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Pharmacology > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

what is vascular tone

A
  • the inward pressure of the blood vessels
    1) vessel smooth muscle contraction/relaxation
    2) vasoconstriction that reflexively occurs in response to stretching
    3) neurotrans effects from ANS on receptors
    4) hormones from nearby tissues effects on vessels
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2
Q

BP terms

A 
SV = stroke volume, blood amount leaving LV with every contraction (bear)
HR = rate of contractions
TPR = total peripheral resistance force against which heart pushes to fill arteries, due to vascular tone of vessels in periphery
SVR = systemic vascular resistance, includes arteries

– if any of these goes up, BP goes up, if any go down, BP goes down

math
BP = CO x TPR
CO = SV x HR
TPR = SVR + venous tone
BP = SV x HR x (SVR + Venous tone)
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3
Q

inotropy and chronotropy

A 
inotropy = ventricular contractility
chronotropy = heart rate
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4
Q

vascular tone and relation to vasocontriction/vasodilation

A

vasocontriction; increases vascular tone

vasodilation: does opposite

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5
Q

one of the most critical things to remember for HTN drugs

A

DO NOT abruptly discontinue, can cause rebound HTN (sudden very high increase in BP)

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6
Q

Numbers for HTN

A 
Normal: 120/80
Prehypertensive: 120-139/80-89
HTN Stage I: 140-159/90-99
HTN Stage II: >160/>100
HTN Crisis: >180/>110 (emergency care needed)
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7
Q

making HTN diagnosis

A

1) after 2 readings seated in char
2) confirm in contralateral (opposite) arm to rule our underlying conditions like aortic coarctation
3) use higher reading (systolic or diastolic) to assign the HTN stage

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8
Q

can’t tell everyone same goal for HTN treatment but what’s the most common?

A

less than 140/90

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9
Q

what’s normal BMI

A

18.5-24.9 (weight kg/height cm)

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10
Q

lifestyle for HTN

A

1) physical activity: 30 minutes all/most days, 4 types
2) normal BMI
3) alcohol consumption: limit to one DE per day, 1-2 for men
4) proper diet: low Na+, adequate K+, veggies/fruits, low-fat dairy, low in sat fat (use DASH)
5) hot tub, avoid OTC drugs that raise BP

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11
Q

homeostasis to maintain a normal BP

A
  • combo of neuro (ANS) and endocrine control
    1) ANS control - balances
  • sympathetic - raises BP through catecholamines release
    a) agonist beta-1: raise force of vent contraction (inotropy( and raise HR (chronotropy) and raise CO
    b) agonist alpha-1: cause vasoconstriction of periph vessels and raises TPR
  • parasympathetic - lowers BP through CNX (vagus)
    a) acetylcholine: on muscarinic receptors lower HR and force of vent contraction
    b) nitric oxide NO cause peripheral vasodilation lowers TPR

2) endocrine - hormones change BP
- renin angiotensin system RAS
- natriuretic peptides

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12
Q

RAS

A

renin angiotensin system - activated when BP is low and kidney has reduced perfusion causing release of 3 hormones

1) angiotensin-II (ang-II): a vasoconstrictor stimulate aldosterone/ADH release, also cardiac effects
2) aldosterone: causes Na+/H2O reabsorption in kidney to increase IV volume
3) antidiuretic hormone ADH: promotes H2O reabsorption in kidney to increase IV volume, called vasopressin or AVP

overall: vasoconstrict periph vessels, increases TPR and increases IV volume (higher SV/CO)

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13
Q

natriuretic peptides

A

1) atrial natriuretic peptide or ANP
2) brain natriuretic peptide or BNP

  • works opposite of RAS, cardiac atria gets stretched when blood volume too high and release ANP to promote diuresis
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14
Q

which hormones retain water and salt of ADH, ANP, and aldosterone?

A

aldosterone, ADH: retain water/salt

ANP: promotes diuresis

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15
Q

what happens when a person has HTN for a long period of time?

A

hypothalamus resets its normal and accepts higher BP value as normal

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16
Q

RAS syste’s relation to clotting systems?

A

if RAS is active patients is more prone to form clots

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17
Q

what would Ang-II cause?

