Cardiology Flashcards

0
Q

What is an intercalated disc and why do we care?

A

This is the division between cardiac cells, gap junctions liver here to allow rapid diffusion of ions. This means that action potentials can travel super easily from one cardiac muscle to the next via the intercalated discs. Thus, cardiac muscle is a synctium

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1
Q

What is the cause of long QT syndrome

A

Congenital: mutations in sodium and potassium channel genes.

Hypocalcemia, hypomagnesemia, hypokalemia

Administration of excess antiarrhythmics like quinidine or fluorquinolones and erythromycin

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2
Q

What are some differences between cardiac and skeletal muscle action potential?

A
  1. Slow calcium channels: After fast sodium channels open, the calcium channels open. These are slow to open, and remain open for longer. This allows for influx of sodium and calcium. This is important becuase it causes plateau phase of action potential
  2. The calcium ions that enter also trigger muscle contraction, whereas in skeletal musclethis comes from sarcoplasmic reticulum
  3. After onset of cardiac AP, the permeability to potassium decreases fivefold. This does NOT happen in skeletal muscle. May be due to excess calcium influx from calcium channels. Anyways, it prevents outflux of potassium ions during plateau phase. When slow calcium-sodium channgels close, then the permeability for potassium increases and potassium leaves cell to restore to resore resting membrane potential
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3
Q

What is the refractory period of cardiac muscle?

A

There is a refractory period, and a relative refractory period. Relative refractory period is when cardiac muscle can be excited by a very strong excitatory signal.

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4
Q

Where does calcium come from for the cardiac muscle contraction? How is it removed?

A

Sarcoplasmic reticulum, but most comes from T tubules themselves. Calcium ions entering cell from T tubules during action potential trigger opening of calcium release channels (ryanodine receptor channels). This triggers release from sarcoplasmic reticulum. The sarcoplasm in the heart is way less well developed than in the skeletal muscle, so without T tubules heart contraction would be much weaker.

At the end of the cardiac action potential, calcium ions in the sarcolemma are pumped out of the muscle fibers into sarcoplasmic reticulum and T tubule ECF space. This is done via calcium ATP-ase

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5
Q

Wigger’s diagram! know this!

A
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6
Q

What is preload?

A

End diastolic pressure when the ventricle has been filled.

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7
Q

What is afterload?

A

Pressure in the aorta - arterial pressure against which the heart must contract

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8
Q

Frank Starling Mechanism

A

Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood. The greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater quantity of blood pumped into the aorta.

Explanation for it;

When extra blood enters heart, this stretches the heart, which causes muscle to contract with greater force because actin and myosin filaments are brought to a more optimal degree of overlap.

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9
Q

Parasympathetic stimulation of the heart?

A
  • Distributed mainly to atria and not ventricles
  • Slows heart rate, but doesn’t really have huge effects on cardiac contraction
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10
Q

Effect of potassium on heart function?

A

Hyperkalemia causes heart to become dilated and flaccid, and slows the heart rate.

Can block condution via AV node. High K depolarizes thecell membrane, and also makes action potential intensitiy weaker

Hypercalcemia is going to make the heart spastic because of effects on calcium in cardiac contraction. Hypocalcium makes heart flaccid.

This is a stupid question!

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11
Q

Resting membrane potential for sinus node?

A

-55 to -60 mV

The reason for this is that the cell membranes of sinus node are naturally leaky to sodium and calcium ions

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12
Q

What causes depolarization of the sinus node?

A

At -55, the fast sodium channels have become inactivated so that only slow sodium calcium channels can open. Thus, the atrial nodal action potential is slower to develop.

The sinus node is leaky to sodium and calcium, so between heartbeats, the sodium slowly leaks into the membrane, becoming gradually more positive. When it reaches a threshold of -40, the sodium calcium channels become activated, causing action potential.

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13
Q

What prevents sinus node from remaining constantly depolarized?

A
  1. Sodium-calcium channels become inactivated very soon after opening
  2. Greatly increasednumbers of potassium chnnels open after sodium calcium channels open. The potassium channels remain open for a little while after depolarization, so makes cell membrane hyperpolarized, which then allows for leakage of sodium and calcium into cell, to make cell more positive, to start new AP
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14
Q

Why is AV node transmission slow?

A

Decreased number of gap junctions causes delay in transission because cells slower to become excited

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15
Q

Why is the sinus node the pacemaker for the heart?

A

Because it’s faster than AV node or Purkinje fibers. So it consistently excites its self before the AV node or Purkinje fibers can reach their thresholds for self-excitation

16
Q

What is the mechanism of vagal effects on the heart?

