Antihypertensive Meds PDF

ANTIHYPERTENSIVE MEDS All these drugs drop the blood pressure and take the workload off the heart - Except DIGOXIN which does not affect BP, but decreases the heart rate and improve cardiac contractility For meds that decrease the BP, we need SLOW POSITION CHANGES - When blood pressure is LO...

ANTIHYPERTENSIVE MEDS All these drugs drop the blood pressure and take the workload off the heart - Except DIGOXIN which does not affect BP, but decreases the heart rate and improve cardiac contractility For meds that decrease the BP, we need SLOW POSITION CHANGES - When blood pressure is LOW, we gotta go SLOW - The goal is to prevent ORTHOSTATIC HYPOTENSION A is for ACE inhibitors and ARBs ACE inhibitors and ARBs - Lowers the blood pressure - But not the heart rate 1st choice to lower the blood pressure are ACE inhibitors - Meds ending in PRIL SECOND CHOICE to lower BP - Angiotensin Receptor Blockers (ARBs) - Meds ending in SARTAN, like losartan QUESTIO N - Do we give PRILS and SARTANS if the heart rate is BRADYCARDIC or below 60? ANSWER YES! ACE inhibitors and ARBs act to  lower the blood pressure only Not the heart rate Renin-Angiotensin-Aldosterone System ​ ​ The renin-angiotensin-aldosterone system (RAAS) maintains fluid and salt levels in the body and, in turn, blood pressure. ​ ​ The two main enzymes involved with the RAAS are renin and the ACE. ​  The body releases renin as a response to low blood pressure  and converts angiotensinogen into angiotensin I, the first step. ​ ​ The next step comes from the ACE, which converts angiotensin I to angiotensin II. Angiotensin II is important in blood pressure control because it can ​ (1) promote sodium and water reabsorption and ​ (2) maintain vasoconstriction. ​ ​ Both actions increase blood pressure. Therefore, we expect a patient with high blood pressure to get medicines that block areas of the RAAS system​ RENIN- ANGIOTENSI N- ALDOSTERO NE SYSTEM (RAAS) ACE and ARBs mechanisms of action  ACE inhibitors block the action of ACE​ ​ stopping the conversion from angiotensin I to angiotensin II. This blocks fluid retention and vasoconstriction, resulting in lower blood pressure. ​  ARBs prevent angiotensin II from binding to receptor sites on the: ​ kidneys ​ and arteries​ resulting in vasodilation and preventing sodium reabsorption.​ Both ACE and ARBs either inhibit or block the Renin- Angiotensin- Aldosterone System Aldostero ne 1. Is BLOCKED from adding sodium and water in 2. And letting potassium out REMEMBER! Sodium and potassium have an INVERSE RELATIONSHIP  if potassium is high, sodium is low  If sodium is high, potassium is low Nurses should WOF hyperkalemi a in patients taking ACE and ARBs DEADLY SIDE EFFECTS OF ACE AND ARBs NOTE:  Angioedema  And cough are side effects that can only be seen in patients taking ACE inhibitors HEALTH TEACHING: AVOID POTASSIUM- RICH FOODS Instruct patients taking ACE and ARBs to avoid fruits and veggies particularly: - Green leafy veggies - Avocados - Melons - And oranges AVOID POTASSIUM -RICH FOODS REMEMBER! Since potassium PUMPS THE MUSCLES - WOF elevated potassium levels (above 5 mEq/L) - Muscle spasms - Peaked T waves - ST elevation NURSING INTERVENTION Any potassium imbalance (high or low) The FIRST ACTION of the nurse should be to attach the patient to a CARDIAC MONITOR REMEMBER the 3 A’s for ACE inhibitors and Angiotensin II receptor blockers THE FIRST DOSE PHENOMENON If you hear:  “First dose”  “Newly prescribed drug”  “first time taking the drug”  DO NOT LEAVE THE PATIENT’S BEDSIDE  ALWAYS ASSESS FOR BIG SIDE EFFECTS For ACEs and ARBs it could be a BIG BP DROP BETA BLOCKERS BETA BLOCKERS are meds ending in LoL Like AtenoLoL For beta blockers think: DOUBLE L’s for DOUBLE LOWS LOW heart rate LOW BP BETA BLOCKERS put the BREAKS on the heart Beta blockers are bad for patients with:  Acute Heart failure Worsening heart failure BETA BLOCKERS MECHANISM OF ACTION Non-selective beta blockers will cause  low BP  slow heart  narrowed bronchi Beta-Blockers There are two beta receptors important to beta-blocker pharmacology: beta-1 and beta-2. Beta-1 receptors are predominantly located in the