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Pharmacology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

name the arteries of the heart

A

Right coronary artery

Left coronary artery - breaks into the circumflex and left anterior descending artery

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2
Q

The right coronary artery supplies what area

A

the R atrium, R ventricle, bottom portion of the L ventricle and back of the septum

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3
Q

The circumflex artery supplies what area

A

The L atrium, side and back of the L ventricle

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4
Q

The left anterior descending artery supplies what area

A

front and bottom of the L ventricle, and front of the septum

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5
Q

what is hyperlipidemia

A

high cholesterol

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6
Q

what is high cholesterol related with

A

increase risk of coronary artery disease such as angina (moderate), or myocardial infarction MI (severe)

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7
Q

What is atherosclerosis

A

Cholesterol accumulation in the vessel wall

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8
Q

What is the progression of atherosclerosis

A

fatty streaks to a fibrous stage leading into lesions involving calcification, ulceration, hemorrhage and eventually thrombosis and occlusion of a vessel

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9
Q

risk factors for atherosclerotic coronary artery disease

A 
DISLIPIDEMIA - high LDL (bad), low HDL (good)
hypertension
diabetes mellitus
smoking
family history
obesity and lack of exercise
male gender and advanced age
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10
Q

what are the three parts to cholesterol

A

LDL - low density lipoprotein
HDL - high density lipoprotein
TG - triglyceride

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11
Q

the skinny of LDL - low density lipoprotein

A

Known as the ‘Bad’ cholesterol
60-70% of total serum cholesterol
LDL transports cholesterol from the liver to peripheral tissue. excessive LDL may deposit onto the walls of the arteries
Forms atherosclerotic plaque which increase risks of CVA

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12
Q

the skinny on HDL - high density lipoprotein

A

known as the ‘Good’ cholesterol
20-30% of total serum cholesterol
HDL transports cholesterol from periphery to the liver for removal from circulation
high HDL is associated with low risk of developing CAD. conversly low HDL increases risk of developing HDL

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13
Q

the skinny on TG - triglycerides

A

10-15% of total serum cholesterol

positive relationship between TG and incidence of coronary artery disease (CAD)

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14
Q

desirable Cholesterol levels

A

Total < 5.2 mmol/L
LDL < 2.6 mmol/L
HDL > 1.5 mmol/L
TG < 1.7 mmol/L

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15
Q

Poor cholesterol levels

A

Total > 6.2 mmol/L
LDL > 4.1 mmol/L
HDL < 1.0/1.3 mmol/L (men/women)
TG > 2.3 mmol/L (up to 5.6mmol/L)

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16
Q

what is the Framingham Risk Score (FRS)

A

risk assessment on when to initiate treatment for hyperlipidemia
High > 20% - consider treatment
Moderste 10-20% - lower LDL < 2 mmol/L (or 50%)
Low < 10%

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17
Q

Statin mechanism of action and therapeutic uses

A

inhibits an enzyme called HMG-CoA reductase which is needed for the final step of cholesterol production
Therapeutic uses: reduce cholesterol, primarily before 1st heart attack, secondly to prevent a 2nd heart attack.

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18
Q

Adverse effects of statins

A

Myopathy (muscle pain/breakdown)
liver dysfunction
nausea
if used in conjunction with fibrates it increases the risk of myopathies

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19
Q

List of the Statin drugs generic names

A 
atorvastatin
fluvastatin
lovastatin
pravastatin
rosuvastatin
simvastatin
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20
Q

risk factors that should be considered for prevention of myopathies when administering statins

A 
> 80 years of age (especially women)
small body frame / frailty
high dose of statin
multiple disease
polypharmacy
hypothyroidism
alcohol abuse
Note: increase risk of myopathy when mixing statin with fibrates
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21
Q

Fibrates mechanism of action

A

primarily to decrease triglyceride production in the liverby interacting with specific receptors in the liver and fat tissues

  • significantly reduces TG’d
  • significantly increases HDL
  • slightly reduces LDL
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22
Q

