Lecture 4: CVP Pharmacology and Lab Values Flashcards
a
venous return???
dilated???
Hypertension drugs:
1) Diuretics - #1 line of treatment
2) Calcium channel Blockers
3) ACE inhibitors - typically prescribed second
4) Short Acting Alpha1 adrengeric blockers
5) Nsaids - can icnrease BP
Common now for hypertensive people to be on 3 or 4 of these
What kind of diuretics are most effective in black patients?
Thiazide diuretics
Asians typically require lower doses of diuretics
Hispanics show an intermittent response to hypertensive pills
* typically on 3-4 combo pills
What do dieutretics do to plasma volume?
* What do they do to CO? - for how long?
Decrease plasma volume
Decrease CO (first 2 months only)
What are the easy going diuretics that are often prescribed first?
Thiazide diuretics
common
What are the 3 classes of diuretics?
Thiazide
Potassium Sparing
Loop
What are the 3 side effects of Thiazide?
1) Fluid/electrolyte imbalance - this happens w/ all diuretics because they’re expelling fluid from your body
2) Erectile Dysfunction
3) Hyperglycemia
Common Thiazide Diuretics:
* Hydrochlorithiazide
* Metolazone
* Benzthiazide
NOTE diuretics expell fluid to work on the pre load on your heart. Less fluid going into the heart so it doesnt have to work as hard
Potasssium sparing diuretics side effects (4)
1) Hyperkalemia (because it leaves potassium in there)
2) GI upset
3) Diarrhea
4) Cardiac irregularities
Common = Spironolatone (Aldactone)
Loop Diuretics side effects
1) Fluid imbalance
2) Hypotension
3) Anorexia
4) vertigo
5) Hearing loss
6) Weakness
Common =
* Bumetanide (Bomex)
* Furosemide (Lasix)
What two ways do calcium channel blockers decrease BP
CO
decreased peripheral vascular resistance
* So this portion works on afterload
2 common calcium channel blockers
Dihydropyridines
Nondihyopyridines
Dihydropyridines (Ca2+) do what?
Vasodilation
nonDihydropyridines (Ca2+) do what
Variation in cardiac contuction (decreased HR) - so I guess this imapcts CO
Adverse effects of Ca2+ blockers
Dizziness, HA, hypotension, flushing, palpitations, LE edema, CHF exacerbation, arrhythmias, AV conduction disturbances, constipation, and gingival overgrowth
Flushing is a very common one
Fatigue/Tiredness is also very common - will imapct ex/hep
Angiotensin-converting Enzyme inhibitors (ACE inhibitors)
* Methidology?
* what way do they decrease BP?
* Common ones?
Inhibit ACE
Vasodilation and reduce PVR (kind of the same thing) - so they work on the after load
Common:
* Benazepril (lotensin)
* Lisinopril (Prinivil/Zestril)
Adverse effects:
* hypotension
* Cough
* Hyperkalemia
* HA
* Dizziness
* Fatigue
* Nausea
* Rash
* taste changes
focus on the main adverse effects for these.
Angiotensin 2 receptor blockers (ARBS) - BP med
* What kind of pts are often put on these?
* How do they help?
For pts that do not tolerate ACE antihypertensives well
Increase vasodilation = decreased TPR
* However it has little affect on CO
Common:
* Candesartan (Atacand)
* Losartan (Cozaar)
* Valsartan (Diovan)
Adverse effects
* Cough, otherwise minimal and similar to ACE
Short Acting Alpha1 adrengeric blockers
* Do they block alpha 1 or 2?
* Methodology?
* Adverse effects?
* What other disease is it used to treat?
