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Pharmacology 2 > Antidysrhythmics and anticoagulants > Flashcards

Antidysrhythmics and anticoagulants Flashcards

1
Q

What makes long QT syndrome dangerous?

A

they can convert into a potentially fatal ventricular tachycardia called torsades de pointes

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2
Q

What test can detect dysrhthmias?

A

Electrocardiogram (ECG)– the only test that directly assesses the conduction of the heart

there are other tests that determine cause but ECG lets you know there is an issue

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3
Q

What type of condition is a risk factors for dysrhythmias?

A

-any condition that alters or interferes with electrical signals following the usual pathways through the myocardium or disruptions in homeostasis that increase or decrease the “excitability” of the myocardium

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4
Q

What are some diagnostics that help to discover the CAUSE of dysrhythmia?

A

-imaging to assess changes in morphology and functioning of the myocardium– echocardiogram
-imaging of the blood supply to the myocardium– angiogram
-blood tests for metabolic imbalances

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5
Q

What are some symptoms of dysrhythmia?

A

-palpitations
-dizziness
-chest pain

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6
Q

What findings support myocardial ischemia? Decreased CO?

A

Ischemia
-chest pain
-pressure
-shortness of breath
-tachycardia
-sweating
-nausea
-atypical signs can be subtle so keep an eye for them

CO
-cardiogenic shock
-really low BP
-mean arterial pressure of about 65 or less shows decreased or no perfusion
-clammy

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7
Q

What is the first line of treatment for Afib?

A

beta blockers (cardio-selective)
ex. atenolol, metoprolol and bisoprolol

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8
Q

What does hemostasis mean?

A

the stopping of blood flow– is an essential mechanism protecting the body from both external and internal injury

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8
Q

Where are thromboplastin and fibrinogen (clotting factor proteins) made?

A

in the liver– they constantly circulate through the blood in an active form

vitamin K is required for the liver to make four of the clotting factors

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9
Q

Disorder to which organ will lead to abnormal coagulation?

A

serious liver disorders

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10
Q

Define fibrinolysis

A

the process of clot removal– initiated 24-48 hours after the clot is formed and continues until the clot is dissolved

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11
Q

When should you test or monitor PTT?

A

before giving heparin and ONLY if the heparin is through IV, NOT for subcut

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12
Q

What is D-dimer?

A

a protein fragment produced during abnormal blood clotting

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13
Q

What is the therapeutic range for INR?

A

2-3

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14
Q

What is the US test for?

A

checking the leg veins for diagnosing DVT

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15
Q

When are direct oral anticoagulants (DOAC) contraindicated?

A

-heart valve disease/replacement
-significant renal impairment (CKD stage 3 or greater)

these pts will get warfarin for an oral anticoagulant

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16
Q

What are the most common indications for long-term anticoagulation?

A

-a-fib
-cardiac valvular disorders or artificial valves
-recurrent DVT

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17
Q

What does the acronym CHADS-65 stand for?

A

A means of predicting the likelihood that a patient in atrial fibrillation will have a stroke. CHADS is a mnemonic for c(ongestive) heart failure; h(ypertension), a(ge) over 75 years, d(iabetes) mellitus, and a previous history of s(troke) (or transient ischemic attack

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18
Q

Describe Beta blockers

A

competes for receptors of catecholamine at the B1-receptor sites in the heart (it blocks these receptors), resulting in decreased heart rate, cardiac contractility, and CO

Indications– antihypertensive, angina (post-MI), heart rate control

ex. metoprolol, atenolol and bisoprolol

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19
Q

What is the difference between a chronotropic and inotropic drug?

A

Inotropic– affects cardiac contractility

chronotropic– affects heart rate

20
Q

What are some of the side effects of beta blockers?

A

-hypotension
-bradycardia
-rebound HTN and tachycardia can occur with sudden discontinuation
-can block SNS response, decreasing the response to and symptoms of hypoglycemia and other conditions (like sepsis)
-non-selective beta blockers increase risk of bronchoconstriction

21
Q

When is a heart rate of 50-55 desirable?

A

for pts with heart failure and ischemic heart disease

22
Q

Why is holding a beta blocker (Ex. metoprolol) not always done when HR is <60?

A

should be held but it more depends on the pts trends and normal HR because the med is what is keeping it so low– it is more important to hold if the pt is symptomatic

23
Q

Define dysrhythmia

A

abnormalities of electrical conduction that may result in disturbances in heart rate or cardiac rhythm– commonly categorized based on area of origin (atrial or ventricular), quality (fib), or conduction pattern

24
Q

What are ectopic pacemakers (foci)?

A

-areas of myocardium (heart muscle cells) other than the conduction pathway that generate action potentials
-may compete with the conduction system
-have the potential to cause dysrhythmias

25
Q

When is the refractory period?

A

-occurs during most of the action potential
-ensures that the myocardial cell finishes contracting before a second AP begins

26
Q

How do antidysrhythmic drugs act on the heart?

