Overview of the cardiovascular and respiratory systems, their diseases and the drugs used to treat them including adverse effects.
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Hypertension
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Heart Failure
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Dysrhythmias
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Angina & Myocardial Infarction
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Lipids
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Coagulation
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Anemia
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1. Diuretics
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Diuretics make you pee
Reduce blood volume through urinary excretion of water and electrolytes (Na+, Ca++, Cl-, K+) Specific mechanism of action varies within the class (thiazide, loop, potassium-sparing) Depends on where (i.e. which part of the nephron) it works Effective, Well tolerated First line treatment for hypertension Due to manipulation of electrolytes, monitoring is important! |
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a.Thiazide diuretics
Hydrochlorothiazide (HCTZ) |
Largest, most commonly prescribed class of diuretics
(‘gentler’ than loop diuretics) Decrease the reabsorption of sodium in the early distal tubule, which increases the production and excretion of urine More sodium (and therefore water) is excreted Treat mild to moderate hypertension and edema that is associated with heart, hepatic, and renal failure |
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b.Loop diuretics
Furosemide |
Are the most effective diuretics
Prevents reabsorption of sodium and chloride in the loop of Henle Reduce edema associated with heart, hepatic, or renal failure Cause large amounts of fluid to be quickly excreted – along with potassium (K+) Used to provide short-term hypotension, not so much for blood pressure maintenance |
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c.Potassium sparing diuretics
Spironolactone |
Block either sodium pump (leaving more sodium in tubule) or aldosterone further along in the nephron (late distal tubule and collecting duct)
Achieve diuresis without affecting blood potassium levels Preferred in patients at high risk of developing hypokalemia Sometimes combined with other diuretics (as an add-on) to minimize potassium loss |
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2.Calcium channel blockers
(CCB) |
Muscle contraction is controlled by calcium moving in and out of channels across cell membranes (Ca++ influx causes contraction)
Blocking the channels limits muscular contraction, relaxing muscle in both the periphery and heart Reduce blood pressure by lowering peripheral resistance and cardiac output |
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Nifedipine
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Mechanism of action: blocks calcium channels in myocardial and vascular smooth muscle (blood vessels > heart) – long-acting dihydropyridine (LA-DHP)
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Anything that causes vasodilation will also cause reflex tachycardia Therefore, anything that causes vasodilation requires heart rate monitoring
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3.Renin-angiotension-aldosterone system
(RAAS) agents |
RAAS is triggered in times of low blood pressure
End result of uninterrupted RAAS is increased blood pressure drugs affecting RAAS Reduce blood pressure by: Reducing peripheral resistance Decreasing blood volume |
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a.Angiotensin-converting-enzyme inhibitors
(ACE Inhibitors) -pril |
Inhibit angiotensin-converting-enzyme (ACE), resulting in less angiotensin II and aldosterone, which reduces blood pressure
Prevents conversion of angiotensin I to angiotensin II, therefore: Prevents aldosterone secretion Prevents the direct vasoconstriction Pregnancy category D |
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b.Angiotensin II receptor blockers
(ARBs) -sartan |
In the same pathway (RAAS), ARBs block angiotensin II from causing vasoconstriction, and block the release of aldosterone at the adrenal gland
Very similar uses and adverse effects as ACE-I **Also newer drugs involved in the RAAS: Aliskiren – renin inhibitor |
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4.Adrenergic agents
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a.β-Blockers
-olol |
β-receptors in heart (β1), lungs (β2), blood vessels (β2) + many others
Cardio-selective: reduce heart rate and slow down myocardial conduction and contractility = reduce cardiac output Non-selective: also produce vasodilation = lower peripheral resistance and reduce cardiac output Because of their action in the heart, their primary use is for angina, arrhythmias, heart failure, and post-myocardial infarction Also used off-label for migraine prevention, or as a performance enhancing drug Drug dependence occurs, so upon abrupt discontinuation = reflex tachycardia (Requires tapering ) |
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b.α1-Blockers
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Block α1–receptors in the periphery – relaxes smooth muscle and reduces peripheral resistance and cardiac output (indirectly)
Vasodilation = ↓ venous return to heart = ↓ cardiac output Primary continuous use is for urinary incontinence and benign prostatic hyperplasia (BPH) Work very quickly to reduce blood pressure |
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Doxazosin
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Blocks vasoconstriction caused by stimulation of α–receptors, therefore reducing peripheral resistance
Used to treat urinary incontinence, BPH, hypertension |
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c.α2-Agonists