Therapeutic uses and A/E’s for Fibrates

A 
Use: reduce triglycerides
A/E: nausea, headaches
liver dysfunction
Gallstones
insomnia
rash
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23
Q

Fibrates important drug interactions, dosing and administration

A

interacts with statins - increases risk of myopathies

dosing: Oral and take with food

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24
Q

Fibrates - drug names

A

Gemfibrozil

Fenofibrate

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25
Q

Bile Acid Sequestrants (Resin)

A

cholestyramine

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26
Q

cholestyramine mechanism of action

A

a large bile acid resin that converts cholesterol to bile acids which lowers blood LDL. Also, slightly increases HDL

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27
Q

cholestyramine therapeutic use and A/E’s

A

USE: hypercholesterolemia
A/E: horrible taste (disliked by Pt’s)
GI discomfort (bloating, indigestion, steatorrhea - fatty pooh)
causes deficiency in lipid soluble vitamins A/D/E/K
CONTRAINDICATED WITH HYPERTRIGLYCERIDEMIA

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28
Q

Nicotinic Acid (Niacin) for hyperlipidemia - mechanism of action and therapeutic uses

A

Mechanism: appears to alter lipid level by inhibiting lipoprotein synthesis
USES: reduce triglycerides
low doses of nicotinic acid are sufficient to raise HDL, unfortunately larger doses are needed to lower LDL
reduces TG 20-40%, reduces LDL 20-35%, elevates HDL 10-20%

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29
Q

Nicotinic acid A/E’s and important drug interactions

A

A/E’s: flushing, rash, pruritis, hepatoxicity
IMPORTANT interaction:
1. Statins - increases risk of liver damage
2. Fibrates - increase risk of gall stones

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30
Q

Ezetimibe mechanism of action

A

Blocks absorption of cholesterol

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31
Q

Ezetimibe therapeatuic uses

A

for elevated LDL
Used alone or in combination with Statins
Reduces LDL by about 20%

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32
Q

Ezetimibe A/E’s

A

Nausea, bloating

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33
Q

What is angina and it causes

A
  • sudden pain beneath the sternum often radiating to the left shoulder and arm.
  • causes by insufficient blood flow to the heart muscle from narrowing of coronary arteries
  • often occurs secondary to athersclerosis which blocks the coronary arteries
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34
Q

goals of therapy for angina

A

to prevent myocardial infarction

to prevent pain

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35
Q

what are the main three families of drugs used to treat angina

A
  1. Nitrates
  2. Beta-Blockers (BB)
  3. Calcium Channel Blockers
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36
Q

what are the three types of angina

A
  1. Stable - usually triggered by increase in physical activity, emotional excitement, large meals, and cold air
  2. Unstable - Present at rest, intensification of existing angina (greater risk of death compared to stable) This is the urgent medical emergency type
  3. Variant (Vasospastic) - coronary artery spasm, can occur at rest or on exertion. Vessels are clean and clear
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37
Q

What are nitrates mechanism of action

A

nitroglycerin acts directly on vascular smooth muscle to promote vasodilation.

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38
Q

Three therapeutic uses of nitrates (nitroglycerin) for angina

A
  1. relieves the attack by using when the attack begins
  2. prevents attacks by using just before an attack is expected to occur
  3. to reduce the number of attacks by using the drug regularly on a long term basis
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39
Q

Nitrates (nitroglycerin) A/E’s (think about it… vasodilator)

A

headache (diminishes over time, or take acetominophen)
hypotension
reflex tachycardia

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40
Q

Nitroglycerin dosing and ways of admin

A 
sublingual / oral tablets
spray
patch (on for 12, off for 12)
paste
intravenous infusion
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41
Q

IMPORTANT drug interaction of nitrates

A

Sildenifil (Viagra) - intensifies the nitrates and causes severe vasodilation which can invoke a heart attack due to life threatening hypotension

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42
Q

nursing implications for nitrates (nitroglycerin)

A

monitor for tolerability, blood pressure and response

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43
Q

types of Beta blockers for angina

A

Beta blocker receptors (several types B1 and B2)
blockade of the receptors cause: 1. reduction in HR and contractility. 2. bronchconstriction

