intotropic

chronotropic

dromotropic

effects

inhibits sodium-potassium ATPase pump which increases cellular sodium and calcium concentrations - overall effect is enhanced myocardial contraction

Augments vagal (cholinergic or parasympathetic) tone: results in increased diastolic filling b/w heartbeats the reduce HR – this further enhances cardiac efficiency and output

Change the electrical conduction properties of the heart: decrease the rate of electrical conduction and prolong the refractory period in the conduction system - this affects the conduction system and cardiac automaticity

Particularly affects conduction b/w the atria and the ventricles (SA node to AV node): Cardiac cells remain in a state of depolarization longer and are unable to start another electrical impulse – reduces the HR and improves cardiac efficiency

What are the 3 "tropic" effects of digoxin (Lanoxin)?

Positive inotropic effect resulting in an increase in the force and velocity of myocardial contraction without a corresponding increase in oxygen consumption.

A negative chronotropic effect producing a reduced HR.

A negative dromotropic effect that decreases automaticity at the SA node, decreases AV nodal conduction, reduces conductivity at the bundle of His, and prolongs the atrial and ventricular refractory periods.

systolic HF, supraventricular tachycardias

Very narrow therapeutic window: normal level is 0.8-2 ng/ml

Bradycardia, A/N/V, colored vision, halo vision are classic!

CV - Any type of dysrhythmia, including bradycardia or tachycardia

CNS - HA, fatigue, malaise, confusion, convulsions

Eye - Colored vision (i.e., green, yellow or purple), halo vision or flickering lights

GI - Anorexia, nausea, vomiting, diarrhea

What electrolyte imbalance increases digoxin toxicity? 

Potassium [K⁼]

High K, low dig therapeutic effects

Low K, high dig therapeutic effects

(hyperkalemia – serum level over 5 mEq/L

hypokalemia - serum level below 3.5 mEq/L)

Antidote: Digoxin immune Fab or Digibind – IV only

Can’t be given unless you know what their dig level is – dosed based on dig level in body.

(order labs before you give med so you know this level)

Additive interactions with other meds that are used to affect the heart.

K+ wasting diuretics increase dig toxicity.

Some antilipemics decrease absorption of dig.  

Antidysrhythmics, sympathomimetics, loop diuretics, laxatives, adrenal steroids and thiazide diuretics - increase dig toxicity

Antacids, antidiarrheals, barbiturates - reduce therapeutic effects

Anticholinergics - increased therapeutic effects

Beta-blockers - enhanced bradycardic effect of dig

Calcium channel blockers - enhanced bradycardic and inotropic effects of dig

Some antidysrhythmics: quinidine, verapamil, amiodarone - increase dig levels (dose should be reduced by 50%)

Why check apical pulse for 1 full min prior to giving digoxin? 

Documentation needed for any irregularities, a pulse rate less than 60 beats/min or more than 100 beats/min as a baseline and identification marker for toxicity.

Why check breath sounds and edema with dig therapy?

This assessment checks for fluid levels – important because of the narrow therapeutic window for dig therapy.

Your client eats 2 bowls of bran cereal every AM with his digoxin.  Is this good or bad?  Why?

This is a bad thing – bran alters the absorption of dig

• Pts should always take radial pulse before admin
• Elderly and physically or mentally challenged are more at risk for interactions with other meds, adverse effects and toxicity.
• Pts should be encouraged to keep a journal with details about med administration and effects/changes in body functioning.
• Pts are encouraged to contact physician with unusual complaints, A/N/V or erratic pulse (<60 beats/min or >100 beats/min)
• Pts should report any changes in vision
• Pts should report any changes in heart beat, dizziness, fainting, blackouts and weight gain (2lbs or more in 24hrs, 5lbs or more in 1 week)
• Pts should weigh themselves daily
• If symptoms worsen, notify HCP
• Pts should wear a medical alert bracelet with up to date information
• Dig should be taken once at day, at the same time every day
• No double dosing, not skipping dose, if dose has been missed by more than 12 hrs: contact HCP.
• Med should not be abruptly stopped
• Consume foods high in potassium, esp if taking a potassium-depleting diuretic
• Avoid using antacids, eating milk products for 2 hrs before or after taking med to avoid interference with drug

nitroglycerin (Nitrostat, Nitro-Bid)

