Cardiovascular diseases
Hypertension |
Heart Failure |
Dysrhythmias |
Angina & Myocardial Infarction |
Lipids |
Coagulation |
Anemia |
Classes of Medication for Hypertension
1. Diuretics |
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! |
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 |
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 |
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 |
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 |
Nifedipine |
Mechanism of action: blocks calcium channels in myocardial and vascular smooth muscle (blood vessels > heart) – long-acting dihydropyridine (LA-DHP) |
Anything that causes vasodilation will also cause reflex tachycardia Therefore, anything that causes vasodilation requires heart rate monitoring |
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 |
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 |
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 |
4.Adrenergic agents |
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 ) |
b.α1-Blockers |
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 |
Doxazosin |
Blocks vasoconstriction caused by stimulation of α–receptors, therefore reducing peripheral resistance
Used to treat urinary incontinence, BPH, hypertension |
c.α2-Agonists |
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 |
d.Miscellaneous |
Labetalol: partial agonist @ β2, blocks @ α1 & β1
Carvedilol: blocks β1&2 and α1 |
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 |
About Action Potentials
Resting State (kind of) |
Na+ and Ca++ are outside cell, K+ is inside cell (+ charge higher outside, than inside – POLARIZED) |
Depolarization |
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) |
Repolarization |
In a further attempt to get back to resting state, the K+ channels open and K+ rushes out |
Remember that calcium also has a role in muscle contraction!
If a patient is asymptomatic with an arrhythmia, we don’t have to treat it
We only treat arrhythmias that affect cardiac output or increase risk of clots
Electric shock / defibrillation – like a reset button for the SA node – hoping to return to normal sinus rhythm in an emergency
Patients with certain types of dysrhythmias are at an increased risk of a clot – therefore, often also on anticoagulants
What are dysrhythmias/arrhythmias ?
Any abnormality of electrical conduction (in the generation or conduction) that results in a disturbance of the heart rate or rhythm
Atrial dysrhythmias are more common and less severe than ventricular dysrhythmias
Diagnose using ECG
Myocardial action potential:
Conduction is sent along the pathway using Na+, K+, and Ca++ channels
Drugs correct dysrhythmias by either:
Manipulating these channels
Altering autonomic activity (α and β receptors) |
Classes of medication for Arrhythmias
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 |
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 |
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 |
Amiodarone |
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 |
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 |
Miscellaneous |
Digoxin |
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 |
Adenosine |
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) |
If it can correct a arrhythmia, it can also cause a arrhythmia
By manipulating the action potential OR the nervous system, we are also manipulating factors / variables that affect blood pressure (cardiac output and peripheral resistance)
Therefore, monitoring would include for ALL:
ECG
Blood pressure
Heart rate
About anemia
Anemia |
occurs when red blood cells (erythrocytes) or hemoglobin have a diminished capacity to carry oxygen Due to: blood loss, excessive destruction, or diminished synthesis |
Erythropoiesis |
the process of making erythrocytes in bone marrow
If we are lacking a substance for erythropoiesis, we won’t have as many RBCs |
Erythropoietin |
– the hormone released by the kidneys that instructs the bone marrow to make RBCs |
Anemias are classified according to appearance of erythrocyte, which tells pathologists which ingredient is missing
General signs and symptoms of anemia
General fatigue
Weakness
Pale skin
Shortness of breath (dyspnea)
Dizziness
Strange cravings to eat items that aren't food, such as dirt, ice, or clay
Tingling or crawling feeling in the legs
Tongue swelling or soreness
Classes of Medication for Anemia
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) |
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 |
Iron |
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 |
Growth Factors |
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 |
Monitoring for Anemia:
B12, folate levels
CBC (RBC, hemoglobin, hematocrit)
Iron, ferritin
Potassium
Neuro status (confusion, etc.)