heart while beta-2 receptors tend to occupy the lungs. When we block the beta-1 receptor, we lower heart rate and likely blood pressure. When we block beta-2, it has more of an adverse effect, since we now constrict the lungs. Because of this, we often avoid first- generation beta-blockers, which can affect the lungs in asthmatics. There are three beta-blocker generations: 1. First generation a. Includes propranolol (Inderal LA) b. Has an -olol stem c. Nonselectively blocks beta-1 and beta-2 receptors d. Avoid using for asthma/COPD patients due to bronchoconstriction 2. Second generation a. Includes atenolol (Tenormin), metoprolol tartrate (Lopressor), and metoprolol succinate (Toprol XL) b. Has an -olol stem c. Selectively blocks only beta-1 receptors 3. Third generation a. Includes carvedilol (Coreg) b. Has a -dil- stem for vasodilation c. Blocks both beta-1 and alpha-1: Alpha-1 blockade leads to vasodilation countering the body’s tendency to vasoconstrict as a response to lower blood pressure DANGEROUS SIDE EFFECTS OF BETA BLOCKERS THE FOUR B’s THE 4 B’s OF BETA BLOCKERS 1. We HOLD THE DRUG for:  BRADYCARDIA LOW BLOOD PRESSURE  Any heart rate LESS THAN 60  Any BP LESS THAN 90 or 100 SYSTOLIC PRESSURE THE 4 B’s OF BETA BLOCKERS 2. Since non-selective beta blockers BLOCK BETA 2 in the lungs patients experience:  bronchospasms (wheezing) DO NOT GIVE in asthma and COPD patients THE 4 B’s OF BETA BLOCKERS 3. Bad for HEART FAILURE patients  new edema  worsening crackles  rapid weight gain  new jugular vein distention All these are signs of heavy fluid accumulation or worsening heart failure THE 4 B’s OF BETA BLOCKERS 4. Do not give in patients with BLOOD SUGAR BELOW 70 mg/dL  because beta blockers can mask the signs and symptoms of hyporglycemia such as TACHYCARDIA, COOL CLAMY SKIN, SHAKINESS  ensure to monitor blood sugar regularly. REMEMBER! HypoGLY, the brain might DIE CALCIUM CHANNEL BLOCKER S Calcium Channel Blockers Smooth muscle requires calcium for vasoconstriction, a narrowing of the vessel. When we block calcium channels in vessels, we can produce the opposite, a vasodilating or vessel opening effect. The heart also needs calcium to function properly and regulate contraction timing. Some calcium channel blockers (CCBs) work to reduce arrhythmias. We then divide CCBs into two main classes:  those that affect the heart and  those that do not. These may not always be the first choice therapeutically due to adverse effects. These two CCB classes, the:  nondihydropyridines and  Dihydropyridines Both vasodilate vessels. Nondihydropyridine CCBs These CCBs blocks calcium channels in the heart and blood vessels, which can help patients with cardiac dysrhythmia, hypertension, and angina pectoris or chest pain. Side effects include constipation and bradycardia. Two nondihydropyridines are  verapamil (Calan) and  diltiazem (Cardizem). Diltiazem (Cardizem): The -tiazem stem identifies diltiazem as a nondihydropyridine. The brand name Cardizem adds the first five letters from cardiac to the last three letters of the generic diltiazem. Verapamil (Calan): The -pamil stem identifies diltiazem as a nondihydropyridine. The brand name Calan takes three letters from the word calcium. Dihydropyridine CCBs Dihydropyridines block calcium channels only in the blood vessels and have no cardiac activity. Thus, we cannot use them for dysrhythmias. Therefore, the most common use for these medications is to treat hypertension. Examples include  amlodipine (Norvasc) and  nifedipine (Procardia). Adverse reactions include peripheral edema and headache. Amlodipine (Norvasc): The -dipine stem comes from dihydropyridine. We can often look at this as a drug that produces a dip in blood pressure. Nifedipine (Procardia XL): Procardia takes the “pro” from promotes and “cardia” from cardiac. Thus, you can remember the brand Procardia XL as promoting cardiac health. Nondihydropyridine Dihydropyridine CCBs Indications: Most often used for hypertension Indications: Most often used for and angina pectoris. hypertension, angina pectoris, and cardiac dysrhythmias. Contraindications: Patients with cardiogenic Contraindications: Patients