Dilate all blood vessels, especially venous vascular beds.  ***Potent dilating effect on coronary arteries.

atenolol (Tenormin)

Block the beta receptors of the heart to slow the HR (slows firing of SA node, slow conduction to AV node and reduce myocardial contractility)

diltiazem (Cardizem)

Blocks Ca++ in the excitation-contraction process of heart and vascular muscle cells >>> promotes contraction of heart and vessels (vasodilation). 

Also decreases automaticity of and conduction thru SA and AV node >>> decreases/slows heart rate. 

Angina

(prevention and treatment

Nitrates: AEs

HA - real common, reflex tachycardia (compensatory mechanism to increase cardiac output).

Nitrate tolerance.  

Patient becomes tolerant to the effects of the nitrate treatment.

Can often occur quickly.

Prevention: a regular nitrate-free period is arranged to allow certain enzymatic pathways to replenish themselves.

Ex- remove transdermal patch at night and apply new patch in the morning (8hr nitrate-free period).

Beta-blockers: Indications

Treatment of typical exertional angina (caused by exercise), MI, HTN, cardiac dysrhythmias and essential tremor

Slow contractility, HR and conduction.

Blocking of beta-1 receptors: decreases in HR, CO and contractility

Blocking of beta-2 receptors: bronchoconstriction and increased airway resistance in pts with asthma or COPD.

Beta blockers mask tachycardia associated with hypoglycemia.

Can cause both hypoglycemia and hyperglycemia

CV - Bradycardia, hypotension, 2^nd or 3^rd degree heart block, HF

CNS - Dizziness, fatigue, mental depression, lethargy, drowsiness, unusual dreams

Metabolic - Altered glucose and lipid metabolism

Other - Wheezing, dyspnea, impotence

First-line drug for: angina, HTN and supraventricular tachycardia

Particularly effective for tx of coronary artery spasms.

Also used for short-term management of A fib. and flutter, migraine, HA and Raynaud’s disease.

dihydropyridine CCB nimodipine is indicated solely for cerebral artery spasms associated with aneurysm rupture.

Peripheral edema, bradycardia, and HF are common.

(Related to the over-expression of the therapeutic effects of CCBs)

• A complete health and medication history should be completed along with wt, ht and vital signs.
• A systolic BP of less than 90mmHg should be reported to the HCP before a dose of these drugs are given
• Pts chest pain should be thoroughly assessed (possible ECG).
• In teaching pt, emphasize significant drug interactions with nitrates and importance of of blood pressure control (esp worsening of symptoms)
• Beta-blockers should not be used in pts with asthma or resp trouble; also concern in pts with hyperthyroidism, impaired renal or liver func, PVD or diabetes
• Assess wt gain (concern: 2lbs or more in 24hrs, 5lbs or more in 1wk)

clonidine (Catapres)

captopril (Capoten)

losartan (Cozaar)

hydralazine HCl (Apresoline)

Antihypertensives: clonidine (Catapres)

Classification and Mechanism of Action

Alpha-2 adrenergic receptor stimulator (agonist)

Works by stimulating the alpha-2 adrenergic receptors in the brain which reduce sympathetic outflow from the CNS which reduces BP  

Classification and Mechanism of Action

Angiotensin-converting enzyme inhibitor (ACE inhibitor)

Inhibit angiotensin-converting enzyme which is responsible for converting angiotensin I (AI) to angiotensin II (AII).

