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Physical Assessment > Pharmachology - CV > Flashcards

Pharmachology - CV Flashcards

1
Q

What is a Cardiac arrhythmia?

A

Change in automaticity, conductivity or both. Heart Without rhythm

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2
Q

What is Dysrhythmia?

A

Abnormal rhythm of the heart

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3
Q

What are Arrhythmias and Dysrhythmia brought on by?

A

Hypoxia
Ischemia
K levels - high or low

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4
Q

What are the 4 types of arrhythmias or Dysrhythmia ?

A

Sinus (bradycardia, tachycardia)
Atrial (fibrillation, flutter)
Nodal or junctional (AV node)
Ventricular (often life threatening: PVC, V tachycardia, V fibrillation)

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5
Q

Classifications of antiarrhythmic Meds:

Class I

A

Class I - Na channel blockers

Lidocaine (Xylocaine)

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6
Q

Classifications of antiarrhythmic Meds:

Class II

A

Class II Beta Adrenergic Blockers

Propranolol (Inderal)

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7
Q

Classifications of antiarrhythmic Meds:

Class III

A

Class III Potassium Channel blockers

Amiodarone (cordarone)

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8
Q

Classifications of antiarrhythmic Meds:

Class IV calcium

A

Channel blockers

Verapamil (calan)

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9
Q

Characteristics of Class I Anti arrhythmics:
Na channel blockers
Lidocaine (Xylocaine)

A

Blocks the movement of Na into cardiac cells
Slows conduction
Tx rapid ventricular arrhythmias.
Cardiac use only.
Must say on label “IV use for ventricular arrhythmias.
Metabolizes by liver and excreted by kidneys

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10
Q

Lidocaine common ADE

A

Hypotension, bradycardia, “lidocaine crazies”

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11
Q

Serious lidocaine ADE

A

Cardiac arrest and seizures

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12
Q 
Lidocaine contraindications 
(1st classification) Na channels blockers
A

Dig toxicity, heart failure/block and allergy to med

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13
Q

Characteristics of Class II Anti arrhythmics:
Beta Adrenergic blockers
Propranolol (Inderal)

A

Blocks the SNS and slows down ventricular conduction.
Neg chronotropic, inotropic. Used to treat rapid ventricular Arrhythmias, HTN and Angina

Common ADE: bradycardia, hypotension, lethargy
Serious ADE: bronchoconstricion

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14
Q

Characteristics of Class III Anti arrhythmics:
K channel blockers
Amiodarone (Cordarone)

A

Slow repolarization and prolongs the refractory period.
Use to treat life threatening arrhythmias ONLY. By ACLS this is the 1st line of defense recommended
Common ADE: tremors, n/v, hypotension
Serious ADE: pulmonary toxicity, exacerbation of arrhythmia, hepatotoxicity.

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15
Q

Characteristics of Class IV Anti arrhythmics:
Calcium channel blockers
Verapamil (Calan)

A

Slows depolarization and decrease ventricular rate
Also used to treat HTN and angina
Common ADE: constipation, dizziness, orthostatic hypotension, edema.
Serious: hypotension, dradycardia.

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16
Q

Non-pharmacological treatment of arrhythmias?

A

Treat underlying disorder. Valsalva or carotid artery massage. Defibrillate. Pacemakers, AICDs. Ablation

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17
Q

What happens in Angina ?

A

Increase myocardial O2 demand. (Exercise, stress, anxiety, smoking and cold weather

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18
Q

What happens in Angina II?

A

Decrease O2 supply to myocardium (atherosclerosis, arteriosclerosis, diabetes)

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19
Q

Types of Angina

A

Most common “classics or stable angina”. Goes away when the patient rests. Patients can tell you intensity, triggers and is very predictable.

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20
Q

Antianginal medications

A

1- nitrates
2- beta blockers
3- calcium channel blockers
All work by decreasing myocardial O2 demand and/or increasing blood supply to the myocardium

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21
Q

Organic nitrates - Nitroglycerine (nitrostat)

A

Dilate veins
Dilates coronary arteries
Dilate arterioles

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22
Q

Preload

A

Think of terms of volume

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23
Q

Afterload

A

Pressure

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24
Q

Nitrates ADE

A

Common: headache, orthostatic hypotension
Serious: severe hypotension
Contraindications: hypotension, phosphodiesterase inhibitors (Viagra)