NOTE: B1 is more specific for the heart so it reduces the risk of bronchoconstriction

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44
Q

Beta 1 blockers affect…

A

The heart as they cause decrease in HR and contractility

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45
Q

Beta 2 blockers affect

A

the lungs as they cause bronchconstriction

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46
Q

Therapeutic uses for Beta-blockers

A 
Angina
Myocardial infarction
hypertension
dysrhythmias
heart failure
hyperthyroidism
pre/eclampsia (high BP during pregnancy)
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47
Q

A/E’s for beta blockers

A

bradycardia and heart block
hypotension
bronchconstriction
fatigue

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48
Q

Beta blockers dosing and administration

A

Various IV and oral doses.

IV route faster onset

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49
Q

types of beta blockers

A 
Acebutolol 
Atenolol
Bisoprolol ***
Esmolol
Metaprolol ***
Nadolol
Oxprenolol
Pindolol
Propranolol
Timolol
***most common
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50
Q

Calcium channel blockers for angina. mechanism of action

A

calcium channels help regulate function of the myocardium, the sinoatrial node, and the atrioventricular node
-CCB’s prevent calcium ions from entering the cell thus reducing BP, HR, electrical conduction, and force of contraction

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51
Q

Therapeutic uses for Calcium Channel Blockers (CCB’s)

A

Angina
Myocardial infarction
hypertension
dysrhythmias

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52
Q

A/E’s for CCB’s

A

bradycardia and heart block
hypotension
dizziness
flushing

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53
Q

nursing implication for CCB’s

A

Contraindicated with heart dysfunction

Monitor BP, HR, ECG and response

Various IV and oral doses

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54
Q

Two CCB agents

A

Dihydropyridines

Nondihydropyridines

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55
Q

list the three CCB dihydropyridines

A

Amlodipine
Felodpine
Nifedipine

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56
Q

list the two CCB nondihydropyridines

A

Diltiazem

Verapamil

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57
Q

What is acute coronary syndrome (ACS)

A

term used to cover a range of clinical symptoms associated with acute myocardial ischemia

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58
Q

ACS includes these three categories

A
  1. unstable angina
  2. Non-ST-elevation myocardial infarction (NSTEMI)
  3. ST-elevation myocardial infarction (STEMI)
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59
Q

What is an ECG (electrocardiogram) used for

A

to view the PQRST Wave voltage of the heart during contraction.
-it can identify angina, NSTEMI, and STEMI

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60
Q

what are caridac biomarkers

A

Cardiac biomarkers are substances that are released into the blood when the heart is damaged or stressed. Measurement of these biomarkers is used to help diagnose, risk stratify, monitor and manage people with suspected acute coronary syndrome (ACS) and cardiac ischemia.
Troponin
Creatine kinase-MB
LDH

61
Q

signs and symptoms of myocardial infarction (MI)

A
  • asymptomatic in 25% (mostly women and those with diabetes)
  • chest pain similar to Angina except, more intense, more persistent, and not releived by palliative measures (nitroglycerin)
  • nausea, sweating, apprehension
  • Pallor
  • Tachycardia
  • signs of congestive heart failure CHF - shortness of breath, swelling, cough
62
Q

List three ‘clot busters’ thromolytics

A

TPA (alteplase)
RPA (Retevase)
TNK (TNKase)

63
Q

what are anti-thrombotic agents (plateletes)

A

ASA (Asparin)
Clopidogrel (plavix)
IIb-IIIa antagonists
-Eptifibitide, Tirofiban, Abciximab

64
Q

list the three anticoagulant agents

A

Warfarin
Heparin
Low molecular weight heparin (LMWH ex. Enoxaparin)

65
Q

drugs used to treat acute coronary syndrome

A 
Thrombolytics
Anti-thrombotic agents
anti-coagulant agents
Beta-Blockers
Calcium Channel Blockers
ACE inhibitors
Statins
66
Q

