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CardioResp > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Describe what a unstable plaque is.

A
  • AKA Thin Cap Fibroatheroma
  • This type of plaque is more likely to rupture
  • More inflammatory cells
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2
Q

Describe what a stable plaque is.

A
  • AKA Thick Cap Firbroatheroma
  • Less Likely to rupture because more stable
  • Less inflammatory cells
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3
Q

Where does a necrotic core form?

A

The intima layer where the lipid core forms → becomes necrotic

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4
Q

Describe post occlusion recanalization

A

Absorption of the thrombus → creates multiple small lumens for blood flow

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5
Q

What is this a picture of?

A

Thin cap fibroatheroma AKA unstable plaque

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6
Q

What is seen here? What is the white substance in the layers?

A

Thick cap fibroatheromas AKA stable plaque

The white substances in the layers is the necrotic core

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7
Q

What can be seen here?

A

Post occlusion recanalization

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8
Q

For nitroglycerin:

  • What is the class?
  • What are the methods of intake and what effects do they have?
  • What is the mechanism of action?
A
  • Class: Nitrate
  • Can take sublingually, po, or IV
    • PO/SL both work on veins
    • IV works on coronary arteries (hence the Nitro drip post-MI)
  • MOA: Nitrates → NO @ vessel walls → stimulates guanylate cyclase → produce cGMP → dephosphorylating of MLC → venodilation → decreases preload
    • REQUIRE THIOL FOR ACTIVATION
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9
Q

For nitroglycerin:

  • What are some side effects?
  • What are contraindications to worry about?
A
  • Side Effects:
    • Hypotension with reflex tachycardia
    • Tolerance can develop
  • Contraindications
    • Keep in glass bottle (reacts with plastic)
    • No Viagra
      • Inhibits PDE 5, which allows for no way to terminate action of cGMP, causing it to accumulate → fatal hypotension
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10
Q

For isosorbide mononitrate:

  • What is the method of ingestion?
  • What class is this drug?
  • What is the MOA?
  • What are some side effects?
  • What is a contraindication?
A
  • Ingested po
  • Class: Nitrate
  • MOA: NO @ vessel walls → stimulates guanylate cyclase → produce cGMP → dephosphorylating of MLC → venodilation → decreases preload
    • Completely bioavailable – no need for metabolism
  • Side Effects:
    • Hypotension with reflex tachycardia
    • Tolerance can develop
  • Contraindications:
    • No Viagra
      • Inhibits PDE 5, which allows for no way to terminate action of cGMP, causing it to accumulate → fatal hypotension
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11
Q

For -olol drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they indicated in?
A
  • Beta-blockers
  • MOA:
    • Act on beta adrenergic receptors in SA/AV node and vessels
    • Decreases HR, contractility, BP (Increasing O2 delivery by increasing diastolic time)
  • Side Effects
    • Hypotension
    • Beta2 blockage is bad for several reasons:
      • Inhibits glycogenolysis (beta 2)
      • Vasoconstriction
      • Bronchoconstriction
  • Indicated in people with cardiac conditions
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12
Q

For -DHP drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they contraindicated in?
A
  • Calcium channel blockers
  • MOA: Works at vessels: blocks Ca2+ from entering cell → blocking constriction of smooth muscles in vessels → arteodilation
    • *decreases afterload
  • Side Effects: hypotension
  • Contraindicated in: patients taking beta blockers
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13
Q

For non-DHP drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they contraindicated in?
A
  • Class: calcium channel blockers
  • MOA: Works at SA/AV nodes: blocks Ca2+ from entering cells → slows contraction of heart → decreased HR
  • Side Effects: hypotension
  • Conraindicated in people taking beta blockers
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14
Q

For Ranolazine:

  • What class are these drugs?
  • What is their MOA? There are two.
  • Side effects?
  • Contraindications?
A
  • Class: Metabolic modifier (used for patients with angina)
  • MOA:
    1. Inhibits late sodium currents → decreased Ca channel activation → therefore decrease Ca2+ in the cell → less diastolic stress → improved coronary blood flow
    2. Partial fatty oxidation inhibitor → tissues switches to glucose metabolism → creates more ATP
    3. *prolongs QT interval
  • Side Effects: Dizziness, headaches, nausea
  • Contraindications: Metabolized by P450s
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15
Q

For aspirin:

  • What is the class?
  • What is the MOA?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Platelet Aggregation
  • MOA: Irreversibly inhibits COX-1/2 → reduces TXA → prevents platelet aggregation
    • *COX-1 found in platelets
  • Side Effects: GI bleeding/GI irritation
  • Contraindications: Patients taking NSAIDS
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16
Q

For clopidogrel:

  • What is the class?
  • What is the MOA?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Platelet aggregation
  • MOA: Prodrug that inhibits to the P2Y (ADP receptor) → allows for Prostacyclin to have anti-platelet activity
  • Side Effects: rash diarreah, bleeding
  • Contraindication: metabolized by CYP540
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17
Q

For Tenecteplase:

  • What is the class?
  • What is the MOA?
  • In what time period should it be administered following an MI?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Thrombolytic:
  • MOA: Binds to fibrin at clot site → activating plasminogen → degrades fibrous clot
  • Administer within 70 minutes
  • Side Effects: Bleeding Thrombocytopenia, allergy/hypotension/fever
  • Contraindicated: patients with active bleeding
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18
Q

Define what is meant by altered impulse formation and by altered impulse conduction.

A
  • Altered impulse formation = decreased automaticity of SA node
  • Altered impulse conduction = conduction block
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19
Q

Explain the ionic process of automaticity.

A
  • Hyperpolarization of SA nodal cell → If (Na+) channels are activated → sloped phase 4 → threshold potential is reached → L-type Ca++ channels open → depolarization → K+ efflux out of the cell →
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20
Q
  • What are the native pacemaker) and their characteristics (including bpm)?
  • What are the latent pacemaker) and their characteristics (including bpm)?
A
  • Native: SA Node (60-100bpm) because it has faster rate, and its repeated discharges prevent spontaneous firing of other potential pacemaker sites
  • Latent: AV node (50-60bpm), Bundle of His (50-60pm), and Purkinje system (30-40bpm)
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21
Q

How the heart rate controlled autonomically? Inhibited and stimulated pathways?

A
  • Cholinergic stimulation
    • Hyperpolarizes the cell, causing less depolarization
  • Adrenergic stimulation
    • Increases the rate of phase 4 diastolic depolarization
    • Causes less hyperpolarization of pacemaker cells
    • Makes the threshold potential for depolarization more negative (lowers the threshold)
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22
Q

Define normal sinus rhythm.

A
  • Normal Sinus Rhythm = 60-100bpm
    • Pw followed by QRS complex
    • QRS complex preceded by Pw
    • Pw is upright in leads I, II, and III
    • The PR interval is between 0.12 seconds and 0.20 seconds
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23
Q

Define sinus bradycardia and sinus tachycardia.

A
  • Sinus Bradycardia = <60bpm
  • Sinus Tachycardia = >100bpm
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24
Q

What does conduction block mean?

A
  • Normal rate of conduction is slowed or completely blocked which leads to slowed ventricular depolarization or bradyarrhythmias
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25
Q

What are the 4 types of conduction block?

A
  • SA nodal exit block
  • First Degree AV Block
  • Second Degree AV Block
  • Third Degree AV Block
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26
Q

What occurs in the SA nodal exit block?

  • What can it initate?
  • What can it be caused by?
  • What is the symptomatic version of this called?
A
  • SA nodal exit block – problem with automaticity
    • Results in sinus pauses, sinus arrest
    • Initiates escape rhythms that require latent pacemakers
    • Can be caused by old age, structural heart disease, cardiac surgery, increased vagal tone, and drugs
    • If symptomatic, sinus node dysfunction is identified as sick sinus syndrome
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27
Q

What occurs in a first degree AV Block?