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25
Q

Heart pumps

A

5-6 L/min

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26
Q

Antianginal medication: Nitrates patch

A

Careful with hairy chest. Need skin contact. Dispose of it carefully. Cleanse the area where the patch was daily. As nurses wear gloves to avoid headaches

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27
Q

Antianginal medication. Beta blockers

A

Propranolol (Inderal). Decrease heart rate, neg chronotropic/neg inotropic.
Decrease BP –> decrease myocardial workload and oxygen demand
Po Long term management of angina. Also tx HTN, arrhythmias
Common: hypotension, bradycardia, lethargy
Serious: bronchoconstricion, heart block

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28
Q

Antianginal med: calcium channel blockers

Verapamil (Calan)

A

Slows the movement of extra cellular calcium in the cell –> coronary & peripheral heart dilation –> decrease Afterload –> increase blood supply to the heart and reduce workload of the heart.
Tx - use to treat Angina when NTG or BB don’t work.

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29
Q

Diuretic medication

A

Diuresis: excretion of fluid, esp water

30
Q

Categories of diuretics

A 
Thiazides (hydrochlorothiazide)
Loop - Furosemide (Lasix)
Potassium sparing or Aldosterone antagonist
-spironolactone (Aldactone)
Osmotic - Mannitol (Osmitrol)
31
Q

Diuretics: Thiazides (hydrochlorothiazide)

A

Not the choice if we need a patient to get rid of fluid immediately. Not for immediate diuresis.

32
Q

Diuretics: Loop - Furosemide (Lasix)

A

Renal diuresis. They give a rapid immediate response if given PO 30- 45 min IV result in 5 min.

33
Q

Diuretics: K+ Sparing

A

Don’t loose K
Uses: HTN, liver disease
Not used in renal disease
Do not use K supplements

34
Q

Diuretics: Osmotics. Mannitol

A

Uses: intracranial pressure (ICP), glaucoma, oliguria/anuria

Short term IV use only

35
Q

Diuretics intervention

A

Watch the potassium K

Normal is 3.5 - 5.2

36
Q

Meaning of weight for patients on Diuretics

A

1 Lt weights 1kg (2.2 lbs)

37
Q

HTN risks

A

MI
CFH (congestive heart failure)
CVA and hemorrhage
Renal disease

38
Q

What is primary HTN

A

90-95% of people. Not one cause. It is a variety of issues

39
Q

What is secondary HTN

A

Hypertension that is secondary to something else. Example: renal issues, central nerves sys issues, renal arteries, use of Meds like long term steroids, Meds retaining water and sodium. To cure you must find the cause

40
Q

Arteriosclerosis

A

Thickening of the vessels. They are not as flexible anymore

41
Q

What are the target organs affected by HTN

A

Heart (MI heart attack)
Brain (CVA stroke)
Kidneys (renal failure)
Eyes (retinopathy)

42
Q

HTN treatment

A 
Stepped : use several different meds to attack the problem and minimized side effects 
Lifestyle modification 
Diuretics
Combination therapy 
Add a third medication 
Maximize drug doses
43
Q

HTN treatment
ACE Inhibitors
Prevents Angiotensin I from becoming II
Captopril (Capoten)

A

Decrease afterload
Decrease preload
Thus decrease the workload of the heart

44
Q

ACE Inhibitors effects?

A

Well tolerated but common side effect:
Dry cough
Serious ADE: angioedema

Black Box: avoid 2nd and 3rd trimester of pregnancy
Note: great to tx DM as it preserves kidney function

45
Q

HTN treatment:
Angiotensin II receptor blockers
Losartan (Cozaar)
ARB

A

Blocks the Angiotensin II
Txs HTN and HF (CHF)
Common ADE: Upper respiratory infection, dizziness, orthostatic, hypotension.
Serious ADE: angioedema

46
Q

HTN treatment:
Calcium channel blockers
Verapamil (calan)

A

Slows the movement of extra cellular Ca into the cell.
Decrease afterload
Good for patients with migraine and asthma (who cannot take beta blockers)
Common ADE: constipation, dizziness edema
Serious ADE: profound hypotension and bradycardia

47
Q

HTN treatment

2nd line Anti-hypertensive drugs

A

Beta blockers
Propranolol (Inderal)
First choice for pt’s with history of MI, stable HF, angina

48
Q

Treatment for Hypertensive Crisis?

A 
HTN BP > 210/120
Sodium nitroprusside (Nitropress)
Decrease BP slowly and systematically
Med must be mixed in IV fluids b/c can cause excessive hypotension 
Cyanide toxicity - almond breath
49
Q

Causes for Heart Failure?