ACS thrombolytics dosing and administration

A

Parental - all IV
TPA - loading dose then infusion
RPA - 2 bolus dose thirty minutes apart (don’t forget the 2nd dose!!!)
TNK - 1 bolus dose (most common now and cost approx. $2500/shot

67
Q

therapeutic uses for thrombolytics in ACS

A 
myocardial infarction (heart attack)
Stroke (brain attack) - TPA ONLY!!
68
Q

Adverse effects for thrombolytics

A

BLEEDING (caution for bleed in head)
repurfusion dysrhythmias (stunned heart when the artery opens up after the blockage)
hypotension

69
Q

Anti-thrombotic agents dosing and administration

A

Oral - ASA, Clopidogrel, Ticlopidine
Parenteral: Eptifibitide, Tirofiban, Abciximab
-loading doses and infusions

70
Q

anti-thrombotic agents mechanism of action

A

decreases the function of plateletes (so they can’t clog the artery)

71
Q

therapeutic use for anti-thrombotic agents

A

Prevents myocardial infarction

prevent stroke - ASA, Clopidogrel, Ticlopidine only

72
Q

Adverse effects for anti-thrombotic agents

A

Bleeding
Nausea
Thrombocytopenia (low WBC count)

73
Q

anticoagulant names

A 
Warfarin
Heparin
low molecular weight heparin (LMWH)
Rivaroxiban
Dabigatran
74
Q

mechanism of action for anticoagulants

A

inhibits clotting factors

-prevents the production of Fibrin

75
Q

Therapeutic uses for anticoagulants

A

Various clotting disorders

  • prevents/treats myocardial infarction
  • treat pulmonary embolism
  • prevent/treat DVT (deep vein thrombosis)
  • prevent stroke
  • atrial fibrillation (ineffective = clots = stroke)
76
Q

Warfarin dosing and administration

A

Oral
takes about 5 days to kick in (need to be on heparin/LMWH until warfarin kicks in
need to carry/wear a bracelet “on blood thinner”
CONTRAINDICATED in pregnant women
Monitor blood work - INR (international normalization ration) target is 2-3 (>3 is too thin. = way too much bleeding)
REVERSE EFFECTS with Vitamin K

77
Q

Adverse effects for warfarin

A

Bleeding
Purple toe
-this syndrome is thought to be secondary to cholesterol crystal emboli released as a result of warfarin-induced bleeding into atherosclerotic plaques
-if warfarin therapy is discontinued, the toe pain will resolve, but the purple discolouration will persist

78
Q

Heparin and LMWH (low molecular weight Heparin) dosing and administration

A

Heparin is Parenteral IV or S/C
-Heparin - IV loading dose and infusion (very short acting)
Monitoring - Use aPTT (activated partial thromboplastin time) - NOT the same as INR

LMWH is S/C injections (no infusion)
Monitoring - no monitoring of clotting times required

79
Q

Adverse effects for Heparin and LMWH

A

Bleeding

Heparin-induced thrombocytopenia (HIT)

80
Q

Anticoagulants - Dabigatran and Rivaroxiban dosing and administration

A

Good alternate to Warfarin as its hard to stabilize patients or poor compliance with monitoring

Oral treatment. - No lab test required
Note: costs lots more than warfarin

81
Q

Adverse effects to Dabigatran and Rivaroxiban

A

bleeding

GI upset

82
Q

Cardiac interventions

A 
Coronary Artery Bypass (artery added around blocked area)
Balloon Angioplasty (balloon inflation to open up artery)
Stent (wire mesh inside artery)
83
Q

What is hypertension

A

high blood pressure

The force against the blood vessel walls

84
Q

what can cause hypertension - risk factors

A 
sedimentary lifestyle
smoking
excess abdominal weight
fatty diet
alcohol consumption
and STRESS
Non-modifiable: family history, heart disease, stroke >45 for men, >55 for women, ethnicity
85
Q

ways to reduce hypertension

A

reduced sodium (intake <88cm)

86
Q

usual blood pressure threshold values for initiation of pharmacotherapy treatment