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Stimulate α2-receptors in the CNS, which causes the identical response as the α1-blockers in the periphery vasodilation reduces peripheral resistance and cardiac output (indirectly)
When α2-receptors are stimulated, the outflow of sympathetic nerve impulses from the CNS to the heart and blood vessels is inhibited α2-agonists and α1-blockers = same clinical result Rarely used for long-term (clonidine, methyldopa) Reserved for patients with hypertension which has been resistant to other therapies |
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d.Miscellaneous
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Labetalol: partial agonist @ β2, blocks @ α1 & β1
Carvedilol: blocks β1&2 and α1 |
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5.Direct-acting vasodilators
Hydralazine, minoxidil, nitroprusside |
Directly relax arteriolar smooth muscle in blood vessels reduce peripheral resistance
Work at cellular level – each differently Quickly reduce blood pressure Generally reserved for acute care to dilate quickly under close monitoring |
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Resting State (kind of)
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Na+ and Ca++ are outside cell, K+ is inside cell (+ charge higher outside, than inside – POLARIZED)
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Depolarization
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Na+ and Ca++ channels open, and both rush into the cell to try and balance out charges (it is mostly the Ca++ increase inside the cell responsible for muscle contraction)
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Repolarization
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In a further attempt to get back to resting state, the K+ channels open and K+ rushes out
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Sodium channel blockers
(class I) Procainamide |
Slow down depolarization by preventing Na+ from rushing into the cell
Lengthen the duration of the action potential Can also suppress ectopic activity (arrhythmias coming from an incorrect source) Similar in structure to anesthetics, therefore potential for CNS effects |
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β-blockers
(class II) |
Slows heart rate
Decreases conduction velocity through the AV node Altering the adrenergic nervous system Usually used for dysrhythmias associated with heart failure (choose cardio-selective ones) Remember: DO NOT STOP ABRUPTLY = reflex tachycardia Contraindicated in clients with heart block, severe bradycardia, asthma, COPD, elderly, diabetics |
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Potassium channel blockers
(class III) |
Delays repolarization and lengthens refractory period
Mostly used for ventricular arrhythmias (repolarization is one of the last steps – in ventricles) Many have multiple actions at other receptors ex. Sotalol – β-blocker and potassium-blocker |
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Amiodarone
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Amiodarone is a potassium channel blocker and a sodium channel blocker, among other mechanisms of action
Widely distributed and stored in tissues, so toxicity can be difficult to get rid of Primarily used to treat resistant ventricular tachycardia and atrial dysrhythmias LOW THERAPEUTIC range |
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Calcium channel blockers
(class IV) |
Reduce automaticity, slows conduction through AV node, slows heart rate
Remember: diltiazem and verapamil were more selective for heart AND it is Ca++ > Na+ that influences cardiac muscle contraction |
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Miscellaneous
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Digoxin
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Decreases automaticity of SA node and slows conduction through AV node – but not by blocking any ion channels
Requires therapeutic drug monitoring Remember to teach signs of toxicity Remember importance of potassium |
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Adenosine
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An endogenous nucleoside that reduces automaticity of SA node and slows conduction through AV node
Sometimes used in diagnosing patients who cannot complete a stress test 10 second half-life (bolus IV injection) |
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Anemia
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occurs when red blood cells (erythrocytes) or hemoglobin have a diminished capacity to carry oxygen Due to: blood loss, excessive destruction, or diminished synthesis
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Erythropoiesis
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the process of making erythrocytes in bone marrow
If we are lacking a substance for erythropoiesis, we won’t have as many RBCs |
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Erythropoietin
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– the hormone released by the kidneys that instructs the bone marrow to make RBCs
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Vitamin B12
Cyanacobalamin |
Required for erythropoiesis
Does not absorb very well from GI tract – must have intrinsic factor present to absorb (genetic differences) Often given by IM injection (monthly maintenance) B12 deficiency presents as memory loss, confusion, unsteadiness, tingling in limbs, delusions, mood disturbances (more CNS effects) |
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Folic Acid
Folate |
Required for erythropoiesis
Does not require intrinsic factor to absorb from GI (more readily absorbed) Deficiency results in anemia, but no neurological symptoms Require folic acid during neural tube formation in pregnancy – suggest supplements in any woman of child-bearing age Green, leafy vegetables – or supplements (1-5mg) Corrected in 2 weeks 1 month |
