Cardio - Physiology - Arrhythmias; Heart Sounds Flashcards by Jason Worley

What rhythym is shown here?

Normal sinus rhythym

(P –> QRS –> T

every time)

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What rhythym is shown here?

Sinus tachycardia

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What is a normal PR interval?

What is a normal QRS interval?

0.12 - 0.20 sec

≤ 0.12 sec

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How much time is represented by each 1 mm box on an EKG?

How much time is represented by each 5 mm box on an EKG?

How much time is represented by five 5 mm boxes on an EKG?

04 second
2 second

1 second

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What is the internationally standardized speed at which EKG paper moves?

25 mm / sec

(so five large boxes = 1 sec)

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If there is one large box (five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

300 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are two large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

150 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are three large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

100 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are four large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

75 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are five large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

60 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are six large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

50 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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If there are seven large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

43 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

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Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:

4 large boxes (twenty 1 mm boxes)

2 large boxes (ten 1 mm boxes)

1 large box (five 1 mm boxes)

3 large boxes (fifteen 1 mm boxes)

(Just 300 divided by the number of large boxes between adjacent QRS complexes)

75 BPM

150 BPM

300 BPM

100 BPM

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Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:

1 large box (five 1 mm boxes)

2 large boxes (ten 1 mm boxes)

3 large boxes (fifteen 1 mm boxes)

4 large boxes (twenty 1 mm boxes)

5 large boxes (twenty-five 1 mm boxes)

6 large boxes (thirty 1 mm boxes)

(Just 300 divided by the number of large boxes between adjacent QRS complexes)

300

150

100

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What arrythmia is shown here?

Atrial fibrillation

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What arrythmia is shown here?

Atrial flutter

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What arrythmia is shown here?

Third degree AV block

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What arrythmia is shown here?

Premature ventricular beat

(ectopic ventricular beat –> this explains why it is opposite in polarity. It may be starting in the right ventricle)

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What are some ways by which arrythmias are classified?

Origin

(SA, atrial, supraventricular, ventricular, etc.)

Pattern & rate

(tachycardia, bradycardia, fibrillation, flutter, etc.)

# of ectopic sites

(unifocal or multifocal)

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How can arrhythmias be classified based on their origin?

Sinus, atrial, supraventricular, ventricular, etc.

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How can arrhythmias be classified based on their pattern and rate?

Tachycardia, bradycardia;

flutter, fibrillation, etc.

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How can arrhythmias be classified based on their number of ectopic sites?

Either unifocal or multifocal

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What is an example arrhythmia that could result in the following finding on EKG examination?

An ectopic site in the left atrium

(the green star in the attached diagram)

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What is an example arrhythmia that could result in either of the following findings on EKG examination?

A supraventricular ectopic site firing

[either in the AV node (no P wave) or adjacent to it]

(the purple circle in the attached diagram)

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What is an example arrhythmia that could result in the following finding on EKG examination? ## Footnote *(Note: the QRS is prolonged and the T wave inverted.)*

An ectopic ventricular firing site ## Footnote *(the red star in the attached diagram)*

Describe the pattern and rate of each of the following: tachycardia bradycardia fibrillation flutter

T \> 100 BPM; regular B \< 60 BPM; regular Fibrillation 300 - 600 BPM; chaotic and irregular Flutter 250 - 400 BPM; regular

If you see multiple morphologies in the same EKG strip, what may be going on? ## Footnote *(See attached image for a simplified version.)*

Multifocal ectopic firing

What arrhythmia is shown here?

Ventricular tachycardia

What arrhythmia is shown here?

Torsade de Pointes ## Footnote *[a polymorphic (multifocal) v. tach.]*

What is Torsade de Pointes?

A polymorphic (multifocal) ventricular tachycardia

What is a very common cause of Torsade de Pointes?

Many, many medications can cause this

What arrhythmia is shown here?

Ventricular fibrillation

≥80% of all clinically relevant arrhythmias are due to what mechanism type?

Reentrant excitation | (or just, *reentry*)

What are two common causes of reentrant excitation in cardiac tissue?

**disturbance in conduction** *(e.g. MI)*; **dispersion of ERPs** (effective refractory periods) *(e.g. due to atrial stretching in CHF)*

What are some examples of arrhythmias for which the mechanism is often reentrant excitation (reentry)?

Ventricular tachycardia (VTach), atrial fibrillation (AFib), ventricular fibrillation (VFib), paroxysmal supraventricular tachycardia (PSVTs), premature ventricular contractions (PVCs)

Name the mechanism common to each of the following arrhythmias: ## Footnote Ventricular tachycardia (VTach), atrial fibrillation (AFib), ventricular fibrillation (VFib), paroxysmal supraventricular tachycardia (PSVTs), premature ventricular contractions (PVCs)

Reentrant excitation | (reentry)

What type of reentrant excitation is associated with ventricular fibrillation and atrial fibrillation?

