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PSA PMCOL 303 > Cardiotoxicity > Flashcards

Cardiotoxicity Flashcards

1
Q

What is direct cardiotoxicity?

A

Direct effects on the myocardium.

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2
Q

What is indirect cardiotoxicity?

A

Indirect effects through vasculature.

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3
Q

What are CV risk factors?

A

Preexisting disease, HTN, age.

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4
Q

What is the pathophysiology of reversible damage?

A

Cellular dysfunction (mito, protein).

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5
Q

What are the diagnostic criteria for reversible damage?

A
  • No injury marker release
  • Reversible contractile dysfunction
  • Reversible arterial hypertension
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6
Q

What are the manifestations of reversible damage?

A
  • Temporary contractile dysfunction
  • Vasoplastic angina
  • Arterial hypertension
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7
Q

What are the results of reversible damage?

A

Normalization of CV function.

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8
Q

What is the pathophysiology of non-reversible damage?

A

Cell loss (necrosis/apoptosis).

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9
Q

What are the diagnostic criteria for non-reversible damage?

A
  • Injury marker release
  • Progressive contractile dysfunction
  • Cardiac remodeling
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10
Q

What are the manifestations of non-reversible damage?

A
  • Cardiomyopathy/HF
  • MI
  • Thrombosis
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11
Q

What are the results of non-reversible damage?

A

Progressive CV toxicity.

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12
Q

What are the effects of cardiotoxicity?

A

1) Cardiac conduction and dysrhythmias - abnormalities in repolarization
2) Systolic/diastolic dysfunction - reduction in ventricular ejection
3) Cardiac structural remodeling - fibrosis
4) Cardiomyopathies - heart failure
5) Systemic and pulmonary vascular dysfunction and altered hemodynamics
6) Hemostasis and thrombosis

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13
Q

Why is the heart vulnerable to injury?

A
  • Limited proliferative capacity of myocytes
  • Promotion of fibroblasts - proliferation/remodeling after injury
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14
Q

What are the cells of the heart?

A
  1. Cardiomyocytes
  2. Endothelial cells
  3. Epicardial cells
  4. Fibroblast
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15
Q

How can we tell there is cardiotoxicity (biomarkers)?

A
  1. Changes in myocardial strain and biomarkers
  2. Assessment of cardiac function
  3. Determination of coronary blood flow reserve, stroke work, VO2 max
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16
Q

What is the most useful tool for diagnosis of cardiac injury?

A

Echocardiography (ECG) is most useful due to safety, availability, reliability, low cost.

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17
Q

What are the markers of cardiac injury?

A

CK-MB (creatine kinase), Troponins (I and TnT), Lactate dehydrogenase (LDH), BNP (B-type natriuretic peptide).

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18
Q

How can we detect markers to look for cardiac injury?

A
  1. Onset of myocardial infarction
  2. Plasma membrane of necrotic myocytes becomes leaky
  3. Molecules leak out cells into circulation
  4. These molecules can be used as biomarkers for diagnosis of MI.
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19
Q

What is reperfusion?

A

Reestablishment of blood flow.

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20
Q

What is ejection fraction?

A

Measurement of the volume percentage of left ventricular contents ejected with each contraction.

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21
Q

How can ejection fraction be measured?

A
  • Echocardiogram (echo) - this is the most common way to check your EF
  • Magnetic resonance imaging (MRI) scan of the heart
  • Nuclear medicine scan (multiple gated acquisition [MUGA]) of the heart.
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22
Q

What is the range of EF for a healthy adult?

A

55% to 70%, ~65%, less than 40% HF.

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23
Q

What is HFpEF?

A

Heart failure with preserved ejection fraction (diastole).

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24
Q

What is HFrEF?

A

Heart failure with reduced ejection fraction (systole).

