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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > CVS Lecture 4, 5, 6 - Electrical activity of the Heart, Understanding the ECG/Identifying some Basic Disturbances of Rhythm > Flashcards

CVS Lecture 4, 5, 6 - Electrical activity of the Heart, Understanding the ECG/Identifying some Basic Disturbances of Rhythm Flashcards

1
Q

What is the Nernst equation and what is it used for?

A

Predict what a potential will be across a semi permeable membrane -> if only permeable to K (diastole) then potential equals E[K] (K+ equilibrium potential = -80mV) -> if membrane only permeable to Na (upstroke of action potential) then potential equals E[Na]=+66mV

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2
Q

What maintains the K+ concentration in the cells?

A

Na/K ATPase -> doesn’t maintain membrane potential, that is due to movement of K out of the cell down it’s conc gradient

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3
Q

How is membrane potential worked out?

A

Goldman-Hodgkin-Katz equation, taking into account relative permeabilities of ions

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4
Q

How does a nerve action potential occur?

A
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5
Q

How does a cardiac action potential differ from a nerve one?

A

Upstroke is caused by Na+ channels opening and membrane depolarisation occurs -> then Na+ channels inactivate so membrane potential repolarises slightly, and very brief Transient outward K+ current (TOKC) -> brief permeability to K+ causes notch at top, and then absolute refractory period occurs (not restimulating cardiac muscle, which is good so it can’t be tetanised), then relative refractory period (can produce another AP) -> both are very long which allows the heart to fill appropriately

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6
Q

What changes in membrane permeability to ions occur in the cardiac action potential?

A

Ca2+ permeability takes place just after upstroke, which is needed for cardiac contraction

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7
Q

What is the refractory period and how does it occur?

A

Occurs as a result of Na+ channel inactivation (recover from inactivation when membrane is repolarised) FRT is when all Na channels are open

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8
Q

How long is the cardiac action potential and why?

A

Long (several hundred milliseconds c.f. 2ms in nerves) -> duration of AP control duration of contraction of heart -> long, slow contraction is required to produce effective pump

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9
Q

What is the full recovery time?

A

The time at which a normal AP can be elicited by a normal stimulus

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10
Q

What is the difference between muscle and cardiac excitation in tetanus?

A

Skeletal muscle repolarisation occurs very early in the contraction phase, so restimulation and summation of contraction is possible -> cardiac muscle isn’t re-excitable until the process of contraction is well underway, so cardiac muscle can’t be tetanised

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11
Q

What are the electrical properties of the heart?

A

Independent generation/propagation of electrical activity; specialised conducting system, so heart can beat independently even after being separated from nerve supply

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12
Q

Where does the extrinsic nerve supply to the heart come from and what does it do?

A

Comes from ANS and serves to modify and control the intrinsic beating established by the heart

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13
Q

What are the phases of the action potential?

A

Phase 0 -> Na+ induced upstroke; Phase 1 -> Early repolarisation by Na+ channels inactivating and K+ channel TOKC Phase 2 -> Plateau, Ca2+ influx Phase 3 -> Repolarisation Phase 4 -> Resting membrane potential (diastole)

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14
Q

What occurs in Phase 2 of CAP?

A

Ca2+ influx required to trigger Ca release from SR, which is required for contraction -> activates rapidly but upstroke dependent more on Na permeability

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15
Q

What inhibits Phase 2 of the CAP?

A

By dihydropyridine Ca channel antagonists -> Nifedipine, Nitrendipine, Nisoldipine (block Ca entry, reducing Ca released from SR -> do the same in SM, so causes vessels to lose some contractility, so vasodilation occurs and reduces BP

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16
Q

What occurs in Phase 3 of CAP?

A

Gradual activation of K currents, so large K current is inactive during plateau and then becomes active once cells have partially repolarised -> IK1 is responsible for fully repolarising the cell

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17
Q

What is IK1 in CAP?

A

Large current and flows during diastole -> stabilises resting membrane potential, reducing risk of arrhythmias by requiring a large stimulus to excite the cell

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18
Q

What are the different AP profiles in the heart?

A

Different parts of the heart have different AP shapes due to different ionic currents flowing and different degrees of expression of ionic channels

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19
Q

What is the difference between AP of the SAN cell and ventricular cell in the heart?