  • What is shown on the EKG?
  • Are there symptoms?
A
  • First Degree AV Block – problem with conduction
    • PR interval is prolonged (>.20 seconds) with no dropped QRS complex
    • Asymptomatic
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28
Q

What occurs with second degree AV blocks?

  • What are the two types?
    • What occurs on the EKG for both types?
A
  • Second Degree AV Blocks – problem with conduction
    • AV nodal block – Mobitz I or Wenckeback Block
      • Pw with progressively lengthening PR interval until there is a Pw with no QRS interval
    • His bundle block – Mobitz II
      • Constant PR interval leading up to a Pw with a dropped QRS complex
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29
Q

What occurs with third degree AV block?

  • What do you end up seeing on the EKG?
A
  • Third Degree AV Block – problem with conduction
    • Ventricle and atria are completely dissociated and are marching to the beat of their own drums
      • Not necessarily sequential p-wave then QRS.
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30
Q

What are the 4 main causes of heart blocks?

A
  • AV nodal fibrosis or calcification
  • Acute MI
  • Structural heart disease
  • Cardiac surgery
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31
Q

How can you tell that a pacemaker is being used based on the EKG?

A
  • Sharp vertical spike before the Pw indicates atrial pacemaker
  • Sharp vertical spike before the QRS complex indicates ventricular pacemaker
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32
Q

For plaque rupture:

  • Do they have minimal lipids or are they lipid rich?
  • What is secreted from the necrotic core that makes plaque more vulnerable to rupture? How does this process start?
  • What does plaque rupture cause exposure of and what does it lead to?
A

Plaque Rupture

  • Lipid rich plaques
  • Vulnerable plaque: plaques with increased necrotic cores have higher levels of inflammatory cells, which secrete lipoprotein-associated phospholipase A2 (Lp-PLA2), and this enzyme oxidizes LDL and thinning of the fibrous cap, making the plaque more susceptible to rupture
  • Plaque rupture causes exposure of subendothelial collagen and tissue factor, activating the intrinsic and extrinsic coagulation cascades respectively
  • Many events are asymptomatic or sub-clinical
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33
Q

For plaque erosion:

  • Do they have minimal lipids or are they lipid rich?
  • When/where does this plaque occur?
  • What is the overal pathophysiology?
  • Who is at more of a risk for this condition and why?
A
  • Lipid poor plaques
  • A plaque that causes ridge in the endothelium disrupts the normal laminar flow
  • Disrupted laminar flow causes endothelial cells to stop producing NO, decreasing vasodilator effect
  • Disrupted laminar flow causes endothelial cells to stop producing prostacyclin, which normally inhibits platelet aggregation
  • More likely to be in smokers because it causes an increase in ROS, further damaging the endothelium
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34
Q

What labs can be used to figure out if cardiac necrosis has occured (2 main labs)?

A
  • Troponins T and I – elevated after 3-4 hours post-MI and peaks around 24 hours, and levels stay elevated for up to 2 weeks
  • CK MB – can be used for 2nd MI because levels of this substance rise and fall rapidly
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35
Q

For the following time ranges, provide the general gross appearance of the heart post-MI:

  • 0-20 minutes
  • < 4 hours
  • 4-24 hours
  • 1-3 days
  • 3-14 days
  • 2 weeks to several months
A

Gross Cardiac Changes Post-MI

  • 0-20 minutes: No changes
  • < 4 hours: No changes
  • 4-24 hours: Dark discoloration
  • 1-3 days: Yellow pallor
  • 3-14 days: Red border emerges as granulation tissue forms
  • 2 weeks to several months: White scar
36
Q

For the following time ranges, provide the general microscopic appearance of the heart post-MI:

  • 0-20 minutes
  • < 4 hours
  • 4-24 hours
  • 1-3 days
  • 3-14 days
  • 2 weeks to several months
A

Microscopic Appearance Post-MI

  • 0-20 minutes: ATP depletion, mitochondria swelling, glycogen depletion
  • < 4 hours: Wavy fibers due to inability to contract; edema
  • 4-24 hours: Few neutrophils and coagulative necrosis
  • 1-3 days: Heavy infiltration of neutrophils
  • 3-14 days: Macrophages with formation of granulation tissue
  • 2 weeks to several months: Fibrosis, with increased collagen and “ghost-like” acellular myocytes
37
Q

At what time is this cardiac muscle post-MI?

