Feb 10 - Electrical Activity of the Heart Flashcards

1
Q

What is the sinoatrial node?

A

It is the normal pacemaker of the heart

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2
Q

What are autorhythmic cells?

A

They are the cells responsible for initiating and conducting cardiac action potentials. These include cells from the sinoatrial node, the atrioventricular node, the Bundle of His, and Purkinje fibres. Autorhythmicity is a consequence of their unique action potential characteristics

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3
Q

Are the all cardiac cell autorhythmic cells?

A

No. The majority of cardiac cells are contractile; they do not fire spontaneously

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4
Q

Different autorhythmic cells fire action potentials at different rates. Explain

A

The fastest rate (70-80 bpm) is observed for the SA node.
The AV node fires action potentials at 40-60 bpm
The Bundle of His and Purkinje fibres fire action potentials at 20-40 bpm
The cells with the highest discharge rate are called pacemaker cells. Those with lower rates are called latent pacemakers

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5
Q

How can two different autorhythmic cells generate action potentials at a different rate?

A

Because one cell has a faster rate of depolarization, it reaches threshold more quickly than the other cell and therefore generates action potentials more rapidly

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6
Q

How can humans adjust their heart rate?

A

Either by changing threshold potential or by changing the rate of depolarization

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7
Q

Describe the spread of cardiac excitation originating from the SA node

A

An action potential initiated at the SA node first spreads throughout both atria and contracts them simultaneously. Its spread is facilitated by interatrial and internodal pathways. The AV node is the only point where an action potential can spread from the atria to the ventricles. The signal goes to the AV nodes, and there is a delay to allow the ventricles to finish filling. From the AV node, the action potential spreads rapidly throughout the ventricles, hastened by a specialized ventricular conduction system consisting of the bundle of His and Purkinje fibres.

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8
Q

How much blood flows passively into the ventricles and how much flows actively (squeezing of the atria)?

A

Passive flow = 80-90%

Active flow = 10-20%

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9
Q

What happens if the atria fail?

A

Atria failure is the most common arrhythmia amongst senior citizens. There are virtually no hemodynamic consequences, however it is treated aggressively to avoid having a stroke)

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10
Q

Explain the train analogy of pacemaker activity

A

There are three engines: the SA node, the AV node and the Purkinje fibres. The remaining 97% of cells are are contractile cells and they just pulled along with the engines. Although the different engines fire at different speeds, however it is the fastest engine that set the heart rate. If everything is normal, the SA node sets the speed (70 bpm). If the SA node fails, the AV node takes over and sets the heart rate (50 bpm). If the AV node fails, the top of the heart and the bottom beat completely independently of each other (70 bpm and 30 bpm, respectively). This is very serious and needs to be treated with a pacemaker

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11
Q

What are ectopic beats?

A

When one part of the heart decides it wants to be the fastest pacemaker and then it takes the remaining bottom part with it. So if the top of the heart is going 140 bpm, so does the bottom. If below of AV node is going 140 bpm, the rest of the bottom does too, but not the top

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12
Q

Where are pacemakers inserted?

A

They are inserted in a patch of fat near the chest. Lead wires are inserted and they go where they need to be

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13
Q

How long is the battery life of a pacemaker?

A

About 10 years

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14
Q

What is an ICD?

A

Intercardiacdefibrillator. It’s an implantable defibrillator

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15
Q

What is fibrillation?

A

It is the most serious arrhythmia. Electrical activity is completely chaotic and there’s no forward movement of the heart. The patient will fall immediately and requires immediate action, or else they will start to lose brain function. It’s treated by shocking the heart with the electrical paddles across the chest (defibrillation)

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16
Q

What causes the majority of cardiac problems?

A

Failure to pump function

Failure of electrical activity (arrhythmias)

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17
Q

Is there much pharmacological interventions for arrhythmias?

A

The CAST study showed that giving patients drugs was more harmful than doing nothing. Since then, the number of anti-arrhythmic drugs have dropped and electrical devices have taken over

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18
Q

Describe the coordination of cardiac contractions

A

Cardiac contractions must be coordinated for efficient pumping. The heart functions as two separate pumps in series (the right side pumps the same amount as the left side). Atrial excitation and contraction must precede ventricular contraction (to avoid blood flowing back). Contraction of each chamber must occur as a unit. Contraction of the pair of atria and the pair of ventricles must occur simultaneously

19
Q

What happens if the contractions are not properly coordinated (mismatched)?

A

It can lead to congestive heart failure and blood pools in the lungs

20
Q

How is coordination of cardiac excitation achieved?

A

The coordination of cardiac excitation is achieved structurally. The SA node initiates contraction in the atria. Excitation occurs throughout the atria via cell to cell contact (gap junctions) and the interatrial pathway. The AV node is excited through the internodal pathway and by cell to cell contact. The atria and ventricles are electrically separated. Transmission of excitation occurs through the AV node (there is no connection between the top and bottom of the heart, except through the AV node). Slow conduction through the AV node ensures a delay between the contraction of the atria and the ventrilces

21
Q

What is Wolff-Parkinson-White syndrome?