A

RAS hormones are agonists mainly, would bind to AT1 receptor and cause a rise in BP/other cardio effects

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18
Q

Steps in the activation of RAS

A

1) first angiotensinogen is produced in the liver, this enzyme is inactive
- > 2) angiotensinogen is broken down by tPA and renin enzyme
3) angiotensinogen becomes angiotensin I (partially active)
- > 4) ACE (angiotensi converting enzymes) and enzymes in the tissue like chymase break down angiotensin I
5) angiotensin I becomes angiotensin II (highly active)
6) then angiotensin II works as an agonist on AT1 receptors to increase BP

*** during this time vasodilators (bradykinins) are being degraded, ACE1 drugs may prevent this and improve vasodilation but can cause cough/angioedema

overall:

a) produces hormones that are vasoconstrictors and volume expanders (salt retention eg)
b) destruction of vasodilators
c) causes overall vasoconstriction and icreased blood volume hence higher BP

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19
Q

AT1 vs AT2 receptors

A

these are receptors that hormones in the RAS bind to as agonists

AT1: causes vasoconstriction, endothelial mitotic effects, and release of ADH/aldosterone (salt/water retention, increased blood volume)

AT2: causes vasodilation, opposite of AT1

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20
Q

essential (primary) vs secondary HTN

A

primary: don’t have underlying medical condition causing HTN, most common in ADULTS
secondary: underlying med condition, more likely in CHILDREN

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21
Q

hypertensive urgency vs hypertensive emergency

A

1) URGENCY
- SBP: >180, DBP: >110
- no organ damage
sx: severe headache, SOB, nosebleed, severe anxiety
tx: readjust meds, no hospitalization/parenteral drugs

2) EMERGENCY
- SBP >180, DBP >120
- could occur at lower leve,s MAIN SIGN is organ damage

examples: stroke, LoC, memory loss, MI, eye/kidney damage, renal failure, aortic dissection, angina, pulmonary edema, eclampsia

tx: in hospital - nursing care ECG tracing
- parenteral meds: nitroprusside IV or substitute nitroglycerin IV, nicardipine IV (postop HTN), fenoldopam/Corlopam IV (vasodilator)

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22
Q

ADPIE of pediatric HTN

A

A/D: look up child’s age sex on table of normal values and if >95th %tile on 3> occasions (preHTN = >90%tile but

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23
Q

How are drugs for HTN classified?

A

by their MOA
INTRO
1) arterioles as site of MOA: drugs working as vasodilators
- review: if arterioles are vasoconstricted, TPR increases, TPR is the force against which the heart pumps when filling arteries, TPR sometimes called afterload, if arterioles are vasodilated then VP will lower

2) capacitance venules as MOA site: drugs here are vasodilators
- review: capacitance venules are veins in lower extremities and viscera capable of storing large amounts of blood; normally blood returned to heart by venous system and provides blood for SV, called preload
- this reduces SV and CO

3) heart site of MOA: drugs here are negative chronotropes and inotropes (remember chronotropy = heart rate, so negative chronotrope means slow the heart rate; inotropy means forceful contraction so negative inotropes make the contractions less forceful)
- lower SV and BP

4) kidney as MOA site: work as RAS blockers and diuretics
- review: if RAS inhibited then no release of Ang-II, aldosterone, ADH
- since RAS causes vasoconstriction/volume retention, these result in vasodilation and reduced blood volume and thus lower BP

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24
Q

what are some common drug clases used to treat HTN?

A

1) Ca+ channel blockers (CCB): vasodilators
2) RAS blockers like ACEIs (ACE inhibitors), ARBs (angiotensin receptor blockers) and DRI (direct renin inhibitors): basodilators and reduce blood volume
3) alpha-blockers: vasodilators
4) beta-blockers: negative chronotropes/negative inotropes
5) diureticsL reduce blood volume and thus SV
6) other: older drugs like clonidine work on CNS site to affect ANS function

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25
Q

Diuretics overview and categories

A

Overview of DIUR

  • diuresis: loss of body water through urination
  • DIUR reduce ECF volume by stimulation natriuresis (salt in urine that drags out water)L urine production reduces blood volume
  • vary by MOA site in kidney
    remember: K+ wasting DUR may need supplements, K+ sparing can lead to hyperkalemia