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25
What is the ejection fraction formula (%)?
(Amount of blood pumped out of the ventricle) / (Total amount of blood in ventricle).
26
What drugs can cause changes in vital signs (toxic syndromes)?
- Sympathomimetics - Anticholinergics - Cholinergics - Opiates - Sedatives
27
What causes heart rate abnormalities due to xenobiotics?
Xenobiotics can directly cause dysrhythmias or cardiac conduction abnormalities usually affecting the cell membranes or indirectly via metabolic effects.
28
What causes bradycardia?
Caused by effects on central or peripheral NS, generation (pacemaker cells) or conduction system, changes to sympathetic outflow, enhanced vagal tone, altered calcium handling.
29
What is bradycardia?
Slow heart rate.
30
What is tachycardia?
Fast heart rate.
31
What is the most common form of tachycardia?
Sinus tachycardia.
32
How does atropine cause tachycardia?
Rise in HR without inhibitory effect of vagal influence.
33
What are the direct effects leading to tachycardia?
Beta-adrenergic agonism.
34
What are the indirect effects leading to tachycardia?
Response to hypotension, hypoxia.
35
What can cardiac poisons cause?
An increase or decrease of HR.
36
What is propafenone?
Sodium channel blocker.
37
What does sodium bicarbonate do?
Increases pH.
38
What is wide QRS?
- Abnormally long duration (>120m sec) - Slowing of ventricular depolarization - Decrease conduction velocity, prolong QT and asystole (no heartbeat).
39
What is substantial QRS prolongation?
One of the most life-threatening EEG warning indicators.
40
What is the main therapeutic treatment for long QRS?
Sodium bicarbonate (only works with sodium channel blockers, via the competitive displacement of binding sites, decreases affinity of propafenone by increasing the pH).
41
What drugs trigger widening of QRS complex?
- Antiarrhythmics (ie., Class Ic propafenone, Class III amiodarone) - TCA's (amitriptyline) - Antipsychotics (phenothiazines, haloperidol) - Calcium channel blockers - Sodium channel blockers - Electrolyte abnormalities.
42
What is bupropion?
Inhibits GAP junctions that inhibit AP movement and can lead to long QRS.
43
What does the P wave represent?
Atrial depolarization.
44
What does the QRS complex represent?
Ventricular depolarization.
45
What does the T wave represent?
Ventricular repolarization.
46
What is the (hERG) human Ether-a-go-go Related Gene?
Encodes pore forming subunit of the rapidly activating delayed rectifier cardiac K+ channel (IKr) (KCNH2).
47
What is hERG?
Voltage-gated potassium channel that contributes to repolarization of cardiac action potential.
48
How is the hERG channel involved in long QTc syndrome?
- Common cause of withdrawal or restriction of drugs is the prolongation of the QT interval - Major effect is loss-of-function (block channel) - Arrhythmias (torsades de pointes).
49
Why are ventricular arrhythmias lethal compared to atrial arrhythmias?
No passive movement of blood like we see in atrial arrhythmia.
50
What is the management of long QTc?
- Correct underlying electrolyte - Asymptomatic - Magnesium sulfate - TdP (defibrillation, MgSO4, isoproterenol, overdrive pacing).
51
What are the mechanisms of drugs that cause hypertension?
1. CNS sympathetic over-activity 2. Increased myocardial contractility 3. Increased peripheral resistance.
52
What are the mechanisms of drugs that cause hypotension?
1. Decreased peripheral resistance 2. Decreased myocardial contractility 3. Dysrhythmias 4. Depletion of intravascular volume.
53
What is more dangerous, hypertension or hypotension?
Hypotension.
54
What do xenobiotics that impact cardiac contractility result in?
- Ejection fraction - Cardiac output - Blood pressure.
55
What are the mechanisms of cardiotoxicity?
Normally multifactorial and/or remain unknown.
56
What are the influencers of contractility (inotropy)?
- Sympathetic NS - Preload - Heart rate - Parasympathetic NS - Catecholamines - Afterload.
57
What drug classes are involved in cardiomyopathy?
- Cardiac glycosides - Beta agonists - Calcium sensitizers - Sympathomimetics.
58
What is an example of a cardiac glycoside and its MOA?
Digoxin, block Na+/K+ ATPase.
59
What is an example of a beta agonist and its MOA?
Dobutamine, isoproterenol, activate beta1AR.
60
What is an example of a calcium sensitizer and its MOA?
Levosimendan, increase troponin affinity for calcium.
61
What is an example of a sympathomimetic and its MOA?
Cocaine, increase catecholamines.
62
What do beta blockers do?
Develop hypotension due to bradycardia and reduced contractility.
63
What is the difference between beta 1 and beta 2?
Increased peripheral vascular resistance (bronchospasm).
64
What do beta blockers interfere with?
Glycogenolysis and gluconeogenesis but rarely cause hypoglycemia.
65
What are the unique properties of beta blockers?
- Intrinsic sympathomimetic activity (ISA) - Membrane stabilizing activity (MSA) sodium channel blockade.