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Iron
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Involved in the oxygen carrying capacity of the erythrocytes
Different formulations (or salts) have different absorptions and bioavailability Ferrous sulfate (red), ferrous gluconate (green), ferrous fumarate Iron interferes with absorption of many other drugs (antibiotics, thyroid meds) It is an ion that binds to some medications, forming a complex too large to absorb It is better absorbed (↑ to 10%) in presence of vitamin C Antacids decrease absorption of iron (by changing the pH of the gastric contents) and need to be separated by ~ 2 hours General recommendation: separate iron supplements from other meds by 2 hours if possible |
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Growth Factors
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When anemia is a result of a lack of growth factor, we can replace the growth factor with biologics
Erythropoietin alfa or darbepoietin alfa = to replace erythropoietin (EPO) Hormone secreted by kidneys – low in kidney failure and cancers EPO = “blood doping” oxygen carrying capacity is increased, boosting endurance |
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Statins
Atorvastatin (Lipitor®) |
Inhibit HMG-CoA-reductase, which is involved in the synthesis of cholesterol in the liver
Reduces the amount of cholesterol made by our body Also increases the amount of LDL removed from the blood First drug of choice; therapy continues for life Very well tolerated DO NOT USE IN PREGNANCY Choice of statin is dependent on lipid profile Some are good at lowering LDL, some better at raising HDL, etc. |
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Fibrates
Fenofibrate |
“Lipid metabolism regulator” – changes production levels of lipoproteins, but different pathway than statins
Lower triglyceride levels and raise HDL levels Some also lower LDL More gastrointestinal adverse effects than statins May be used with a statin in some cases |
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Niacin
Nicotinic acid / nicotinamide / niacinamide / vitamin B3 |
Available without a prescription (OTC)
Exact mechanism is unknown, but reduces synthesis of LDL, VLDL, and increases HDL Also causes peripheral vasodilation flushing More gastrointestinal effects than statins |
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Bile Acid Resins
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Bind to bile acid made by the liver to enhance excretion of cholesterol
Bile acid then does not absorb through intestinal wall (forms a complex, too big to pass through plasma membrane), so once bile acid is bound, it is excreted with feces The liver responds by getting rid of even more cholesterol Drug of choice in pregnancy (no absorption occurs!) |
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Miscellaneous
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Ezetimibe
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inhibits intestinal cholesterol absorption – used along with a statin
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Orlistat
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doesn’t allow fats to be absorbed from intestine – anal discharge (anti-obesity drug)
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Omega-3
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insufficient evidence for cholesterol, but likely no harm
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Psyllium (Metamucil®)
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similar mechanism to bile acid resin
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PCSK9 Inhibitors
Alirocumab, evolocumab |
Class of biologics for very high-risk patients (of a cardiovascular event) who have not reached targets with statins
Monoclonal antibodies for PCSK9, which promotes LDL degradation – reduce LDL substantially Administered SC every 2 weeks (q2w), monitor within 4-8 weeks |
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Thiazide Diuretics
Hydrochlorothiazide (HCTZ) |
Electrolyte imbalances (especially loss of potassium - hypokalemia) – monitor all electrolytes
Hyperglycemia – monitor blood glucose Dizziness – monitor upon standing Hypotension – monitor blood pressure/vitals Some drug interactions – most mild and require ↑ monitoring; sulfa drug Important to warn patient about ↑ peeing! AM dosing! |
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Calcium Channel Blockers
Nifedipine |
Dizziness, hypotension, headache, flushing, reflex tachycardia*, constipation, peripheral edema
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ACE Inhibitors
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electrolyte imbalances (esp. potassium)
first-dose syncope orthostatic hypotension unexplained persistent dry cough Theory: due to high levels of bradykinin usually broken down by ACE angioedema (rare) |
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Angiotensin II Receptor Blockers
(ARBs) |
Same adverse effects as ACE-I
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α1-Blockers
Doxazosin |
orthostatic hypotension (first-dose syncope), dizziness, headache
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α2-Agonists
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more CNS adverse effects than α1-blockers:
Sedation, depression, fatigue, + orthostatic hypotension, dizziness, headache, etc |
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Direct Vasodilators
Hydralazine, minoxidil, nitroprusside |
Multiple dangerous side effects limit use to emergencies and acute care:
Reflex tachycardia, lupus-like syndrome (hydralazine), pericardial effusions (minoxidil), sodium and fluid retention * arthralgia, arthritis, fever, myalgia, pleural effusions; resolves upon discontinuation |
