Renal Cardio Drugs Lecture Notes PDF

Renal Regulation 4 Main jobs of the Kidneys - Fluid and electrolyte balance - Acid-base balance - RBC production - Blood pressure Kidneys take part in erythropoiesis! - Secrete renin- for blood pressure regulation - Erythropoietin- to stimulate red blood cell production - Calci...

Renal Regulation 4 Main jobs of the Kidneys - Fluid and electrolyte balance - Acid-base balance - RBC production - Blood pressure Kidneys take part in erythropoiesis! - Secrete renin- for blood pressure regulation - Erythropoietin- to stimulate red blood cell production - Calcitriol- active form of vitamin D for bone homeostasis *When the kidneys fail in a person, they won’t have any of these things^ - May even be anemic because no stimulation of RBC production Nephron - Nephrons are the functional units of the kidneys - Blood enters the nephrons and its filtered through the glomerulus - Water and small molecules pass into proximal tuble - Filtrate passes through loop of henle, then distal tubule - Filtrtate empties into collecting docs and leaves nephron as urine! - Two different processes start: reabsorption and secretion - Once blood reaches the nephron, it’s called filtrate! - Active ingredients of drugs are absorbed into the filtrate, go to nephron and are excreted. - Those that are bound to plasma proteins DONT because they’re too big to fit. Once the blood gets filtered through the bowman’s capsule, reabsorption of fluid and electrolytes such as glucose, water, amino acids, sodium, chloride, calcium, and bicarbonate are sent back to the bloodstream (fluid and electrolyte balance is through reabsorption). Some substances are able to pass to be filtrated, potassium, phosphate, hydrogen, ammonium, and some acid drugs secreted into filtrate. - Loop of henle is solely reabsorption. Renal Failure (CKD) -Decrease in the kidney’s ability to function. -Leading causes: untreated hypertension and diabetes mellitus -drugs will accumulate to high levels -meds will need to be adjusted by dosages -admin of an AVERAGE dose to a person with renal failure can be fatal Diagnosis of Renal Failure - Urinalysis - Serum creatinine: when your kidneys don’t process creatinine or get rid of it, the levels will rise. (Obvs means that the kidney function isn’t working well). - Blood urea nitrogen: influenced by many things, ratio kinda, hydration status is important! If a person is very dehydrated, their blood will be concentrated, which means their BUN will be up. If someone is too hydrated, their blood will be dilute, and BUN will go down. If you have a patient, and their creatinine is normal, but BUN is high, the patient is dehydrated and they have kidney failure. - Diagnostic imaging - Renal Biopsy Glomerular filtration rate (GFR) - Best marker for estimating renal/kidney function. Doesn’t have to do with hydration or muscle function. - Measures volume of filtrate passing through the bowman’s capsule per minute. - If you have fewer functioning nephrons/bowman's capsule, less is flowing through → kidney damage. Acute Renal Failure Most common cause of acute renal failure is hypoperfusion (not perfusing the kidneys well enough). - Heart failure leads to acute renal failure, not because there isn’t enough volume in the bloodstream- the heart is just too weak to push it through. The heart needs to work better in order to compensate for the lack of volume in the bloodstream (say someone got shot or something). - Medications can cause acute renal failure Chronic Renal Failure - May go undiagnosed for a long time - May be caused by nephrotoxic drugs - Cause kidney failure and absolute contraindications to people who have kidney failure. - Exception: ACE inhibitors! We use these for people who have insufficient renal insufficiently/kidneys aren’t working. BUT NOT FOR PEOPLE WITH KIDNEY FAILURE. Treatment of Renal failure - Address the cause - Pharmacological management of cause - Diuretics to increase urine output - Cardiovascular drugs to treat hypertension or heart failure - Pharmacological management of loss of kidney function -Dietary management (restriction of protein, reduce sodium, potassium, phosphate, magnesium) -Dialysis  If your patient is in renal failure, what med would you use to make up for what the kidney isn’t doing? Diuretics, ACE inhibitors, Beta-blockers, etc. ○ Fluid and electrolyte balance is one of their