A

-they alter ion movement during the myocardial action potential (AP)

27
Q

Describe what happens in each phase of an action potential (AP)

A

0– AP begins when threshold potential is met and plasma membrane sodium channels open– sodium rushes INTO the cell and causes rapid depolarization and calcium enters the cell

1– cardiac muscle cell is depolarized (short period)

2– K+ channels open and K+ rushes OUT of the cell which begins repolarization but Ca2+ in cell maintains depolarization

3– Ca2+ channels close and K+ channels open which repolarizes the myocyte– muscle contraction will end shortly after

muscle is unable to generate another AP during depolarization and repolarization– refractory period

28
Q

What ion generates depolarization?

A

calcium entering the cell through calcium channels

29
Q

What are the 4 classes of antidysrhythmics?

A

Class 1– sodium channel blockers

Class 2– beta-adrenergic blockers

Class 3– potassium channel blockers

Class 4– calcium channel blockers

30
Q

Describe sodium channel blockers

A

slows the rate of impulse conduction across the heart by blocking Na+ channels, which blocks Na+ entry and cell depolarization

31
Q

Describe beta-adrenergic blockers

A

slow the heart rate (negative chronotropic effect on SA node) and conduction velocity through AV node by blocking sympathetic activity

32
Q

Describe potassium channel blockers

A

prolong the heart’s refractory period by blocking K+ channels, which prevents K+ exit and cell repolarization

33
Q

Calcium channel blockers

A

-slows the heart rate (negative chronotropic effect on SA node) and conduction velocity through AV node by blocking Ca2+ channels
-actions and effects similar to beta blockers

34
Q

What is long QT syndrome?

A

-congenital
-acquired (meds are the biggest risk factor)
-SNS activation increases risk
-if persists, can convert into a lethal ventricular tachycardia called torsades de pointes (can cause sudden cardiac death in young people)
-repolarization takes longer which is often related to an interference with the ability for K+ channels to open
-Amiodarone carries a high risk for long QT syndrome

35
Q

What diagnostic test is needed to diagnose dysrhythmias?

A

ECG– the gold standard being a 12-lead ECG

36
Q

What are some common conditions that alter myocardial morphology or conduction pathways?

A

MI–forms scar tissue that interferes with conduction

Myocardial remodeling– dilation and hypertrophy (as seen in HF)

37
Q

What are common acute conditions that alter the excitability of the myocardium?

A

-potassium or magnesium imbalances
-conditions that activate SNS (stress or stimulants)
-hypoxia
-acidosis

38
Q

What diagnostics are used to discover the CAUSE of the dysrhythmia?

A

-imaging to assess changes in morphology and functioning of the myocardium, such as an echocardiogram

-imaging of the blood supply to the myocardium, such as angiogram

-blood tests for metabolic imbalances, such as electrolyte imbalances or troponin

39
Q

Describe myocardial perfusion imaging

A

MIBI, nuclear stress test

-evaluates blood flow to the heart at rest and under stress
-blood flow from coronary arteries to the heart– decreased myocardial perfusion is one cause of dysrhythmias
-MIBI uses radiopharmaceutical tracer (make sure pt is not pregnant or breastfeeding)
-STOP all caffeine 24 hours before test (note caffeine is found in many analgesics ) and remain fasting for 4 hours after the test
-if pt becomes distressed (angina, dizziness, etc.) during the stress test portion then the physical test will be stopped and in the case of med test the antidote will be given

40
Q

How does tachycardia put someone at risk for myocardial ischemia?

A

increases myocardial oxygen demand and decreases myocardial oxygen supply

41
Q

How does tachycardia and bradycardia effect CO?

A

tachy– less filling time that leads to less blood being in the LV for each beat <SV

brady– a slower rate decreases CO (CO=SVxR)

SV– stroke volume

42
Q

What is the advantage of using an immediate release med q6h over a OD ER?

A

for beginning the medication it easy easier to titrate and find the correct dose when giving it 4 times a day rather than waiting for the next day’s dose

43
Q

What does Amiodarone do?

A

it has the POTENTIAL to vonvert the pt back into a normal sinus rhythm and can control ventricular rate

44
Q

What are the 3 basic steps of hemostasis?

A
  1. vessel spasm
  2. coagulation and clotting
  3. fibrinolysis
45
Q

Define hemostasis

A

the process of stopping blood flow (an essential mechanism to protect the body from external and internal injury)

46
Q

Define fibrinolysis

A

the process of clot removal– initiated 24-48 hours after clot formation and continues until the clot is dissolved

47
Q

What are thrombolytics used for?

A

also called fibrinolytics

used to dissolve life-threatening clothes by promoting fibrinolysis

48
Q

What are the most common indications for long-term anticoagulation use?

A

-Afib
-cardiac valvular disorders or artificial valves
-recurrent DVT

Pharmacology 2 (12 decks)

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