A

MI
HTN
Anything that decrease the pumping ability or increase the workload of the heart and drops the CO

50
Q

Drug therapy for heart failure

A 
ACE
Beta blockers
Diuretics (decreasing preload)
Inotropic: Digoxin
Antianginal meds
Vasodilators
51
Q

What happens in blood coagulation?

A

Thrombus - blood clot

Embolus - piece of blood clot breaks off and travels to the heart, brain and lungs.

52
Q

Drugs affecting blood coagulation

A

Anticoagulants: best in preventing venous thrombus

53
Q

Drugs affecting blood coagulation

A

Anti platelet drugs are best in preventing arterial thrombus

54
Q

Drugs affecting blood coagulation

A

Thrombolytics: lyse (break off) thrombus

55
Q

Anticoagulants IV or subq?

A

Prototype: Heparin
Use to treat deep vein thrombosis, pulmonary emboli
ADE: bleeding
Serious: more bleeding, drop in platelets
Pt need labs for PTT: Norm 25-35 sec
Therapeutic PTT : 1 1/2 to 2 times normal 38 to 70 sec
Metabolize in liver and excreted in the kidneys

56
Q

What is an antidote for heparin?

A

Protamine sulfate

57
Q

Anticoagulant oral use?

A 
Warfarin (Coumadin)
PT - 12-13 seconds
Therapeutic 18 seconds 
ADE: bleeding
Serious: bleeding from anywhere (bloody nose, vomiting blood, coughing blood, in the urine/stool, bruising). 
Antidote: vitamin K
58
Q

Antiplatelet drugs?

A

Prevent arterial thrombus. Interferes with platelet adhesion
ASA- aspirin (one a day and usually 81mg)
NSAID- bind with platelet only as long as the NSAID is in the system (about 4 hours)
Clopidogrel (Plavix)
ADE: bleeding

59
Q

Thrombolytic drugs?

A

Alteplase (Activase)
Dissolve or lyse the clot
Treatment acute thromboembolic events: MI, PE, femoral thrombus
Goal: re establish blood flow and prevent tissue damage
“Limit time”

60
Q

Drugs for hyperlipidemia

A

This meds are gonna lower lipids level in the blood which reduces mortality and morbidity.

61
Q

Blood lipids? What do we talk about?

A 
Cholesterol  60 (healthy one - preventitive)
LDL N:
62
Q

Drugs for hyperlipidemia

A

Lovastatin (Mevacor)
Common ADE: v/d, constipation
Pt teaching: continue w lifestyle changes. Take at bed time

63
Q

Drugs for hyperlipidemia

Lovastatin (Mevacor)

A

Serious ADE:

Rhadomyolysis, Hepatotoxicity

64
Q

Current recommendations for AHA for all patients with CVD

A 
Statin
ACE inhibitor
Beta blocker 
ASA daily 
Nitro sl prn
65
Q

What is the physiology of the CV system?

A

It is composed of: heart, blood vessels and blood.
Function: transport supplies to the cell and remove waste products.
Efficiency of CV system: ability to pump, patency of blood vessels, quality of blood and quantity of blood.

66
Q

What is the conduction of the heart?

A

SA : 60-100 bpm
AV : 40-60 bpm
Ventricles: 20-40 bpm
ANS

67
Q

What is the composition of blood?

A

55% plasma

45% solid particles
RBC (erythrocytes) - hct male 42% - 50% female 40% - 48%. Hgb male 13-18 and female 12-16
WBC (leukocytes) 5,000 to 10,000
Thrombocytes (platelets) 100,000 to 400,000

68
Q

What do inotropics do?

A

They increase the force of myocardial contraction

Prototype: digoxin (lanoxin)

69
Q

Uses of inotropic Digoxin?

A 
Tx of heart failure
Tx of atrial arrhythmias
Tx sinus tachycardia 
Common ADE: n/v, anorexia, blurred vision, diplopia, halos, bradycardia, tachycardia 
Serious: ventricular fibrillation
70
Q

What is digoxin toxicity?

A

N/v, confusion, blurred vision, bradycardia
Treatment: stop digoxin.
KCL, anti-arrhythmic, atropine for bradycardia and digibind

71
Q

Who is at high risk for dig toxicity?

A 
Hypokalemia (low K)
Renal or liver failure
Large loading dose
Large maintenance dose
Infants and aged
Hypothyroidism
Hypoxia

Physical Assessment (5 decks)

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