• Influence the contractility of muscular tissue
• "Squeeze" effect
• Positive or Negative

• Influence the heart rate
• Positive or Negative

• Influence the conduction velocity of nerve or muscle fibers
• Positive or Negative

Hypertension Drugs

Beta Blockers

• Beta-Blockers: Beta-Adrenergic Blocker

• Block the sympathetic nervous system (especially sympathetics to the heart)

• Produces a slower HR and lowered BP

• 5 different classes of blocking agents

Hypertension Drugs - Beta Blockers

Beta-Adrenergic Blocker

Prototype: Propranolol (Inderal) "LOL"

Indications

- HN, angina, prevent cardiac arrhythmias, migraines

- Once the most widely prescribed

Actions

- Blocks beta-adrenergic receptors in the nervous system and blocks beta-receptors of the heart

- Inhibits catecholamine binding at beta one and beta two receptor sites

- Decreases HR, contractility, and excitability, which reduces cardiac workload

Side Effects

- Hypotension, bradycardia, fatigue, weakness, syncope, GI, decreased libido, pulmonary edema, allergic reaction

Teaching/Nursing Implications

- Side effects

- Daily pulse and BP

- Avoid sudden discontinuation

- Hold for a stress test

Hypertension Drugs

Diuretics

• Increase volume of urine produced
• Increase Na excretion
• Na causes increased intravascular volume, therefore increased BP
• "Water Pill"
• Vasodilating effect
• Watch labwork (especially K+)
• S/Sx of dehydration
• Use cautiously with renal pts
• Advantages: CHEAP
• Disadvantages: risk for electrolyte imbalances
• Best way to measure effectivenss is loss of wt (fluid)

Hypertension Drugs - Diuretics

Thiazides

Prototype: hydrochlorothiazide (Hydrodiuril) HCTZ

Indications

- HN, HF, liver, and renal disease

Actions

- Blocks the Cl pump in the kidney (keep Cl in kidney to be excreted and Na moves out with Cl)

- Mild diuretic

Side Effects

- orthostatic hypotension, hypokalamia, muscle cramps/spasms

Teaching/Nursing Implications

- Teaching

- Watching labs

- I&O, daily wts

- S/Sx of dehydration and hypotension

Hypertension Drugs - Diuretics

Loop Diuretics: work in the Loop of Henle

Prototype: furosemide (Lasix)

Indications

- More diuresis than others (up to 20lb a day)

- HF, HN, renal disease

Actions

- Blocks Cl pump in the Loop of Henle and brings Na with it

- Loop of Henle reabsorbs 30% of all filtered Na

Side Effects

- Hypokalemia, alkalosis, hypocalcemia, bladder spasms, hypotension, constipation

Teaching/Nursing Implications

- Watch labs

- Make sure they have a K+ supplement

- S/Sx of dehydration and hypotension

-BSC, foley, daily wts, I&O

- K+ rich foods

- Consider changing BID times

Hypertension Drugs - Diuretics

Potassium-Sparing Diuretics

(do not excrete as much K+)

Prototype: spironolactone (Aldactone)

Indications

- HN, HF, cirrhosis

- when pt is susceptible to hypokalemia

Actions

- Blocks K+ secretion by blocking the effects of aldosterone in the kidneys, while allowing for Na secretion

Side Effects

- hyperkalemia

Teaching/Nursing Implications

- Monitor K+ levels

- S/Sx of hyperkalemia (LOC changes, cramps, heart arrhythmias)

- Avoid foods high in K+

Hypertension Drugs

ACE Inhibitors & Calcium Channel Blockers

• Angiotensin-Converting Enzyme Inhibitors: acts on renin angiotension system (compensates to ensure adequate blood flow and perfusion to the kidneys)

1. Low BP or lack of oxygenation to kidneys
2. Kidneys secrete renin
3. Renin goes to liver and converts angiotensinogen to angiotensin I
4. Angiotensin I travels to the lungs and combines with ACE to make angiotensin II
5. Angiotensin II causes vasoconstriction
6. Vaso constriction raises peripheral resistance & BP
7. Increased BP allows kidneys to get blood and oxygen it needs

