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184 Cards in this Set

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  • Back
The heart beats in absence of what? Why?
The heart beats in absence of any nervous connection. This is due to the property of specialized cells (pacemaker cells) with pacemaker activity (auto-rhythmicity).
What leads to cardiac muscle contraction?
Electrical (pacemaker) activity generated by the heart itself leads to cardiac muscle contraction. Requires electrical events.

So the pacemaker cells have the ability to create Action Potentials independently.
What conducts electrical activity in the heart?
Specialized conduction tissue.
What allows rapid spread of electrical activity?
Cardiac muscle synctia.
A heart or ? ? can beat on it's own.
A heart or heart cell can beat on it's own.
The cardiac muscle cells are ? cells. What does this allow them to do?
They are contractile cells. Allows them to perform mechanical work of pumping blood flow thru cardiovascular system.
What allows for the coordinated contraction of the heart?
Excitation-contraction coupling.
What are arrythmias an interruption of?
The normal impulse generation and conduction in the heart.
What does the conduction system within the heart allow?
Rapid, organized near-synchronous depolarization and contraction of ventricles.
The conduction system w/n the heart allows rapid, organized near-synchronous depolarization and contraction of ventricles:

List 2 things this property is essential to.
1. Allow sufficient rest time for filling of ventricles.

2. Generate pressure efficiently during ventricular contraction and pumping of blood into arterial system.
The electrical activity of the heart begins with what?
Electrical activity of the heart begins with the pacemaker cells of the SA node.
The transmission of electrical activity in the heart is essential to what?
Essential to stimulate the heart to contract.
The heart cannot contract and pump unless what occurs first?
unless an electrical stimulus occurs first.
Pacemaker cells possess the ability to produce what? This is referred to as what?
To produce a spontaneous electrical stimulus initiating an impulse. This is referred to as automaticity.
The pacemakers cells include what 4 components?
1. SA node

2. AV node

3. Bundle of His

4. Purkinje fibers
The automaticity of pacemaker cells are ALTERED by what?
1. Sympathetic NS

2. Parasympathetic NS

(they are altered not dependent upon these...these give additional control)
Sympathetic stim. does what to the heart rate?
Increases heart rate.
Parasympathetic stim. does what to the heart rate?
Slows heart rate.
Electrical activity is aka what?
Electrical activity = impulses = action potentials (terms can be used interchangeably)
What is the primary area for pacemaker cells?
SA node (there are other but this is the main one)
What is an autorhythmic cell?
Pacemaker cell
Each group of autorhythmic cells has its own what?
Each has its own rate of AP initiation.
The heart cells with the fastest rate of AP initiation are localized where? What does this mean?
They are localized in the SA node. Thus, the SA node drives the rest of heart at its rate (~70-80APs/min). So the SA node is the pacemaker of the heart.
How many APs/min is the heart's normal rate?
~70-80APs / min
The AV node and Purkinje fibers could be referred to as the ? pacemakers.
The latent pacemakers.
The AV node initiates APs at what pace?
40-60/min
The purkinje fibers initiate APs at what pace?
20-40APs/min
Why don't you have different heart rates in different parts of your heart?
Because the SA node suppresses the pacemaker activity of the other areas.
If the SA node suppresses the other areas of pacemaker activity then what is the point of them?
If the SA node is damaged the next highest would take over. So the AV node would become the pacemaker of the heart. (not optimum but better than nothing)
List the order of the pathway of impulse conduction. (7)
1. SA node