functions; the patient will have anemia, hyperkalemia, hyperphosphatemia, hypervolemia, hypocalcemia, metabolic acidosis. Hypervolemia: The patient will have too much volume because the kidneys aren’t getting rid of fluid → give diuretics! Help them PEE! Hyperkalemia: when a patient’s kidney fails, they will have high potassium levels, as they can’t excrete it. Hyperphosphatemia: Kidneys aren’t able to excrete phosphate; calcium and phosphate run oppositely *teeter totter*. SO, you would give them more calcium to increase calcium levels, in order for the phosphate levels to decrease. (give these drugs only with food). If you boost up the calcium levels in the blood, and the patient eats things with phosphate, the body won’t absorb phosphate because the calcium level is too high. Diuretics -Increase rate of urine flow - Excretion of excess fluid used to treat: hypertension, heart failure, kidney failure, liver failure or cirrhosis, pulmonary edema. All about increasing rate of urine flow: helps decrease volume^ Adverse Effects -All have the possibility of causing dehydration and orthostatic hypotension -Fluid and electrolyte disturbances, potassium and sodium imbalances. Loop Diuretics Mechanism of Action: to block reabsorption of sodium and chloride in a loop of henle. Primary use: to reduce edema associated with heart failure, hepatic cirrhosis, or renal failure -Furosemide (severely depletes potassium) → hypokalemia runs the risk of cardiac dysrhythmias. and torsemide is also approved for hypertension. Black Box warning: in excessive amounts, may lead to profound diuresis with water and electrolyte depletion. Contraindications: include hypersensitivity/allergic to furosemide or sulfonamides; anuria (who don’t pee); hepatic comal and have severe fluid or electrolyte depletion, hypotension (Hold for SBP 20 mmHg below baseline) Hold for K+ < 3.5 (med will make the patient’s potassium level go down, so if their levels are low, don’t give it to them or else they’ll get dysrhythmias without supplementation (patient is not receiving extra potassium through meds or diet). Loop (High-ceiling) diuretics - Obtain baseline weight and monitor, get their I & Os. → “Am I diuresing them too much? Or are there not enough meds and they are holding onto fluid?”  - If a patient says they’ve gained or lost 2lbs in a 24 hr period or 5lbs in a week, these are signs they’re holding onto too much fluid or losing too much fluid. THESE NEED TO BE REPORTED → teach patients:D - Give in AM to avoid nocturia. - Monitor lab values - Potassium other electrolytes, including sodium and chloride (loop diuretics inhibit reabsorption of K+, Na+, and Cl) - Blood urea nitrogen/ creatinine - Uric acid - Blood-glucose levels - Loop diuretics will make uric acid and blood glucose levels go up a bit. - If your patient has gout or diabetes pay special attention! -A patient taking a loop diuretic will lose dangerous amounts of potassium when taking digoxin. -May reduce effectiveness of anticoagulants, antidiabetic drugs (drug-drug interaction). Adverse effects: Serious: Hypokalemia, circulatory collapse, dysrhythmias, hearing loss, ototoxicity (damage nerve), renal failure (lol kinda ironic). Other: orthostatic hypotension (syncope), hyponatremia, rash or puritis, anemia, polynuria, nocturia Patient teaching: take diuretics in the morning, change position slowly, monitor weight, take potassium supplements, consume potassium rich food, know how to take BP and hold parameters. Loop Diuretics: role of the nurse (monitor these) KNOW THESE FOR THE TEST - Laboratory electrolyte values, especially potassium level - Daily weights: Am I diuresing them too much or too little? Gained or lost 2lbs in a 24 hr period or 5lbs in a week. - Intake and output - Assessment of edema and signs of fluid overload - Patient’s ability to ambulate safely - Photosensitivity: sunscreen; they are more susceptible. - Hearing loss (these drugs are ototoxic) - Glucose and uric acid levels Thiazide Diuretics - For people who hypertension - Largest, most commonly prescribed class of diuretics. - Less effective than loop diuretics/Like loop diuretic but to a lesser degree - Not effective in patients with severe renal failure, or heart failure. Mechanism of Action: to block Na+ reabsorption in the distal tubule and increase potassium and water excretion. (water follows Na+!!!!) Primary use: to treat mild to