with shock and use with caution in patients with heart failure or who are post–myocardial infarction. hypotension, severe left ventricular dysfunction or hypersensitivity. Adverse effects: Peripheral edema and Adverse effects: Side effects include headache. constipation and bradycardia. Patient education and care: Patients Patient education and care: If a patient needs may have significant constipation and a low-dose CCB to prevent uterine contractions, nifedipine (Procardia XL), a dihydropyridine, is a should alert their provider. proper choice because it does not suppress the mother’s and fetus’s hearts as the nondihydropyridines would. NONDIHYDROPYRIDI NES KEY NURSING CONSIDERATIONS FOR CALCIUM CHANNEL BLOCKERS particularly nondihyropyridines MNEMONIC: C-C-B MNEMON IC is CCB 1. Always before giving, count the HEART RATE and BP  If systolic BP is 90 or 100 mmHg…WE HOLD THE DRUG!  If heart rate is 60 or less… WE DON’T GIVE THE DRUG! Except for amlodipine and nifedipine MNEMONIC is CCB 2. Change position S-L-O-W-L-Y. Just like any meds that DECREASES BP we want to prevent:  FAINTING  ORTHOSTATIC HYPOTENSION MNEMONIC is CCB 3. BAD HEADACHE, which is typically NORMAL WHEN DO WE HOLD GIVING CCB? 1. Heart rate below 60 bpm 2. Systolic BP below 90 or 100 mmHg 3. Slow or stop any IV drip that is DROPPING the BP TOO QUICKLY DIGOXIN DIGS for a DEEPER CONTRACTION (increasing the force of the heart’s contraction) - Usually given to patients with SYSTOLIC HEART FAILURE  Digoxin is a NEGATIVE CHRONOTROPIC. Meaning it DECREASES HEART RATE CAUTION! Digoxin is a TOXIN!  Very narrow therapeutic index THREE NURSING CONSIDERATION S FOR DIGOXIN THREE NURSING CONSIDERATIONS FOR DIGOXIN MNEMONIC: A T P 1. Always check apical pulse for A FULL 60 SECONDS “if heart rate is LESS THAN 60, it gets RISKY “  don’t give the drug! THREE NURSING CONSIDERATIONS FOR DIGOXIN MNEMONIC: A T P 2. Toxicity – Anything over 2.0 could be TOXIC!  Normal level is 0.8-2.0 ng/mL Early signs of digoxin toxicity: 1. Vision changes 2. Nausea and vomiting 3. Anorexia 4. Dizziness or light headedness NOTIFY DOCTOR IMMEDIATELY! REMEMBER! OLDER PATIENTS WITH DECREASED KIDNEY FUNCTIONS are at high risk for TOXICITY!  Check for BUN and Creatinine levels  Between the two, Creatinine is the No.1 kidney lab  Normal creatinine level (0.6 – 1.2 mg/dL) Creatinine OVER 1.3, means KIDNEY INJURY! THREE NURSING CONSIDERATIONS FOR DIGOXIN MNEMONIC: A T P 3. Low potassium  Potassium level below 3.5 mEq/L increases the risk for DIGOXIN TOXICITY CLARIFICATION:  Digoxin does not cause low potassium  But low potassium does increase DIGOXIN TOXICITY NITRATE S Nitroglycerin converts to nitric oxide, a vasodilator.  Make sure the patient sits when taking the medication because it causes significant dizziness.  With Nitroglycerin, think “nitrous” from sports cars—the patient and blood pressure drop “stat.” NITRO makes the blood pressure GO LOW KILLER CONSIDERATIO N! Indications: Anginal pain. Contraindications: 1. Watch for PDE-5 inhibitors such as sildenafil (Viagra). 2. The combination can create dangerously low blood pressure. Adverse effects: Severe hypotension. Patient education and care: The patient should carry nitroglycerin at all times. The patient should be asked for the bottle at every visit to check the expiration date and remind the patient specifically how to take the medication. KILLER CONSIDERATIO N! STOP NITRO IF: 1. Systolic BP is less than 90 or 100 mmHg 2. Or if we see a drop of 30 POINTS or more  s/sx  confusion  Agitation  Pale  Cold clammy skin  diaphoresis NORMAL SIDE EFFECTS 3 H’s Usually present after very first dose Health Teaching: 1. Slow position changes 2. Always check BP before giving this drug TWO FORMS OF NITROGLYCERIN Pill  Given for stable angina  Stress induced  angina that ceases when at rest Nitro Patch  Given for UNPREDICTABLE ANGINA  angina that can happen anytime  Sleeping/awake, at home/at work TAKE NITRO BEFORE ANY STRENUOU S ACTIVITY IMPORTANT INFO ABOUT NITRO PILL 1. Call EMERGENCY HOTLINE if there is still pain 5 MINS AFTER FIRST DOSE 2. Give only MAXIMUM OF THREE DOSES 5 MINS APART 3. No swallowing (given SUBLINGUALLY) 4. Storage: NO light, NO heat  Replace nitro EVERY SIX MONTHS IMPORTA NT INFO ABOUT NITRO PATCH DIURETIC S The order of diuretics would then be: 1. Osmotic diuretics such as mannitol (Osmitrol) work by increasing osmotic pressure inside the lumen (tube) of the PCT. This action increases water diuresis and in turn, decreases blood volume and lowers blood pressure. 