Block alpha 1 (1 heart)
* makes sense, alpha 1 receptors do sympathetic stimulation which causes vasoconstriction
Methodology: Inhibit catecholamine induced vasoconstriction (decreased vasoconstriction = decreased BP because the TPR is lower)
Common agents:
* Doxazosin (Cardura)
* Prazosin (Minipress)
* Terazosin (Hytrin)
Adverse effects:
* Orthostatic hypotension
* First-dose response - everytime you take it for the first time/increase dose you’re going to have more of those adverse effects
Also used to treat benign prostatic hypertrophy
* Decreases that sympathetic stimulation = less pressure on urethera
Beta-andergenic Receptor antagonists (Beta blockers)
* What do they block?
* Do they use this later or earlier in treatment?
* What does the second generation of this medication do?
* Common agents?
* Adverse effects?
* What is the suffix on these medications?
They sit in the beta 1/2 binding sites (antagonists) and block epi/nor from binding
* So essentially block that sympathetic stimulation to the heart (meaning theres less contractility and it doesnt have to work as hard)
Use to be first line of defense (no longer is)
Often used for younger pts, pts with intolerances to ACEI and ARB
2nd generation (cardioslective) beta blcokers spare B2 blockers to the lungs
* So when you block beta at the lungs you decrease sympathetic stimulation to the lungs meaning they don’t widen as much which is bad for pts w/ asthma and stuff
all end in -olol
Common agents:
* Propranolol (inderal)
* Metroprolol (lopressor, toprol)
* Carvedilol (Dilatrend, Eucardic)
Adverse effects:
* Fatigue
* HA
* Dizziness
* Diarrhea
* Sexual dysfunction
* Proke angina when stopped suddenly
* Acute MI when stopped suddenly - so important that pts don’t miss a dose
Short acting alpha 1 end in what suffix?
-osin
What is the suffix for angiotensin 2 receptor blockers?
-rtan
* its a spartan wht the last line of defense in the RAAS system
What do ACE inhibitors end in?
-Pril
“I aced an exam in April”
What do calcium channel blockers end in?
-Pine
How do you know a medication is an antianginal agent?
It has the word “Nitro/nitrate” in it somewhere
What kind of medication aims to provide symptomatic and prophylactic treatment?
Antianginal agents
What is the gaol of antianginal agents?
Rude myocardial O2 demand
These drugs can be used for chronic/stable angina to halt progression of atherosclerosis, and thrombus formation
Mechanism: Relax vascular smooth muscle by increasing nitric oxide (NO), leading to vasodilation
Long term management of angina:
* BEta blockers
* Calcium channel blockers
* Ranolazine
Antianginal agents
Nitroglycerin - remember, keep in OG container, throw out after 3 months, keep out of direct sunlight
* check becuase she said 6
* When O2 binds to it it starts breaking it down
Amly nitrate (inhaled)
Drugs used to treat CHF
* Afterload reducers (doesnt have to pump as hard to get blood systemically)
* Aldosterone antagonists
* Preload reducers
* Positive Inotrophic agents - make heart pump harder
Afterload reducers:
ACE inhibitors
* Block RAAS which causes vasodilation = decreased TPR
Beta Blockers
* Decreases Sympathetic Stimulation to vessels = decreased TPR (so systemically, not at the heart)
* make it easier on the heart to pump systemically
Angiotensin 2 receptor blockers
* Prevent Rass system from causing vasoconsttriction = vasodilation = decreased TPR
Vasodilators
* decreased TPR
Aldosterone Antagonists
Reduce Fluid retention in the kidneys
* its a diuretic (less fluid = decreased TPR)
Names:
* Spironolactone (Aldactone)
* Eplerenone (Inspra)
Preload Reducers - reduce amount of fluid going back into the heart
Diuretics
* Promote excretion of excess fluid in vascular system - so decreased fluid comes back to the heart aka afterload reducer
* Decrease workload
What are our 2 kinds of positive ionotrophic agents?
Cardiac Glycosides
Phosphodiesterase inhibitors
Common Cardiac Glycosides (Positive Ionotrophic agent)? - what 2 things does this drug do?
* adverse effect?
Digoxin is most common
* It increases force and velocity of systolic contraction and decreases SNS activity
* So i guess it works w/ Ca2+ somehow instead of sympathic NS
Adverse:
* Toxicity
* Afib may not be controlled w/ beta blockers - so it can cause a fib?