A

Most channels exist in the SAN to some extent -> EXCEPT IK1; also very little Na iflux, upstroke produced by Ca influx -> T-type Ca channels activate at more -ve potentials than L-type. TOKC is very small and pacemaker current is present

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20
Q

What is the pacemaker current?

A

SAN cells -> control AP is changed by ANS stimulation -> SNS causes pacemaker potential to become steeper, reaching threshold potential faster, so increases HR; PSNS causes pacemaker potential to decrease gradient, so slows HR as threshold potential isn’t reached quickly

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21
Q

What are the 4 components of the heart’s conduction system?

A

SAN, inter-nodal fibre bundles, AVN, ventricular bundles (bundle branches and Purkinje fibres)

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22
Q

How is the heart’s conduction carried out?

A

Excitation begins in SAN and moves across the atria via the internodal fibre bundles -> then reaches the AVN where the conduction is carried through the Bundle of His and down the Purkinje fibres in the interventricular septum and then divides into 2 large branches (R/L bundle branches), and from the apex upwards to the base, causing ventricular contraction

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23
Q

What is the SAN?

A

Small mass of specialised cardiac muscle situated in anterior aspect of RA -> located in aterolateral margin between the orifice of SVC and the atrium -> fibres of SAN are fused with surrounding atrial muscle fibres

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24
Q

What is the function of the SAN?

A

It has automatic self-excitation, initiating the beat of the heart, so is the pacemaker of the heart

