Cardio Vascular Medications Flashcards
Diuretics what does it do
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
Diuretics med
Thiazide Loop Potassium-sparing -Aldosterone antagonists -Non-aldosterone antagonists
=↓ circulating volume and venous return to heart. ↓SVR.
Loop diuretics medication Med: Action: Uses: SE: NS: Evaluation:
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
Thiazide diuretics Med: Action: Uses: SE: NS: Evaluation:
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
Potassium-sparing: aldosterone antagonist Med: Action: Uses: SE: NS: Evaluation:
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
Potassium-sparing: non aldosterone antagonists
Med:
Action:
SE:
Med: triamterene
Action: This class of medications directly blocks the reuptake of Na and the excretion of K
SE: Can cause elevated K levels
Drugs that act on the Renin-Angiotensin-Aldosterone System
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)
what does angiotensin do?
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)
By vasodilation and decreasing blood volume we can:
- drop blood pressure 2. improve circulation to the heart muscle 3. reduce the workload of the heart
- prevent nephropathy by dropping pressure in the glomerulus
By blocking the evil effects of angiotensin 2 we can
- improve outcomes after MI
- reduce cardiac death
- reduce remodeling of heart muscle
Direct Renin Inhibitors
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
ACE Inhibitors: “pril" Med: Action: Uses: SE: NS: Evaluation:
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
Angiotensin II Receptor Blockers (ARBS): “sartan”
Action?
Effects?
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
Drugs that interfere with the RAAS
Basic effect of all drugs in this class is vasodilation, increased excretion of salt and water, and prevention of A2 damage to tissues
Calcium Channel Blockers
CCBs grow in the “pines”
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
Calcium Channel Blockers
Short version
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)
By turning off (or turning down) the “on switch” CCBs can:
- dilate arteries (tx HTN, angina)
- ↓force of cardiac contraction, 3. slow HR
- treat arrhythmias
- ↓conduction thru AV node.
Calcium Channel Blockers Med: Action: Uses: SE: NS: Evaluation:
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
Alpha blocker short version
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
Beta blocker the short version
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)
Adrenergic blockers: Med: Action: Uses: SE: NS: Evaluation:
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
3 groups of beta blockers
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,
Direct Vasodilators the short version Effects Action Use SE Med
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
Centrally-acting antihypertensive the short version Effects Action SE Med
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)
HMG-CoA Reductase Inhibitors: “statins” Med: Action: Uses: SE: NS: Evaluation:
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
Bile-Acid Sequestrants
Use
Action
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
Fibric Acid Derivatives
Med
Effects
SE
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
Niacin
action
SE
NSG
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
Fish Oil
contains?
Action?
Fish Oil
Contains EPA & DHA (omega 3 fatty acids)
Lower TG levels; prevent platelet aggregation, reduce inflammation, plaques; ↓BP
Platelet aggregate inhibitors
Med:
Uses:
SE:
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
Anticoagulants what does it do
reduce formation of fibrin by:
prevent synthesis of clotting factors
OR
inhibit the activity of clotting factors
Warfarin (Coumadin) Med: Action: Uses: SE: NS: Evaluation: Antidote;
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
Heparin derivatives Med: Action: Uses: SE: NS: Evaluation: Antidote;
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
Nitroglycerin Med: Action: SE: NS:
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
Positive inotropes: digoxin Med: Action: Uses: SE: NS: Evaluation:
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