Phosphodiesterase inhibitors (positive ionitrophic agent) - does what 2 things?
* Most common 1
* Adverse effects
Milirinon (primacore): Increase contractility and vasodilation
Adverse effect:
* Arrhythmias
* Hypotension
* Hypokalemia
Which of the following medications has adverse effects if abruptly discontinued?
a) calcium channel blockers
b) diuretics
c) beta-adregenic receptor antagonists (beta blockers)
d) Nitroglycerin
C
causes that acute MI/angina
Drugs Post-MI
Neurohormonal blocking agents: BEta-Blockers, ACEI, ARBs
Statins
Antiplatelets and anticoagulants
What is the goal w/ stantins?
* When are they often perscribed?
* Goal for LDL?
Often perscribed following a MI, but are also a BP medication
Goal is to reduce LDL and increase HDL
Goal is LDL <70 mg/dL
They are Antihyperlipidemic Agents
What are the 2 antiplatelets and anticoagulant agents?
* What is perscribed if neither can be tollerated?
* When are these drugs often perscribed?
Aspirin
Clopidogrel (if asprin is not tolerated)
Warfin if can’t tolerate either
Often perscribed following a MI
What do antiarrhythmic agents do/work on?
Work on the myocardial AP
Need to work on different sections of AP to decrease the arrythmia that is happening
All the different classes of antiarrhthmic agents work on different portions of that AP.
* this makes sense because of which chemicals they are letting in / blocking
Class 1 Antiarrhthmic agents
* called what?
* block what
called membrane depressants
Block fast forward NA+ channels
* so sodium channel blcokers
Class 2 antiarrhythmic agents
* called what
* block what?
Autonomic inhibitors and activators
Beta blockers
Class 3 antiarrhythmic agents
* what do they do?
K+ channel blockers and openers
Prolonged repolarization and refractory period
These are the most effective
Class 4:
* called what?
* What do they do?
Ca2+ handling modulators
Slow conduction through the AV node
She said we don’t have to know specifics of the antiarrhythmic agents but be able to dilinate between classes
Which antiarrhythmic drug is most effective?
Class 3 - K+ channel blockers
these make sense based on suffix
Dyslipidemia Medications:
* Statins - most common
* Bile Acid Sequestrants: block bile; Gi and absorption issues
* NIcotinic Acid (niacin and B3): flushing and hepatoxicity
* Fibric acid derivatives: + statins; GI upset, gallstones
* Cholesterol absorption inhibitors: newer, + statin; diarrhea, joint pain
What do statins sometimes cause?
Muscle pain
So check this if they have high pain level
How much do statins reduce LDL?
20-50%
When should statins be taken?
In the evening
remember they can cause muscle pain
Antiplatelets:
* Aspirin
* Clopidogrel (Plavix)
* Tirofiban (Aggrast)
Anticoaglants
* Heparin - LMW Heparin (lovenox)
* Warfin (Coumadin)
EX: Before starting a PT session, a pts vital are recorded as HR - 102, SpO2 - 84%, RR - 18, RPE 2/10. What is the most likely cause of these numbers
a) Normal vitals
b) pt is mildly deconditioned
c) COPD
d) Acute respiratory distress syndrome
Shedidnt answer but it seems like C is the only possible answer
What condition would rapid, shallow respirations from respiratory depression most likely lead to?