Arrhythmias
Resolving of symptoms (fatigue, pale colour)
GI adverse effects with iron
Classes of medication for lipids
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. |
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 |
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 |
Bile Acid Resins |
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!) |
Miscellaneous |
Ezetimibe |
inhibits intestinal cholesterol absorption – used along with a statin |
Orlistat |
doesn’t allow fats to be absorbed from intestine – anal discharge (anti-obesity drug) |
Omega-3 |
insufficient evidence for cholesterol, but likely no harm |
Psyllium (Metamucil®) |
similar mechanism to bile acid resin |
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 |
Adverse effects of Cardiovascular medication
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! |
Calcium Channel Blockers
Nifedipine |
Dizziness, hypotension, headache, flushing, reflex tachycardia*, constipation, peripheral edema |
ACE Inhibitors |
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) |
Angiotensin II Receptor Blockers
(ARBs) |
Same adverse effects as ACE-I |
α1-Blockers
Doxazosin |
orthostatic hypotension (first-dose syncope), dizziness, headache |
α2-Agonists |
more CNS adverse effects than α1-blockers:
Sedation, depression, fatigue, + orthostatic hypotension, dizziness, headache, etc |
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 |
β-Blockers |
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 |
Cardiac Glycosides
Digoxin |
dysrhythmias, nausea, vomiting, anorexia, visual disturbances Narrow therapeutic range = toxicity |
Digoxin Toxicity |
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 |
Loop Diuretics
Furosemide |
hypokalemia, dysrhythmias (related to K+), dehydration, hypotension |
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 |
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 |
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) |
Warfarin |
Hemorrhage – of any type Upper and lower GI tract (gums --> rectum) Respiratory Genitourinary tract Skin
All other adverse effects are rare |
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 |
Thrombolytics |
high bleeding risk, watch for cognitive change which could be a sign of cerebral hemorrhage |
Anti-fibrinolytics |
Most common adverse effect = infusion site reactions
They also slow down blood flow = bradycardia, hypotension |
Vitamin B12 |
Rare adverse effect: low potassium |
Iron |
All oral supplements can cause nausea, dyspepsia, GI bleeding, constipation, black stool (Take with food) |
Statins
Atorvastatin (Lipitor®) |
intestinal cramping, diarrhea, constipation and rarely liver damage, rhabdomyolysis
All adverse effects (even nausea and vomiting) are rare |
Fibrates
Fenofibrate |
heartburn, abdominal pain, diarrhea, nausea, flatulence, skin reactions (itchiness, redness, rash), rhabdomyolysis, liver damage
Not as well tolerated as statins |
Niacin |
: flushing, nausea, abdominal pain, hyperglycemia, gout, flatulence, rhabdomyolysis |
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) |
PCSK9 Inhibitors
Alirocumab, evolocumab |
local injection site reactions, upper respiratory tract infections, itch |
Nitroglycerin |
headache, reflex tachycardia, flushing, hypotension
ANYTHING THAT CAUSES VASODILATION WILL CAUSE REFLEX TACHYCARDIA |
β-Blockers |
hypotension, bradycardia, hypoglycemia, hyperglycemia, etc. |
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The 3 Variables of Blood Pressure
Blood Volume |
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. |
Peripheral resistances |
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. |
Cardiac output |
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. |
These are the different things that we can manipulate (with drugs), in order to affect blood pressure
Hormones and Neurotransmitter involved in BP
Antidiuretic hormone (ADH) |
released by hypothalamus and pituitary that:
Keeps fluid in the body Constricts blood vessels |
Epinephrine and norepinephrine |
both constrict blood vessels via adrenergic receptors |
Aldosterone |
released by adrenal glands that tells kidney to keep sodium (and therefore water) in the body |
Remember Wherever sodium goes, water follows
Homeostasis
Detected by: |
1.chemoreceptors |
measure CHEMICALS levels like pH, levels of oxygen, carbon dioxide |
2. baroreceptors |
measure PRESSURE levels |
Controlled by: |
1.Autonomic nervous system |
2.Renin-angiotensin-aldosterone system (RAAS) |
Kidneys and Diuretics
Filtration |
when urine is first created, substances are filtered from blood --> urine |
Reabsorption |
substances move back from urine -->blood through tubules |
Secretion |
– substances move from blood --> urine through tubules |
Urine = Filtration- Reabsorption +Secretions |
What is heart Failure ?