moderate hypertension (also indicated to reduce edema associated with heart, hepatic, and renal insufficiency). Contraindications: include anuria and prior hypersensitivity/allergy to thiazides or sulfonamides. Thiazides are contraindicated in pre-eclampsia or other pregnancy-induced HTN. - Hold for SBP 20 mmHg below baseline (SHOULD BE ON MEDSHEET FOR EVERY MED THAT AFFECTS BP) - Hold for K+ 5. -Black box warning: tumors in animals in clinical studies, therefore should only be used in specific indications. K+ sparing: spironolactone (aldactone) Administration Alerts: -Give with food to increase absorption of the drug. -Do not give potassium supplements Adverse effects: -Hyperkalemia (worse with potassium supplements or ACE inhibitors at the same time), orthostatic hypotension, muscle weakness, gynecomastia, impotence and diminished libido, menstrual irregularities, hirsutism, breast tenderness because it affects aldosterone hormone. Potassium-sparing diuretics: -Report signs and symptoms of hyperkalemia. -Spironolactone may decrease effectiveness of anticoagulants. (drug drug interaction) Patient teaching: -Take in AM -Avoid use of potassium-based salt substitutes -When in direct sunlight, use sunscreen. -Do not eat excess amounts of foods high in potassium (oranges, bananas, dried fruit, legumes) -Report to provider: muscle cramps, lethargy, thirst, HA, rash, menstrual irregularities, nausea, numbness. -How to take BP and hold parameters Miscellaneous Diuretics: carbonic anhydrase inhibitors: - Example: Acetazolamide (Diamox): med for glaucoma/ weak diuretic. Mechanism of Action: to inhibit formation of carbonic acid Primary use: to decrease intraocular fluid pressure in patients with open-angle glaucoma. Adverse effects: avoid giving to patients with allergic reaction (contain sulfa), fluid and electrolyte imbalances. Miscellaneous Diuretics: osmotic diuretics -Example: mannitol (osmitrol) Mechanism of Action: raises osmotic pressure; inhibits reabsorptions of water and electrolytes Primary use: to reduce intracranial pressure due to cerebral edema. Also used to maintain urine flow in prolonged surgery, acute renal failure, or severe renal hypoperfusion. (mainly used in operation or ICU) -Can worsen peripheral edema, used with caution. Because its weak, and its MOA^ USE ATI PHARM BOOK FOR PRACTICE QUESTIONS Drugs for Cardiovascular disorders (pt1) Drugs for lipid disorders Lipids and cardiovascular disease - Hyperlipidemia (high levels of hyperlipidemia) - High levels of lipids in the blood- major risk factor for cardiovascular disease. - Most patients asymptomatic until cardiovascular disease produces symptoms, - Genetic and lifestyle contributors: - Diets high in saturated fat and lack of exercise contribute - Genetics determines ability to metabolize lipids Three types of lipids: 1. Triglycerides a. Three fatty acids attached to glycerol b. Energy source c. Amount for 90% of total lipids in body 2. Phospholipids a. Essential to building plasma membranes i. Necessary for production of: Vitamin D, bile acids, cortisol estrogen, progesterone, testosterone. 3. Steroids a. Cholesterol is the most widely known type of steroids. i. Natural and vital component of plasma membranes ii. Body makes about 75% of cholesterol needed. iii. Remaining 25% comes from diet (animal products) 1. Limit to < 300 mg/day. Lipoproteins -Remember lipids are not soluble in the blood and need carriers. -Consist of cholesterol, triglycerides, and phospholipids with protein carrier -Three types of carriers of cholesterol: Low-density lipoprotein (LDL) (we want it to be LOW) ○ Transports cholesterol from liver to tissues and organs- to cause damage. Contributes to plaque deposits and coronary artery disease High-density lipoprotein (HDL) (we want it to be HIGH) ○ Assist in transport of cholesterol away from the body tissues and back to the liver. Transport cholesterol for destruction and removal from body. Very low-density lipoprotein (VLDL) ○ Primary carrier of triglycerides in blood- to cause damage. Don't give to patients with diabetes since they have high levels of triglycerides already.  ○ Through bodily processes becomes HDL Lifestyle changes: - Should always be included in any treatment plan for reducing blood lipid levels. - Many patients can control dyslipidemia entirely through non-pharmacologic means. - Monitor blood-lipid levels - Maintain weight - Implement a medically supervised exercise plan - Dietary changes (teach patients) - Replace saturated fats with polyunsaturated fats from vegetable oil. - Consume healthy protein sources such as low fat poultry, no skin, fish, seafood, low-fat dairy products, and nuts. - Limit intake of sugar sweetened beverages and tropical vegetable oils. - Increase soluble fiber in diet - Eliminate tobacco use HMG-CoA reductase inhibitors (statins) (for high cholesterol patients) (work in liver) Interfere with the synthesis of cholesterol. First drugs of choice to reduce blood-lipid levels, with the goal of reducing risk of MI and stroke. Examples: atorvastatin (lipitor), fluvastatin (lescol), lovastatin (mevacor), rosuvastatin (crestor), simvastatin (zocor) ★ Interferes with an enzyme that is necessary to make cholesterol. ★ THINK ABOUT the LIVERRRRRRRRRRRRRRRRRRRRRRRRRRRRRRR (very damaging to the liver) - Prototype drug: atorvastatin (lipitor) - Mechanism of action: inhibits HMG-CoA reductase (an enzyme necessary for the production of lipids) - Primary use: antihyperlipidemic - Contraindications: do not use on Pregnancy or breast-feeding (pregnancy category X), serious liver disease; hypersensitivity. Administrative alerts: give at HS (body makes most cholesterol at night); may be given with dinner if GI discomfort; may be taken with dinner if GI upset occurs. Adverse effects: Hepatotoxic; muscle or joint pain; GI complaints, such as intestinal cramping, diarrhea and constipation; rare, but possible – rhabdomyolysis (very damaging; muscle tissue breaks down and releases proteins and electrolytes into the bloodstream). - MONITOR LIVER FUNCTION TESTS Patient teaching: avoid drinking grapefruit juice because it inhibits metabolism, report to provider: blurred vision , GI symptoms, muscle pain, weakness. - Muscle pain may indicate liver problems! Bile Acid Sequestrants: hold onto cholesterol to poop it out so your body doesn't reabsorb as much cholesterol. - Can be used in combination with statins - Prototype: cholestyramine (prevelite) - Mechanism of action: bind with bile acids, increasing cholesterol excretion in stool. - Primary use: to lower serum lipid levels - Contraindications: biliary obstruction; hypersensitivity. - Administration alerts: Mix thoroughly with 60 to 180 mL liquid or else it’ll clog up the GI tract; give separately from other meds: 4 hours before or 2 hours after most meds because other meds could be fat soluble, the bile acid sequestrant will hold on to it and it’s not going to get reabsorbed. - Adverse effects: GI tract, such as bloating and constipation; can bind other drugs, increasing potential for drug-drug interactions (particularly lipid-soluble drugs/vitamins). Cholesterol Absorption Inhibitor: also has effects in the liver, and causes muscle problems. Ezetimibe (zetia) work in GI tract Mechanism of Action: Inhibits absorption of cholesterol in the small intestine, resulting in small reduction in LDL. Side effects: serious side effects uncommon; minor side effects nasopharyngitis, myalgia (muscle pain → problems in the liver when given with statins), upper respiratory tract infection, arthralgia, and diarrhea. Potential to affect nutritional status Myopathy and rhabdomyolysis are possible. Niacin (Nicotinic acid): Much higher dose when used to decrease cholesterol/triglycerides. (liver) - B-complex vitamin (lower dose) - Niacin (Niaspan) KNOW SIDE EFFECTS!!! - Decreases VLDL levels - Has numerous adverse effects: flushing, hot flashes, nausea, excess gas, diarrhea; more serious effects like hepatotoxicity and gout possible - Monitor patients liver function - Monitor uric acid levels, if predisposed to gout - Monitor blood-sugar levels if diabetic - Patient teaching: Take ASA ½ hour before med to decrease flushing Fibric-Acid Agents: work mostly on triglycerides - Prototype drug: gemfibrozil (lopid) - Mechanism of action: unknown (decreases hepatic triglycerides production; accelerates removal of cholesterol from the liver; and increases excretion of cholesterol into the feces) - Primary use: severe hypertriglyceridemia  - Contraindications: hepatic impairment, severe CKD, gallbladder disease, hypersensitivity. - Administrative alerts: 30 minutes before meals - Adverse effects: gallstones, decreased liver function; GI distress: dyspnea, diarrhea, nausea, and abdominal pain. - Drug-drug interaction: Use with warfarin may potentiate anticoagulant effects. Use with statins increases the risk of myopathy and rhabdomyolysis. Drugs for hypertension: Hypertension: classified into three categories -Consistent elevation of systemic arterial blood pressure - Normal B/P varies with age -Three categories (JNC-VIII) -Prehypertension -Stage 1 (patient may be taking 1 or 2 meds) -Stage 2 (patient will be taking multiple meds) ★ Hypertensive: you cannot be on more than one antihypertensive in the same class. Three factors responsible for blood pressure - Cardiac output: heart rate affected by SNS, PNS, and epinephrine. - Peripheral resistance: diameter of vessel is smaller, there will be more pressure on the walls. Increase in blood viscosity. - Blood volume: if volume is high BP will be high. Fluid loss = dehydration, Fluid retention = aldosterone and ADH. Factors responsible for BP - Blood volume - Increased blood volume increases blood pressure - Medications affect blood volume to lower BP - Peripheral resistance - Friction and resistance in arteries as blood flows through vascular system - ANS helps regulate peripheral resistance - Medications widen blood vessels to lower BP - Cardiac output - Volume of blood pumped per min - Stroke volume x heart rate - Medications that affect stroke volume, heart rate will affect blood pressure. Hormones that affect BP: -Natural hormones affect blood pressure daily -Epi and norepinephrine raise B/P -Antidiuretic hormone (ADH) raises B/P by raising blood volume. -Renin-angiotensin-aldosterone system is a primary homeostatic mechanism for controlling blood pressure. (low bp triggers the RAA system→ bp will go up). If you inhibit the RAA, blood pressure will not go up. Types of Hypertension - Primary hypertension: no identifiable cause (much more common) - Primary antihypertensives can be used alone. - Secondary hypertension: cause identified - Secondary antihypertensives cannot be used alone. - Cushing’s syndrome - Hyperthyroidism - Chronic renal disease - Certain drugs - Treat the cause - Pharmacological management individualized to patient’s risk factors, medical conditions, degree of blood pressure elevation. Target organs Affected by untreated hypertension - Heart - Brain - Kidneys - Retina - Blood Pressure > 140/90 mmHg damages target organs. Non Pharmacological methods to control hypertension - Limit alcohol intake - Restrict sodium consumption - Reduce saturated fat and cholesterol; increase fresh fruit and veggies intake - Increase aerobic physical activity - Discontinue tobacco use - Reduce stress - Maintain optimum weight. First-Line Antihypertensive Drugs - Primary antihypertensive agents - Thiazide diuretics - Angiotensin-converting enzyme (ACE) inhibitors: better because they work a little earlier in the system so they’ll have a better effect. If you give an ACE inhibitor to a patient, it is renal protective! - Angiotensin receptor blockers (ARBs) - Direct Renin Inhibitors: work in the very beginning, stopping renin from being excreted.  - Calcium channel blockers (CCBs) - ALL of these have the potential to block angiotensin II, which is used for vasoconstriction. (So, in other words, it does not allow vasoconstriction, peripheral resistance). - Primary effect: vasoconstriction, secondary effect: diuresis = lower blood pressure - Prescribing two antihypertensives results in additive or synergistic blood pressure reduction. - However, NEVER use more than one medication from a single class (whether it’s 1st or 2nd line med). - When there's a drop in BP, the body secretes renin → renin makes angiotensin I → ACE makes angiotensin II. If we inhibit ACE, angiotensin I does not become angiotensin II. ★ Anything that vasodilates has the issue of orthostatic hypotension Second-line Antihypertensive Drugs - Beta-adrenergic receptor blockers (in heart) - Alpha1- adrenergic receptor blockers (in arterioles) - Alpha2- adrenergic agonists - Direct-acting vasodilators - Peripherally acting adrenergic neuron blockers - Direct renin inhibitors - Loop and potassium-sparing diuretics - Second-line antihypertensives are never used alone for hypertension. Diuretics - Increase urinary excretion of water and electrolytes, thereby reducing blood volume. - Used for mild to moderate hypertension - Potassium-sparing diuretics, thiazide and thiazide-like diuretics, loop/high-ceiling diuretics Drugs Affecting