Cardiovascular Drugs Flashcards
2 most common diseases of heart
Congestive Heart Failure (CHF)
&
Coronary Artery Disease (CAD)
Congestive Heart Failure (CHF)
Contractibility of heart decreases
- heart pumps out less than it receives, blood accumulates, heart enlarges.
- less blood goes out to organs
- pooling may lead to formation of clots
- kidneys (sensitive to decrease flow) retain Na and H2O=edema
- *causes chronic HTN, MI, valve disease, aging
Coronary Artery Disease (CAD)
General term for several things that involve insufficient flow of blood to heart muscle
- arteriosclerosis - aging/narrowing
- atherosclerosis - fatty deposits/plaque
- angina - clinical condition - chest pain
- myocardial infarction - ischemia or death of some heart muscle
Compensatory reflexes
- cardiac enlargement-remodeling
- sympathetic reflexes - effort to increase blood flow/BP and decrease congestion (release epi/norepi & vasoconstriction/increase HR/force)
- kidneys retain Na/H2O to increase BP and volume
- *may help slightly but will eventually weaken the heart
Generalized symptoms of active heart failure
- tiredness
- weight gain
- fatigue
- SOB
- peripheral edema
- rapid HR
4 classes of heart failure symptoms
Class 1 - symptoms noted with significant exercise or a symptomatic
Class 2 - symptoms noted with mod activity
Class 3 - Symptoms noted with min. Activity
Class 4 - symptoms noted while at rest
A= at risk, D= advanced disease
Left ventricular failure
- pulmonary congestion: blood backs up from L heart into the lungs
- dyspnea, orthopnea, tachypnea, pulmonary edema, coughing, nocturnal dyspnea
Right ventricle failure
“Venous congestion”
- Fluid backs up into the body first
- pitting edema
- ascites (fluid in abdomen)
Congestive heart failure symptoms
-right and left sided failure symptoms;
Fatigue, cardiomegaly, periph edema, arrhythmias
-arrhythmias - dead
Pharmacological goals for CHF
- help heart pump more efficiently
- make work easier for heart; less resistance to blood flow (decreased peripheral resistance)
- usually multi drug approach
Cardiac Glycosides
Digoxin (Lanoxin)
Digitalis derivative
+inotrope, -chronotrope, -dromotrope
Cardiac Glycosides Uses
- heart failure
2. Arrhythmias - atrial fibrillation, tachycardia
Pharmacological effects of Cardiac Glycosides
- decrease Hr (-chronotropic)
- increase force of contraction (+inotropic)
- slow conduction through AV node (lengthen PR interval)
- improved CO>improves kidney flow, diuresis
MOA of Cardiac glycosides
- inhibits Na/K pump from resetting - slows AV node conduction
- accelerates entry of Ca, leads to increase Ca in heart muscle - greater myocardial contraction
**maintaining normal K and Ca levels is very important to avoid toxicity.
Pharmacokinetics of cardiac glycosides
- large volume of distribution - loading dose needed aka digitalizing dose
- narrow therapeutic index
- long 1/2 life - about 36 hours
Side/Adverse effects of Cardiac glycosides
- anorexia, NVD
- visual disturbances (green/yellow vision, halos Van Goh)
- Dig toxicity (arrhythmias)
- enhanced by hypokalemia (low K) or hypercalcemia (high Ca)
**be careful w/ puts on diuretics (lasix) - eat bananas and other food w/ K
Do not give digoxin if pulse is less than ______ or greater than ______
60;100
The 6 Rights
- Right Patient
- Right Drug
- Right Dosage
- Right Route
- Right Time
- Right Documentation (HR)
Ischemia
Inadequate O2 supply to tissues > can lead to necrosis
Coronary Artery Disease is caused by
- ischemia
- coronary artery obstruction; plaques or clots
- decreased blood flow to hear muscle due to coronary artery blockage leads to oxygen demand exceeding the oxygen supply
Arteriosclerosis
- due to aging
- vessels are constricted>decrease blood flow
Atherosclerosis
Fatty deposits accumulate in the walls of the arteries
Angina (pectoris)
Chest pain due to arteriosclerosis and atherosclerosis
**chest pain resulting from imbalance between oxygen demand & oxygen supply
Myocardial Infarction - MI
- complete ischemia to a section of heart
- if not restored, piece of heart muscle will die
- depending on size/location, may cause long term impaired function
What are the 3 types of angina
- Stable classic angina
- Unstable angina
- Vasospasm of coronary artery
Stable classic Angina
Less serious, from fixed obstruction - usually worsened with exercise
Unstable Angina
Sudden interruption; partial or complete blockage, may develop at rest (medical emergency)
**plaque fissuring - inflammation, clot formation
What 3 drugs are used to treat anginas
- Nitrates-nitroglycerin
- Beta Blockers - “olol”
- Calcium Channel Blockers
Desired result of anti-anginal drugs?
Decrease oxygen demand and increase oxygen delivery so the heart always has O2 it needs.