2. Bachmanns bundle

3. Internodal pathways

4. AV-node

5. Bundle of His

6. Bundle branches (Right and left)

7. Purkinje fibers
Pacemaker cells have ?.
CONDUCTIVITY
Electrical activity/impulses are conducted in an ? ? throughout the heart.
In an orderly sequence throughout the heart.
As electrical activity is conducted cardiac cells undergo a cycle of what?
Depolarization and Repolarization.
As waves of depolarization and repolarization are transmitted through myocardium what does it cause?
It causes sequential contraction and relaxation of heart chambers.
Depolarization causes what?
Contraction
Repolarization causes what?
Relaxation
The heart contracts in what way?
As a unit.
In the pathway of impulse conduction what component has the highest conduction velocity?
Purkinje fibers
The purkinje fibers connect with ? myocytes.
Connect with ventricular myocytes.
The ventricles are the "?" of the heart.
"powerhouse"
The high conduction velocity of the Purkinje Fibers and their connection to ventricular myocytes allows for what?
Allows for efficient contraction and emptying of ventricles. (Right ventricle = blood to lung)
(Left ventricle to body)
In the pathway of impulse conduction what component has the lowest conduction velocity?
The AV node.
The AV node is the only what between the atria and the ventricle?
The only electrical bridge.
The AV node is the only electrical bridge between the atria and ventricle and it has the lowest conduction velocity. What does this allow for?
It allows time for complete atrial depolarization, contraction and emptying of atrial blood into ventricles prior to ventricular depolarization and contraction. So, basically you need a gap so you have room or atrial blood to enter the ventricles.
The atria pumps blood to where?
Only to the ventricle.
The ventricles pump blood to where?
To the body.
The different speeds in the pathway of impulse conduction allows for what (besides the filling of the ventricles)?
Allows for the 'wringing' contraction of the heart.
Conduction velocity can be ?. (drugs do this)
Conduction velocity can be altered.
List 5 extrinsic factors that increase the rate of impulse conduction w/n the heart.
1. Sympathetic stimulation

2. Muscarinic receptor ANtagonist

3. B1-adreonceptor agonists (ex. dobutamine)

4. Circulating catecholamines

5. Hyperthyroidism
List 5 extrinsic factors that decrease the rate of impulse conduction w/n the heart.
1. Parasympathetic stim.

2. Muscarinic receptor agonist

3. Beta-blockers

4. Ischemia/Hypoxia

5. Sodium and calcium channel blockers
As impulses are transmitted and cardiac cells undergo a cycle of depolarization and repolarization what are generated in different heart regions?
Characteristic Action Potentials (AP) are generated in different heart regions.
An AP generated during the depolarization-repolarization cycle has what?
It has unique phases.
Each phase of an AP is the result of what?
The result of specific ions moving through unique ion channels.
During APs ion movement creates a ? and alters what?
Creates a current and alters membrane potential of the caridac cell.
What essentially does an EKG machine do?
It reads the electrical activity of the heart and can tell us what unique part of the heart is contracting and relaxing.
All AP impulse on an EKG reading have what?
All have unique shapes.
The pacemaker APs (that include what components of the heart?) do not have a what?
The pacemaker APs (SA and AV-node, Bundle of His, Purkinje) do not have resting membrane potentials. They are always trending towards depolarization.
The slow depolarization of pacemaker APs is generated by what?
Na+ into cell
The slow depolarization of pacemaker action potentials can also be referred to as what?
The pacemaker potential.
The slope observed during a pacemakers action potential is the reason why components like the SA, AV, purkinje, and His can do what?
The slope (the pacemaker potential) is the reason why these components can independently cause APs. It allows Ca2+ to enter into the cells. So they never rest.
The ventricle's AP is triggered by what?
Triggered by depolarizing currents from adjacent cells.
The non-pacemaker APs are observed in what components of the heart?
In the atria and ventricles.
What do the atria and ventricles have that the pacemaker APs do not? What is the reason for this?
They have a true resting membrane potential (~90mV). This is maintained by potassium (K+) channels.
? = Na+ = non-resting.
Pacemaker
? = K+ out fast maintains resting.
Non-pacemaker
The duration of cardiac potentials (pacemaker and non-pacemaker) is longer than what? Why?
Longer than the AP of a neuron and skeletal muscle. This ensures that contractions don't occur too close together.
Describe phase 4 of the SA node?
Phase 4 = diastole (resting)

The pacemaker current --> SLOW sodium ion channels open.

Sodium moves slowly into cell.
Describe phase 0 of the SA node?
Depolarization

Voltage-dependent calcium channels open (L-type, T-type)

Calcium moves into the cell.
Describe phase 3 for the SA node?
Phase 3 = repolarization

Voltage-gated potassium channels open - delayed rectifier current.