The inability of the heart to pump enough blood to meet the body’s metabolic demands
A weakened heart
Pre-load ǂ Afterload
Classic Presentation = FED
Fatigue, Edema, Dyspnea
If Heart Failure is in the left, it will back up into the lungs (congestion and pulmonary edema)
If Heart Failure is in the right, it will back up into periphery (peripheral edema, leg edema)
Classes of medication for Heart Failure
ACE inhibitors (ACE-I) |
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 |
Angiotensin II receptor blockers (ARBs) |
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 |
β-blockers |
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) |
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 |
Diuretics |
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 |
Vasodilators |
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 |
Bleeding disorders
Can be due to disease of bone marrow (where we make blood cells), or genetics |
Hemophilia's |
there are lots of types, depending on which factor they lack |
Von Willebrand’s Disease |
lack von Willebrand factor |
We focus treatment on trying to get the blood to clot, or stopping bleeding |
VIP clotting factors
Factors involved in forming a blood clot: |
Platelets |
Prothrombin |
--> (prothrombin activator) --> thrombin--> fibrinogen --> fibrin strands |
Vitamin K |
Factors involved in dissolving a blood clot (fibrinolysis): |
Plasminogen --> (tissue plasminogen activator) --> plasmin |
Thrombus |
=a stationary clot |
Embolus |
=a travelling clot |
Deep Vein Thrombosis
(DVT) |
= clot in veins of leg (calf) |
Pulmonary Embolism
(PE) |
= clot that has travelled to the lung |
Cerebrovascular Accident
(CVA) (Stroke) |
= clot that has travelled to the brain a stroke can also be caused by a bleed in the brain |
Clinical presentation of Clot
Swift neurological status change
Swollen, red, sore calf (DVT)
Signs of myocardial infarction (chest pain)
Signs of stroke (one-sided weakness or numbness, sudden confusion, trouble speaking, difficulty understanding speech, vision loss, loss of balance and coordination)
Dyspnea, chest pain, coughing up blood (pulmonary embolism)
Colour changes in skin
Classes of medication for bleeding disorders
Anticoagulants |
Prevent a clot from forming, either by inhibiting a specific clotting factor or by inhibiting platelet action
NOT = BLOOD THINNERS |
a.Unfractionated heparin |
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 |
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 |
c.Warfarin |
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 |
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 |
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 |
ASA |
Irreversibly binds to cyclo-oxygenase in platelets, which prevents it from aggregating
Effects of one dose lasts 7-10 days (irreversible binding) |
Thrombolytics |
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 |
Antifibrinolytics |
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 |
About coronary artery disease
Atherosclerosis |
= narrowing or occlusion of an artery due to plaque |
Plaque |
= 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 |
Coronary Artery Disease
(CAD) |
= narrowing or occlusion of the coronary arteries |
Angina Pectoris |
= chest pain caused by insufficient oxygen to a portion of the myocardium |
Types of Angina |
1.Stable Angina – when symptoms are predictable as to frequency, intensity and duration |
2. Variant Angina – when the chest pain is caused by spasms of the smooth muscle of coronary arteries rather than atherosclerosis |
3. Unstable Angina – when symptoms are more intense and occur during periods of rest; unpredictable |
Classes of Medication for Angina
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 |
β-Blockers |
Reduces cardiac workload
Slows heart rate and reduces contractility
Used for prevention of chronic angina (if occurring often or unstable)
Cardio-selective preferred |
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) |
Respiratory diseases
Asthma |
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 |
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 |
Common Cold |
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 |
Inhalers
Advantages |
Large surface area for absorption, Direct to site of action, resulting in fast onset, Reduces systemic side effects (does not eliminate) |
Disadvantages |
Precise doses dependent on patient condition/abilities, Correct use of devices critical, Some oral absorption due to inadvertent swallowing |
Types of Inhalation Devices |
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 |
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 |
3. Nebulizers |
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 |
Classes of Medication for Respiratory diseases
Bronchodilators |
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) |
1. β-Agonists |
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 |
2. Anticholinergics |
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 |
Ipratropium (Atrovent®) |
Used mostly in COPD
Must be dosed quite often due to short duration of action (~q4h – approximately every 4 hours) |
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 |
Anti-inflammatories |
1. Corticosteroids |
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 |
Fluticasone (Flovent®) |
Produces anti-inflammatory and immunosuppressive effects reduces inflammation and secretion
Used in both asthma and COPD |
2. Leukotriene Receptor Antagonists |
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 |
Miscellaneous |
Omalizumab |
a monoclonal antibody (biologic) that attaches to IgE to prevent inflammation from triggers |
Roflumilast |
oral phosphodiesterase-4 inhibitor (PDE4); taken daily to prevent inflammation associated with COPD |
Acetylcysteine |
a mucolytic: dissolves or breaks up mucous in lungs, making easier to get out (less viscous) |
Pulmonary vasodilators |
specific for receptors in lungs; use potent vasodilators such as nitric oxide; will still have systemic effects (hypotension --> reflex tachycardia) |
Cold symptom relief Medication |
Antitussives
dextromethorphan (DM), codeine |
suppress cough by stimulating opioid (sigma) receptors |
Decongestants
pseudoephedrine, phenylephrine |
stimulants that cause vasoconstriction and shrinks swollen mucous membranes |
Expectorants
guafenesin |
increases mucous flow/movement so it can be expelled by coughing |
Anti-histamines
diphenhydramine, chlorpheniramine |
antagonize histamine receptors (involved in allergic response); better for allergy symptoms than common cold; may help sneezing |
Acetaminophen |
fever or aches/pains, included if product says “…& Flu”; an extra ingredient in most combo products |
Adverse effects of Respiratory Medication
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 |
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 |
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 |
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 |
Leukotriene Receptor Antagonists |
Few adverse effects/well tolerated: headache, cough, GI upset |
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