Categories

1) thiazide diuretics
2) loop DIUR
3) aldosterone antagonists (aldoANT)
4) osmotic diuretics
5) carbonic anhydrase inhibitors
6) AVP (arginine vasopressin) (ADH) antagonists)
7) synthetic hyman B-type ANP

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26
Q

thiazide DIUR

A
  • K+ wasting though very mild so may not need K+ supplements
  • don’t work in patients with kidney disease (creatinine >1.5)

MOA: site in proximal nephrone (proximal tubule) to inhibit Na+ reabsorption - allows natriuresis (Na+ exretion and diuresis)

DRUGS

1) hydrochlorthiazide (HCTZ, Diuril)
2) chlorthalidone (Hygroton)
3) metolazone (Zaroxolyn, Mykrox, unsual/powerful)
4) methyclothiazide (Enduron)
5) indapamide

Usefulness: treat HTN, treat edema; reduce calciuria so prevent Ca+ kidney stones

AEs: aside from mild a) hypokalemia b) high dose AE on cholesterol c) patients with sulfa allergy may be allergic d) increased blood glucose and could develop DM2 e) gout may develop since thiazides may raise uric acid levels

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27
Q

Loop DIUR

A
  • more powerful DIUR, work even in kidney disease
  • K+ wasting and may cause more severe hypokalemia -> supplements

MOA: in loop of Henle of kidney and block Na+ reabsorption promoting atriuresis

Drugs
1) furosemide (Lasix)
2) ethacrynic acid (Edecrin)
3) bumetanide (Bumex, shorter acting)
4) torsemide (Demadex)
(available PO and IV/IM)

Usefulness: not just for HTN, also for severe edema

AEs aside form hypokalemia
a) sulfa allergy except for ethacrynic acid

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28
Q

aldoANT

A

alodsterone antagonists
- K+ sparing can severe hyperkalemia causing life-threatening cardiac arrhythmias

MOA: distal nephrone as aldosterone antagonists so Na+ ot reabsorbed and natriuresis occurs

Drugs

1) amiloride (Midamor)
2) spironolactone (Aldactone)
3) triamterene (Dyrenium)
4) combos
5) newer = eplerenone (Inspra): used only for severe cardiac failure

Other uses: tumors producing aldosterone (Conn’s syndrome); off-label - treatment of hirsutism (excessive facial hair)

Combo drugs
1) often combined with K+ wasting diuretics such as triamterene + HCTZ or spirinolactone + HCTZ etc

AEs
a) severe hyperkalemia - never add K+ supplements and CAUTION with RAS blockade drugs

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29
Q

Osmotic Diuretics

A
  • not usually for HTN
    MOA: act as a particle in the renal tubules to to drag water out of body in urine

Drugs
1) mannitol (Resectisol, Osmitrol)

usefulness: edema syndromes, intra-cranial pressure, keep blood flowing in transplanted kidneys

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30
Q

carbonic anhydrase inhibitors

A
  • also not usually for HTN
  • mildly K+ wasting

MOA: bocks enzyme needed for sodium bicarbonate (NaHCO3) reabsorbtion promoting natriuresis - ALSO reduces aqueous humor formation in anterior chamber of eye

Drug
1) acetazolamide (Diamox)

Usefulness: managing glaucoma since drug reduces IOP
- others based on other effects, metabolic alkalosis, aspirin overdose, prevent acute mountain sickness, catamenial epilesy

AEs

a) kidney stones
b) hypokalemia
c) sulfa allergy may
d) may worsen liver failure encephalopathy (increases serum ammonia)

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31
Q

AVP antagonsists

A

what is ADH
- has 2 names: both ADH and AVP
when AVP: thinking ability to cause vasoconstriction
when ADH: thinking of action on kidney to cause reabsorption of water

MOA: antagonize ADH and promote water excretion in urine

Usefulness: treating SIADH (syndrome of inappropriate ADH secretion) which can occur after head trauma or from ANY CNS lesion; treating hyponatremia

Drugs
OLDER
1) demeclocycline (tetracycline derivative, Declomycin)
2) lithium salts (Lithonate, Lithotabs, Eskalith)
NEWER
3) conivaptan (Vaprisol) IV: for severe hyponatreia