Potassium moves out of the cell.
Phase 4 for the SA node is resting but moving towards what?
Moving towards depolarization.
In phase 3 for the SA node what channels open and what movement does this cause?
K+ channels open and K+ moves OUT of SA node. (repolarization)
In phase 0 for the SA node what channels open and what movement does this cause?
The Ca2+ channels open and causes a huge INFLUX of Ca2+ into the SA node. (depolarization)
Phase 4 for the SA node is the ? ?.
pacemaker potential.
During phase 4 for the SA node there is a ? trend towards depolarization.
Slow trend.
During phase 4 for the SA node why is there a slow trend towards depolarization?
Because Na+ channels are slow to open and allow orderly flow of sodium into the SA node
Describe phase 0 for the purkinje fibers.
Phase 0 = depolarization

FAST voltage-dependent Na+ channels open.

Sodium moves rapidly into cells. This very fast speed is the speed at which AP is conducted.
Describe phase 1 for the purkinje fibers?
Phase 1 = Early repolarization

Sodium channels CLOSE

Transient outward potassium channels open.

Potassium flows OUT RAPIDLY

(peaks, then trends towards repolarization b/c K+ channels start to open, so some K+ escapes)
Describe phase 2 for the purkinje fibers?
Phase 2 = Plateau

Voltage-dependent L-type calcium channels open.

Ca2+ ions move INTO the cell.

Potassium rectifying channels open.

Potassium flows OUT.

(So calcium channels open, calcium flows into purkinje, this is significant b/c it is reqd for muscle contraction)
Describe phase 3 of the purkinje fibers.
Phase 3 = Repolarization

Calcium channels close.

Potassium flows out RAPIDLY.

(so K+ channels open, leads to full repolarization)
Describe phase 4 of the purkinje fibers.
Phase 4 = diastole

Pacemaker current

(generate own AP... so have pacemaker potential...same ion channels present as in SA node)
Compared to purkinje fiber's phases what can be said about the ventricle cell's phases?
In ventricle cell Phases 0-3 are the same as the purkinje's. BUT phase 4 has a negative potential maintained via potassium channels (inward rectifying).
Generally speaking, what returns the ions that have moved in and out of the cardiac cell during APs?
Ion pumps and exchangers return the ions. This maintains the concentration gradients for each of these ions and returns membrane potential back to baseline.
List the 3 ion pumps and exhangers that return the ions that have moved in andn out of the cardiac cell during an AP.
1. ATP-dependent calcium pump

2. Na+/Ca++ exchanger (3:1)

3. Na+/K+-ATPase pump (3:2)

(see 1st slide pg 9)
The action potentials of cardiac cells have ? periods.
They have refractory periods.
What is an ARP?
Absolute Refractory Period. It is unexcitable to stimulation.
What is an ERP?
Effective Refractory Period. Brief period beyond ARP where stimulation produces weak depolarization that does not propagate.
What is an RRP?
Relative Refractory Period. Stimulation produces a weak AP that does propagate but more slowly than usual.
If another impulse comes along during the ARP what happens?
The cardiac muscle can't generate an AP.
How do the refractory periods protect the heart?
They limit how quickly APs can occur in sequence.
What is a tetanic contraction?
When the muscle lock up in 'contract mode'.
The electrical activity of contraction of heart muscle is recorded by what?
An EKG
What does the P wave represent in an EKG?
Atrial depolarization (and contraction)
What does the QRS wave of an EKG represent?
Ventricle depolarization (and contraction)
What does the T wave of an EKG represent?
Ventricle repolarization.
What is the P-R interval on an EKG?
Time from atrial depolarization to spread of impulse through the AV node.
What is the QT interval on an EKG?
Time from ventricular depolarization to repolarization.
What is the ST segment on an EKG?
End of ventricular depolarization and beginning of ventricular repolarization.
An electrical impulse goes from the ? to the ? only.
From the AV node to the ventricle only.
Why might one refer to K+ as the "teenager" of all the ions?
Always wants to go out...always flows out of cell through channels
What ion channels is responsible for phase 0 in purkinje?
Na+ (fast in for depolarization)
What ion channel is responsible for phase 1 in purkinje?
K+ (slow out)
What ion channel is responsible for phase 2 in purkinje?
Ca2+ (slowly opens...in)
What ion channel is responsible for phase 3 in purkinje?
K+ (flow out)
What are cardiac arrhythmias?
They are disorders of rate and rhythm of the heart, which can occur as the result of abnormal impulse generation or abnormal impulse conduction.
What does radiofrequency ablation do?
Kills tissue that is depolarizing incorrectly.
The drugs used in the tx of arrhythmias are aimed at correcting what?
Aimed at correcting the mxms of abnormal impulse generation and conduction.
Where can arrhythmias originate?
1. Specialized Conduction systems : SA node, AV node, His bundle, Purkinje fibers.