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25
What are the inter-nodal fibres?
Interspersed among the atrial muscle fibres, they conduct the action potential to the AVN with a greater velocity then ordinary atrial muscle
26
What is the AVN?
Located at the border of the RA near lower part of the interatrial septum, electrically connecting the conduction system between the atrial and ventricular chambers
27
What is the purpose of the AVN and internodal fibre bundles?
Produce a short delay in transmission of the impulse to the ventricles -\> occurs within the fibres of the AVN and in the special junctional fibres that connect the node with ordinary atrial fibres
28
Why is the 0.1s delay from atrial AP to ventricle AP important?
Permits the atria to complete their contraction and empty their blood into the ventricles before the ventricles contract
29
What are the bundle of His and bundle branches?
Comprise of specialised muscle fibres called Purkinje fibres which terminate in a finger-like fashion on the working myocardial cells -\> very large, conducting the AP at about 6x velocity of ordinary cardiac muscle
30
What are Purkinje fibres?
Terminal PF extend beneath endocardium and penetrate 1/3 of distance into myocardium, ending on ordinary cardiac muscle within the ventricles and impulse proceeds through the ventricular muscle
31
How is the impulse propagated?
Propagation of the AP is due to a combination of passive spread of current and the existence of a theshold -\> coupling resistance of the cells determines the extent of spread of current
32
What do gap junctions do in the cardiac AP?
They help intercellular communication and impulse conduction from one cell to the next -\> form at intercalated discs
33
What is the basis of the ECG?
Effects of wave of depolarisation are detected as p.d. between 2 electrodes -\> wave of depolarisation moving towards +ve electrode causes UPWARD deflection; wave of depolarisation moving away from +ve electrode causes DOWNWARD deflection; repolarisation wave moving away from +ve electrode causes UPWARD
34
What happens if there is a repolarising current on an ECG?
Opposite polarity to depolarising current
35
What are the ECG lead configurations?
Limb lead and chest leads -\> can predict waveform that should record if heart is normal
36
How does the excitation sequence appear on the ECG and why?
1) SAN produces depolarisation towards electrode. (up of P) 2) Depolarisation moves away from electrode. (down of P) 3) Depolarisation moves toward electrode (QR) 4) Depolarisation moves away from electrode (RS) 5) Repolarisation occurs from outside of heart epicardial to endocardial surface, producing T-wave
37
What happens during ventricular repolarisation to the ECG?
38
What is the utility of ECG?
Tachyarrhythmias, Bradyarrhythmias, myocardial infaction/ischemia, cardiomyopathy, assessment of pacing, electrolyte distrubances
39
What is the function of an ECG?
Sensing the heart's electrical activity via electrodes
40
What are the 4 limb electrodes?
Present on the LHS of the ECG
41
What is Lead I?
R arm to L arm (slight positivity)
42
What is Lead II?
R arm to L leg (normal heart direction, so positive)
43
What is Lead III?
L arm to L leg (no positivity)
44
What is Einthoven's triangle?
45
What sign is P and QRS in leads I and II?
Positive
46
How are the augmented leads obtained?
Using the average voltage of any 2 points on skin as a negative pole and regarding the third electrode (positive pole)
47
What is Lead aVR?
R -\> right arm
48
What is Lead aVL?
L -\> left arm
49
What is Lead aVF?
F -\> left foot
50
What are the axes of the limb leads?
51
What are the axes of the augmented leads?
52
What is the frontal QRS axis?
-30 to 90 is normal QRS axis
53
How do you calculate QRS axis?
+ve is up and -ve is down and then -\> Tan (x)= aVF/lead I -\> anything less than -30 is left axis and anything more than 90 is right axis
54
How are the planes different between chest leads and the limb/augmented leads?
Limb are on the frontal plane and the chest leads are on the horizontal plane
55
Where are the pericordial leads placed?
56
What are the pericordial leads?
6 unipolar leads, V1-6 and for each lead the chest lead is the positive pole -\> negative pole is Wilson's central terminal, made up of the R arm, L arm and L leg
57
Which part of the heart are the pericordial leads placed over?
58
Which leads are bipolar and which are unipolar?
59
What are some common cardiac arrhythmias?
Bradycardia, tachycardia, cardiac conduction abnormalities, supraventricular arrhythmias (atrial fibrillation, atrial flutter, AVNRT), ventricular arrhythmias (ventricular tachycardia, fibrillation)
60
What is an ECG, how are the squares read?
61
How do you approach an ECG - 12 steps?
62
What are some normal ECG values for each of these components?
63
What does sinus tachycardia look like on an ECG and how is it defined?
64
How are sinus tachycardia ECG different?
P waves have normal morphology, with atrial rate 100-200bpm -\> regular ventricular rhythm of 100-200bpm -\> one P wave precedes every QRS complex
65
What is the physiological response to sinus tachycardia?
Hypovolaemia, sepsis, stress
66
What does atrial fibrillation look like on an ECG and how is it defined?
Atria are contracting but not in a synchronised way
67
How are atrial fibrillation ECG different?
P waves absent, oscillating baseline waves -\> atrial rate: 350-600 bpm; irregular irregular ventricular rhythm, with rate 100-180bpm
68
What does atrial flutter look like on an ECG and how is it defined?
x
69
How are atrial flutter ECG's different?
Undulating sawtoothed baseline F waves -\> atrial rate 250-350bpm with regular ventricular rhythm at a rate of 150bpm (2:1 atrioventricular block, 4:1 is also common)
70
What is AV nodal reentrant tachycardia?
Narow-complex tachycardia, with regular QRS complexes and P waves often buried within QRS or just after QRS -\> re-entrant circuit within AVN; responsive to adenosine
71
What does pre-excitation syndrome look like on an ECG and how is it defined?
72
How are pre-excitation syndrome ECG's different?
Accessory pathway (connect atrium to ventricle), short PR interval, ventricular pre-excitation -\> predisposes to accessory pathway tachycardias -\> accessory pathways: 1/3 conduct antergradely, 2/3 can only conduct retrogradely -\> ablation of accessory pathway
73
What are the 3 degrees of heart block?
1st degree: prolonged PR interval; 2nd degree: Mobitz Type I (Wenckebach) [progressive prolongation of PR interval] or II [2:1 AV block, so every other one is absent]; 3rd degree: Complete Heart Block [no electrical impulse from atrium to ventricle]
74
What is Bundle branch block?
One of the cause for axis deviation -\> depolarisation of BB and PF are seen as QRS, so QRS complex widens and morphology changes
75
Why does the QRS complex widen in bundle branch block?
When the conduction pathway is blocked, it will take longer for the electrical signal to pass throughout the ventricles
76
What QRS morphology is characteristic of Right bunble branch block?
Wide QRS complex assumes a unique shape in lead V1 and 2 as it overlies the right ventricle -\> bunny ears
77
What QRS morphology is characteristic of Left bunble branch block?
Wide QRS complex assumes change in shape in leads V1 and 2 -\> broad deep S waves
78
What does a ventricular tachycardia ECG look like?
QRS are broad and rapid -\> deadly, leading to drop in CO and BP then cardiac arrest
79
What does a ventricular fibrillation ECG look like?
Ventricles are not contracting -\> no pulse, no CO

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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