Multifocal (many simultaneous rentrant loops) *(atrial shown in the attached image)*

What type of reentrant excitation is associated with paroxysmal supraventricular tachycardia (PSVT)?

AV nodal reentry

What is a 'dispersion of ERPs' in regards to reentrant excitation in cardiac tissue?

Different sections of cardiac tissue have varying effective refractory periods ## Footnote *(flow is not even through the tissue and may loop around and 'reenter' slower tissues)*

What are EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?

Abnormal automaticity in cardiac tissue (i.e. ectopic pacemaker(s) that is(are) repeatedly firing)

What is the cause for most EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?

Medications; they are most commonly drug-induced arrhythmias

Describe the changes in extracellular potassium and intracellular pH in infarcted cardiac tissue in the following timeframes after infarction has occurred: the first 0 - 5 minutes 15 - 40 minutes ≥ 40 minutes

**The first 0 - 5 minutes** Rapid efflux of potassium; rapid decrease in pH **15 - 40 minutes** Plateaued potassium level; rapid decrease in pH **≥ 40 minutes** Continued efflux of potassium; plateaued pH

In the graph below, cardiac intracellular pH and extracellular potassium are shown plotted against time after infarction. What is the significance of the potassium plateau between 10 and 40 minutes? What is the significance of the rising levels of potassium after 40 minutes?

The changes are reversible; cell necrosis has begun

How long does it typically take for cardiac myocytes to begin to die in ischemic conditions?

30 - 40 minutes

What happens to extracellular K⁺levels during infarction? Why?

They increase; lack of ATP --\> no inhibition of K_ATP channels;

What type of channel are K_ATP channels? Where are they found?

K⁺ channels that are inhibited by ATP; cardiac tissue, the pancreas, smooth muscle

What happens to K_ATPchannels if ATP levels fall?

They are unihibited; massive efflux of potassium out of cardiac cells

What effect do ischemic conditions have on cardiac myocyte resting potentials?

Depolarization; Na⁺ channel inactivation

What effect do ischemic conditions have on Na⁺ channels? What is the result?

Depolarization --\> Na⁺ channel inactivation --\> conduction block

What happens when cardiac tissue action potentials run headlong into one another?

They extinguish one another | (due to ERPs)

The attached image shows a subendocardial infarction in the apex of the heart. Indicate the accepted route that might be taken for a reentrant excitation (reentry) arrhythmia to take place.

What are the three requirements that must be met for a reentrant excitation (reentry) arrhythmia to occur?

1. ≥ Two parallel pathways 2. Unidirectional block 3. Conduction time of the circuit \> ERP for the circuit * (Basically, all just requirements so that the action potential(s) can double back from its normal route and circle around between healthy and affected tissues)*

Why is each of the following necessary to the development of a reentrant excitation (reentry) arrhythmia? 1. ≥ Two parallel pathways 2. Unidirectional block 3. Conduction time of the circuit \> ERP for the circuit

1. So there is an unrefractory path 'backwards' if the action potential swings around and goes back the way it came 2. So that when the action potential swings around to go back, it isn't blocked going backwards 3. If the effective refractory periods (ERPs) of some cells were longer, the circuit action potentials would simply hit them and dissipate (i.e. the circuit would not keep flowing around and around)

For a _slow-moving_ reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?

(Single or multiple) premature ventricular contractions (PVCs) *(the current can get caught in this loop)*

For a _fast-movin_g reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?

Ventricular tachycardia *(the current can get caught in this loop)*

Describe the mechanism by which atrial or ventricular tachycardia operate. How does this differ from non-sustained ventricular tachycardia (\> 2 beats; \< 30 sec)?

A single loop of quick conduction goes around in a reentry (reentrant excitation) pathway *(the attached image shows an example in the ventricles)*; NSVT = one _transient_ circuit

What is the simple mechanism for atrial or ventricular fibrillation? What is atrial flutter's simple mechanism?

Large number of reentry circuits (reentrant excitation) a single, large reentry circuit (reentrant excitation)

What is the accepted mechanism for paroxsymal supraventricular tachycardia?

AV nodal reentrant excitation ## Footnote *(reentry arrhythmia --\> the conduction current goes around some differential in conduction speen and keeps reexciting its circuit by traveling back up the faster end)*

What predisposes individuals to paroxysmal supraventricular tachycardias (PSVTs)?

Large differences in speed and effective refractory period (dispersion of refractoriness) between at least two pathways in the AV node

How do paroxysmal supraventricular tachycardias (PVSTs) often present? How are they treated? Why?

Palpitations, dizziness --- no P waves on EKG; calcium channel-blockers --- AV nodal dysfunction

In atrial flutter (a macroreentry arrhythmia), why is the atrial rate so much higher than the ventricular rate (i.e., why doesn't each atrial action potential make it to the ventricles)?