2. Loop diuretics such as furosemide (Lasix) inhibit sodium and chloride reabsorption in the ascending loop of Henle. 3. Thiazide diuretics such as hydrochlorothiazide (Microzide) inhibit sodium and chloride resorption in the DCT. 4. Potassium-sparing diuretics such as triamterene (Dyrenium) and spironolactone (Aldactone) work at the collecting duct. They exchange sodium for potassium and inhibit potassium excretion, “sparing” potassium or keeping more of it in the body. Diuretics produce less diuresis as they continue down. The order from most to least diuresis is: osmotic loop thiazide potassium sparing Osmotic Diuretic Mannitol (Osmitrol) is an osmotic diuretic that reduces intraocular and intracranial pressure, usually in an emergency. It acts on the PCT, preventing reabsorption of sodium and water, increasing urine volume. Adverse reactions can include: The brand name Osmitrol combines the class of medication, osmotic, and adds that it helps control brain swelling. Indications: Generally, we use osmotic diuretics for elevated cerebral or intraocular pressures, whether from trauma or disease. Also, they are used if the patient is in danger of acute renal failure. We give POTASSIUM-WASTERS if potassium level is within NORMAL RANGE  3.5-5.0 mEq/L Encourage patients to eat:  melons  Bananas  green leafy veggies  liver  AVOID licorice root (lowers potassium) Loop Diuretic Furosemide (Lasix) is a loop diuretic named after the loop of Henle. It prevents sodium from being reabsorbed in the loop and the water follows the sodium’s lead, staying in the tube and exiting as urine. Prescribers often use loop diuretics for edema. Hypokalemia (low potassium) and ototoxicity (damage to hearing) are potential side effects. The -semide stem indicates a furosemide-type loop diuretic. The brand name Lasix indicates it lasts six hours. Indications: Most often used for hypertension and edema. Contraindications: Watch for hypokalemia, anuria, and hypovolemia. Adverse effects: May include diarrhea, nausea, ototoxicity presenting as tinnitus (ringing in the ears) or hearing loss, orthostatic hypotension, hyperglycemia, and electrolyte imbalances. Thiazide Diuretic Hydrochlorothiazide (Microzide)— Thiazide diuretics get their class name from the stem of generic drugs such as hydrochlorothiazide. Prescribers often abbreviate hydrochlorothiazide as HCTZ. Thiazides don’t produce as much diuresis as loop diuretics, but are good for initial hypertension treatment. They work by preventing sodium reabsorption in the DCT. Water once again follows sodium, and urine volume increases. While the “hydro” in hydrochlorothiazide stands for the hydrogen atom, you can think of “hydro” as “water” for diuretic to remember its use. Indications: Most often used for hypertension and edema. Contraindications: Watch for hypokalemia and anuria. LOOP DIURETICS Are the FIRST DRUGS USED in:  Acute Heart Failure or  Worsening Heart Failure We give –IDEs to make the body DRIED - IDEs block reabsorption of sodium in the kidneys  LESS SODIUM means less swelling REMEMBER! Potassium-wasting diuretics can can HYPOKALEMIA which can result to abnormal ECG findings FOR POTASSIUM REPLACEMENT  we never give potassium via IV PUSH, this would result to INSTANT DEATH! Dsf  Always give potassium in an IV bag and give for over:  for OVER AN HOUR or more  typically for FOUR HOURS BLOCKS ALDOSTERONE DIRECTLY “Lets fluid OUT OF THE BODY and INTO THE POTTY”  Avoid potassium-rich foods POTASSIUM- SPARING DIURETICS Can cause SEVERE HYPERKALEMIA ANY POTASSIUM ABNORMALITY The FIRST nursing action is to attach the patient to a CARDIAC MONITOR Potassium-Sparing Diuretic Spironolactone (Aldactone) is one potassium-sparing diuretic, but this drug can cause gynecomastia, an enlargement of male breasts. Spironolactone