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β-Blockers
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IF a β–blocker is stopped abruptly = REBOUND TACHYCARDIA + Tachycardia, headache, tremor, chest pain, arrhythmia or myocardial infarction
IF a β–blocker needs to be discontinued, it should be tapered slowly over 1-2 weeks Hypotension, Bradycardia, Hyper/hypoglycemia (depends on individual agent), Hyperlipidemia, Nausea, Shortness of breath, fatigue, diminished libido, Dizziness Depending on the selectivity of the individual agent, β-blockers can cause both hypoglycemia AND hyperglycemia In addition, they can also MASK symptoms of hypoglycemia (things like tachycardia, tremor, and anxiety)(see Module 6) The only symptom that remains unopposed is SWEATING |
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Cardiac Glycosides
Digoxin |
dysrhythmias, nausea, vomiting, anorexia, visual disturbances Narrow therapeutic range = toxicity
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Digoxin Toxicity
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Acute Toxicity: anorexia, nausea, vomiting, lethargy, confusion, weakness, hyperkalemia, dysrhythmias
Chronic Toxicity: abdominal pain, anorexia, dysrhythmias, confusion, delirium, disorientation, headache, hypokalemia, hypomagnesemia, nausea, vomiting, ocular disturbances |
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Loop Diuretics
Furosemide |
hypokalemia, dysrhythmias (related to K+), dehydration, hypotension
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Sodium Channel Blockers
Procainamide |
nausea, anorexia, diarrhea, vomiting, abdominal pain, headache, dysrhythmias, hypotension
High doses may result in confusion or psychosis Lupus effect – agranulocytosis, bone marrow depression, anemias – 30-50% of patients using > 1 year |
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Potassium Channel Blockers
Amiodarone |
pneumonia-like syndrome, blurred vision, photosensitivity, nausea, vomiting, anorexia, fatigue, dizziness, and hypotension
Corneal microdeposits = blurred vision = permanent blindness Neurological abnormalities in 20-40% patients (Delirium, confusion, tremors, sleep disturbances) Pulmonary abnormalities in 10-15% GI – 25% Further dysrhythmias Elevated liver enzymes = Cirrhosis Blue/grey skin abnormality; photosensitivity; alopecia (hair loss) Hypo- or hyperthyroidism |
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Calcium Channel Blockers
(CCBs) Verapamil or diltiazem (cardioselective) |
headache, constipation, hypotension, peripheral edema, dizziness
Less peripheral effects than nifedipine (vessels > heart) Avoid grapefruit juice (possible toxicity due to CYP3A4 inhibition) |
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Warfarin
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Hemorrhage – of any type Upper and lower GI tract (gums --> rectum) Respiratory Genitourinary tract Skin
All other adverse effects are rare |
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Antiplatelets
ASA (acetylsalicylic acid) |
Can cause GI upset because they also inhibit prostaglandin synthesis in the stomach, which ↓ mucosal lining
nausea, dyspepsia, increased risk of bleeding 81mg = “Baby Aspirin”- often recommended to prevent cardiac event in high risk patients We do not give Aspirin to babies |
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Thrombolytics
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high bleeding risk, watch for cognitive change which could be a sign of cerebral hemorrhage
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Anti-fibrinolytics
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Most common adverse effect = infusion site reactions
They also slow down blood flow = bradycardia, hypotension |
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Vitamin B12
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Rare adverse effect: low potassium
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Iron
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All oral supplements can cause nausea, dyspepsia, GI bleeding, constipation, black stool (Take with food)
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Statins
Atorvastatin (Lipitor®) |
intestinal cramping, diarrhea, constipation and rarely liver damage, rhabdomyolysis
All adverse effects (even nausea and vomiting) are rare |
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Fibrates
Fenofibrate |
heartburn, abdominal pain, diarrhea, nausea, flatulence, skin reactions (itchiness, redness, rash), rhabdomyolysis, liver damage
Not as well tolerated as statins |
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Niacin
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: flushing, nausea, abdominal pain, hyperglycemia, gout, flatulence, rhabdomyolysis
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Bile Acid Resins
Cholestyramine |
Adverse effects limited to gastrointestinal reactions:
constipation (ensure sufficient water intake), bloating, gas, nausea, steatorrhea Drug interactions: May potentially alter absorption of any drug, vitamin, or mineral Separate by 2 hours (you will see variations of this) |
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PCSK9 Inhibitors
Alirocumab, evolocumab |
local injection site reactions, upper respiratory tract infections, itch
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Nitroglycerin
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headache, reflex tachycardia, flushing, hypotension
ANYTHING THAT CAUSES VASODILATION WILL CAUSE REFLEX TACHYCARDIA |
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β-Blockers
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hypotension, bradycardia, hypoglycemia, hyperglycemia, etc.