The AV node acts as a filter, only letting through 1 for every 3 or 4 atrial beats (3:1 or 4:1)

What arrhythmia is known for relapsing and recurring?

Atrial fibrillation ## Footnote *("Afib begets afib")*

What tissues are ablated to try and treat atrial fibrillation?

Areas with especially short effective refractory periods (ERPs)

How will a patient with ventricular fibrillation present? Why?

Unconscious (cardiac arrest); no successful systole --\> virtually no blood being pumped

Are the atrial contractions in atrial fibrillation regular? Are the ventricular contractions in atrial fibrillation regular?

**No**; **no** (occur at irregular, random rates --\> but may appear regular at first glance!)

In first degree AV node block, how prolonged is the PR interval?

\> 0.20 sec (larger than 1 large box on the EKG strip)

**True/False.** First degree AV blocks can devolve into third degree AV block without passing through second degree block.

True.

Which type of AV block is most likely to devolve into third degree AV block?

Mobitz type II second degree AV block ## Footnote *(dropped QRS complexes with no change in PR interval)*

**True/False.** Wenckebach AV block (Mobitz type I second degree AV block) is more likely to devolve into third degree than Mobitz type II second degree AV blocks.

**False**. Mobitz type II second degree AV blocks is more likely to become third degree.

In what disorder are atrial depolarization and ventricular depolarization regular but completely out of sync with one another?

Third degree AV block

What arrhythmia is shown here?

Mobitz type I 2° AV block

What arrhythmia is shown here?

Atrial fibrillation

Third degree (complete) AV block

Describe the conditions that are risk factors for Torsade de Pointes in regards to the following: Extracellular ionic concentrations Gender Heart rate QT interval

**Hypo**magnesia **Hypo**kalemia Female Bradycardia Prolonged QT interval

Drugs that block what channel can predispose an individual to Torsade de Pointes? How?

I_KR (Inward-rectifier potassium channel); the QT interval is lengthened

Early after-depolarizations (EADs) occur when in the cardiac cycle?

Phase 3

What is the basic pathophysiology of an early after-depolarization (EAD)?

A prolonged repolarization *(slow or blocked I_KR channels)* allows incoming ion flow *(L-type calcium channels, sodium channels, sodium-calcium exchangers)* to create extra upbeats during phase 3

Congenital early after-depolarizations (EADs) are most often due to: Acquired early after-depolarizations (EADs) are most often due to:

Long QT syndromes; medication use (e.g. quinidine)

**True/False.** Torsade de Pointes is a type of delayed after-polarization (DAD).

**False**. Torsade de Pointes is a type of _early_ after-depolarization (EAD).

Early after-depolarizations (EADs) are most likely to occur in what cardiac cells?

Purkinje fibers

Delayed after-depolarizations (DADs) occur when in the cardiac cycle?

Phase 4

Delayed after-depolarizations (DADs) occur when in the cardiac cycle? Early after-depolarizations (EADs) occur when in the cardiac cycle?

Phase 4; phase 3

What is the basic pathophysiology of a delayed after-polarization (DAD)? ## Footnote *(Note: the DAD is the small bump in the EKG strip after the previous beats)*

Increased intracellular calcium (often due to blockage of the sodium-calcium exchanger) --\> SR overloads and ejects calcium

Describe delayed after-polarizations (DADs) in terms of: intracellular ions heart rate phase involved

Increased intracellular calcium --\> mechanism Tachycardia --\> increases severity Phase 4 event

Describe the differences in early after-polarizations (EADs) and delayed after-polarizations (DADs) in terms of: major ions involved phase involved heart rate

D. Tissue hyperkalemia

Physiological levels of enhanced vagal tone, such as that produced by carotid artery massage or a Valsalva maneuver can reproducibly produce this condition.

B. First degree AV block

A condition that can enhance Purkinje fiber (ectopic) automaticity more than automaticity of the SA node. A cause for ventricular tachyarrhythmias.

C. Hypokalemia *(causes more hyperpolarization-activated (I_h or I_f) pacemaker current to be activated)*

If a portion of cardiac tissue has a conduction defect that does not prevent conduction in either direction (bidirectional conduction block), will this be a potential site for reentrant excitation (reentry) arrhythmias?

No; the site must have a **_uni_**directional block (so the conduction can swing around and enter from the opposite side)

Conditions of intracellular calcium overload caused by hypercalcemia or excessive catecholamine stimulation (e.g. in a patient on digoxin or toxic levels of amphetamines) can result in arrhythmias due to:

A. Delayed after-depolarizations (DADs)

Drugs or ion channel mutations that reduce the rate of phase 3 repolarization and prolong the QT interval can result in an arrhythmia associated with sudden death. A cellular mechanism believed to be responsible for this type of arrhythmia is:

B. Early after-depolarization (EADs)

Torsade de pointes is a potentially fatal arrhythmia that can be caused by more than 40 different drugs. Which of the following clinical conditions is also associated with an increased risk of this arrhythmia? Female gender Hyperkalema Hypermagnesia Tachycardia

Female gender (and **hypo**kalemia, **hypo**magnesia, and **brady**cardia)

Do men or women typically have a longer QT syndrome?