a) Respiratory acidosis
b) Respiratory alkalosis
c) Metabolic acidosis
d) Metabolic alkalosis
She didnt answer
Airway patency is maintained via endogenous B2 adrenergic stimulation
* meaning the airway stays open if it has this
This relaxes smooth muscle and promotes bronchodilation
B2 adrenergic agonists are also called _
Other effects:
* Inhibition of inflammatory cells or substances, reduction of bronchial mucosal edema, improved mucociliary clearance of secretions, and anticholinergic effects
FOR LUNGS
Parasympathetic innervation
* rest and digest
* Muscarinic and cholinergic receptors –> bronchoconstriction
* These are stimulated when you dont need blood going to the lungs right now
Sympathetic innervation
* fight, fright, or flight
* Beta 2 adrenergic receptors –> bronchodilation (want more air to use systemically)
Sympathomimetics
* so its an agonist meaning that it sits in the B2 receptors and causes the response = vasodilation = opens airway more
Below are medications often used for COPD/Asthma
Meter Dose Inhalers:
Bronchodilators
* Sympathomimetics
* Anticholinergics
* Xathine derivatives
Anti-inflammatory agents
* Corticosteriods
* Leukotriene modifiers
* Mast cell stabilizers - stabilize histamine
Often used in some combination with each other
how to use an inhaler
This is a discus inhaler. Good for pts w/ limited dexterity in fingers / weakness
Bronchodilators: SABA - short acting beta 2 agonist
Fast acting:
* Beta 2 agonists/short acting (SABA)
* “Rescure inhaler”
* How long does it last? How long does it take to start working
* common one?
* Use = asthma, exercise-induced asthma, COPD, acute shortness of breath
* MOA?
* Side effects
lasts 4-6 hours, takes 5 minutes to start working
Albuterol is common (ventolin, proventil, proair, xopenex)
MOA = relaxes smooth muscle surrounding the bronchioles
Side effects = heart palpitations (because of the excess sympathetic stimulation), tachycardia/tremors (same reason)
ProAir Respiclick
* What is it?
* How old do you have to be to use it?
* Why is it good?
Albuterol sulfate powder (so im guesing fast acting inhaler)
Children over 4 y/o
Good because theres no spacer, priming, shaking, or hand-breath coordination needed
* So its simple and good for younger/advanced aged pts who can’t follow simple directions
Bronchodilators: LABA
Long Acting
* Beta 2 Agonists/Long Acting (LABA)
* How long does it take to work?
* Lasts how long?
* Common agents?
Takes up to 30 minutes to take effect
Lasts up to 12 hours
Goal = maintence bronchodilation
Used for: Exercise-induced bronchoconstriction, long term management of asthma
Common agents: Salmeterol (in diskus), Formoterol, Foradil, Brovana, Performomist, Arcapta Maleate
Never used as a monotherapy - typically combined w/ one of the other agents
No Pulmonary pharmacology, No lab values on quiz
Just cardiac medications on quiz
Whats faster acting, short-acting muscarinic receptor antagonists, or short acting beta 2 agonists (SABA)?
SABA is faster acting, so we use the other one when we don’t need it immediately
How long do short acting muscarinic receptor antagonists take to work?
* common one?
* MOA?
NOTE: this is a bronchodilator
30 minutes (note, its a bronchodilator)
* so these are not considered a rescure inhaler
Common = Ipratropium Bromide (Atrovent)
Inhibitirs airway constriction, decreases mucus prodiction
* so its an anticholinergic, meaning when the muscarinic receptor is stimulated it causes vasoconstriction, so it sits as an antagonist in the receptor and blocks it from recieving epi/nor, leading to increased vasodilation
Side effect = dry mouth
* because its inhaled
Long-acting Muscarinic antagonists
* What do muscarinic receptors do when stimulated w/ their agonist?
* How often is it used?
* What is it primarily used for?
Cause bronchoconstriction
* this long acting agent sits in the receptor and acts as an anatgonist to block this mechanism
* used 1x/day
Priamrily used for COPD, and is less effective for asthma
Common agents = Spiriva
Side effects: systemic side effects associated w/ atropine include dry mouth, constipation, urinary retention, tachycardia, blurred vision, and confusion
NOTE: typically LAMA and LABA are used together. (Long acting muscarinic anatgonists / Long acting beta 2 agonists)
Stiolto (Triotropium Bromide and Olodaterol)
These are typically more bronchodilators, less inhaled steriod
Indications: COPD, Chronic bronchitis, emphysema
Long term, not rescure inhaler
Short acting anticholinergic (SAMA) plus B2-Agonist (IB/SABA) - often combined
* What does it do?
