Cardio Vascular Medications Flashcards

1
Q

Diuretics what does it do

A

Work mainly by interfering with reabsorption of Na & Cl and passive reabsorption of water remember: water follows salt
This means less circulating volume and less resistance for the heart to work against

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diuretics med

A
Thiazide
Loop
Potassium-sparing 
-Aldosterone antagonists
-Non-aldosterone antagonists

=↓ circulating volume and venous return to heart. ↓SVR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
Loop diuretics medication
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

furosemide
bumetanide
Action: block reabsorption of Na & Cl in the loop of Henle so it prevents passive reabsorption of water
Reduces ECF volume and venous return to heart

Uses: HF, Edema of cardiac, hepatic, or renal origin, HTN that can’t be controlled with thiazide diuretics

SE: ↓ Na, ↓Cl, ↓K, dehydration, ↓BP, orthostatic hypotension, ototoxicity

NS: teach gradual position change, K diet sources, S/S of lyte imbalances/dehydration, BP & wt record

Evaluation: weight, edema, intake/output, labs monitor lytes: K, Na, Cl and hydration: BUN & Creat, ortho BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
Thiazide diuretics
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: metolazone, hydrochlorothiazide

Action: Works in distal tubule to increase renal excretion of Na, Cl, K and water. Dependent on adequate kidney function. Not as “strong” as loops

Uses: HTN, edema

SE: ↓ Na, ↓Cl, dehydration, ↓BP, orthostatic hypotension, ↓K

NS: teach gradual position change, K diet sources, S/S of electrolyte imbalances/dehydration, BP & wt record

Evaluation: weight, edema, intake/output, labs monitor electrolyte: K, Na, Cl and hydration: BUN & Creat, ortho BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
Potassium-sparing: aldosterone antagonist
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: spironolactone

Action: blocks the action of Aldosterone in nephron, so ↑Na excretion ,↑ K reabsorption = limited diuresis. Also blocks aldosterone effects in heart & vessels

Uses: HTN ,or edema (often in combination with loop or thiazide diuretic), HF, hyperaldosteronism

SE: ↑K, endocrine effects (steroid derivative), N & V

NS: teach effect delayed, never combine with K supplements (including salt substitutes), recognize ACEs, ARBs, & renin inhibitors can ↑K RT ↓aldosterone

Evaluation: monitor K levels, wt., edema, endocrine effects: gynecomastia, impotence, menstrual irrg, hirsutism (condition in women that results in excessive growth of dark or coarse hair in a male-like pattern), deepening of voice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Potassium-sparing: non aldosterone antagonists
Med:
Action:
SE:

A

Med: triamterene

Action: This class of medications directly blocks the reuptake of Na and the excretion of K

SE: Can cause elevated K levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Drugs that act on the Renin-Angiotensin-Aldosterone System

A

ACE inhibitors (ACEIs)
Angiotensin Receptor Blockers (ARBs)
Direct Renin Inhibitors
Aldosterone Antagonists

Interfere with RAAS effects
(vasoconstriction, ↑ blood volume, electrolyte changes, damage to heart & vessels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does angiotensin do?

A

These meds prevent the formation of Angiotensin II (ACEI) or block its action (ARB). So we keep the blood vessels from getting tight (we stop vasoconstriction)
AND
We stop release of ALDOSTERONE that says to the body “SAVE SALT SO THAT WATER WILL FOLLOW” (we drop volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

By vasodilation and decreasing blood volume we can:

A
  1. drop blood pressure 2. improve circulation to the heart muscle 3. reduce the workload of the heart
  2. prevent nephropathy by dropping pressure in the glomerulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

By blocking the evil effects of angiotensin 2 we can

A
  1. improve outcomes after MI
  2. reduce cardiac death
  3. reduce remodeling of heart muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Direct Renin Inhibitors

A

aliskiren (Tekturna)

Prevent conversion of angiotensinogen into angiotensin I
This acts earlier in the RAAS than the ACEIS and ARBS do.
Approved to treat HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
ACE Inhibitors: “pril"
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: lisinopril, captopril

Action: 1) prevents conversion of angiotensin I to II: : so blocks vasoconstrictor, & aldosterone release & reduces hypertrophy & remodeling in CV & kidneys
2) ↑bradykinin (vasoodilator)

Uses: : HTN, HF, MI, nephropathy, prevent MI & stroke

SE: hypotension, ↑K, renal failure, fetal injury, cough, angioedema, renal failure

NS: NSAIDS ↓effectiveness, diuretic enhance drug effects, teach to report cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Angiotensin II Receptor Blockers (ARBS): “sartan”
Action?
Effects?