Classification and Mechanism of Action

Angiotensin II receptor blocker (ARB)

Block binding of AII to type 1 AII receptors, thereby block vasoconstriction and secretion of aldosterone

Vasodilator

Directly elicit peripheral vasodilation – reduction of SVR (hypotensive effects)

Adrenergic Agents: Key drug 

(adrenergic agents include: alpha1 blockers, centrally acting agents, peripherally acting agents)

Key drug: clonidine (Catapres) - an alpha-2 adrenergic receptor stimulator (agonist)

Pts experience sedation and drowsiness -  sympathetic outflow from CNS is reduced which reduces BP

(body is less stimulated, systems are slowed)

Orthostatic hypotension - a sudden drop in BP during changes in position.

CNS depressants - Alcohol, benzodiazepines and opioids

(enhance CNS depression)

These drugs block the angiotensin-converting enzyme (ACE) - ultimately prevents vasoconstriction and aldosterone secretion.

(Aldosterone - responsible for reabsorption of salt and water and excretion of potassium in the kidneys)

ACE Inhibitors (the "prils"): Indications

Drug of choice for what population?

HTN, stop progression of ventricular remodeling post MI (“cardioprotective effect”).

“Pro-drug” – not effective until metabolized by the liver.

Drug of choice for:

Hypertensive patients with HF and diabetic pts

(protect/preserve the kidneys)

Persistant, non-productive cough is a classic side effect – “ACE” cough (coughing all the time).

CNS - Fatigue, dizziness, mood changes and HA

CV - Significant decrease in BP - hypotension

Other - Loss of taste, proteinuria, hyperkalemia, rash, pruritus, anemia, neutropenia, thrombocytosis and agranulocytosis

Pts with severe HF: renal failure

Potentially fatal: angioedema (strong vascular reaction involving inflammation of submucosal tissues, which can progress to anaphylaxis)

ACE Inhibitors (the "prils"): Interactions

Any ideas why hyperkalemia may occur when ACE inhibitors are given with K+ sparing diuretics or K+ supplements?  (Hint: take a look at RAAS - what does aldosterone do?)

Lots of drug interactions. 

Aldosterone increases renal excretion of potassium – ACE inhibitors block its secretion from the adrenal gland and so K+ builds up in the body, leading to hyperkalemia.

Pregnancy, lactation

Hyperkalemia

Known allergy or hypersensitivity

captopril (Capoten)

Angiotensin II receptor blocker (ARB) ("sartan" drugs): Key drug

Do not protect the heart and kidneys like the ACE Inhibitors do

Don't cause the classic cough like ACE-I do  

But they do cause:

Most common: upper respiratory infections and HA.

Occasionally: insomnia, dizziness, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigue.

Rarely: Anxiety, muscle pain, sinusitis, cough and insomnia.

3 negative tropic effects: HTN, Angina, tachydysrhythmias, prevention of cerebral artery spasms post-CVA

Block intracellular calcium influx

furosemide (Lasix) – most effective diuretic

Block chloride absorption – blocks sodium – water follows sodium and is peed out (unfortunately, potassium is also peed off)

Run the risk of hypokalemia

Increase renal prostaglandins – kidneys work more effectively

Potency depends where the diuretic works – strongest are the loop diuretics (Loop of Henle), least effective are in the distal collecting duct

Used for rapid diuresis, with kidney failure and FVE

Treat HF and HTN by vasodilation (pee extracellular fluid off)– decreasing blood pressure and preload

Reduce afterload, BP and preload

Antihypertensives: Diuretics

Nursing Considerations

Check BP, I&O (urine output) and daily weights

Antagonized by NSAIDs

Antihypertensives: Diuretics

Contraindications

Allergy

End stage liver failure

Severe electrolyte imbalances

Antihypertensives: Diuretics

AEs

Electrolyte imbalances: hypokalemia

CNS – HA, dizziness, tinnitus

Antihypertensives: Diuretics

Toxicity

Tx: fluid and potassium

Hypokalemia – heart gets irritable without potassium (PVCs)

Neurotoxicity and nephrotoxicity

Best test of nephrotoxicity – check creatinine level (high=something wrong with kidneys)

Ototoxicity (cranial nerve toxicity) – permanent hearing loss

Antihypertensives: Vasodilators

Key Drug

hydralazine HCl (Apresoline)

Antihypertensives: Vasodilators

What else can this class of drugs be used for?