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Blood Volume
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Blood volume is regulated by the kidneys.
Blood volume measurement may be used in people with congestive heart failure, chronic hypertension, kidney failure and critical care. |
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Peripheral resistances
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the resistance of the arteries to blood flow.
As the arteries constrict, the resistance increases and as they dilate, resistance decreases. Peripheral resistance is determined by three factors: 1.Autonomic activity: sympathetic activity constricts peripheral arteries. 2.Pharmacologic agents: vasoconstrictor drugs increase resistance while vasodilator drugs decrease it. 3.Blood viscosity: increased viscosity increases resistance. |
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Cardiac output
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the amount of blood pumped by each ventricle per minute.
To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by the heart rate (HR) in beats per minute. Use following equation: CO = HR × SV. |
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Antidiuretic hormone (ADH)
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released by hypothalamus and pituitary that:
Keeps fluid in the body Constricts blood vessels |
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Epinephrine and norepinephrine
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both constrict blood vessels via adrenergic receptors
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Aldosterone
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released by adrenal glands that tells kidney to keep sodium (and therefore water) in the body
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Detected by:
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1.chemoreceptors
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measure CHEMICALS levels like pH, levels of oxygen, carbon dioxide
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2. baroreceptors
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measure PRESSURE levels
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Controlled by:
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1.Autonomic nervous system
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2.Renin-angiotensin-aldosterone system (RAAS)
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Filtration
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when urine is first created, substances are filtered from blood --> urine
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Reabsorption
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substances move back from urine -->blood through tubules
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Secretion
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– substances move from blood --> urine through tubules
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Urine = Filtration- Reabsorption +Secretions
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ACE inhibitors (ACE-I)
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Reduce afterload = improve cardiac output
Dilate vessels = decreasing preload Interrupts the RAAS, which enhances excretion of sodium and water Lowers peripheral resistance and reduces blood volume Drug of choice for heart failure because it interrupts both compensatory mechanisms |
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Angiotensin II receptor blockers (ARBs)
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Reduce afterload = improve cardiac output
Indirectly dilate vessels = decreasing preload Block angiotensin II from causing vasoconstriction and block adrenal glands from releasing aldosterone Same pathway as ACE-I, different place in the pathway Like ACE-Is, interrupt both compensatory mechanisms used in clients who have not responded to ACE-I |
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β-blockers
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Slow heart rate and reduce blood pressure = reduce cardiac workload and provides rest
Negative inotropic effect Decreased heart contractility Blocks the over-stimulation of sympathetic nervous system (fight-or-flight) that occurs in patients with heart failure Must be introduced slowly and NEVER abruptly stopped Generally, we avoid β–blockers in patients with Diabetes (Type 1 & 2) and patients who are at a high risk of hypoglycemia (ex. elderly) |
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Cardiac glycosides
Digoxin |
Slows heart rate by acting on SA and AV nodes = improves cardiac output
Requires steady levels of potassium for action Positive inotropic effect Increases heart contractility Second-line treatment for heart failure (primary treatment for arrhythmias) NARROW THERAPEUTIC RANGE DRUG Requires drug monitoring to ensure proper loading dose, digitalization, and doses to maintain steady state Mechanism of action: increases the contractility of myocardial contraction (+ inotropic) – requires steady levels of potassium for action Used for dysrhythmias and heart failure IF other drugs fail |
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Diuretics
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Work in different places in the nephron of kidney
Reduce blood volume and cardiac workload ALSO reduce edema and pulmonary congestion Mostly for symptom relief of excess fluid Used in addition to other heart failure drugs As heart failure progresses, we see the stronger loop diuretics (furosemide) used more often, at higher doses Mechanism of action: prevents reabsorption of sodium and chloride, primarily in the Loop of Henle to increase urine flow, reduce blood volume and cardiac workload For symptomatic relief of excess fluid |
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Vasodilators
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Relax blood vessels = lowers blood pressure = reduces afterload and preload