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32
Q

Synthetic Human B-type atrial natriuretic Peptide (ANP)

A
  • IV infusion of the same hormone that the atria normally make in conditions of volume overload

Usefulness: in severe edematous heart failure

potential AE: hypotension

drugs
1) nesitiride (Natrecor IV)

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33
Q

types of adrenergic antagonists

A

also called blockers, block sympathetic nervous sytem

1) beta-blockers (BB)
2) alpha-blockers

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34
Q

Beta-blockers (BB)

A

MOA: block catecholamine (sympathetic effects at the beta receptors

phys review
beta-1: receptors on heart, positive chronotropy and positive inotropy (some beta-1 on kidney and can activate RAS)
beta-2 receptors on lung, bronchodilate
beta-3: metabolic effects on glucose and lipids

THING TO KNOW
1) blockade can be non-selective or selective
selective: for beta-1 only
non-selective: for beta-1 and 2
2) some BB also block alpha-1, called alpha-beta blockers

AEs of beta-blockade:

1) bronchoconstriction due to beta-2 blockade
2) adverse metabolic effects on glucose and lipids (beta-3 blockade)

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35
Q

which beta receptor is blocked when treating HTN?

A

beta-1
causes negative chronotropy, negative inotropy
and blockade of renin release (reduce RAS activity)

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36
Q

which BB crosses the BBB? what implication does this have? list the two examples of BB’s that don’t cross the BBB

A

1) lipophilic BB
2) can cause CNS side effects
3) non-lipophilic: atenolol (Tenormin), nadolol (Corgard)

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37
Q

selective BBs do what? what’s the benefit of them? name the main example

A

1) beta-1 blockade
2) less chance of pulmonary bronchoconstriction
3) metoprolol (Lopressor) and atenolol (Tenormin); another is the ocular glaucoma drug betaxolol (Betopic)

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38
Q

what’s a big side effect of non-selective BBs? examples?

A

1) bronchoconstriction

2) propranolol (Inderal), nadolol (Corgard), glaucoma ocular BB timolol (Timoptic)

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39
Q

adverse _____ effects may occur with BBs, what are some that pertain

A

1) lipid effects

2) lipid neutral: pindolol (Visken)&acebutolol (Sectral), and metoprolol (Lopressor)

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40
Q

ISA

A

intrinsic sympathomimetic activityL means drug can stimulate as well as block the beta-1 receptor, may cause raised HR and BP and hurt cardiac patients

examples: pindolol (Visken)&acebutolol(Sectral) and the ocular glaucoma drug careteolol (Ocupres)

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41
Q

what’s a long-acting BB that allows once-daily dosing

A

propranolol-XL

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42
Q

what’s special about nadolol (Corgard)?

A

can be used in liver failure since not hepatically degraded

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43
Q

what’s special about the alpha-beta blockers?

A

can improve HTN by periph vasodilation

ex: carvedilol (Coreg, Coreg-CR), labetolol (Normodyne, Trandate)

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44
Q

what’s special about nebivolol (Bystolic)

A

had additional oxide vasodilation

45
Q

Clinical uses for BB

A

1) Ischemic Cardiovasc Disease
- HTN, ischemic heart disease, angina since BBs will reduce MVO2
2) post-MI
- prolongation of survival after MI (but not diabetic) and limiting infarct size
3) cardiomyopathy
- eg IHSS since BBs reduce contractility and lengthen time of vent ejection, so more blood can get out of left ventricle per beat increasing SV
4) cardiac arrhythmias
- BBs one of Vaughn-William anti-arrhythmic drug classes
5) LVH & heart failure (HF) and LVD
- reduce MVO2
- not given if patient is hemodynamically unstable
- used only in compensated HF (not symptomatic)
5) Diseecting Aortic Aneurysm
- lowers BP and limits dissection rate
6) thyroid storm
- hyperthyroidism causes excessive production of catecholamines as well as upregulation of adrenergic recptors –BBs block this
- help periph conversion of T4-T3
- propranolol used, unless a selective drug is required due to history of asthma