Minoxidil (Rogaine): in topical form, used to restore hair growth.

 dizziness, HA, anxiety, tachycardia, edema, nasal congestion, dyspnea, etc.

Minoxidil: 

T-wave changes on ECG

Cardiac tamponade

Breast tenderness or gynecomastia (men grow breasts)

Nipride:

Potential for cerebral steal and/or coronary steal - can causes profound hypotension

Cyanide toxicity – metabolized down to cyanide

Severe HTN

Parenteral form is generally reserved for treatment of severe or malignant HTN

Hypotension

CAD or AMI – steals blood from organs

Assessment parameters (monitor the following)

• Pulse, BP, resp – hold parameters
• Want to keep BP about 130/80
• Serum electrolytes
• Potassium and sodium
• Renal and hepatic func
• ACE inhibitors are highly metabolized in these areas
• Importance of ophthamoscopic exam
• Blood is pulled away from retinal - retinopathy
• Peripheral edema
• Blood pools in extremities when drug is working too well
• I&O and daily weights
• Dilation is causing weight gain – drug is working too well

Why assess respiratory status and K+ serum levels prior to giving captopril (Capoten)?

ACE inhibitors have the AE of a dry, hacking, chronic cough.

Antihypertensives: Vasodilators

You are preparing to administer hydralazine (Apresoline) to your elderly client.  What is important to assess first?

Baseline neurologic assessment with noting of level of consciousness and cognitive ability – elderly are esp sensitive to drug’s ability to lower BP (more problems with hypotension, dizziness and syncope)

Diuretic Agents: Carbonic Anhydrase Inhibitors

Effects

Sodium is exchanged for hydrogen ions in the proximal tubules of the nephrons of the kidney.

Water follows sodium in the exchange.

Without hydrogen, the salt exchange and the retention of water that follows the sodium cannot occur.

Carbonic anhydrase helps make hydrogen available for this exchange.

Diuretic Agents: Loop Diuretics

Key Drug

Diuretic Agents: Loop Diuretics

Mechanism of Action

Advantage: work even if creatinine clearance is low (< 25 mL/min; nl is 125 mL/min) and if there minimal kidney function (3% or more)

Diuretic Agents: Loop Diuretics

Indications

Edema with HF and hepatic or renal disease

HTN

Diuretic Agents: Loop Diuretics

AEs

CNS - Dizziness, HA, tinnitus, blurred vision

GI - Nausea, vomiting, diarrhea

Hematologic - Agranulocytosis, thrombocytopenia, neutropenia

Metabolic - Hypokalemia, hyperglycemia, hyperuricemia

Diuretic Agents: Loop Diuretics

Drug Interactions

Aminoglycosides, capreomycin, chloroquine, vancomycin - increased neurotoxicity, esp ototoxicity

Corticosteroids, digoxin - additive hypokalemia, increased dig toxicity

lithium - increased lithium toxicity

NSAIDs - decreased diuretic activity

Sulfonylureas - hyperglycemia

Diuretic Agents: Loop Diuretics

What happens when given with ibuprofen (NSAID)? 

Inhibits full effect of diuretic

Diuretic Agents: Loop Diuretics

What happens when given with digoxin?

Additive hypokalemia and increased dig toxicity.

Diuretic Agents: Osmotic Diuretics

Key Drug

Produces osmotic pressure in the GF >>> pulls fluid into tubules >>> diuresis

Osmotic diuretic of choice.

Non-absorbable – leaches out fluid and promotes diuresis

(No significant electrolyte block)

Effective in getting rid of fluid – esp. fluid on the brain (cerebral edema – closed head injuries)

Early, oliguric phase of acute renal failure, increased incranial pressure and cerebral edema.