Minor role in heart-failure treatment Hydralazine: arteries > veins (afterload) Isosorbide: veins > arteries (preload) For heart failure, sometimes are used together for highest effect |
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Can be due to disease of bone marrow (where we make blood cells), or genetics
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Hemophilia's
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there are lots of types, depending on which factor they lack
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Von Willebrand’s Disease
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lack von Willebrand factor
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We focus treatment on trying to get the blood to clot, or stopping bleeding
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Factors involved in forming a blood clot:
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Platelets
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Prothrombin
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--> (prothrombin activator) --> thrombin--> fibrinogen --> fibrin strands
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Vitamin K
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Factors involved in dissolving a blood clot (fibrinolysis):
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Plasminogen --> (tissue plasminogen activator) --> plasmin
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Thrombus
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=a stationary clot
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Embolus
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=a travelling clot
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Deep Vein Thrombosis
(DVT) |
= clot in veins of leg (calf)
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Pulmonary Embolism
(PE) |
= clot that has travelled to the lung
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Cerebrovascular Accident
(CVA) (Stroke) |
= clot that has travelled to the brain a stroke can also be caused by a bleed in the brain
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Anticoagulants
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Prevent a clot from forming, either by inhibiting a specific clotting factor or by inhibiting platelet action
NOT = BLOOD THINNERS |
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a.Unfractionated heparin
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Does not dissolve a clot, but prevents them from getting bigger and new ones from forming
Binds to multiple clotting factors SC or IV only - no oral or IM Do not massage injection site (bleeding & bruising) Short half-life (1.5h) – used in situations where we need it to work quickly, or have the ability to stop it quickly (like pre-surgery) Antidote = protamine – works within 5 minutes Dose is dependent on condition |
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b.Low molecular weight heparins
(LMWH) Tinzaparin, enoxaparin, dalteparin -parin |
Longer duration of action and more predictable response, so often a choice for discharge (can teach patient to do SC injection)
Doses are decided according to patient weight and what we’re treating (post-surgery, treat DVT, prevent clot for dialysis) – so, DOUBLE OR TRIPLE CHECK CORRECT DOSAGE SC injection or directly in hemodialysis catheter; no IM Still use protamine as antidote, but not as effective |
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c.Warfarin
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Inhibits the synthesis of multiple clotting factors
Oral therapy for people with a long-term need for anticoagulation (atrial fibrillation, valve replacement, treatment of DVT or PE) Warfarin takes ~ 3 days to reach a therapeutic level, so when transitioning from heparin/LMWH to warfarin, there must be an overlap of therapies Even higher risk of bleeding during overlap Antidote = vitamin K – works in a few hours This is why we caution foods high in vitamin K, because we want stability of anticoagulation Important to take at same time each day (most institutions will give all warfarin at the same time – like supper) MUST GIVE CORRECT DOSE Patient must be consistent with checking for drug interactions and signs of bleeding |
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d.New Oral anticoagulants
(NOACs) |
Inhibit more specific clotting factors Rivaroxaban (Xarelto®), apixaban (Eliquis®) = inhibit Factor Xa
Dabigatran (Pradaxa®) = thrombin inhibitor Pros: No INRs, predictable response, one dose less chance of error Cons: No antidote, need dosage adjustment in kidney failure, $$, more dyspepsia than warfarin, more difficult to individualize therapy with restricted doses All still cause bleeding, many drug interactions |
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Antiplatelets
ASA, dipyridamole, clopidogrel, ticlopidine |
Can be given along with anticoagulants, because affect different places in clotting cascade
+++ bleeding risk if combined Can cause GI upset because they also inhibit prostaglandin synthesis in the stomach, which ↓ mucosal lining |
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ASA
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Irreversibly binds to cyclo-oxygenase in platelets, which prevents it from aggregating
Effects of one dose lasts 7-10 days (irreversible binding) |
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Thrombolytics
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TPA = tissue plasminogen activator OR other drugs that do same thing (alteplase)
Convert plasminogen --> plasmin, which breaks down many clotting factors Destroy a clot that’s already formed --> used in emergency situations (like stroke, MI, DVT, PE) If the patient is actively bleeding DO NOT GIVE Dosed according to weight Only administered by RN with special training and in facility with appropriate equipment to monitor for hemorrhage |
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Antifibrinolytics
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Promote clotting, to prevent bleeding during surgery or emergency
