactivation gates close when membrane depolarizes
Partial role in the early repolarization of the AP (phase 1)
Within the range of positive voltages, a very small INa remains: prolongs plateau phase (phase 2)
Magnitude of INa: impacts regenerative conduction of APs

51
Q

Sodium at the SA and AV nodes

A

If = “funny” or “pacemaker” current
Activated on hyperpolarization
Non-specific channel: ↑ Na+ and K+ currents
Increased Na+ influx is primarily responsible for initiation of slow depolarization phase (phase 4)

52
Q

Calcium

A

ICa: all cardiac myocytes
Majority: L-type Ca2+ channel (Long-lived, DHPR)
Fewer T-type Ca2+ channels (Transient)

53
Q

Calcium at SA and AV nodes

A

ICa contributes to pacemaker activity (phase 4)
ICa (influx) contributes to upstroke (phase 0)
ICa is smaller than INa
Nodal cells: slower upstroke vs. atrial & ventricular m.m.
APs in nodal cells: slower conduction velocity because the smaller ICa depolarizes adjacent cells more slowly

54
Q

Calcium at the Ventricular m. Atrial m. and purkinje fibers

A

Smaller ICa adds to INa during the upstroke (phase 0)
Ca2+ channels are closed at negative RMP
Activate at more positive voltages (near upstroke peak, ∼1 ms) Inactivate (slower than Na+ channels, ~ 10 to 20 ms, time-dependent)
Small ICa prolongs plateau (phase 2) 1° via L-type Ca2+ channels
Ca2+ entering through L-type Ca2+ channels activates release of Ca2+ from SR via calcium-induced Ca2+ release in atrial & ventricular m.m.

55
Q

Potassium

A

All cardiac myocytes:
Slow, delayed IK also contributes, in part, to relatively long cardiac APs
IK: contributes to repolarization in all cardiac myocytes (phase 3)
2 major IK contribute to repolarization (there are other K+ currents):
IKR : relatively rapid
IKS : relatively slow
IK: very small at negative voltages
Slowly activates with depolarization (~ 20 to 100 ms), does not inactivate

56
Q

Potassium at SA and AV node

A

IK decreases at the end of phase 4, contributing to pacemaker activity (decreasing K+ efflux promotes depolarization)

CV (15 decks)

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