A

<4 hours: “Wavy” fibers due to inability to contract; edema

38
Q

At what time is this cardiac muscle post-MI?

A

4-24 hours: Few neutrophils and coagulative necrosis

39
Q

At what time is this cardiac muscle post-MI?

A

4-24 hours: Dark discoloration

40
Q

At what time is this cardiac muscle post-MI?

A

1-3 days: Heavy infiltration of neutrophils

41
Q

At what time is this cardiac muscle post-MI?

A

4-14 days: Macrophages with formation of granulation tissue

42
Q

At what time is this cardiac muscle post-MI?

A

4-14 days: Red border emerges as granulation tissue forms

43
Q

At what time is this cardiac muscle post-MI?

A

2 weeks to several months: Fibrosis, with increased collagen and “ghost-like” acellular myocytes

44
Q

At what time is this cardiac muscle post-MI?

A

2 weeks to several months: white scars

45
Q

Name 7 post-MI complications

A
  • Papillary muscle dysfunction: leads to mitral valve regurgitation
  • Heart wall rupture: leads to cardiac tamponade
  • Interventricular septal rupture
  • Arrhythmia: can lead to death
  • Mural thrombosis: can lead to stroke or other embolic event
  • Pericarditis: inflammation of the myocardium can lead to inflammation of the pericardium
  • Cardiac aneurysm: thinning of myocardial muscle/wall can cause high blood pressure in ventricle to push out the wall of the heart
46
Q

What are the causes of sudden cardiac death? (3)

A
  • Post-MI complication of fatal arrhythmia
  • Aortic dissection with rupture
  • Massive pulmonary embolus from akinetic heart wall
47
Q

What are the causes of non-atherosclerotic MIs? (4)

A
  • Congenital (abnormal anatomy of coronary arteries)
  • Inflammation (vasculitis, Kawasaki disease)
  • TTP/HUS/DIC
  • Vasospasms
48
Q

Tachyarrhythmias

Definition?

A

Definition: HR > 100 bpm

49
Q

Supraventricular Tachycardias

A
  • Supraventricular Tachycardias – not dangerous
    • Originate in atrium
    • Narrow QRS <120ms
50
Q

Ventricular tachyarrhythmias

A
  • Ventricular tachyarrhythmias – dangerous
    • Originate in ventricle
    • Wide QRS >120ms
51
Q

Tachyarrhythmias

Symptoms/Complications

A
  • Symptoms
    • Heart racing, palpitations, syncope
  • Complications
    • Stroke, heart failure
52
Q

Mechanisms of

Tachyarrhythmias

A

automaticity, triggered, reentry

53
Q

Explain automiticity

A
  • Increased native pacemaker activity – sinus tachycardia
  • Enhanced latent pacemaker activity – premature atrial contractions, junctional tachycardia
  • Abnormal non pacemaker cells – ventricular, atrial tachycardia
54
Q

Explain triggered abnormal impulse formation

what are the two types?

A
  • Triggered – abnormal activity is stimulated by a preceding depolarization
    • Early Afterdepolarizations (EAD)
      • Repetitive depolarizations during the repolarization phase of cardiac AP due to membrane potential being more positive
        • Caused by channelopathies, drugs, prolonged QT interval
    • Delayed Afterdepolarizations (DAD)
      • Repetitive depolarizations after repolarization phase of cardiac AP due to HIGH intracellular Ca2+
        • DIGOXIN toxicity
55
Q

Explain Reentry

What are the required conditions?