Enhances the action of albuterol
* makes sense because its short acting
What do Xanthine Derivatives do?
* What disease
* How do they help it
* When is it used
* 1 important side effect
* common one
Reverse bronchoconstriction in pts w/ asthma
* Usually as an anti-inflammatory agent
Use: acute asthma that has failed b2-agonist and anticholinergic treatment
side effects: tremor, anxiety, agitation, insominia, arrhythmias, and GI
* because of those arrythmias when taking these drugs you would want to avoid anything w/ caffine in it
Common drug = Theophylline- narrow therapeutic window and risk for toxicity
Anti-inflammatory agents:
* Inhaled corticosteriods, leukotriene modifiers, and mast-cell stabilizers inhibit production of inflammatory cells and suppress inflammatory mediators
Use: bronchospasm, asthma, pulmonary edema
here are some s/s of acute respiratory distress syndrome
* what is a common medication that is administered w/ this?
Anti-inflammatory agents
What are inhaled corticosteriods primarily perscribed to treat?
* how do they treat lung pathologies?
* Side effects
* Common
Asthma
They decrease inflammation in airways
Side effects: hoarseness, fungal infections in mouth (thrush), nasal irritation, dryness, sneezing, and bloody mucus
Common agents: Qvaar, pulmicort, aerobid
she touched on Budesonide and AeroBid are common ones
These are inhaled corticosteriods (sone = steriod)
She said to know the highlighted ones
Know that they can come orially, inhalation
Leukitrienes:
* MOA:
* What are they used for? over what age?
* Side effects?
* Common
MOA: Leukitrenes inhibit the lipoxygenase enzyme, thereby reducing the production of leukotrienes (which are inflammatory agents)
Uses: Long term control of persistent asthma > 12 years old
Side effects: relatively low, liver dysfunction
* Which is why they can be on it for a long time (think years)
Common agents: Zyflo (zileuton), singular (montelukas)
Mast cell stabilizers:
* Other name?
* Used for?
* If they can’t tolerate what drug we use this?
* Side effects
* Common agents
* Thing thats special about them
Cromones
Uses: seasonal allergies, persistent asthma in children, anyone unable to tolerate side effects of other antihistamine drugs
* so remember, these essentailly block allergies by keeping those mast cells from exploding and shooting histamine everywhere - essentially the same effect as those other anti histamine drugs
Side effects: Bronchospasm, throat and ansal irritation, cough, GI distress
Common agents: Nasalcrom, intal
NOTE: remarkably free of serious adverse reactions, some irritation of the nasal and upper respiratory passages may occur following inhalation
* So this is like the medication w/ the least side effects if she asks that question
Combo inhalers:
Corticosteriod and Long acting beta 2 agonist is a common combo
Common agents: Advair, Symbicort, Dulera, Breo, and Ellipta
Antihistamines
* MOA
* First genreation
* Second generation
* Side effects
Block the effects of histamine and result in decreased congestion, mucosal irritation, and symptoms of common cold/allergies
First generation = Bendryl (makes you sleepy)
Second generation: cetirizine (Zyrtec), loratadine (claritin), and fexofenadine (allegra)
Side effects: arrythmias, postural hypotension, sedation, fatigue, dizziness, blurred vision, incoordination, and GI distress
Expectorants:
* MOA
* Uses
* Side effects
Facilitate the production and ejection of mucus
* can be used anytime you have a productive cough and have extra mucus
Uses: cough associated with RTI, sinusitis, pharyngitits, bronchitits, and asthma
* mucus plugs - blobs of mucus - helps clear these
Side effects: Gi distress, drowsiness
NOTE: these dry you out so much that it would be a precaution for a woman thats lactating