Renin-Angiotensin system - Angiotensin-converting enzyme (ACE inhibitors) - Angiotensin receptor blockers (ARBs) - Direct renin inhibitor- aliskiren (Tekturna) - All ultimately block effects of angiotensin II (a potent natural vasoconstrictor) lowering peripheral resistance and decreasing blood volume. - Hold for SBP < 100 or > 20 mmHg below baseline. Drugs affecting renin-angiotensin system Angiotensin-converting enzyme ACE inhibitor - prototype drug: lisinopril (prinivil, zestril) - Mechanism of action: inhibit angiotensin converting enzyme (vasodilation) and decrease aldosterone secretion (mild diuretics)  - Primary use: hypertension, post MI, neuropathy - Adverse effects: first dose hypotension (a patients first time taking the drug and we don’t know how they’ll react to it), dry cough, HA, Dizziness, hyperkalemia (aldosterone holds onto K+ more than Ca+), renal failure, angiodema. - Black box warning: fetal injury and death may occur when ACE inhibitors are taken during pregnancy. When pregnancy is detected they should be discontinued as soon as possible. Drugs affecting renin-angiotensin system Angiotensin-receptor blockers ARBs - prototype drug: Iosartan potassium (cozaar) - Mechanism of action: block binding of angiotensin II in arterial smooth muscle and adrenal glands (vasodilation and mild diuresis) - Primary use: hypertension, nephropathy - Adverse effect: weakness, fatigue, dizziness, hypoglycemia, hyperkalemia, orthostatic hypotension. - Avoid grapefruit - Lower risk of angioedema, no dry cough - Concurrent use of Iosartan with aliskiren is contraindicated - Black box warning: pregnancy Calcium Channel Blockers - Used to treat hypertension and other cardiovascular diseases. - Block calcium ion channels, which limits muscle contractions, leading to vasodilation and lower B/P - CCBs also affect chronicity (therefore used for dysrhythmias) - Some selectively target calcium channels in the arterioles; others also affect cardiac muscle. - Teach patient to avoid drinking grapefruit juice. Beta-Adrenergic Blockers - Decrease heart rate and contractility by blocking sympathetic stimulation of the heart (block beta-1 receptors in juxtaglomerular apparatus; may also affect beta 2- receptors) - Cardioselective beta blockers have much greater effect on beta1 receptors than beta2, therefore much lower risk of bronchoconstriction. - Reduce cardiac output and lower systemic BP. Heart failure - Inability of ventricles to pump enough blood for the body's needs. - Weakening of heart muscle due to aging or disease. - Associated with: - Coronary artery disease - Mitral stenosis  - Myocardial infarction - Chronic hypertension - Diabetes mellitus - THERE IS NO CURE ONLY PREVENTION AND SLOWING OF PROGRESSION Preload and Afterload - Preload - Affects cardiac output - The degree myocardial fibers are stretched prior to contraction– more fibers are stretched, more forcefully they will contract. - Drugs that increase preload contractility will increase cardiac output - Positive inotropic agents. - Afterload -affects cardiac output -pressure in aorta that must be overcome before blood is ejected from left ventricle Lowering blood pressure creates less afterload, resulting in less workload for the heart Etiology and patho of HF: -Left sided heart failure -blood accumulates in left ventricle -Left ventricle thickens and enlarges: hypertrophy -cardiac remodeling -blood backs up into lungs -cough shortness of breath results -Right sided heart failure -blood backs up into veins -peripheral edema and organ engorgement -less common than left-sided HF Management of HF - Slowing the heart rate - Increasing contractility - Reducing myocardial workload ACE inhibitors -Reduce afterload -Drug of choice for heart failure -Enhance excretion of sodium and water -Lowers peripheral resistance and reduces blood volume -Increases cardiac output Nurse’s role: -Precautions, administration, and adverse effects are the same as when used for hypertension. -Evaluation of effectiveness -Therapeutic response time: weeks or months Angiotensin II receptor blockers (ARBs) - Actions very similar to ACE inhibitors - Usually used for patients who are unable to tolerate the adverse effects of ACE inhibitors Nurse’s role: - Precautions, administration, and adverse effects are the same as when used for hypertension. - Evaluation of effectiveness different - Therapeutic