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Prehospital Pharmocology > EMS Pharmacology Test 1 > Flashcards

EMS Pharmacology Test 1 Flashcards

1
Q

acute coronary syndromes

A

refers to a group of clinical diseases occurring as a result of myocardial ischemia.

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2
Q

Name the different types of acute coronary syndromes

A

unstable angina, stable angina, non ST segment elevation myocardial infarction, ST segment elevation myocardial infarction.

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3
Q

stable angina (SA)

A

chest discomfort that is transient, episodic, resulting from myocardial ischemia.

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4
Q

Describe an SA attack

A

discomfort is predictable, reproducible, constant, resolves spontaneously with rest and nitroglycerine. Attacks can occur from physical and psycho. stress, exertion, anemia, and dysrhythmias.

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5
Q

ischemia

A

deprivation of oxygen

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6
Q

angina attacks typically occur from

A

physical and psychological stress, exertion, anemia, and dysrhythmia

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7
Q

Unstable angina pectoris usually occurs (vascular)

A

when a partially occluding thrombus produces symptoms of ischemia.

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8
Q

NSTEMI

A

acute process in which ischemia effects the myocardium with no elevation in ST segment on the ECG. (Symptoms identical to UA)

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9
Q

UA

A

Angina occurring when patient is at rest.

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10
Q

How does UA differ from NSTEMI

A

In NSTEMI cardiac enzymes will be elevated which indicates necrosis of the cardiac tissue.

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11
Q

STEMI

A

actual infarction of the cardiac tissue secondary to oxygenation deprivation. Cell death occurs and there is permanent, irreversible damage to the cardiac muscle cells.

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12
Q

Why should Oxygen be administered to ACS patients?

A

When a patient as angina pectoris, the oxygen demand exceeds the body’s ability to deliver adequate oxygen to the heart muscle. Providing oxygen loads the red blood cells for delivery to the heart muscle.

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13
Q

What is the mechanism of action of oxygen along with the side effects?

A

Oxygen facilitates cellular energy metabolism. Side effects can cause decreased LOC and respiratory depression in patients with COPD.

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14
Q

What are the anti platelet drugs indicated for ACS patients?

A

aspirin and plavix

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15
Q

State the mechanism of action and the side effects of aspirin.

A

Irreversibly inhibits platelets. Prevents the formation of thromboxane A2 which causes platelets to clump together and for plugs that cause obstruction or constriction of small coronary arteries. Anaphylaxis, bronchospasm, and GI bleeding.

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16
Q

State the mechanism of action and the side effects of Plavix/Clopidogrel

A

Thienopyridines (Plavix) are more potent platelet inhibitors than aspirin. Preferred agent of the anti platelets because of its rapid onset. Nausea, abdominal pain, bleeding.

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17
Q

What is the mechanism of action and the side effects of nitrates?

A

Nitrates decrease myocardial preload and subsequently afterload. They increase vein capacity and vein pooling which decreases preload and oxygen demand. Headache and hypotension.

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18
Q

What is the mechanism of action and what are the side effects of morphine?

A

Morphine is a potent opioid analgesic with weak sympathetic blockade, systemic histamine release, and anxiolysis. Side effects include respiratory depression, hypotension, and allergic reaction. (Tends to make people itchy.)

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19
Q

When is morphine appropriate for an ACS patient? Why?

A

When the patient is unresponsive to NTG or has recurrent symptoms despite anti ischemic therapy. Morphine is good because it decreases pain which calms the patient down, reducing oxygen consumption.

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20
Q

What are Beta Blockers?

A

Drugs that bind to beta adrenoreceptors and thereby block the bonding of catecholamines to these receptors. Inhibit normal sympathetic effects that act through these receptors.

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21
Q

What types of ACS are beta blockers effective in treating?

A

v fib, increased contractility, heightened myocardium oxygen demand.

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22
Q

What are the cardiac effects of beta blockers?

A

decreases contractility, decreases relaxation rate, decreases heart rate, decreases conduction velocity.

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23
Q

What is the vascular effect of beta blockers?

A

smooth muscle contraction. (mild vasoconstriction.)