• Calcium Channel Blockers: prevent movement of calcium into the cardiac muscle, interfering with the heart's ability to contract

Hypertension Drugs - ACE Inhibitors

prototype: captopril (Capoten)

Indications

- HN, HF, left ventricular problems after MI

Actions

- Blocks conversion of angiotensin I to angiotensin II by inhibiting the release of renin

- Different types of ACE inhibitors exist and disrupt system at different steps

Side Effects

- Tachycardia, MI, bone marrow suppression (RBC, WBC, platelets), "Cardiac Cough" (cause unknown)

Teaching/Nursing Implications

- Caution in pregnancy

- Baseline tests (renal function, BP, HR)

- Teaching need for compliance

Hypertension Drugs - Calcium Channel Blockers

prototype: diltiazem (Cardizem)

common drugs: Cardizem & Norvasc

Indications

- HN and angina

Actions

- Inhibits calcium movement across the membranes of the heart and arterial muscle cells

- Inhibits the action potential and cell contraction

- Lower contractility, slows cardiac impulses (HR), relaxes and dilates arteries - causes fall in BP and decrease in venous return

Side Effects

- Hypotension, bradycardia, heart arrhythmias, CNS effects, liver damage, flushing of skin (from decrease in venous return causing blood pooling in the extremities)

Teaching/Nursing Implications

- No crushing or chewing

- S/Sx of hypotension

- Avoid grapefruit juice (increases effect)

- Take daily, even if late DO NOT SKIP DOSE

• Inotropic drugs

1. Increases Ca levels in heart muscle
2. Increased contractility
3. Increases CO
4. Increases renal blood flow
5. Decreases renin production
6. Prevent activation of reninangiotinsen system
7. Increases urine output
8. Decreased blood volume
9. Decreases heart workload

Cardiotonic Agents - Cardiac Glycosides

prototype: digoxin (Lanoxin) "Dig"

(originally derived from the foxglove plant)

Indications

- HF and atrial fibulation

Actions

- Positive inotrope

- Diuretic effect (not a diuretic)

- Negative chronotrope

- Negative dromotrope

Side Effects

- Hypotension, bradycardia, weakness, drowsiness, headache, vision changes ("yellow halo", blurring, spots/threads), arrhythmias, GI upset

Teaching/Nursing Implications

- Dose is 0.125mg-0.25mg

- Therapeutic dose close to toxic dose

- Monitor for SE, pregnancy/lactation, MI

- Apical pulse for 1 min, if HR <60 hold, retake pulse 1 hr later, if still <60 hold and call doctor (document, may be indicator of dig toxicity)

Cardiotonic Agents - Digoxin Antidote

prototype: Digoxin Immune Fab (Digibind)

• Digoxin stays in system 6-8 days. Doses can "build-up" and cause too high of a level
• Normal value of digoxin: 0.8-2 ng/ml

Indications

- Digoxin toxicity: >10 ng/ml and symptomatic

- K+ >5 mEq/L

- S/Sx: acute (N/V/D and lethargy); chronic (SE of digoxin)

Actions

- Binds molecules of digoxin, making them unavailable at their receptor site

- Antibody found in sheep

Side Effects

- allergic response, reemergence of HF and AFib, hypokalemia

Teaching/Nursing Implications

- Get pt off your floor

- Continuous heart monitoring, no telemetry, crash cart by the door

- Do not look at labs after giving (serum level will remain high and give false high reading)

- IV only

Cardiotonic Agents - Phosphodiesterase Inhibitors

prototype: inamrinone (Inocor)

Indications

- end stage HF (not responding to Dig, diuretics, or vasodilators)