blocks aldosterone, an important steroid hormone in retaining sodium and water under hypotensive conditions. Indications: Most often used for hypertension, heart failure, hypokalemia (low potassium), and edema associated with CHF and nephrotic syndrome. Potassium-Sparing Diuretic Contraindications: With increased potassium comes the danger of other medications that raise potassium levels, including angiotensin-converting enzyme (ACE) inhibitors such as  lisinopril or  enalapril. Adverse effects: May include  gynecomastia, a swelling of breast tissue in men and  irregular menses or amenorrhea in women as well as electrolyte imbalances. Patient education and care: Watch for electrolyte and fluid imbalances by monitoring weight and intake and output ratios. May need to watch diet for potassium-rich foods that may contribute to electrolyte imbalances. THREE IMPORTANT NSG CONSIDERATION S BEFORE GIVING DIURETICS: (B- B-P) THREE IMPORTANT NSG CONSIDERATIONS BEFORE GIVING DIURETICS: 1. B for Blood pressure  You hold diuretics for low blood pressure  Anything less than 100 systolic THREE IMPORTANT NSG CONSIDERATIONS BEFORE GIVING DIURETICS: 2. B for BUN and Creatinine  The kidney labs, we always check before giving since it can hurt the kidneys by giving TOO MUCH or TOO QUICKLY THREE IMPORTANT NSG CONSIDERATIONS BEFORE GIVING DIURETICS: 3. P for potassium imbalances Since POTASSIUM PUMPS THE HEART, we always put patients on a cardiac monitor WOF: Muscle spasms Cramps Weakness parethesia  FIVE GENERAL TIPS ABOUT DIURETICS FIVE GENERAL TIPS ABOUT DIURETICS 1. Give in the morning not at night Rationale: this made drains fluids, we do not want potty breaks all the time during the night FIVE GENERAL TIPS ABOUT DIURETICS 2. This medication makes patients dizzy (just like any BP meds) Slow position changes to avoid fainting (orthostatic hypotension/postural hypotension) FIVE GENERAL TIPS ABOUT DIURETICS 3. Monitor patient’s weight DAILY (not weekly)  REPORT if patient gained 2-3 lbs of weight in a single day  Usually indicates fluid accumulation in the body FIVE GENERAL TIPS ABOUT DIURETICS 4. Risk for sunburn  Advice patient to wear sunblock FIVE GENERAL TIPS ABOUT DIURETICS 5. Low sodium diet Rationale: The principle of osmosis teaches that… “where salt goes, water follows: Avoid:  Chips  Fried foods  No canned foods  No packaged foods AVOID THESE MEDS WHEN TAKING DIURETICS Mnemonic is: C-A-A-N These meds contain high amount of sodium which SWELLS THE BODY CAUTION ABOUT FUROSEMIDE: If given too fast.. CAUTION ABOUT FUROSEMIDE: Given too much for long-term this medication can cause 1. Renal damage, monitor BUN and creatinine levels 2. Long-term doses may cause HYPOKALEMIA Alpha-2 Adrenergic Agonist CLONIDINE Oppose the effects of the Sympathetic Nervous System When to give Clonidine? 1. Clonidine is USED LAST because it is a VERY POTENT blood pressure lowering drug 2. Given to lower blood pressure when the ELEVATED BLOOD PRESSURE US PERSISTENT and is not responsive to other medications REMEMBE R! For Clonidine think… “CARDIAC DOWN for CLONIDINE”  the C in Clonidine stands for CARDIAC  the D in clonidine stands for DOWN Alpha-2 Adrenergic Agonists  Reduces sympathetic outflow in the brainstem  The brainstem also contains THE CARDIOVASCULAR CENTER which: 1. controls heart rate 2. and blood pressure. CLONIDINE’s MECHANISM OF ACTION 1. Decreases heart rate 2. Decreases cardiac output 3. Decreases blood pressure TWO FORMS OF CLONIDIN E: HEALTH TEACHING ABOUT CLONIDINE PATCH 1. Change patch EVERY SEVEN DAYS 2. Apply patch on:  hairless  intact skin  on upper arm REMEMBER! Do not stop taking SUDDENLY because this can cause: 1. Severe rebound hypertension  Systolic BP over 180 mmHg (hypertensive crisis) which can cause Heart attack or stroke REMEMBE R! 2. Nurses should SLOWLY TAPER OFF Clonidine REMEMBE R! “When the blood pressure is LOW, we gotta go SLOW” 3. Nurses should teach patients and relatives to change positions veery slowly to prevent: Postural hypotension Orthostatic hypotension AVOID OTHER CNS DEPRESSANTS WHILE TAKING CLONIDINE 1. NO alcohol 2. NO sedatives Which can drive blood pressure even lower