response time: weeks or months Diuretics - Increase urine flow - Reduce blood volume and cardiac workload - Reduce edema and pulmonary congestion - Prescribed in combo with other drugs (NOT MONOTHERAPY FOR HEART FAILURE) Nurse’s role: - Precautions, administration, and adverse effects are the same as when used for hypertension. - Evaluation of effectiveness different - Therapeutic response time: weeks or months Beta-Adrenergic Blockers Slow heart rate and reduce blood pressure - Positive inotropic effect (makes the heart muscle contract stronger); negative chronotropic effect (slows heart rate) - Reduce workload of heart - Nurse’s Role: - Precautions, Administration, and Adverse Effects are - the same as when used for hypertension - Evaluation of effectiveness different Not used as monotherapy for heart failure (often combined with an ACE inhibitor or an ARB) Vasodilators Hydralazine with isosorbide dinitrate (BiDil); Nesiritide (Natrecor) Minor role in heart-failure treatment Lower blood pressure; relax blood vessels  PO med (not the IV for htn emergencies) High incidents of adverse effects - Tachycardia - Orthostatic HTN Nurse’s Role: Precautions, Administration, and Adverse Effects are the same as when used for hypertension Evaluation of effectiveness different Dysrhythmias -Abnormalities of electrical conduction or rhythm in heart, -Range from harmless to life threatening -ECG the only way to diagnose a dysrhythmia -symptoms range from none to sudden death -dysrhythmias estimated to be quite common -Persistent/severe dysrhythmias increase risk of stroke and heart failure. -Occurence of dysrhythmias -Can occur in both healthy and diseased hearts -Can disrupt regulation of the heart -May decrease cardiac output Etiology and classifications -Diseases and conditions associated with dysrhythmias -hypertension -cardiac valve disease such as mitral stenosis -coronary artery disease -medications such as digoxin, dobutamine, and amiodarone -low potassium or magnesium levels in the blood -stroke -Diabetes mellitus -heart failure Supraventricular classification of dysrhythmias: -Originate in the atria or AV node -Most common type Ventricular classification of dysrhythmias: - Originate in the ventricles - Generally more serious Nonpharmacologic therapies for dysrhythmias - Cardioversion and defibrillation - Serious types of dysrhythmias - Electrical shock stops all electrical impulses in the heart and allows SA nodes to regain control. - Catheter ablation – identify and destroy aberrant cardiac cells that cause dysrhythmias - Cardiac pacemaker- paces heart at set rate - Implantable cardioverter defibrillator– combination of pacemaker and defibrillator. Generation of Action potentials - Electrical impulses across myocardium - Cell membrane with negative membrane potential = polarized - Negative membrane potential - Na+ and Ca++ outside cell - K+ inside cell - Sodium channel opens and sodium ions rush in, cause depolarization. - Calcium channel opens and calcium ions enter cell and stimulate cardiac muscle contraction - SA and AV cells depolarize in response to calcium-ion influx. - Repolarization -Return to polarized state -Sodium pump removes Na+ -Potassium ion channels allow K+ to move back into cell Pharmacologic strategies to terminate dysrhythmias - Block potassium, sodium, or calcium ion channels - Prolong refractory period - Brief period in conduction cycle when myocardial cells cannot produce another action potential. - Primary mechanisms of action -Blocking flow through ion channels (conduction) - Altering autonomic activity -Use is declining significantly for two reasons -They can worsen or create new dysrhythmias -Nonpharmacologic therapy is improving Antidysrhythmic drug groups - Drug classes - Class 1: sodium channel blockers - Delay or accelerate repolarization; slow conduction velocity, may alter duration of action potential - Class 2: Beta-adrenergic antagonists - Slow conduction velocity through AV node, decrease automaticity, prolong refractory period. - Class 3: Potassium channel blockers - Delay repolarization, increase duration of action potential, lengthen refractory period – stabilize dysrhythmias. - Class 4: calcium channel blockers - Slow conduction velocity, decrease contractility, prolong refractory period -Miscellaneous antidysrhythmic drugs: slow conduction through AV node and/or decrease automaticity of