- short term tx

Actions

- Increases Ca levels in cardiac cell

- Results in stronger contractions

- Vasodilation

Side Effects

- Hypotension, arrhythmias, burning at injection site

Teaching/Nursing Implications

- Telemetry

- S/Sx of hypotension

- Initiated in CCU/Short Stay and then monitored

- Gradually increase tapering

- Frequent VS when starting

• Goal: restore oxygen supply/demand balance to the heart by

1. Dilating vessels: increasing supply of O2 to heart
2. Decreasing workload of the heart: decrease the heart's demand for O2
3. Drugs used are: Nitrates, Beta-Blockers, and Calcium Channel Blockers

• Not used only as anti-hypertensives, but also to relieve angina

Anti-Angial Agents - Nitrates

prototype: nitroglycerin (Nitro-Stat)

Indications

- prevention and treatment of angina pectoris

Actions

- Relaxes and dilates veins and arteries, increasing blood flow and decreasing BP

- Vasodilation causes blood to pool in veins, decreasing the amount of blood the heart has to pump (preload) and the resistance that the heart has to pump against (afterload)

Side Effects

- H/A, hypotension, flushing of the skin, perspiration

Teaching/Nursing Implications

- Sublingual: fast acting tx and most common; mouth should be moist, do not swallow, bottle out of light, expiration 6 months, cotton out, 3x5 rule

- NTG spray: (Nitrolingual) make sure it is used under the tongue, do not inhale

- NTG po: (Nitrogard, Nitrocot) not for emergency use, scheduled times to prevent chronic angina

- NTG IV: (Nitrobid-IV, Tridil) do not give on floor, needs to be titrated

- Transderm: dose measured application papers, squeeze ointment on measure scale on paper; apply on non-hairy spot, do not massage, use dressing over it, do not get on hands, remove previous patches, rotate sites, long acting

• Hyperlipidemia: increase in level of lipids in blood (increases risk for CAD)
• Lipid: group of fat or fat-like substances, insoluble in water (alcohol, fatty acids, glycerol, cholesterol)
• Cholesterol: one of the groups of lipids, main component in plaques in arteries/veins; body needs it to maintain normal function (hormones, cell formation and maintenance). Sources are dietary, but can be made by the body if needed

1. HDL: "good cholesterol" <40 risk for heart disease, >60 goal
2. LDL: "bad cholesterol" <100 optimal, >160 risk for CAD
3. Triglyceride: combination of glycerol and 3 fatty acids, called neutral fats; combined with proteins form lipoproteins. <150 normal and >220 high

Lipid-Lowering Agents - HMG-CoA Inhibitor

prototype: atorvastatin (Lipitor)

Indications

- Hyperlipidemia, usually with 1 other risk factor (with pts who had poor results with diet changes)

Actions

- Blocks formation of cellular cholesterol

Side Effects

- hard on the liver, lot of GI Sx, rhabdomyolysis (muscle breakdown; hurts, can shut down kidneys)

Teaching/Nursing Implications

- S/Sx of SE

- Frequent monitoring of liver enzymes and cholesterol levels

• Coagulation: process of forming a solid state of blood, purpose of maintaining stability of cardiovascular system
• Clot resolution: body must also have a system to stabilize coagulation in order to keep vessels open and blood flowing
• Delicate balance
• Coagulation involves a complex process involving vasoconstriction, platelet clumping, and a cascarde of clotting factors

• Blood vessel injury causes vasoconstriction in attempt to "seal off" the injured site, and promote healing
• Sometimes this is good enough, and sometimes not

• Platelets circulating through blood "stick" to the site of injury and release a chemical (ADP) that attracts other platelets to the site ("stick" to collagen, which is exposed from the injured vessel lining)
• ADP also causes further vasoconstriction
• Plug is formed, keeping the cardiovascular intact
• Sometimes this is good enough, and sometimes not

• Injured vessel wall exposes collagen and Factor XII (Hagemen Factor) is activated and stimulates a complex series of coagulating substances, culminating in the activation of thrombin. (Clot resolution process also starts at this time, as well as the inflammatory process)
• About 12 factors that effect coagulation
• Thrombin breaks down fibrinogen to form fibrin threads. These are what form a clot inside of the vessel at the site of the injury
• Clot = thrombus