Nitrate MOA
Relaxes vascular smooth muscle; (dilates vessels) - makes it easier to push blood out of the heart
Nitrate Uses
Angina/hypertensive crisis
Nitrates Clinical Effect
- reduced O2 demand; reduced work load due to reduced vascular resistance
- increased O2 delivery by dilating coronary arteries
Nitrate Drugs
- nitroglycerin (Nitro-Bid, Transderm Nitro, Nitro Stat)
- isosorbide (Idordil)
What is the most common administration of Nitrates?
Sublingual - acts w/ in 5 minutes. (Repeat 2more times, seek medical attention of symptoms do not get better)
Is nitrate sensitive to air and light?
Yes - must be stored properly for best effects of drug
What are other ways of administering nitrates
As a patch or orally for prophylaxis
What is the 1/2 life of nitrates?
30-60 min
T or F - Nitrates skip the hepatic first pass
True
Nitrate Side effects
- headaches
- faintness/lightheadness - hypotension
- orthostatic hypotension; reflex tachycardia
- tolerance
Beta Blocker Drugs
- propranolol (Inderal)
- nadolol (Corgard)
- atenolol (Tenormin)
- metoprolol (Lopressor)
- carvedilol (Coreg)
- nebivolol (Bystolic)
T or F: beta blockers can’t be used with nitrates
False - they can be used together
Why do beta blockers slow the heart down?
Bc they work well to..
- decrease work load
- decrease HR
- allow for better refill
- help with symptoms and longevity
- fewer arrhythmias
What happens when organs receive less O2 or blood from heart?
- fluid buildup
- brain: dizziness, drowsiness, less alert
- lungs: SOB, cough
How do kidneys compensate when organs receive less blood?
Kidneys retain water by retaining Na
**edema occurs everywhere
How do we treat water retention from the kidneys?
With diuretics
Beta Blocker MOA
Decrease O2 consumption of heart.
- negative chronotropic
- negative inotropic
Beta Blocker side effects
- hypotension
- bradycardia
- bronchospasm
- some have black box warning
- some bleed over to alpha
**discontinue slowly to avoid tachycardia
What are the 2 classes of Ca Channerl Blockers?
Dihydropyridines and Nondihydropyridines
Dihydropyridines
“Dipine”
- Nifedipine (Procardia or Adalat)
- Amlodipine (Norvasc)
- Nisoldipine (Sular)
Nondihydropyridines
- verapamil (Calan)
- diltiaszem (Cardizem or Tiazac)
Ca channel blocker MOA
Inhibit movement of CA to reduce heart work load
What is the role of Ca?
- responsible for force of contraction
- HR
- regulates contraction in vascular arteries/arterioles
Dihydropyridines MOA
Block entry of Ca into smooth muscle
-allows for the muscles to relax and causes vasodilation > decrease BP
- lowers arterial pressure > easier work
- coronary artery vasodilation > more O2
Use of Dihydropyridines
Angina and hypertension
MOA of Nonhydropydridines
- Effect on the pacemaker cells of the heart. > blocks Ca > decreases rate of SA node & decreases the conduction velocity of the AV node.
- negative chronotropic/dromotropic
- blocks entry of Ca into the cardiac muscle > decreases FOC
- neg inotropic
Use of Nonhydropyridines
Angina
HTN
Arrrhythmias
CHF
Side effects of Ca channel blockers
- HA
- facial flushing
- dizziness
- hypotension
- reflex tachycardia
- constipation/swelling
- Xerostomia: dry mouth
Drug types used to treat angina
- nitrates
- beta blockers
- Ca channel blockers
Diseases that can result from an MI
- HF
- cardiac arrhythmias
Immediate treatment for an MI
Rest MONA -morphine -oxygen -nitroglycerin -aspirin
Long term MI treatment
Rest Oxygen Diet change Stool softener Treat other complications: HTN/CHF & arrhythmias
CHF treatment goal
-improve profusion & reduce excess volume
Meds: ACE inhibitors, diuretics, glycosides, BB
CAD treatment goal
Decrease O2 demand & increase O2 supply
Meds: BB, CCB & nitrates
hypertension is the leading cause of…
Stroke, heart attack and kidney disease
Risk factors for HTN
- over age of 60
- men & postmenopausal women
- family history
- increased cholesterol
- diabetes
- smoking
Cause of secondary HTN
Renal disease, pregnancy, drug induced
Cause of primary HTN
Cause unknown but associated factors:
- family history
- racial disposition
- obesity
- stress
- smoking
- sedentary life-style
- high fat diet
Non drug therapy for HTN
DASH diet - dietary approaches to stop HTN
- weight reduction
- moderate alcohol intake
- increase physical activity
- rest
- decrease fat intake
- avoid tobacco use
Pharmacologic approach to HTN
-drugs that impact heart, blood vessels, and kidneys
Drug types used to treat HTN
- diuretics
- beta blockers
- vasodilators
- CCB
- ACE inhibitor
- ARBs
- Renin inhibitors
If BP is down, kidneys will…
Retain Na/H2O to increase BP
If BP is up, kidneys will…
Excrete Na/H2O to decrease BP
MOA of diuretics
Increase excretion of Na by inhibiting tubular reabsorption of Na
**where Na goes, H2O follows
Thiazides type diuretics
Hydrochlorothiazide (Hydrodiuril)