66
What do calcium channel blockers do?
Develop hypotension due to bradycardia and reduced contractility, decreased inotropy, decreased chronotropy (conduction blocks and delays), decreased vascular resistance.
67
What are dihydropyridines?
Vascular selective (due to slower opening/closing channels).
68
What are non-dihydropyridines?
Myocardium selective (due to faster opening/closing channels).
69
How are calcium channel blockers metabolized?
- CYP3A4 (drug interactions) - Protein bound (high distribution, not good for ECMO).
70
What happens in DHP OD?
Initial baroreceptor mediated reflex tachycardia.
71
What does amlodipine cause?
Profound vasoplegic shock resistant to vasopressor support.
72
What is a hyperglycemia side effect of calcium channel blockers?
Due to effect of decreased calcium influx in pancreatic cells limiting insulin release.
73
Which is more toxic, CCB or BB?
CCB, more cardiogenic shock and vasogenic shock.
74
What xenobiotics cause a combination of bradycardia and hypotension?
- Alpha2 adrenergic agonists - Beta blockers - Calcium channel blockers - Cardioactive steroids - Cholinergic agents - Imidazolines - Opioids - Withdrawal from sympathomimetic use.
75
What is loperamide?
- Antimotility opioid agonist to mu opioid receptor - Abused to attain euphoric state.
76
What can OPR stimulation do?
- Inhibit beta1 and beta2 adrenergic receptor activity in cardiomyocytes - Restrict inotropic and chronotropic effects - interfering with excitation contraction coupling.
77
What predisposition can lead to development of LQT and TdP?
Cardiac dysrhythmia.
78
What does cocaine affect?
CVS 2 major pathways (sympathetic output and local anesthetic effect).
79
What is believed about cocaine usage?
- Provokes AMI - Increases myocardial oxygen demand (ischemia) - Coronary vasoconstriction and vasospasm, accelerate atherosclerosis and thrombosis.
80
What are the key components of cannabis?
THC and CBD.
81
What are the key receptors for cannabis?
CB1R and CB2R.
82
What may consequences of cannabis toxicity stem from?
- Inhalation of combustion products - Direct effects of THC - Indirect effects of THC related to acute anxiety, hallucinations and/or psychosis.
83
Where are cannabinoid receptors found?
Directly on the heart and in the vasculature.
84
What are the CV adverse effects from cannabis?
- Sudden and unexpected strain on the body with hallucinations - Stimulated SNS (increased tachycardia, HTN, catecholamine) - THC primarily responsible.
85
What is cardio-oncology?
- Rapid development of anticancer treatments - Aging population - more often CVD and cancer in the same patient - Use of multiple chemotherapeutic agents - Increased survivorship.
86
What are examples of chemotherapeutics that may influence cardiac function?
- Anthracyclines (doxorubicin, epirubicin, idarubicin) - Non-anthracyclines (mitoxantrone, mitomycin, bleomycin) - Topoisomerase II inhibitors (etoposide) - HER2 - Antibody (Trastuzumab) - HER2 - Tyrosine Kinase inhibitors (TKI).
87
What is doxorubicin?
- Quinone containing anthracycline antibiotic - Treats a variety of cancers - Clinical use is associated with increased risk of cardiomyopathy or congestive heart failure - Antitumor properties involve inhibition of both topoisomerase and DNA synthesis.
88
What are the cardiomyopathy effects associated with doxorubicin?
Increase LDH, CPK, troponin T Loss of myofibrils Cytoplasmic vacuolization Mitochondrial damage Oxidative stress Reduced systolic function T-wave flattening ST-T wave changes Decrease voltage Tachycardia.
89
What are the long-term CV effects of doxorubicin?
- Cardiomyopathy - Congestive heart failure.
90
What is COX1?
Constitutive.
91
What is COX2?
Inducible.
92
What are NSAIDs?
Nonsteroidal anti-inflammatory drugs, non-specific to COX.
93
What is COXIB?
COX-2 inhibitor.
94
What does PGE2 do?
Inflammatory response.
95
What does PGI2 do?
Inhibits platelet adhesion, vasodilator (prostacyclin).
96
What does TXA2 do?
Vasoconstrictor, inflammatory response, produced by activated platelets and is prothrombotic, increases platelet aggregation (thromboxane).
97
What are the cardiovascular effects of COXIB?
- Promoted thrombosis (inhibit COX2 derived PGI2) - Platelet aggregation (inhibit COX2 block suppression of thrombin - augment platelet activation) - Gradual - constant inhibition of neutrophils and platelets - promotes initiation and early progression of atherosclerosis - Does not inhibit COX1 (TXA2 effects are exaggerated, vascular tone, cardioprotection).
98
What happens with overall inhibition of COX2 derived metabolites?
Will augment the response to pro-thrombotic and hypertensive stimuli.
99
What is myocarditis?
Inflammation of the myocardium.
100
What is classic myocarditis?
Refers to inflammation of the heart muscle occurring as a result of exposure to either discrete external antigens or internal triggers.

PSA PMCOL 303 (7 decks)

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