7) Delirium Tremes
- prevents sympathetic nervous system discharge during withdrawal syndrome
8) Migraine H/A prophylaxis: unknown
9) Portal vein HTN
- BBs prevent rebleeding, thus as prophylaxis for bleeding
- usually nadolol (Corgard) since not hepatically degraded
8) Stage fright
- prophylactic use of tiny does of short-acting like propranolol 10 mg
- take drug 30 minutes before performace
9) glaucoma
- reduced aqueous humor production
10) familial benign tremor: reduces it
11) prior to surgery (may change soon)
- cardioprotective, high-risk CVD patient and during vascular surgery but DON’T start at high doses immediately before surgery (start one-seceral weeks prior at low dose and tritrate up to targeting resting pulse of 60-80)
- maintaing pulse target during surgery and one month postop then taper down
12) PTSD
13) infantile hmangioma
- liquid propranolol to reduce size of hemangioma

46
Q

Toxicity concerns of BBs

A

1) pulmonary (receptor activity on smooth muscle function)
- cautionL bronchospastic illness eg asthma/COPD due to beta-2 pulmonary blockade causing bronchoconstriction
- occurs with selective BBs too (no such thing as 100% selectivity)
2) dyslipidemia (thouse with ABL)
- may worse lipid profile b/c beta-3 receptors on adipocytes
3) diabetes
- hyperglycemia due to beta-3 effects
- may cause hypoglycemia
- remember catecholamines and sympathetic NS counter-regulate hypoglycemia so blockade of their effects blocks this response
- blunts patients symptoms and awareness of hypoglycemia
4) Depression/CNS effects
5) geriatric
- existing bradyarrhythmis, bradycardia
- disposition to syncope and confusion
6) CV concerns
- may decompensate HF but in mild/moderate compensated HF, beta-blcokers are indicated since reduce MVO2

47
Q

what is MVO2

A

myocardial oxygen demand

48
Q

drug-drug interactions of BBs

A
  • do not use with non-DHP calcium channel blockers (arrhytmia, CHS, hypotension)
  • remember: DON’T USE BLOCKERS TOGETHER, too much of combine negative inotropic effect; danger of bradycardia esp if with Non-DHP CCBs (diltiazem and verapamil)
  • certain CCBs due to bradycardia
49
Q

Alpha-blockers

A

phys review
- most slpha receptors are alpha-1 receptors: in response to catecholamines (norepinephrine and epinephrine), these recptors cause smooth muscle contraction - thus vasoconstriction of blood vessels and contractility of genitourinary smooth muscle

MOA: blockade of alpha-1 receptors REVERSES catecholamine (sympathetic) effect and results in smooth muscle relaxation

  • THUS periph vasodilation and lower TPR (for HTN)
  • also obtain reduced tone of prostatic urethra for decrease resistance to urine flow (benign prostatic hypertrophy, BPH)

selective alpha- blockers: if selective, only work on one sub-sub-type of alpha receptors

1) alpha-1B receptors: found on bascular smooth muscle
2) alpha-1A receptorsL found elsewhere including prostatic urethra

50
Q

reasons to use alpha-blockers

A

1) treat HTN though rarely used for this purpose b/c of AEs
2) treat BPH, usually newer version of ABs
3) treat tumors that release epi (pheochromocytoma tumor)
4) antidote for accidental admin of vasoconstrictors

51
Q

older alpha blockers, newer alpha blcokers

A

OLDER

  • nonselective, immediate release
  • originally for HTN and now used off-label for BPH
    1) prazosin (Minipress)
    2) terazosin (Hytrin)
    3) doxazosin (Cardura)

Toxicity

  • hypotension: severe periph vasodilation causing sudden drop in BP, often with syncope
  • due to low BP, a reflex tahcycardia could occur putting stress on heart, raise MI chance

NEWER

  • selective, long-acting alpha-1 blockers for BPH
    1) tamsulosin (Flomax)
    2) alfuzosin (Uroxatral)
    3) xl doxazosin (Cardura-XL)

TOXICITY OF ANY ALPHA-BLOCKER

1) intraoperative floppy iris syndrome (IFIS): occurs during cataract surgery in patients taking alpha-1 blockers - requires special surg tech to manage or patient can lose iris during surgery
2) even alpha-1A super-selective drugs for BPH have risk of hypotension