2. Atrial muscle

3. Ventricular muscle
Arrhythmias that develop can cause the heart to do what?
1. Beat too slowly

2. Beat too rapidly

3. Respond to APs that travel down pathways outside the conduction system (genetic mutation to create paths thru atria and ventral or MI)

4. Respond to impulses originating from SA node sites (causes heart to beat out of sync)
All arrhythmias result from alterations in what?
1. Impulse formation (prob. with pacemakers)

2 Impulse conduction (prob. with signal from pacemaker failing to reach non-pacemaker tissue)

3. Both impulse formation and conduction.
List the 3 main categories of arrythmias?
1. Atrial Arrhytmias

2. Supraventricular Tachycardias

3. Ventricular Tachycardias
What are Atrial arrhythmias? List 4 examples and note which is the most common.
Disorders of atrial rhythm or conduction.

1. Sinus tachycardia

2. Paroxysmal tachycardia

3. Atrial fibrillation (more common)

4. Atrial flutter
What are supraventricular tachycardias? List 3 examples.
Disorders of atrial rhythm conduction OR AV node conduction where impulses from atria to ventricles are disrupted.

1. AV node reentry

2. Wolf-Parkinson White syndrome

3. Paroxysmal and acute supraventricular tachycardias
What are ventricular tachycardias? List 4 examples.
Disorders of ventricular rhythm or conduction.

1. Paroxysmal ventricular tachycardia

2. Monomorphic ventricular tachycardia

3. Polymorphic ventricular tachycardia (Torsade de pointes)

4. Ventricular flutter and fibrillation
What is an arrythmia of atrioventricular conduction? List 3 examples.
Disorders of AV node conduction where impulses from atria to ventricles are blocked.

1. First degree AV block

2. Second degree AV block

3. Third degree AV block
What is sinus tachycardia?
Rhythms resulting from abnormalities in impuls rate (in atria). SA node paces at faster rate than it should.
Heart rate is defined as what (relative to QRS complexes).
Distance between two consecutive QRS complexes. This is the beat to beat heart rate.
How is tachycardia defined?
"fast heart"...heart rate of more than 100 beats/min
How is bradycardia defined?
"slow heart"...heart rate of fewer than 60 beats/min.
What is atrial fibrillation?
Rhythms resulting from abnormalities in impulse conduction.
In whom may atrial fibrillation occur?
May occur in patients with coronay artery disease, mitral valve disease, ischemic heart disease, pericarditis, htn, MI, heart failure, digitalis toxicity, hyperthyroidism.
What is the mxm behind atrial fibrillation?
Continous rapid firing of multiple ectopic foci of atrial cells. (instead of SA node impulse)
When the atria pumps too fast what can it not do?
It can't pump the blood.
What are the two main characteristics of Atrial fibrillation?
1. Atrial contractions are chaotic and asynchronized

2. Atrial rate > 400-600 bpm
What are supraventricular tachycardias?
Rhythms resulting from abnormalities in impulse conduction.
What is the mxm of AV nodal reentry?
1. Continous reentry of impulse through AV junction region.

2. Depolarizing stimulus to atria and ventricle each time it passes through.
List 4 characteristics of AV nodal reentry.
1. Palpitations

2. Rate = 170-250 bpm - atria and AV node at high frequency

3. Rhythm = ventricular rhythm very regular

4. P waves hidden, narrow QRS (so short time b/w contraction and relaxation)
Can reentry occur in the ventricles during supraventricular tachycardias?
yes
During supraventricular tachycardias the AV node signal follows what kind of pattern?
A circular pattern called re-entry arrythmia. Atria and ventricles beat out of sync.
What needs to be present for reentry?
Two conducting pathways need to present. Occurs around scar tissue from an MI or by an abnormal genetically inherited pathway for conduction.
Describe reentry process?
1. Two conducting pathways reqd