They also slow down blood flow --> bradycardia, hypotension Tranexamic acid most common (can give orally) All are rarely prescribed compared to anticoagulants Many biologics developed for genetic conditions that lack a clotting factor (products very specific to type of hemophilia) Used to both prevent and treat bleeding – treatment would continue for life (most intervals every 3-4 days, longer intervals with newer products) but dosages change Most developed using recombinant DNA to replace missing factor |
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Atherosclerosis
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= narrowing or occlusion of an artery due to plaque
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Plaque
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= a fatty, fibrous material that accumulates gradually due to high cholesterol – attracts WBCs, platelets, remnants of dead cells, fibrin that narrows and then eventually occludes the artery
Also makes the vasculature less elastic, which means it can’t respond to dilation |
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Coronary Artery Disease
(CAD) |
= narrowing or occlusion of the coronary arteries
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Angina Pectoris
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= chest pain caused by insufficient oxygen to a portion of the myocardium
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Types of Angina
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1.Stable Angina – when symptoms are predictable as to frequency, intensity and duration
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2. Variant Angina – when the chest pain is caused by spasms of the smooth muscle of coronary arteries rather than atherosclerosis
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3. Unstable Angina – when symptoms are more intense and occur during periods of rest; unpredictable
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Nitrates
Nitroglycerin |
Potent vasodilator
Relaxes arterial and venous smooth muscle – opens up everything Decreases workload of the heart and myocardial oxygen demand --> chest pain alleviated Short acting formulations: nitroglycerin sublingual spray or tablets – for emergencies Long acting formulations: isosorbide – for prevention of frequent angina episodes; nitroglycerin patch Can be given sublingual (SL), orally, IV, transdermally, topically; SL = relief in 4 minutes |
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β-Blockers
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Reduces cardiac workload
Slows heart rate and reduces contractility Used for prevention of chronic angina (if occurring often or unstable) Cardio-selective preferred |
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Calcium Channel Blockers
(CCB) |
Reduce cardiac workload and dilate coronary arteries, and reduce peripheral resistance (depends on selectivity)
Bring more oxygen to myocardium Both types (cardio-selective and non) work First choice for prevention of variant angina because they help prevent the cardiac muscle spasm For those intolerant/contraindicated for β-blockers (elderly, diabetic, asthma/COPD) |
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Asthma
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Chronic inflammatory disease of the airway with 2 components
Inflammation treat w/ anti-inflammatories Bronchoconstriction treat w/ bronchodilators Often have triggers that cause exacerbations Environmental (pets, foods, pollens), NSAIDs, cold weather |
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Chronic Obstructive Pulmonary Disease
COPD |
Lung disease that includes chronic bronchitis and emphysema
Chronic bronchitis: airways are swollen and filled with mucous Emphysema: air sacs are damaged, leaving less surface area for oxygen to enter blood stream COPD patients have frequent lung infections and exacerbations – frequent hospitalizations |
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Common Cold
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Viral infection of upper respiratory tract (URTI)
Antibiotics not indicated or appropriate Treat symptoms only – resolves by itself Cough Congestion Fever Body aches, mild headache |
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Advantages
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Large surface area for absorption, Direct to site of action, resulting in fast onset, Reduces systemic side effects (does not eliminate)
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Disadvantages
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Precise doses dependent on patient condition/abilities, Correct use of devices critical, Some oral absorption due to inadvertent swallowing
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Types of Inhalation Devices
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1. Metered Dose Inhaler
(MDI) |
Deliver drugs via a propellant (drug is in a solution)
Requires hand-eye co-ordination Spacers and aerochambers improve distribution |
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2. Dry Powder Inhalers
(DPI) |
Delivers medication in a powder form, using patient’s own inhalation (no propellant)
Requires ability to inhale quickly and deeply Leaves slight residue in mouth Cannot use spacers with these devices |
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3. Nebulizers
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Vaporize a liquid into a fine mist
Requires a machine Takes a long time to deliver one dose (time-consuming) Inconvenience of being near machine for every dose |
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Bronchodilators
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Target the bronchoconstriction component
Used in both asthma and COPD (or any time bronchodilation is needed) Literally open up the airway to let air in (make airways bigger) |
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1. β-Agonists
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Open up the airway very quickly