52
Q

alpha-1 blockers with additional alpha-2 blocker effects

A
  • used for presurg treatment of pheochromocytoma tumor
  • antidote for vasoconstricted blood vessels exposed to epi during local anesthesia admin

1) phentolamine (Regitine)
2) phenoxybenzamine (Dibenzyline)

53
Q

direct-acting vasodilators

A
  • direct effects on vascular smooth muscle causing periph vasodilatoin; lower periph resistance and BP

clinical uses: angina, HF, HTN esp if parenteral needed

Fo HTN and HF: hydralazine (Apresoline), available IM, PO, IV
- often used in HTN of pregnancy
- longterm use may cause AEs
AEs
1) vitamin B6 neuropathy, lupus-like syndrome
- new combo drug BiDil (hydralazine plus isosorbide dinitrite) for HF in Af-Am patients, combines 2 vasodilators

Older drug: originally for HTN, now for hair loss restoration

  • minoxidil (Loniten): older BP drug, no longer for HTN
  • AE is reason we use drug, like topical Rogaine

NITRATES

  • release nitric oxide (NO) gas like the parasympathetic nervous system resulting in vasodilation
  • short-acting drugs are diazoxide (Hyperstat), nitroprusside (Nipride IV), nitroglycerin (NTG, Nitrostat - sublingual paste)
  • long-acting drugs: oral isosorbide dinitrate (Ismo, Isordil, Imdur)
  • usefulness in angina syndromes where vasoconstriction of coronary arteries, vasodilate coronary

PDEI drugs

  • inhibit phosphodiesterase enzyme which normally degrades cGMP
  • cGMP hangs around longer and causes vasodilation
    1) dipyridamole (short-acting Persantine)
    2) long-acting dipyrimadole with aspirin (Aggrenox) for cardiovasc prophylaxis
54
Q

CCBs overview

A

calcium channel blockers
MOA: indirect vasodilators, decrease periph resistance
- some negative chronotropic effects (slow HR)
- some negative inotropic effects (reduce contractility)
- block entry of Ca_ into smooth muscle cless, preventing contraction (cause vasodilation) and causes cardiac effects

possible AEs

older: abrupt vasodilation with transient myocardial ischemia from coronary steal
newer: safer, long-acting; wometimes worsens HF b/c of - inotropic effects; worsens bradyarrhythmias since slow HR, periph edema

label-indicated for: angina from CAD, some cardiac arrhythmias, HTN

off-label:

a) Raynaud’s (nifedipine most commonly used);
b) primary pulmonary HTN (PPH): used for vasodilating MOA; c) peyronie’s disease: plaque develops causing extreme ventral curvature of penis; topical verapamil gel dissolves plaque

55
Q

what are the two clinical categories of CCBs?

A

1) non-DHPs: special caution when combined with beta-blockers (severe bradycardia)
a) diphenylalkylamines - verapamil
b) benzothiapines - diltiazem

2) dihydropyridines (DHPs): largest category
a) older ones are short-acting (not for routine use)
b) long-acting for routine use/safer

56
Q

Info on the Two non-DHP CCBs

A
  • DO NOT COMBINE WITH BB - severe bradycardia

1) verapamil: available in multiple long-acting version
- anti-arrythmic for tachys, angina, HTN
- includes Calan SR, Verelan SR, ISOPTIN SR, Covera HS, Verelan PM

AEs

  • some negative inotropic effects (reduces force of cardiac contraction)
  • increase digoxin levels (another drug for HF)

SPECIAL: ones ending in HS and PM for bedtime to be more active in early morning when BP levels are normally highest

2) Diltiazem
- HTN, angina
- short-acting: diltiazem (Cardizem)
- long-acting: diltiazem XR (Cardizem CD, Dilacor XR, Tiamate, Tiazac)

AEs
- may increase digoxin levels

Contraindicated

  • bradyarrhythmias like AV block, sick sinus syndrome
  • pulmonary fluid syndromes like edematous HF
57
Q

DHP

A

dihydropyridine

58
Q

DHP CCBs

A
  • largest group of CCBs
    prototype: nifedipine

older short-actingL long longer routine b/c of coronary steal syndrome

newer long-acting

1) amiodipine (Norvasc)
2) felodipine (Plendil)
3) isradipine control release (DynaCirc CR)
4) nicardipine sustained release (Cardene SR)
5) nisoldipine XR (Sular)
6) nifedipine XR (Adalat CC, Procardia XL)
7) IV nicardipine (Cardene) and clevidipine (Cleviprex): in OR for HTNcrisis

UsefulnessL HTN, some angina

AEs
- vasodilatory side effects including flushing, headache, periph edema

59
Q

CCB combos?