Women

Delayed after-depolarizations (DADs) result from activation of which transport mechanism? ## Footnote **L-type Ca channel** **Na/Ca exchange** **Na/K pump** **Sodium channels**

**Na/Ca exchange**

How many ions does the cardiac sodium-calcium exchanger move and in what directions?

Three sodium ions in; one calcium ion out

The patient with the EKG results below mentions during his history & physical that he inhaled an excessive amount of organophosphate insecticide (cholinesterase inhibitor) an hour before arriving at the hospital. What drug could you give to increase his heart rate & provide relief from his symptoms? A. Acetylcholine B. Atropine C. Lidocaine D. Norepinephrine E. Nicotine

B. Atropine

A patient on sotalol (a class III antiarrhythmic) for atrial fibrillation presents with the following EKG reading. What is your diagnosis?

Torsade de Pointes | (medication-induced)

**True/False.** Even though it results in calcium efflux, increased Na/Ca exchanger activity can result in diastolic depolarization (resulting in DADs).

True.

**True/False.** Cardiac disease can be due to either issues in the electrical system or the pump system of the heart.

True.

The S1 heart sound is caused by: The S2 heart sound is caused by: The S3 heart sound is caused by: The S4 heart sound is caused by:

Closure of the AV valves Closure of the aortic-pulmonic valves Increased ventricular filling Forced blood flow into stiff ventricle

How is the intensity of a systolic heart murmur described? How is the intensity of a diastolic heart murmur described?

On a scale of 1/6 - 6/6. On a scale of 1/4 - 4/4.

What is 1/6 heart murmur? What is 2/6 heart murmur? What is 3/6 heart murmur? What is 6/6 heart murmur? (Note: all systolic)

Difficult to hear Clearly audible (S1 and/or S2 is(are) still louder) Louder than S1 and S2 Audible without a stethoscope

What is a cardiac murmur? What is a gallop?

Turbulence over the heart valves; extra heart sounds (S3, S4)

Highly irregular S1 sounds might indicate what condition?

Atrial fibrillation

Murmurs indicate problems in the: Gallops (extra heart sounds) indicate problems in the:

Valves; chambers (stiff or floppy)

A pathologic S3 sound indicates what about the ventricles? When in the cardiac cycle is it heard?

They are enlarged and floppy; in early diastole *(bum, bum-bum)*

Which is sometimes normal, an S3 or an S4 heart sound?

S3 (pregnant women, children, athletes after exercise)

Dilated cardiomyopathy often presents with what gallop?

Describe the murmur associated with aortic or pulmonic stenosis.

Crescendo-descendo during systole

S4 heart sounds are due to what change in the ventricle(s)? When in the cardiac cycle does it occur?

They are stiff; late diastole (bu-dum, bum)

Describe the murmur associated with aortic or pulmonic regurgitation.

Normal S1, descendo following S2

When does the S3 gallop occur in the cardiac cycle? When does the S4 gallop occur in the cardiac cycle?

Early diastole (**bum, bu**-dum); late diastole (bu-**dum, bum**)

How can a murmur associated with left-sided valve stenosis be increased in intensity?

Squatting

How can a murmur associated with right-sided valves be increased in intensity?

Inspiration

What method can be used to increase **forward** flow over the left-sided cardiac valves? What method can be used to increase **forward** flow over the right-sided cardiac valves?

Squatting; inspiration

What method can be used to resist forward flow over the cardiac valves?

Hand grip

What murmur can be increased by increasing hand grip?

Aortic regurgitation | (increased TPR)

The valsalva manuever (increasing intraabdominal pressure) increases what cardiac murmur?

Hypertrophic cardiomyopathy

Describe both the effect of each of the following on heart murmurs and also the mechanism by which it occurs: Hand grip Valsalva maneuver Squatting Inspiration

**Aortic regurgitation** - Increases TPR that the LV is pushing against **Hypertrophic cardiomyopathy** - Increases intraabdominal pressure **Left-sided valve stenosis** - Brings the heart closer to the periphery **Right-sided valve murmurs** - Increased venous return to the RA

What clinical maneuver can increase the murmur of hypertrophic cardiomyopathy?

The Valsalva maneuver (bear down)

What clinical maneuver can increase the murmur associated with aortic regurgitation?

Hand grip (increase TPR)

What clinical maneuver can increase the murmurs associated with right-sided valves?

Inspiration