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24
Q

inotropy

A

agent that alters the force of muscle contractions

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25
lusitropy
myocardial relaxation
26
chronotropy
changes the heart rate
27
dromotropy
affects the conductivity of a nerve fiber
28
What is the mechanism of action and the side effects of Metoprolol.
(Beta blocker) Selective inhibitor of beta 1 receptors. Competitively blocks beta 1 receptors with little to no effect on beta 2 receptors at doses less than 100 mg. Side effects are bradycardia, bronchospasm, and hypotension.
29
What are the three types of anticoagulants discussed in class?
1) Heparin 2) Glycoprotein 2b/3a inhibitors 3) Direct thrombin inhibitors
30
How does unfractionated heparin work?
Binds to antithrombin III, forming a complex that is able to inactivate factor II (thrombin) and activated FACTOR X (10). This prevents the conversion of fibrinogen to fibrin thus inhibiting clot formation.
31
True or False, Heparin has anticoagulant properties?
False. Heparin by itself has no anticoagulant properties, it indirectly effects thrombin (responsible for fibrinogen to fibrin) which inhibits clot formation.
32
What are the potential side effects of heparin?
bleeding, HIT, and allergic reactions
33
What is HIT?
heparin induced thrombocytopenia. Thrombocytopenia is a disorder where there is an abnormally low amount of platelets.
34
What is low molecular weight heparin?
They have a small effect on the activated partial thromboplastin time and strongly inhibit factor Xa. Used as an anticoagulant.
35
Enoxoparin
(LMWH) Effects the activated partial thromboplastin time and strongly inhibits factor Xa. Side effects include Bruising around injection side, bleeding, HIT.
36
Describe glycoprotein 2b/3a inhibitors
Block the glycoprotein 2b/3a receptor, the binding site for fibrinogen. Reversibly blocks platelet aggregation and prevents thrombosis.
37
Eptifibatide
Glycoprotein 2b/3a inhibitor. Reversibly prevents fibrinogen from binding thus blocking platelet aggregation and thrombosis. Side effects include bleeding, hypotension, anaphylaxis.
38
Direct thrombin inhibitors
acts as a specific and reversible thrombin inhibitor.
39
Bivalirudin
Direct thrombin inhibitor, that is used for STEMIs. Binds to thrombin bound to clots and thrombin circulating. Side effect is bleeding.
40
What are the examples of ACE inhibitors discussed in class?
lisinopril, enalapril, captopril
41
What is the mechanism of action and the side effects of ACE inhibitors?
Decrease preload and afterload by inhibiting the conversion of angiotensin 1 to angiotensin 2. This causes lower levels of angiotensin 2 which increase renin and decrease aldosterone. Aldosterone directly increases preload. Side effects include category X (no for pregnant patients) cough, angioedema, and hyperkalemia.
42
Why is angioedema a concern when giving ACE inhibitors?
Angioedema is when the airway swells shut, there is no known reason for it. It can happen the first time the patient takes the medication or the 500th time.
43
HMG-CoA reductase inhibitors
Prevent cholesterol from being formed. Reduce the level of LDL LDVL and triglycerides in circulation while increasing the amount of HDL.
44
Simvastatin
HMG-CoA reductase inhibitor. Cholesterol inhibitor. Side effects include abdominal pain and rhabadomyolysis. (muscle breakdown.)
45
What are the two types of Reperfusion therapy?
Fibronylitics and PCI
46
Reperfusion therapy
Restores blood flow to blocked arteries and is most beneficial in STEMIs. Most effective way to preserve myocardial function and limit infarct size.
47
Fibronylitics
Clot busters. They dissolve clots by converting plasminogen to plasmin, an enzyme that digests the fibrin meshwork holding clots together. Alteplase is the most effective when initiated 4 to 6 hours after onset.
48
PCI
Percutaneous Coronary Intervention. (Balloon angioplasty.) Balloon inserted and inflated to push plaque against the walls of the artery, making a wider channel for blood flow.
49
CABG
Coronary artery bypass graft surgery. Arteries and veins are taken from somewhere else in the body and attached to the myocardium to bypass blocked vessels and increase blood flow to the heart.
50
What causes a dysrhythmia?
result from alterations of electrical impulses that regulate cardiac rhythm.
51
arrhythmia
absence of cardiac rhythm
52
Describe normal conduction of the heart
Impulses originate in SA node and travel through the AV nodes to reach the ventricles. Impulses that arrive at the AV nodes are delayed before reaching the ventricles. The His- purkinje system conducts impulses rapidly throughout the ventricles.
53
Fast potentials and slow potentials
The heart employs these two types of action potentials., fast potentials occur in the His-P system, the ventricles and the atria. The slow potentials in the AV and SA node.
54
Phase 0 of cardiac cycle
Generated by rapid influx of sodium. Fast potentials generate fast depolarization.
55
Phase 1 of cardiac cycle
Fast potentials. Calcium enters myocardial cells, thereby producing contraction.
56
Phase 2 of cardiac cycle