A
  • Reentry – formation of abnormal impulse conduction circuits
    • Required conditions
      • Initial premature/abnormal impulse/beat
      • Unidirectional block
        • Functional: interaction with cells still in refractory period (can be caused by certain anti-arrhythmics)
        • Fixed: interaction with cells affected by fibrosis or myocardial scar
      • 2 pathways with different conduction properties
        • 1 with faster conduction or a slower refractory period (normal – non-injured tissue) i.e. alpha
        • 1 with slower conduction or faster refractory period (unidirectional blocked – damaged tissue) i.e. beta
56
Q

Sinus Tachycardia

Description & Mechanism

A
  • Description: sinus rhythm with bpm >100
  • Mechanism: increased automaticity
57
Q

Premature Atrial Contractions/Beats

Description & Mechanism & Tx

A
  • Description: early than expected p-wave
  • Mechanisms: automaticity, triggered, reentry (occurring outside of SA node)
  • Treatment: lifestyle changes or beta-blockers if symptomatic
58
Q

Paroxysmal SVT

Description & Mechanism

A
  • Description:
    • Sudden onset and termination of arrhythmia
    • Atrial rates of 140-250 bpm
    • Narrow QRS complex
  • Mechanism: reentry
59
Q

AV nodal reentrant tachycardia (AVNRT)

EKG & Mechanism & Tx

A
  • Mechanism: Reentry via dual AV node pathways with functional unidirectional block creation reentry loop within node –> repetitive depolarizations –> tachycardia
  • Treatment: block AV node, ablation (stimulates vagal tone), antiarrhythmics
  • EKG: no p waves
60
Q

Atrioventricular reentrant tachycardia (AVRT)

Mechanism & Tx

A
  • Mechanism: Reentry pathway where one pathway in from the AV node and the other by congenital accessory pathway (abnormal band that connects atrial to ventricular tissue)
  • Treatment: : block AV node, ablation
  • most commonly associated with Wolff-Parkinson-White syndrome
61
Q

Ventricular Pre-Excitement/ Wolff Parkinson White Syndrome (WPW)

Two types?

A
  • Accessory pathway known as Bundle of KENT
    • Manifested (bidirectional) – slurred upward QRS (delta wave) EKG
      • Can induce V-fib
    • Concealed (unidirectional) – normal EKG
62
Q

Focal Atrial Tachycardia

Description & Mechanism & Tx

A
  • Description: abnormal p-waves with SVT
  • Mechanism: reentry or automaticity of non-pacemaker atrial tissue
  • Treatment: underlying cause (can be elevated sympathetic tone)
63
Q

Atrial Flutter

Description & Mechanism & Tx

A
  • Description: Atrial rates of 180-350 bpm resulting in saw-tooth pattern EKG
  • Mechanism: Reentry circuit that around the ring of the tricuspid valve (isthmus) not effecting AV node
  • Treatment: AV nodal blockers, ablation, cardioversion
64
Q

Atrial Fibrillation

Description, Mech, and Tx

A
  • Description: no discrete p-waves with varying R-R intervals
  • Mechanism: automatic (pulmonary veins) and reentry mechanisms
  • Treatment: ablation
    • Rate control: AV nodal blockers – beta blocker, ca2+ channel blocker, digoxin
    • Rhythm control: anti-arrhythmics
65
Q

Ventricular Tachycardia

Description, Mech, and Tx

A
  • Description: series of 3 or more premature ventricular beats – wide QRS complex with tachycardia
  • Mechanism: usually re-entrant from fibrosis or prior MI
66
Q

Ventricular Tachycardia

Types

A
  • Sustained: more than 30 seconds with severe symptoms
    • Treatment: Cardioversion, anti-arrhythmics
  • Benign: rare exception
  • Torsade de pointes: associated QT intervals with polymorphic QRS complexes
    • Mechanism: Triggered – early afterdepolarizations
67
Q