• Basically the same as intrinsic pathway only it forms a clot on the outside of the blood vessel
• Injured vessel is vasoconstricted (by 2 different processes) and there is a clot on the inside of the vessel and one on the outside of the vessel
• If that doesn't work = problem

• Blood plasma has anti-clotting substances to inhibit clotting reactions that could lead to obstruction due to clots
• Antithrombin III: prevents formation of thrombin, prevent fibrin threads from forming
• Plasmin: dissolves clots (high levels of plasmin are found in lungs and uterus) and can be stimulated throughout body when intrinsic pathway is started
• Anticoagulants: drugs that interfere with normal coagulation process
• Different drugs affect the process at different steps to slow, prevent, or dissolve clot formation
• Antiplatelet drugs: affect formation of platelet plug (platelet aggregation)
• Anticoagulants: interfere with clotting cascade (intrinsic and extrinsic pathways)
• Thrombolytic drugs: break down clots, once formed
• NOT "Blood Thinners"

Drugs Affecting Coagulation - Antiplatelets

prototype: aspirin (Aspirin)

• Decrease the formation of the platelet plug by decreasing the responsiveness of platelets to stimuli - messes up ADP process, factor VII, prostoglandin production and intrinstic pathways

Indications

- prevent stroke, MI, occluded vessels, intermittent claudification, analgesic, anti-inflammatory, anti-pyretic

Actions

- inhibits platelet adhesion and aggregation

- prevents formation of the plug

Side Effects

- bleeding (GI and dental), tinnitus, aspirin toxicity, heartburn, rash

Teaching/Nursing Implications

- S/Sx of SE

- Bleeding precautions

- Monitor INR

- Promote enteric coated

- "Stool check"

Drugs Affecting Coagulation - Anticoagulants

prototype: heparin (Heparin)

• interfere with the clotting cascade (intrinsic and extrinsic pathway) preventing clot formation

Indications

- prevention of PE (given through IV drip), DVT, cardiac embolus (AFib:risk) MI, and IV and dialysis line from clotting

Actions

- prevents conversion of prothrombin to thrombin, thus preventing fibrin from forming

- does NOT dissolve clots

Side Effects

- bleeding (GI and dental), heartburn, rash, toxicity

Teaching/Nursing Implications

- Monitor for SE

- When starting usually give a IVP bolus, then start IV rate

- IV line care: hold pressure longer when DCing, triple lumen subclavian over a stick for lab draws, patency/maintainence

• Inhibit clot formation by blocking different blood clotting factors (X and II)
• Less SE
• Do not affect thrombin, clotting due to Factor VII or PT
• Use to prevent/slow down CA
• Used postop and when on long term bedrest
• Do not use with other heparin Tx = death
• Usually given in the abdomen, sub-q
• Fragmin, Lovenox, Arixtra

Drugs Affecting Coagulation - Anticoagulants

prototype: warfarin (Coumadin)

always po

• interfere with the clotting cascade (intrinsic and extrinsic pathway) preventing clot formation

Indications

- preventing clot formation - maintenance, long term Tx AFib, artificial heart valves, DVT, post MI/PE

Actions

- works differently than heparin

- prevents production of vitamin K dependent clotting factors (vitamin K causes clotting enhancement)

Side Effects

- bleeding (GI and dental)

- More severe; antidote: vitamin K subq, po

Teaching/Nursing Implications

- Monitor labs (PT/INR)

- Compliance with meds

- Onset of action is 3 days (not for acute situation)

- Effect lasts 4 or 5 days (hold before surgery)

- Do not use if pregnant

- Watch herbals

- "Stool check"

Drugs Affecting Coagulation - Thrombolytic Agents

prototype: streptokinase (Streptase)

Indications

- coronary thrombosis, PE, DVT, some strokes

Actions

- Actually dissolve an existing clot

Activates plasminogen to plasmin, which breaks down the fibrin threads

Side Effects

- deferred

Teaching/Nursing Implications

- deferred