A

The action is similar to ACEIs – ARBs prevent action of A II. These meds produce vasodilation & excretion of salt and water.

The effects are similar to ACEIS but delayed effect & less angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drugs that interfere with the RAAS

A

Basic effect of all drugs in this class is vasodilation, increased excretion of salt and water, and prevention of A2 damage to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Calcium Channel Blockers

CCBs grow in the “pines”

A

by blocking the calcium channel, we allow less calcium into the cell which dials down the strength and length of contraction in the smooth muscle cells of the heart and vessel walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Calcium Channel Blockers

Short version

A

They work by preventing calcium from entering the cell

Calcium is a big part of the “on switch” for the contraction of cells in the heart and arteries. (selective)

Work to control the heart muscle, SA & AV nodes (they effect electric & pump function of the heart) & contraction of smooth muscle in arteries (entry of calcium causes vasoconstriction)

17
Q

By turning off (or turning down) the “on switch” CCBs can:

A
  1. dilate arteries (tx HTN, angina)
  2. ↓force of cardiac contraction, 3. slow HR
  3. treat arrhythmias
  4. ↓conduction thru AV node.
18
Q
Calcium Channel Blockers
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: amlopidine, verapamil

Action: selective –in vessels cause vasodilation, in heart cause↓ HR, contractility & conduction

Uses: HTN, angina, arrhythmia

SE: bradycardia, exac of heart failure, heart block, vasodilation can = dizziness, HA, & edema

NS: some can cause reflex tachycardia, can intensify the effect of beta blockers or digoxin

Evaluation: monitor BP, chest pain, edema, daily wts, heart rhythm

19
Q

Alpha blocker short version

A

Med: tamsulosin, terazosin, doxazosin

Alpha blocker “osin” stop the effect of the sympathetic nervous system on vessels that cause vasoconstriction These drugs VASODILATE. Can be used for urinary smooth muscle to treat BPH.

Side effects can be excess effect: orthostatic hypotension (vein effect),reflex tachycardia or blockage of sympathetic symptoms in other places: nasal congestion, impotence

20
Q

Beta blocker the short version

A

Beta blockers “olols” stop the effect of the sympathetic nervous system that tells the CV system to “work harder, work faster & vasoconstrict” & beta receptors in kidney →renin release, selective classes
Used to treat HTN, angina, dysrhythmias, MI, HF
Side effects can be excess effect: bradycardia, reduced conduction, contractility, or cardiac output or bockage of sympathetic symptoms in other places: suppress glycogenolysis (liver), block beta 2 receptors in lung → bronchoconstriction or mask S/S of hypoglycemia in diabetics, block treatment w/Epi
(careful use in asthma, HF and DM)

21
Q
Adrenergic blockers:
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med:

alpha: tamsulosin.
beta: propanolol, metoprolol, carvedilol

Action: Block the effect of the sympathetic NS

Uses: HTN, HF, angina, dysrhythmias, MI

SE: bradycardia, heart block, heart failure, rebound tachycardia & dysrhythmia if DC’d, ↓ability to deal with ↓BS & blocks S/S of hypoglycemia

NS: teach gradual position change, monitor BP, HR, teach do not stop suddenly, S/S HF

Evaluation: BP & HR with each dose, angina, heart rhythm,
orthostatic BPs

22
Q

3 groups of beta blockers

A

NONSELCTIVE: propanolol (INDERAL) block beta one and two

CARDIOSELECTIVE: selective blockade of beta 1 at usual doses

VASODILATING: act on blood vessels to cause dilation by exerting alpha effect, may cause nonselective or selective beta blockade

Side effects: bradycardia, AV heart block, HF due to reduced contractility, teach worsening HF, rebound tachycardia and dysrhythmias , postural hypotension,

23
Q
Direct Vasodilators the short version
Effects
Action
Use
SE
Med
A

Effect of vasodilators varies due to site of action arterioles, veins or both

Most direct vasodilators act on arterioles:
(↓ afterload/resistance)
Used for HTN, HF, angina, and MI

Major SE: reflex tachycardia, fluid retention

Examples: hydralazine, minoxidil, nitropress

24
Q
Centrally-acting antihypertensive the short version
Effects
Action
SE
Med
A

Work on the brainstem to suppress outflow of impulses from the sympathetic nervous system

↓HR, ↓contractility, & vasodilates

Side effects will be very similar to beta blockers

Example: clonidine (Catapress)

25
Q
HMG-CoA Reductase Inhibitors:  “statins”
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: pravastatin, lovastatin, simvastatin

Action: ↑LDL receptors on liver & production of VLDL (very-low-density lipoprotein)

Uses: ↓LDL & total cholesterol, triglycerides, & ↑HDL

SE: myopathy/rhabdomyolosis, hepatotoxicity

NS: teach to report muscle pain, liver stress, combined effect with other lipid lowering agents ↑ risk of SE, teach avoid grapefruit juice, teach diet & lifestyle

Evaluation: lipid panel, liver function

26
Q

Bile-Acid Sequestrants
Use
Action

A

Used primarily as adjuvant to statins

Reduces LDL by preventing reabsorption of bile acids – form an insoluble, undigestible clump with bile acids & they are excreted.
Body uses up LDL to make bile.

