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PHARM250 Cardiovascular & Respiratory Cheat Sheet by

Overview of the cardiovascular and respiratory systems, their diseases and the drugs used to treat them including adverse effects.

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

Normal sinus rhythm

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.
 

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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