Mucolytics:
* MOA
* Used for
* 2 kinds
Decrease the viscosity of respiratory secretions, can be administered by a nebulizer
Uses: Viscous mucus in pneumonia, emphysema, chronic bronchitits, and cystic fibrosis
Acetylcysteine (mucomyst, mucosil)
* Splits the disulfide bonds of respiratory mucoproteins, this forming a less viscious secretion
GUaofenesin
* Not fully understood
* You can just increase fluids - this effect might just be due to the pt drinking more water (as recommended w/ this medication) instead of the emdication actually owkring well
Which of the following drugs MOST likely indicate a diagnosis of asthma
a) Mucolytics
b) Expectorants
c) Inhaled corticosteriod
d) Antihistamine
C
NOTE: You wouldnt take this if you just had a cold
Your pt w/ a past medical history of asthma begins to exhibit wheezing and shortness of breath. Which of the following medications would BEST mange their current symptoms
a) Albuterol
b) Salmeterol
c) Acetylcysteine
d) Expectorant
A - key is that they have asthma and they’re wheezing - so its acute
* so we use the short acting rescue inhaler t
serium chemistry for cardiac lab values is made up of what 3 things
1) Lipid profile - assocated w/ hyperlipidema (high choleserol)
2) cardiac markers
3) thyroid function
what value should your total cholesterol be under?
under 200
HDL #’s for M/F
M = >40 mg/dL
F = >50 mg/dL
remember these are the good ones
what should LDL #’s be?
<100 mg/dL
Triglyceride #’s
<150 mg/dL
What shoulder your total HDL ratio be?
<4:1
you want HDL High (they’re cardioprotective)
you want LDL Low
what should fasting glucose be
what should unfasted glucose be
70-110
<200
what does increased cholsterol put you at risk for?
athrosclerosis
What should HbA1C be? (this is hemoglobin) - tells us how well pt has managed their diabetes
<5.7%
troponin I norm
<0.03
troponin T norm
<0.1
High sensitivity Cardiac Troponin
* M
* F
M = < 22
W = <14
this means theres cardiac breakdown, typically as result of an MI
need to be trending down 3 measurements for ex
BNP
* norm
* HF likely value
norm < 100
HF > 400
More of a chronic thing opposed to the MI causes tropnin
NT-pro-BNP norm
< 300
Creatine kinase norm
* when does ck-mb elevate, what causes it to elevate, how long does it take to drop back down
30-170 U/L
a certain kind of creatine kinase called MB normally elevates 4 hours after infarct and declines over 48-72
women = higher glucose due to diseases like sarcopenia / oteoprosis (so less lean mass i guess)
TSH
* gives you info about what organ?
* Norms?
thyroid
0.4-4.5 mU/L
Thyroxine (T4)
* what organ does it pretain to?
* Norms
thyroid
5-12
Free T4
* what organ does this pretain to
* norms?
thyroid
0.75-1.5
Triiodothyronine (T3)
* what organ does this pertain to?
* norms for 20-50 y/os
* norms >50
thyroid
20-50 = 70-205 ng/dL
> 50 = 40-180 ng/dL
what mental illness does hypothyroidism cause?
depression
what mental illness does hyperthyroiism cause
anxiety
Hyperthyroidism
* what hormone is trending down
* which 2 are trending up
down = TSH - becuase your bodies trying to compensate for too much thryoid hormone
up = T3/T4
Hypothyroidism
* what 2 hormones trending down
* what 1 trending up or normal
down = t3/4
up/normal = tsh - because your body is trying to add mroe thyroid hormone
what 5 things make up a complete blood cell count
1) WBCs
2) RBCs
3) Platelets
4) Hematocrit
5) Hb
Partial Thromboplastin time norm
21-35s
info about clotting
Prothrombin Time
11-13
clotting info
INR norm
0.8-1.2
clotting info
which of the following autonomic receptors would most likely cause vasodilation of vascular smooth muscle or bronchodilation in the resp system?
a) beta2
b) beta1
c) Nicotinic
d) Alpha1
a