A

Parasympathetic fibers distributed to AV node, SA node, and atria

Acetylcholine released from parasympathetic nerve endings increases permeability of fiber to potassium ions, so potassium leaks out of cell, becoming hyperpolarized

17
Q

What are the effects of sympathetic stimulation on the heart?

A

Increased heart rate- increased sinus node discharge. Increased rate of conduction, increases force of contraction

NE stimulates beta-1 receptors, which MAY increase permeability of the fiber membranes to sodium and calcium

18
Q

What causes increased voltage of QRS?

A

hypertrophy of the heart muscle

19
Q

Decreased voltage of the QRS complex?

A

old myocardial infarctions with diminished muscle mass?

Also things that muffle electrical current conduction: pericardial effusion, pleural effusion, pulmonary emphysema (lungs and chest get bigger and this deceases conduction of electrical current).

20
Q

What can cause left axis deviation on ECG?

A

hypertension causing hypertrophy of left ventricle, or anything causing left ventricular hypertrophy (aortic stenosis, aortic insufficiency, etc)

21
Q

What can cause right axis deviation on ECG?

A

anything causing right heart hypertrophy: pulmonic stenosis, tetraology of Fallot, interventricular septal defect, etc.

Also RBBB

22
Q

What is sinoatrial block?

A

When the impulse from the sinus node is blocked even before it enters atrial muscle. This means there are no P waves on ECG. But AV node will trigger

23
Q

Where do electrical signals for heart contraction come from when there is AV block?

A

Usually from AV node or AV bundle.

24
Q

What is stokes-adams syndrome?

A

This is when you have overdrive suppression it can take ventricles 5-30 seconds after cessation of AV conduction to pick up. This will result in syncope in humans periodically, called stokes adams syndrome

25
Q

What is overdrive suppression?

A

Ventricular excitability is suppressed because they have been driven by atria at a greater rate than their normal rate of rhythm.

26
Q

What causes electrical alternans?

A

In dogs we think of pericardial effusion

This is when the conduction in the Purkinje system is blocked. And electrical alternans causes partial intraventricular block every other heartbeat. Cases could include tachycardia, ischemia, myocarditis, digitalis toxicity.

27
Q

What is QT syndrome?

A

It is anything that cause delayed depolarization of ventricular muscle following action potential can cause prolonged ventricular action potentials, and thus, long QT intervals.

Major reason it’s of concern is that it increases a person’s susceptibility to torsade des pointes.

28
Q

What is ventricular fibrillation?

A

This occurs when the cardiac action potentials have gone berserk within ventricle, stimulation one portion, then another, then another, and feeding ack to re-excite ventricular muscle without stopping. When this happens, many small portions of ventricular muscle will be contracting at same time, while equally as many are relaxing.

29
Q

Describe re-entry

A

Normal cardiac impulse in heart dies out after being conducted ot ventricles because the muscles are refractory and cannot conduct impulse further. However, in some conditions this doesnt occur and can initiate re-entry and circus movements.

30
Q

What three things can predispose the heart to circus movements or re-entry?

A
  1. pathway around circle is too long- then by the time the impulse returns to starting point, the stimulated muscle will no longer be refractory so impulse can keep going round and round in circles. Ex: dilated heart
  2. Velocity of conduction around pathway becomes decreased- thus it’s out of refractory period and go round and round. Ex: ischemia of the heart, blockage of purkinje system, hyperkalemia, etc.
  3. Refrctory period of muscle gets shortened. Ex: drugs like epinephrine
31
Q

What things occur when the heart starts to fibrillate that sets it up for continued VFIB?

A
  • Block of impulses in some directions but successful transmission in other directions creates situation where re-entrant signal can develop
  • Rapid stimulation of the heart causes change in velocity of conduction (decreases), refractory period of muslce gets shortened, allowing for re-entry
  • Division of impulses: When a depol wave reaches a refractory area, it splits in two to get around that. That causes many circutious routes for impulses to travel, greately lenghthening the cardiac conductionpathway= propagate vfib.
32
Q

Why does the ECG look like it does in VFIB?

A

Because the ventricular muscle is contracting all at the same time, the ECG potentials are changing constantly and spasmodically so you can’t really get anything organized on your ECG

33
Q

Why does defibrillation work for VFIB?

A

Strong, high voltage alternating electrical current will make all the ventricles refractory simultaneously. Of course, when refractory period stops you may go right back into fibrillation.

34
Q

What are the immediate consequences of AFIB?

A

Decreased pumping of blood into ventricles decreases efficiency of ventricular pumping by 20-30%

35
Q
A