Convulsions, thrombophlebitis, pulmonary congestion.

End-stage renal disease (ESRD)

Active intracranial hemorrhage

Keep it warm and push through a filter – it crystallizes just below room temp

Diuretic Agents: Potassium-Sparing Diuretics

Key Drug

Binds to aldosterone receptors (blocks aldosterone) >>> blocks resorption of Na+ and water, spare potassium

Hyperaldosteronism

HTN

Reverse potassium loss caused by potassium-wasting (i.e., loop, thiazide) diuretics

Used in combo with potassium-wasting drug to keep therapeutic levels

Provide diuresis without causing electrolyte imbalance

Cardio-protective

CNS -Dizziness, HA

GI - Cramps, nausea, vomiting, diarrhea

Other - Urinary frequency, weakness, hyperkalemia, dysamennorhea in women and men grow breasts

Admin of ACE-I or potassium supplements in combination with potassium-sparing diuretics can result in hyperkalemia.

ACE-I block secretion of aldosterone (hormone that promotes K+ wasting)

Potassium-sparing diuretics keep K+ from being excreted

Potassium supplements increase serum K+ levels

All these factors can lead to build-up of K+ in the serum without proper excretion, which can lead to hyperkalemia.

Diuretic Agents: Thiazides

Key Drug

hydrochlorothiazide (HydroDIURAL)

Inhibit resorption of Na+, K+, Cl^- >>> osmotic water loss.  Direct relaxation of arterioles >>> reduces afterload.

Works best with adequate creatinine clearance (> 50 mL/min).

HTN

Edematous states

Idiopathic hypercalciuria

Diabetes insipidus

Orthostatic hypotension

Dehydration

Impotence, decreased libido

Reduced K⁼ levels (hypokalemia)

Elevated levels of: Ca²⁼, lipids, glucose and uric acid

Interactions

Corticosteroids, dig and oral hypoglycemics

• Administration: PO – give with food to minimize gastric upset; IV– confirm rates and use infusion pump.
• Baseline vitals (BP, pulse, I & O [hydration status], capillary refill, daily weights) and continue to be monitored as well as heart rate and rhythm.
• Assess for signs and symptoms of constipation (FVD), cardiac irregularities, nocturia and hyperkalemia (nausea, vomiting, diarrhea, and abdominal cramping)

• Physical assessment with documentation of baseline fluid volume levels, postural BPs, skin turgor, status of moisture levels of mucous membranes and capillary refill; kidney and liver function.
• Labs: serum potassium, sodium, chloride, magnesium, calcium, uric acid and creatinine levels should be measured and documented; ABGs and blood pH.
• Discuss cautions, contraindications and interactions associated with the diuretics (esp loop diuretics – adversely react with other meds that are ototoxic or nephritic)

• Maintain proper nutritional intake and fluid volume status – eat potassium-rich foods.
• Foods high in potassium: bananas, oranges, dates, raisins, plums, fresh veggies, potatoes (white and sweet), meat, fish, apricots, whole grain cereals and legumes.
• Potassium supplements may be recommended.
• Frequent lab tests at the beginning of therapy.
• Pts need to change positions slowly (orthostatic hypotension) and give meds at night (nocturia).
• Forcing fluids may be needed to keep levels therapeutic.
• Pts should report any unusual effects of problems to their HCP immediately.
• Pts should keep a daily journal to monitor changes (if any).
• Prevent constipation with an increase in fiber, bulk, roughage and fluids (if not contraindicated)
• Pts should avoid hot climates and spaces (saunas, hot tubs) that may cause excessive fluid loss.
• Pts educated about signs and symptoms of hypokalemia – weakness, leg cramps, and other cramping.
• Pts educated on monitoring pulse when taking dig and diuretics and be educated on dig toxicity.
• Pts with diabetes mellitus who are taking thiazide and/or loop diuretics must be educated about close monitoring of blood glucose levels.