A

if Diabetic = 130/80
high risk = 140/90 (if CV risk)
low risk = 160/100 (if no CV risk)
very elderly = 160/na

87
Q

Therapeutic uses for Ace inhibitors

A

hypertension
heart failure
myocardial infarction
diabetic nephropathy

88
Q

Adverse effects of ACE inhibitors

A 
hypotension
dizziness
electrolyte abnormalities (may need to increase K)
Cough
Angioedema (swelling of the throat)
89
Q

list some ACE inhibitors (PRIL’s)

A 
Benazepril
Captopril
Cilazapril
Enalapril
Fosinopril
Lisinopril
Perindopril
Ramipril
Tandolapril
90
Q

Therapeutic uses for diuretics

A

hypertension

heart failure

91
Q

Adverse effects for diuretics

A

hypotension/dizziness
Metabolic/Electrolyte abnormalities
-increase Uric Acid levels (Thiazides) will form crystals that lead to gout in the joints
-increase Na+
-increase/decrease of Potassium (usually decreases except with K-sparing)
Gynecomastia (Spironolactone) = man boobs
NSAIDS reduce the effectiveness of diuretics as they cause the body to retain salt

92
Q

what needs monitoring when on diuretics

A

Electrolytes
Kidney function
Blood pressure

93
Q

mechanism of action for Thiazides (diuretics)

A

Causes diuresis (decreased plasma volume)
Reduce peripheral vascular resistance
Works in the distal part of the kidney

94
Q

mechanism of action for Loop diuretics

A

Causes more profound diuresis than thiazides
not generally used for chronic management of hypertension
works in the Loop of Henle in the kidney

95
Q

mechanism of action for Potassium sparing diuretics

A

Weak diuresis

usually combined with a thiazide to prevent potassium loss

96
Q

List the generic thiazides diuretics

A

Chlorthalidone
Hydrochlorothiszide
Indapamide
Metolazone

97
Q

List the generic Loop diuretics

A

Ethacrynic Acid

Furosemide **most common

98
Q

List the generic Potassium Sparing diuretics

A

Amiloride
Spironolactone
Triamterene

99
Q

List the generic Angiotensin Receptor Blockers (ARB’s) (SARTAN’s)

A 
Candesartan
Eprosartan
Irbesartan
Losartan
Telmisartan
Valsartan
100
Q

Alpha 1 Antagonists (blockers) mechanism of action

A
  • prevents stimulation of alpha1 receptors on the blood vessels thereby preventing vasoconstriction
  • relaxes smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow
101
Q

Therapeutic uses for Alpha 1 antagonists

A 
Hypertension
Prostatic hypertrophy (enlarged prostate in men)
102
Q

Adverse effects of alpha 1 antagonists

A

hypotension
dizziness
fluid retension
nasal congestion

103
Q

list the 3 alpha 1 antagonists generic names

A

Prazocin
Doxazocin
Terazocin

104
Q

Mechanism of action for Alpha 2 agonists

A
  • Acts within the brainstem to suppress sympathetic (norepinephrine) outflow to the heart and blood vesssels
  • Results in vasodilation and reduced cardiac output
105
Q

Therapeutic uses for Alpha 2 Agonists

A

hypertension

Pre/Eclampsia (methyldopa) - hypertension plus protenuria after 20 weeks gestation

106
Q

Alpha 2 agonists adverse effects

A

hyoptension / dizziness (do not withdraw Clonidine abruptly as it will lead to rebound hypertension)
fluid retention
dry mouth
sedation

107
Q

list the two alpha 2 agonists

A

Clonidine and Methyldopa

108
Q

Mechanism of action for Direct Acting Vasodilators (Minoxidil and Hydralazine)

A

primarily causes vasodilation in the arteriole

Limited effect on the veins (therefore minimal orthostatic hypotension)

109
Q

Therapeutic uses for Direct Acting Vasodilators (Minoxidil and Hydralazine)

A

Hypertension
Baldness (Minoxidil = Rogaine)
Pre/Eclampsia (Hydralazine)

110
Q

adverse effects for Direct Acting Vasodilators (Minoxidil and Hydralazine)