2. PREMATURE atrial depolarization arrives at AV node

3. One pathway is still refractory (conduction slowed) but other can conduct impulse normally

4. Reentry into atrium occurs when SLOWED impulse undergoes retrograde (backward) conduction into atrium

5. Reentry may occur with coronary artery disease cardimyopathy or MI
What is Wolff Parkinson White Syndrome (WPWS)?
(congenital) Rhythms resulting from abnormalities in impulse conduction.
Describe the mxm of Wolff-Parkinson-White Syndrome?
1. Presence of abnormal accessory pathway connecting atria with ventricle. Bypasses AV conduction.

2. Short circuits the usual delay at AV node.
Describe the characteristics of WPWS?
1. Rate = normal unless Afib present

2. Rhythm = regular - unless afib present

3. Short PR - interval, delta wave, wide QRS complex
What is WPWS?
(supraventricular tachycardia)

Congenital rhythm disorder, observed in young children and adults ages 20-35.

WPWS = Wolff-Parkinson-White syndrome.
What are the two most common tachydysrhtymias seen in WPW syndrome?
Paroxysmal Supraventricular Tachycardia (PVST) and Atrial Fibrillation.
What is the name of the extra path that leads to WPWS?
Bundle of kent
What can be used to get rid of the bundle of kent in WPWS?
KF ablation
What are monomorphic ventricular tachycardias?
Rhythms resulting from abnormalities in impulse conduction. (vent. fib)
What is the mxm of monomorphic ventricular tach.s?
Presence of ectopic focus in either ventricles.
What are the characteristics of monomorphic ventricular tach.s?
1. Rate > 100-250 bpm, lethal beat, interferes with pumping action of heart (rest time for ventricular filling)

2. Rhythm : Essentially regular

3. Bizarre QRS complex via fusion beat
Monomorphic Ventricular tachycardia (V Tach) can be caused by what?
Early or late complication of MI, cardiomyopathy, valvular heart disease, myocarditis, following heart surgery, low blood potassium, pH changes, or insufficient oxygenation, anti-arrythmic medications.
V Tach can deteriorate into what?
Can deteriorate into V fibrillation...Polymorphic VT = Torsade de pointes.
What are torsades de pointes?
Rhythms resulting from abnormalities in impulse conduction. Polymorphic ventricular tachycardias. So the ventricles are contracting erratically. Torsades de pointes translates to "twisting of the points".
How are APs characterized during polymorphic ventricular tachycardias (torsades de pointes)?
Prolonged AP duration caused by early after-depolarizations. (EADs)
How are QT waves characterized during polymorphic ventricular tachycardias (torsades de pointes)?
Prolonged QT wave. Ventricular rate of 150-250 beats per minute.
What is the cause of polymorphic ventricular tachycardias (torsades de pointes)?
Many possible:

1. Congenital

2. Anti-arrythmic meds

3. Calcium channel blockers

4. Digitalis

5. Haloperidol

6. Erythromycin

7. Electrolyte imbalances

8. MI

9. HIV

10. Cocaine
How long will an Early Afterdepolarization continue?
These Self-sustaining APs will continue until medically stopped.
Where do after-depolarizations occur?
In non-pacemaker cells.
After-depolarizations are ? depolarizations.
Spontaneous
After-depolarizations can trigger what?
Self-sustaining APs
Early after-depolarizations occur during what phase of AP? Via what?
During phase 3 of AP via excess Ca2+ flowing into cardiac cell and too littl K+ flowing out. (so increase K+ in ventricles causes contractions)
What is heart block?
Rhythms resulting from abnormalities in impulse conduction. (arrythmias)
A heart block is a failure to transfer what?
Failure to transfer an impulse from the atria to the ventricles (either partially or completely).
What are the degrees of heart block?
1 (not too serous), 2, 3 (very serious)
During primary (1) heart block what will be observed on an EKG?
EKG will have a longer p to r interval.
During complete (level 3) heart block what will be observed on an EKG?
A complete failure of the impulse to move from atria to ventricle.
In complete heart block what is surprisingly still observed on an EKG? What is the reason for this?
QRS waves are still observed. These are generated by the non-pacemaker cells causing the ventricles to depolarize and contract.
A heart block results from a defect in what?
Results from defects in the cardiac conducting system.
During a heart block, the atria do what? What about the ventricles?
The atria beat regularly, but the ventricles occassionally fail to be stimulated.
During heart block impulses between atria and ventricles can be blocked to ? ?.
Can be blocked to varying degrees. For example, once every second or third atrial impulse = 2:1 or 3:1 block.
A Complete heart block is a total disssociation between what?
A total dissociation between atrial and ventricular activity. The impulses from atria to ventricles are not conducted at all.
Describe the difference between the atria impulses and the ventricle impulses during complete heart block?
Atrial impulses from the SA node are normal, but ventricles generate their own, much slower impulses.
Describe the ECG characteristics of a complete heart block?
P waves normal, and QRS and T waves occur regularly, but at a much slower rate, completely independent of P wave rhythm.
List some causes for heart blocks.
1. Scar tissue