SA node Thrombolytics - Dissolve clots obstructing coronary arteries - In cases of acute MI, used to restore circulation to myocardium - Narrow margin of safety between dissolving clots and producing serious adverse effects, particularly excessive bleeding. Clotting Process - Blood vessel injury causes vessel spasm (constriction) - Platelets are attracted to and adhere to injured area - Aggregation of platelets forms plug - Formation of insoluble fibrin strand and coagulation (coagulation cascade) - Normal clotting occurs in 6 minutes - Clotting disorders: thromboembolic disorders- caused by thrombi and emboli  - Thrombocytopenia Lab tests that measure coagulation disorders - Activated clotting time - Prothrombin time - Activated partial thromboplastin time - International normalized ratio - Also considered: - Liver function tests - Bleeding time - Platelet count Anticoagulants: Inhibit clotting factors, prevent thrombus growth Antiplatelets: Inhibit platelet actions, prevent thrombi growth Thrombolytics: Dissolve existing thrombi Anticoagulants - Used to prolong bleeding time - Prevent thrombi from forming or enlarging - Heparin, low-molecular-weight heparins, and related drugs -Heparin- traditional drug of choice -given SUBQ (at home too) -Duration of action 2 to 4 times longer -Fewer follow up lab tests needed - ASSESS FOR BLEEDING Antiplatelet Drugs Prolong bleeding time by interfering with aggregation of platelets Mechanism of action : to alter the plasma membrane of platelets so they cannot aggregate (permanently) Primary use: to prevent thrombi formation after stroke or myocardial infarction Include Aspirin Adenosine diphosphate (ADP) receptor blockers (clopidigril -Plavix) Glycoprotein 11b/111a receptor antagonists (eptifibatide – Integrillin, abciximab – RePro) Drugs for intermittent claudication (cilostazol - Pletal, pentoxifylline – Trental) Role of the Nurse: Antiplatelet Agents Monitor for bleeding Risk increases if given with anticoagulants Prolonged pressure needed to control bleeding at puncture sites Monitor for gastrointestinal upset with ticlopidine (Ticlid) May increase menstrual bleeding Thrombolytics (Fibrinolytics) Used to dissolve life-threatening clots (myocardial infarction, cerebrovascular accident) Mechanism of action: to convert plasminogen to plasmin, which digests fibrin and dissolves clots Primary use To treat acute myocardial infarction, deep vein thrombosis To treat cerebrovascular accident, pulmonary embolism, arterial thrombosis To clear IV catheters Adverse effects: abnormal bleeding; Contraindications: patients with bleeding disorder, recent trauma, or surgery (past 14 days) Hematopoiesis - Process of blood-cell formation - Begins with stem cell in bone marrow - Homeostatic control maintained by hormones and growth factors - Demands of the body affecting hematopoiesis - White blood cells WBC can increase concentration up to 10 times normal to combat infection. - Red blood cells (RBC) can increase concentration up to 5 times in presence of blood loss or hypoxia - Pharmacological growth factors  - Recombinant DNA technology - Used to stimulate production of erythrocytes, leukocytes, platelets Erythropoietin - Hormone that stimulates red blood cell production - Secreted when kidneys sense reduction in oxygen (hypoxia or hemorrhage) Epoetin in alfa (epogen, procrit) Uses: To treat disorders caused by a deficiency in RBC formation (lack of endogenous erythropoietin). Patients with chronic kidney disease, cancer, chemo. Black Box Warning: risk of serious cardiovascular and thromboembolic events is increased with epoetin alfa (TIA, MI, stroke). Contraindications: uncontrolled htn, myeloid cancers Administration:SQ route 3 times per week. Adverse effects:Hypertension, peripheral thrombiosis, headache, fever, nausea, diarrhea, edema. Colony-Stimulating Factors CSFs increase the production of new leukocytes in response to antibodies Also activate existing WBCs to work more effectively (migration of leukocytes to the bacteria; antibody toxicity; phagocytosis) CSFs as pharmacotherapy Reduce duration of neutropenia associated with chemotherapy or organ transplant Shortens the length of time patients are susceptible to life-threatening infections due to low numbers of neutrophils (neutropenia) By raising neutrophil counts, CSFs help keep antineoplastic dosing regimens on schedule (and more effective)