A

hypotension
dizziness
fluid retention
Hydralazine - systemic lupus erythromatosis SLE - arthritis autoimmune disease that attacks the joints in the body
Minoxidil - hypertrichosis (excessive hair growth)

111
Q

list the generic names of the two Direct Acting Vasodilators

A

Minoxidil

Hydralazine

112
Q

what is heart failure

A

condition in which the heart is unable to adequately pump blood throughout the body

generally, heart failure is a process that occurs over time, when an underlying condition damages the heart or makes it work too hard, weakening the organ

113
Q

Stats for heart failure

A

affects 1% of people aged 50 and older and about another 5% of those aged 75 years and older

about 10% of patients diagnosed with heart failure die within 1 year, and about 50% die within 5 years of diagnosis

114
Q

top 4 causes for heart failure (in order)

A
  1. myocardial infarction
  2. Coronary artery disease
  3. Valve disease
  4. Idiopathic cardiomyopathy
    others: viral/bacterial cardiomyopathy, myocarditis, pericarditis, arrhythmias, chronic hypertension
115
Q

what is ejection fraction

A

the percentage of blood pumped out of the left ventricle with each contraction

measuring the ejection fraction using Echocardiography is a way to determine left ventricle function

116
Q

what are normal ejection fraction amounts and abnormal

A

normal is about 60%
40-45% indicates mild dysfunction
30-40% indicates moderate dysfunction
10-25% indicates severe dysfunction

117
Q

List some symptoms of heart failure

A 
Fatigue
Heart palpitations
Loss of appetite
Memory loss, confusion
Nausea
Persistent coughing/wheezing
Shortness of breathe (dyspnea)
Swelling (edema) of the feet, legs, or abdomen
118
Q

Mechanism of action for Digoxin

A

increases the pumping force of the heart (positive inotrope) - Binds to the NA-K-ATPase (sodium pump)
slows conduction through the heart
Comes from the Fox Glove Plant (Latin: Digitalis)

119
Q

Therapeutic uses for Digoxin

A

Congestive Heart Failure

Dysrhythmia’s

120
Q

Adverse effects to Digoxin

A

Bradycardia
Nausea
Vision disturbances
**Amiodarone and Verapamil - significantly increases Digoxin blood levels
NOTE: measure serum blood concentration and chech HR prior to administration (must be >60bpm)

121
Q

what is a dysrhythmia

A

abnormal rhythm of the heart

The atriums and ventricles are not contracting in sync

122
Q

how does the normal rhythm of the heart work

A

normally generated by the pacemaker cells within the sinoatrial (SA) node, which is located within the wall of the right atrium.
The SA node governs the rhythm of the atria and ventricles. Atrial contraction is always followed by ventricular contraction.

123
Q

types of dysrhythmias

A 
too fast (tachycardia)
too slow (bradycardia)
frequency of the atrial and ventricular beats are different
124
Q

what can cause dysrhythmias

A

changes in the pacemaker cells
abnormal generation of impulse at sites other than the SA node - (Ectopic Foci - a tissue in the heart becomes hyperactive and triggers the muscle to fire/contract out of rhythm)

125
Q

types of tachy-dysrhythmias

A

Supraventricular (above the ventricles)
-Atrial fibrillation / flutter

Ventricular

 - Premature Ventricular Contractions (PVC's)
 - Tachycardia or Fibrilation
126
Q

types of brady-dysrhythmias

A

atrioventricular block

  • first degree
  • second degree = type I and type II
  • third degree (will lead to death)
127
Q

what do anti-dysrhythmic drugs do

A

act primarily by altering ion fluxes within tissue of the myocardium.
-the three main ions are: Na+, Ca2+, K+

Anti-dysrhythmic drugs can be classified by their ability to directly or indirectly block flux of one of these ions

128
Q

types of antidysrhythmic agents

A

Class 1a - atrial fibrilation
Class 1b - ventricular dysrhythmias
Class 1c - Severe ventricular dysrhythmias
Class II - general myocardial depressants for both supra-v and ventricular dysrhythmias
Class III - Life threatening ventricular tachycardia
Class IV - Paroxysmal supraventricular tachycardia