Relax bronchial smooth muscle – selective for β2 (stimulating sympathetic) We don’t give orally because 1) would not act as fast, and 2) tachycardia Short acting are “rescue” agents – salbutamol Long acting are used more as disease progresses for maintenance therapy – salmeterol, formoterol, indacaterol, vilanterol |
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2. Anticholinergics
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Bronchoconstriction that occurs in both asthma and COPD is largely caused by stimulation of muscarinic receptors – so blocking this pathway makes sense
Don’t work as fast as β-agonists Does NOT make any clinical difference in secretions Could either provide a benefit OR an adverse effect Acute and maintenance therapy – Newer agents better for long term |
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Ipratropium (Atrovent®)
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Used mostly in COPD
Must be dosed quite often due to short duration of action (~q4h – approximately every 4 hours) |
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3. Methylxanthines
Theophylline, aminophylline, oxtriphylline |
Induces Fight-or-flight response
Stimulants, similar in structure to caffeine stimulate the CNS relax bronchial smooth muscle Narrow therapeutic range (requires monitoring), adverse effects (stimulant!), and numerous drug interactions limit its use to severe asthma that has not responded to other treatments Oral or IV route |
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Anti-inflammatories
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1. Corticosteroids
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Anti-inflammatory and immuno-suppressive
Used to prevent exacerbations and progression of disease Suppress airway inflammation and secretions Must be used daily to work; won’t provide “rescue” if used as needed (PRN) by patient Dose is increased OR switched to oral during exacerbation Inhaled route minimizes numerous systemic steroid side effects |
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Fluticasone (Flovent®)
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Produces anti-inflammatory and immunosuppressive effects reduces inflammation and secretion
Used in both asthma and COPD |
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2. Leukotriene Receptor Antagonists
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Reduce inflammation by blocking leukotrienes in inflammation cascade; also useful in allergies
Preventative – not “rescue” Not as effective as corticosteroids Must be taken daily to work Oral |
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Miscellaneous
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Omalizumab
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a monoclonal antibody (biologic) that attaches to IgE to prevent inflammation from triggers
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Roflumilast
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oral phosphodiesterase-4 inhibitor (PDE4); taken daily to prevent inflammation associated with COPD
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Acetylcysteine
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a mucolytic: dissolves or breaks up mucous in lungs, making easier to get out (less viscous)
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Pulmonary vasodilators
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specific for receptors in lungs; use potent vasodilators such as nitric oxide; will still have systemic effects (hypotension --> reflex tachycardia)
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Cold symptom relief Medication
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Antitussives
dextromethorphan (DM), codeine |
suppress cough by stimulating opioid (sigma) receptors
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Decongestants
pseudoephedrine, phenylephrine |
stimulants that cause vasoconstriction and shrinks swollen mucous membranes
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Expectorants
guafenesin |
increases mucous flow/movement so it can be expelled by coughing
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Anti-histamines
diphenhydramine, chlorpheniramine |
antagonize histamine receptors (involved in allergic response); better for allergy symptoms than common cold; may help sneezing
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Acetaminophen
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fever or aches/pains, included if product says “…& Flu”; an extra ingredient in most combo products
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β-Agonists
Salbutamol (Ventolin®) |
tachycardia, anxiety, arrhythmias, nervousness, restlessness, tremor, vertigo, headache, hypokalemia
Typical dose: 1-2 puffs up to QID PRN Caution if arrhythmias or on β-blockers |
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Anticholinergics
Ipratropium (Atrovent®) |
hoarseness, dry mouth, cough, bitter taste (rinse mouth after use)
Caution in conditions contraindicated to anticholinergic use (elderly, incontinence, glaucoma, kidney disease) – may still be used due to little systemic absorption but will still monitor |
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Methylxanthines
Theophylline, aminophylline, oxtriphylline |
Narrow therapeutic range (requires monitoring),
adverse effects (stimulant!), and numerous drug interactions limit its use to severe asthma that has not responded to other treatments |
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Corticosteroids
Fluticasone (Flovent®) |
hoarseness, change in voice, thrush, watch for systemic steroid effects (hypertension, hyperglycemia, osteoporosis)
MUST RINSE MOUTH AFTER USE TO PREVENT THRUSH (ORAL CANDIDIASIS – FUNGAL INFECTION) DUE TO IMMUNO-SUPPRESSIVE QUALITIES |
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Leukotriene Receptor Antagonists
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Few adverse effects/well tolerated: headache, cough, GI upset
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