Fast potential repolarization generated by rapid extrusion of potassium
57
Phase 3 of cardiac cycle
Slow potentials. Slow depolarization caused by slow influx of calcium.
58
Phase 4 of cardiac cycle
Spontaneous depolarization confers the automaticity. (REST) Normally determines the heart rate.
59
P wave
Occurs in atria. Caused by depolarization of the atria.
60
QRS complex
Caused by the depolarization of the ventricles.
61
Which tachycardias have atrial origin?
supraventricular tachycardia, Atrial fibrillation, sinus tachycardia
62
Which tachycardias have ventricular origin?
ventricular ectopy, ventricular tachycardia, ventricular fibrillation
63
Which drug is used for supraventricular tachycardia?
Adenosine
64
What is adenosine's effect?
Slows the impulse formation in the SA node, slows conduction time through the AV node. Interrupts pathways through the AV node. Depresses left ventricular function.
65
Which three drugs are recommended for atrial fibrillation?
diltiazem, verapamil, metoprolol
66
How does diltiazem work and what are it's side effects?
Blocks the calcium influx during depolarization of cardiac and vascular smooth tissue. Decreases peripheral vascular resistance and causes relaxation of vascular smooth muscle resulting in the decrease of systole and diastole. Bradycardia, hypotension and heart block.
67
How does verapamil work and what are it's side effects?
Blocks the flux of calcium into arterial smooth muscles. Reduces vascular resistance and promotes selective vasodilation of peripheral arteries. Inhibits coronary spasm and relaxes arteriole muscles. Side effects include bradycardia and heart block.
68
How does one treat sinus tachycardia?
Treat the cause: anxiety, stress, infection/fever, dehydration
69
Describe Class 1 of the V-W scheme
Sodium channel blockers, slow the impulses in the ventricles, atria, and his-p system. (Largest class of antiarrythmics)
70
Describe Class 2 of the V-W scheme
Beta Blockers, reduce calcium entry and depress phase 4 depolarization.
71
What three effects do beta blockers have on the heart?
SA node, reduce automaticity. AV node, they slow conduction velocity, in atria and ventricles they reduce contractility.
72
Describe class 3 of the V-W scheme
Potassium channel blockers. Drugs that delay repolarization.
73
Describe class 4 of the V-W scheme
Calcium channel blockers, reduce automaticity in the SA node, delay conduction in the AV node, reduce myocardial contractility.
74
Which 2 drugs classify as "other" on the V-W scheme?
Adenosine and digoxin. surpress dysrhythmias by decreasing conduction through the AV node and reducting automaticity of the SA node.
75
What is the goal of treatment with antidysrhythmic drugs?
Terminate the dysrhythmia
76
What is the important concept of treatment with antidysrhythmic drugs?
Treat only if there is clear benefit, and then only if the benefits outweigh the risks.
77
What are the class 1 A drugs?
procainamide quinidine
78
What is the class 1B drug?
LIDOCAINE! Accelerates repolarization
79
What are the class 3 drugs and what do they do?
Block the potassium channels. AMIODARONE, dronaderone, bretylium
80
Class IV drugs
block the calcium channels, effects identical to beta blockers. Example diltiazem, verapamil.
81
What drugs are recommended for ventricular tachycardia?
amiodorone, lidocaine, procainamide. Choose amiodorone after the SHOCK!
82
Torsades de Pointes
Give magnesium, it is an electrolyte that stabilizes the heart.
83
What do you do in v fibrillation?
Shock immediately and then give amiodarone.
84
In fine v fib what is happening?
The heart is not getting ATP, it is almost asystole.
85
What are the bradycardia rhythms?
1st degree AV block, 2nd degree AV block (1 and 2), 3rd degree AV block, PEA, asystole.
86
What drugs should be considered for bradycardic dysrhythmias?
atropine sulfate, epi, dopamine, vasopressin
87
What is the effect of atropine sulfate and the side effects?
Speeds up the heart. Parasymatholytic. Inhibits the smooth muscles and glands. Decreased secretions.
88
What is the effect of epinephrine and the side effects?
Effectively causes vasoconstriction, induces bronchial smooth muscle relaxation. Vasoconstriction, hypertension, anxiety, tremors, chest pain.
89
What is the effect of dopamine?
Increases heart contractility and blood pressure. Side effects include hypertension, vasoconstriction, and dysrhythmias.
90
Describe PR complex in 1st degree AV block
PR complex is elongated
91
Describe PR complex in 2nd degree AV block 1
Progressive lengthening of the PR interval occurs from cycle to cycle, then one P wave is not followed by QRS. (dropped beat) Wenkeback 1
92
Describe PR complex in 2nd degree AV block 2
Some P waves not followed by QRS complex. (more than one)
93
Describe the Rhythm of 3rd degree AV block
both atrial and ventricular rhythm are are regular but independent. (dissociated) Ps and Qs don't agree.
94
In which brady dys. situations do you use atropine?
First degree and second degree type 1.
95
What do you give a patient with PEA?
epinephrine.

Prehospital Pharmocology (2 decks)

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