Ventricular Fibrillation (life threatnening)

Description, mech, & tx

A
  • Description: chaotic rhythm with no discrete p-waves and no contraction/cardiac output
  • Mechanism: initiated by an episode of V-tachycardia – reentry circuit becomes overwhelmed
  • Treatment: ACLS, defibrillator
68
Q
A

Premature Atrial Contractions/Beats

69
Q
A

Ventricular Pre-Excitement/ Wolff Parkinson White Syndrome (WPW)

70
Q
A

Atrial Flutter

71
Q
A

Atrial Fibrillation

72
Q
A

Ventricular Tachycardia

73
Q
A

Torsade de pointes

74
Q
A

Ventricular Fibrillation

75
Q

What would ealry afterdepolarization look like?

A
76
Q

What would delayed afterdepolarization look like?

A
77
Q

Adenosine

MOA? Effects? Use? Adverse Effects?

A

MOA: Blocks Ca++ channels at SA and AV nodes

Effects:

  • Prolonged QT interval because prolonged Phase 0 depolarization

Use:

  • Acute reentrant supraventricular tachycardia

AE:

  • Bronchospasm
78
Q

Digoxin

MOA? Effects? Use? Adverse Effects?

A

MOA: Blocks Na+/K+ ATPase

Effects:

  • Increases vagal activity
  • Slows AV conduction

Use:

  • AV reentrant arrhythmias
  • Chronic AFIB

AE:

79
Q

Non-DHP CCBs (verapamil and diltiazem)

Type? MOA? Effects? Use? Adverse Effects?

A

Type: IV

MOA: Blocks calcium channels at SA and AV nodes

Effects:

  • Prolonged Phase 0 depolarization in nodal tissue
  • Prolonged QT interval

Use:

  • AFIB

AE:

  • Bradycardia
  • Hypotension
80
Q

Dofetilide

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks K+ channels

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Continuing atrial tachycardia after ablation

AE:

  • QT prolongation – contraindicated for hypokalemia
81
Q

Sotalol

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks K+ channels and beta-blocker

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Atrial and ventricular tachycardia

AE:

  • Bradycardia, bronchospasm
82
Q

Amiodarone

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks Na+, Ca++, and K+ channels

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Sustained life-threatening arrhythmias

AE:

  • Thyroid issues
  • “Smurfism”
83
Q

Beta Blockers

Type? MOA? Effects? Use? Adverse Effects?

A

Type: II

MOA: Blocks beta-adrenergic receptors

Effects:

  • Slows conduction velocity
  • Decreases automaticity, thus increasing PR interval (due to slowed AV conduction)

Use:

  • Atrial tachycardia because slows conduction at AV node
  • Ca++ dependent arrhythmias at AV and SA nodes

AE:

84
Q

Flecainide

Type? MOA? Effects? Use? Adverse Effects?

A

Type:Ic

MOA: Na+ channel blocker (potent)

Effects:

  • AV Node: prolonged refractory period
  • Atrial, ventricular, Purkinje fibers: prolonged Phase 0 with no change in refractory period
  • Raises depolarization threshold

Use:

  • Ventricular arrhythmias
  • AFIB
  • Paroxysmal supraventricular arrhythmias

AE:

  • Metallic taste
  • Visual disturbances
85
Q

Quineidine

Type? MOA? Effects? Use? Adverse Effects?

A

Type:Ia

MOA:Na+ channel blocker and K+ rectifier channel blocker

Effects:

  • Prolonged Phase 0 depolarization and prolonged Phase 3 repolarization
  • QT and QRS prolongation
  • Raises depolarization threshold

Use: Historic drug for reentrant arrhythmias

AE:

  • QT prolongation – Torsades de Pointes
  • Anticholinergic properties
  • Cinchonism – tinnitus, dizziness, blurred vision, headache,

CardioResp (14 decks)

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