A

An accessory pathway that causes arrhythmias. It connects the top and the bottom of the heart outside of the AV node. It’s fairly dangerous. It’s treated electrically to burn the pathway (create a lesion)

22
Q

Explain ventricular conduction

A

The ventricular conduction system is highly organized. It’s an extremely fast event that is mediated by some of the fastest conducting cells in the body.Ventricular excitation is rapidly conducted from the AV node through the Bundle of His to the Purkinje fibres. Excitation of the large ventricular mass then proceeds by cell to cell contact (gap junctions). The ventricular action potential has different characteristics than that of the SA and AV nodes

23
Q

Describe the propagation of action potentials in autorhythmic cells

A

Autorhythmic cells do not have a stable resting membrane potential; they are constantly drifting towards a threshold potential then they fire. At -60 mV, permeability to K goes down and Na stays the same. As membrane potential rises towards threshold, T type calcium channels increase intracellular Ca. At threshold, we switch to L type calcium channels. At 0 mV, K permeability rises and membrane potential begins to fall

24
Q

Describe the propagation of action potentials in contractile cells

A

Contractile cells have a stable resting membrane potential (-90 mV; no excitation, nothing happens). Excitation causes an explosive increase in intracellular Na; membrane potential raises to +30 mV. Then [Na] lowers, intracellular Ca rises, intracellular K lowers. There is a prolonged plateau caused by the slow entry of Ca by the efflux of potassium. When K permeability exceeds calcium, membrane potential returns to resting membrane potential

25
Q

What is excitation-contraction coupling?

A

In cardiac muscle, an electrical signal is converted into a contractile signal. The signal for contraction is an elevation of cytosolic Ca. Ca is derived from two sources: ECF and the sarcoplasmic reticulum. The elevated Ca leads to cross-bridge cycling between actin and myosin. The relationship between the electrical event and the mechanical event prevents tetanus

26
Q

Describe the result of an action potential in a cardiac contractile cell

A

The action potential travels down the T tubules, causing entry of small amount of Ca from the ECF, which causes the release of a large amount of Ca from sarcoplasmic reticulum. Both of these events causes a rise in cytosolic Ca. Ca binds to troponin-tropomycin complex in thin filaments, which pulls them aside. This allows cross-bridge cycling between thick and thin filaments. Thin filaments slide inward between thick filaments, causing contraction

27
Q

What has the most effect on heart contraction?

A

Calcium. At low levels of Ca, there is virtually no force. At 1 uM, 50% contraction. At 10 uM, 100% contraction. People who have failing hearts typically have a problem with diastole (too much calcium, the heart can’t relax, can’t fill with blood completely) or with systole (not enough calcium, not very forceful contractions, blood not pumped well)

28
Q

How is intracellular calcium concentration raised?

A

Calcium flows in from the ECF into the cell via L type calcium channels and signals RyR. This opens up and releases even more Ca (calcium-induced calcium release).

29
Q

How is intracellular calcium removed?

A

This relaxes the heart. It’s done by NCX, PMCA (ATPase pump) and SERCA (resequesters Ca out of the cell)

30
Q

Describe the relationship between the electrical and the mechanical event

A

The cardiac action potential and contraction is prolonged. The action potential precedes contraction. This relationship protects the heart from tetanization. It can’t tetanize because there is a refractory period (200-300 ms) where the heart can’t contract. About 1/3 of the time is spent contracting, the other 2/3 is the refractory period meant for filling

31
Q

Why is tetany a bad thing in the heart?

A

It is an intermittent pump that requires continual contraction, otherwise there won’t be any forward movement of blood.

32
Q

What an electrocardiogram do?

A

The ECG records the overall spread of electrical activity in the heart. It measures electrical signals from the heart conducted by body fluids. It is not a direct measure of cardiac electrical activity. The ECG represents the sum of all electrical activity in the heart, not the activity of single cells. It measures the difference in electrical potential between two different points on the body.

33
Q

What does the P wave represent?

A

Atrial depolarization

34
Q

What does the QRS complex represent?

A

Ventricular depolarization

35
Q

What does the T wave represent?

A

Ventricular repolarization

36
Q

What does the PR segment represent?

A

AV nodal delay

37
Q

What does the ST segment represent?

A

It occurs when the ventricles are completely depolarized

38
Q

What does the TP interval represent?

A

It occurs when the heart is at rest

39
Q

What does a flat line represent?

A

When there’s no difference; when the whole heart is relaxed or when the whole heart is contracting

40
Q

Why are ECGs important?

A

The ECG can be useful for diagnosing abnormal heart rates (tachyarrhythmias, bradycardias), arrhythmias (atrial flutter, fibrillation, heart block, extrasystoles, ventricular fibrillation, cardiac myopathies), and damage to the heart muscle

41
Q

What is extrasystole?

A

Premature or extra heart beats. Occasional extrasystoles are very common and not all that dangerous. Recurrent extrasystoles predisposes the patient to other arrhythmias

42
Q

What is ventricular fibrillation?

A

The most serious arrhythmia. Total chaos of the heart. Ther is not longer forward movement of the blood. If it is not corrected within minutes (ideally seconds), there’s a 10% decline in brain function per minute

43
Q

What is complete heart block?

A

There are regular P waves and regular QRS complexes, but there is not relationship between the P wave the QRS complex. This is typically treated with a pacemaker

44
Q

Name the three types of AV block

A

First-degree AV block (prolongation of the time between atrial and ventricular contraction)
Second-degree AV block (the atrial signal is not passed to the ventricles)
Third-degree AV block (no relationship between the top and the bottom of the heart)