Not absorbed from GI so safe & SE limited to GI (constipation, bloating etc)

Can bind other drugs

27
Q

Fibric Acid Derivatives
Med
Effects
SE

A

Med: gemfibrozil, fenobric acid

Effects: Effective for TG (triglycerides) and raise HDL but minimal impact on LDL (lowers VLDL level)

SE: GI disturbances, ↑risk of gallstones, myopathy, liver injury

28
Q

Niacin
action
SE
NSG

A

Niacin = ↓LDL & TG (triglycerides), ↑significant HDL

Acts by ↓VLDL production

SE: Flushing, itching of skin, GI tract :N,V,D; liver toxicity; hyperglycemia, gouty arthritis

NSG: teach ASA before dose can ↓ flushing

29
Q

Fish Oil
contains?
Action?

A

Fish Oil
Contains EPA & DHA (omega 3 fatty acids)
Lower TG levels; prevent platelet aggregation, reduce inflammation, plaques; ↓BP

30
Q

Platelet aggregate inhibitors
Med:
Uses:
SE:

A

Med: ASA, clopidogrel

Uses: Used to prevent MI, CVA, (stenosis of stents)
3 types of drugs that have different actions but same effect

ASA SE: GI bleeding & ↑ hemorrhagic stroke risk

clopidogrel SE: cautious use with NSAIDS & anticoagulants, GI effects, PPIs (proton pump inhibitor) may ↓effectiveness

31
Q

Anticoagulants what does it do

A

reduce formation of fibrin by:
prevent synthesis of clotting factors
OR
inhibit the activity of clotting factors

32
Q
Warfarin (Coumadin)
Med:
Action:
Uses:
SE:
NS:
Evaluation:
Antidote;
A

Med: Warfarin
Action: Inhibits the synthesis of vitamin K-dependent clotting factors

Uses: long-term prevention of DVT & PE, a fib, pts with mechanical heart valves

SE: bleeding

NS: delayed onset: many interactions with other meds; requires adherence with med schedule, lab testing, and dietary consistency with vitamin K intake; can be dangerous if liver disease or bleeding disorders

Evaluation: PT/INR

Antidote: vitamin K or fresh frozen plasma

33
Q
Heparin derivatives
Med:
Action:
Uses:
SE:
NS:
Evaluation:
Antidote;
A

Med: Heparin

Action: Inhibits the activity of clotting factors

Uses: Used for acute treatment due to its rapid onset
Uses: embolism, evolving CVA, DVT treatment, DVT prevention with lower doses, during procedures

SE: bleeding, heparin-induced thrombocytopenia, hypersensitivity

NS: low molecular wt versions (lovenox) are more consistently bioavailable and don’t need lab monitoring

Evaluation: aPTT , and monitor platelets

Antidote: protamine sulfate

34
Q
Nitroglycerin
Med:
Action:
SE:
NS:
A

Med: Nitroglycerin

Action: Directly vasodilates and ↓ cardiac oxygen demand in stable angina and can ↓ spasm and ↑oxygen supply in variant angina

Many dose forms, routes, durations of action
Quickly available but rapid metabolism by liver

SE: HA, Hypotension, reflex tachycardia

NS: tolerance can develop quickly, monitor BP carefully, especially with changes or short-acting

35
Q
Positive inotropes: digoxin
Med:
Action:
Uses:
SE:
NS:
Evaluation:
A

Med: digoxin

Action: increases force of ventricular contraction by causing calcium to accumulate in heart cell
Improves cardiac output, ↓HR, heart size declines, ↓vasoconstriction; ↓fluid overload; alters electrical
Potassium competes with dig for binding sites so if hypokalemia exists much ↑risk of dig toxicity

Uses: HF, dysrhythmia

SE: dysrhythmias, visual (halos, blurred vision, yellowing), and GI (anorexia, N, V), fatigue

NS: NARROW THERAPEUTIC RANGE, carefully consider med changes, apical pulse every time you give it, teach S/S of toxicity, monitor K