2. Fibrosis

3. Medications (B-blockers, digitalis, calcium-channel blocking agents, anti-arrhythmic meds [class 1a]

4. Electrolyte imbalances

5. Cardiac surgery

6. Inflammatory disease
?kalemia can act as a mxm of arrhythmia.
HYPERkalemia can act as a mxm of arrhythmia.
Changes in ECF [K+] can have a profound effect on what?
The heart. Changes in ECF [K+] can alter the concentration gradient between ICF and ECF.
Elevated ECF [K+] does what to the gradient between ICF and ECF? What is the normal situation?
It reduces the gradient b/n ICF [K+] and ECF [K+].

Normally,
ICF [K+] =~ 150mmol/L
ECF [K+] =~ 4mmol/L
An elevated ECF [K+] reduces the gradient b/n ICF and ECF...what does this do to the resting membrane potential? What does this indicate?
The resting membrane potential is reduced. This means the membrane is less neg. inside than normal. This indicates a very excited heart cell.
How does elevated ECF [K+] relate to APs?
The difference in magnitude from normal resting membrane potential to AP is reduced. So K+ can't move out of the cell. The cell can't repolarize. So the AP gets longer. QRS complex gets wider. Essentially the heart contracts but doesn't relax.

This ultimately results in the heart not beating.
Hyperkalemia =

? AP duration =

? ventricular contraction =

? QRS complex =

? sequence cardiac conduction =

? cardiac rhythms
Hyperkalemia =

PROLONGS AP duration =

SLOWING ventricular contraction =

BROADENING QRS complex =

ABNORMAL sequence cardiac conduction =

ABERRANT cardiac rhythms

(she compared the appearance of the heart in this situation to a 'pile of squirming maggots')
Reducing a membrane potential does what to depolarization?
A cell would be ready to depolarize faster.
Is K+ suppose to be higher inside or outside of the cell?
Suppose to be higher ICF.
Normal impulse conduction is highly ordered along a highly specialized what?
Conduction system.
Normal impulse formation is initiated by the what?
The SA node.
Cells that have automaticity include what?
SA node, AV, pacemaker cells, bundle of his, purkinje fibers.
The APs in the AV node and the purkinje fibers have how many different phases? What are these caused by?
5 different phases caused by different ion currents.
In the SA node Phase 4 is the result of what? Phase 0? Phase 3?
Phase 4 = Na+ ions

Phase 0 = Ca2+ ions

Phase 3 = K+ ions
In the purkinje fibers phase 1 is the result of what? Phase 2? Phase 3? Phase 4?
Phase 1 = K+ ions

Phase 2 = Ca2+ ions

Phase 3 = K+ ions

Phase 4 = Na+ ions
ALL arrhythmia result from alterations in what?
ALL result from alterations in impulse generation and conduction or both.
Give two examples of arrhythmias that affect the atria?
Sinus tachycardia and Atrial flutter
Give examples of arrhythmias that affect the ventricles?
Ventricular tachycardia, heart blocks, ventricular defib., torsades de pointes.
List 2 characteristics of Ventricular tachycardias?
1. Increased rate

2. Bizarre QRS complex
List 2 characteristics of Atrial fibrillation.
1. Chaotic contractions

2. No P-wave
List 3 characteristics of AV node reentry.
1. Palpitations

2. Narrow QRS

3. Hidden P-wave