129
Q

Class I Antidysrhythmic agent

A

Procainamide

130
Q

Therapeutic uses for Procainamide (class 1 antidysrhythmic agent)

A

atrial and ventricular dysrhythmias

131
Q

Adverse effects of Procainamide

A 
Dizziness
Hypotension
Rash (Systemic Lupus Erythromatosis SLE - same as hydralazine)
bradycardia
vision disturbances
132
Q

Procainamide (antidysrhythmic agent) dosing and nursing implications

A

Oral or Parenteral
Measure serum blood concentration
Monitor for tolerability, HR and response (ECG)

133
Q

Class Ib Antidysrhythmic agent

A

Lidocaine

134
Q

therapeutic use for Lidocaine (class Ib antidysrhythmic agent

A

Ventricular dysrhythmias

135
Q

Adverse effects of Lidocaine (class 1b antidysrhythmic agent)

A

Dizziness
hypotension
bradycardia

136
Q

Lidocaine (antidysrhythmic agent) dosing and nursing implications

A

Parenteral

Monitor for tolerability, HR and responses (ECG)

137
Q

Class Ic antidysrhythmic agent

A

Propafenone

138
Q

Therapeutic uses for Propafenone

A

atrial dysrhythmias

139
Q

Adverse effects for Propafenone (antidysrhythmic agent)

A

dizziness
hypotension
bradycardia
SOB (shortness of breath) in asthma Pt’s

140
Q

Propafenone dosing, administration and nursing implications

A

Oral, and loading does for conversion out of atrial fibrillation
CAUTION in patients with CHF and asthma
Monitor for tolerability, HR and response (ECG)

141
Q

IMPORTANT drug interactions with Propafenone (antidysrhythmic agent)

A

Digoxin - significantly increases the digoxin blood levels

Warfarin - significantly increases the warfarin levels (increases risk of bleeding) - check the INR

142
Q

Class III antidysrhythmic agent

A

Amiodarone

143
Q

Therapeutic use for Amiodarone

A

Atrial and ventricular dysrhythmias

144
Q

Adverse effects for Amiodarone (antidyshythmic agent)

A 
dizziness / hypotension / bradycardia
HYPO/HYPERthyroidism
BLUE SKIN (Smurf drug)
Pulmonary fibrosis (scars in the lungs)
Liver toxicity
nausea
145
Q

Amiodarone dosing, administration and nursing implications

A

Oral and parenteral. Loading dose for conversion out of atrial fibrillation

  • may be used safely in patients with CHF.
  • Monitor for tolerability, HR and response (ECG)
  • Thyroid function tests
  • Chest X-ray
146
Q

What is acute ischemic stroke and the two types

A

Brain attack where a blood vessel breaks or clogs

  1. Ischemic (most common 85%)
    a. Thrombotics - clot in a brain blood vessel
    b. Embolic - clot between heart and brain
  2. Hemorrhagic (bleed in brain)
    a. intracerebral (inside) or subarachnoid (outside)
147
Q

goal of therapy for acute ischemic stroke

A

minimize brain damage
prevent complications
reduce the risk of recurrence
restore function of the individual

148
Q

signs/symptoms of Acute Ischemic Stroke

A

Weakness - sudden loss of strength, numbness, tingling
Trouble speaking - sudden confusion (even if temporary)
Vision problems - sudden (and sometimes temporary)
Headache - sudden, severe and unusual
Dizziness - sudden loss of balance with any of the above signs

149
Q

goal of care for those experiencing a stroke

A

4hr window from signs to drug administration or threshhold would have passed for benefits from meds

  1. identify signs
  2. EMS assessment
  3. Immediate general assessment and stabilization (CT scan of brain)
  4. Immediate neurologic assessment by stroke team
  5. review CT scan for hemorrhage
  6. no bleed = consider fibrinolytic therapy (TPA)
    - Bleed = consider transfer to neurosurgeon

Pharmacology (7 decks)

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