A
  • often mised with other fixed-dose drugs
    1) with ACEIs: like amiodipine and benazepril (Lotrel), felodipine and enalapril (Lexxel), and verapamil-XR and trandolapril (Tarka)
    2) with ARBs (angiotensin receptor blockers): amiodipine and valsartan (Exforge); amiodipine and olmesartan (Azor)
60
Q

What are the three classes of RAS blockade drugs

A

1) ACEIs, angiotensin coverting enzyme inhibitors
2) ARBs: angiotensin receptor blockers
3) DRIs: direct renin inhibitors

61
Q

MOA of RAS Blockade Drugs

A

ACEIs and DRIs: ENZYME inhibitors that prevent FORMATION of Ang-II

ACEIs: prevent formation of Ang-II by clocking ACE enzyme needed for converting from Ang-I to Ang-II

DRIs: prevent formation of Ang-II by blocking renin enzyme at very begninning of biosynthetic pathway (so angiotensinogen doesn’t get converted to angiotensin I)

ARBs: RECEPTOR blocker that prevents ACTION of Ang-II at receptor

ARBs: prevent action of Ang-II on AT1 receptor, AT1 receptors cause vasoconstriction, and release of aldosterone & ADH

62
Q

ACEIs

A 
PROTOTYPE: captopril (Capoten)
***all drugs end in PRIL 
later drugs...
1) lisinopril (Zestril, Prinivil)
2) enalapril (Vasotec)
3) benazepril (Lotensin)
4) fosinopril (Monopril)
5) quinapril (Accupril)
6) ramipril (Altace)
7) moexipril (Univasc)
8) perindopril (Aceon)
9) trandolapril (Mavik

NOTE: captopril not used very much since AE is low WBC and needs CBC, no others need this

  • combined with diuretics and with CCBs
63
Q

the ARBs

A 
angiotensin receptor blockers
**** ALL END IN ARTAN
Drugs
1) losartan (Cozaar)
2) valsartan (Diovan)
3) irbesartan (Avapro)
4) telmisartan (Micardis)
5) eprosartan (Teveten)
6) olmesartan (Benicar)
7) candesartan (Atacand)

–combined with diuretics and CCBs

64
Q

combining ACEIs and ARBs?

A
  • may see in clinical practice but NOT RECOMMENDED due to increase AEs; two separate Rxs needed as no fixed-dose combo
65
Q

DRIs

A
  • rather new to market

Drugs

1) aliskiren (Tekturna)
2) combo with diureticL aliskiren + HCTZ (Tekturna-HCTZ)
3) aliskiren + amlodipine (Tekamlo)

  • little info, know it works with HTN, but other benefits and uses of RAS blockade drugs
66
Q

important in monitoring with RAS blockade drugs

A
  • electrolytes and renal function tests RFTs like BUN and Creatinine
  • may cause hyperkalemia
67
Q

uses for RAS blockade drugs

A

1) HTN (combo with DIUR, CCB, BB)
2) HF: ACEI DoC, ARB second-line
3) post-MI: ACEI or ARB
4) LVH (cardiomegaly/enlarged heart): ACEI or ARB
5) LV dysfunction improvement
6) prevent stroke
- ramipril (Altace), many think class effect of ACEIs
7) preven diabetic nephropathy (kidney damage)
- DM1 or DM2 can reduce risk of en-stage renal disease (ESRD) by protective effect on glomerulus
- may reverse pathology of Kimmelstiel-Wilson kidney
- ACEI or ARB therapy first-line for diabetics with HTN (if preg, CCB, avoid BBs and DIUR in diabetes)
8) managing chronic renal failure (CRF)
- excess RAS activation bad renal
- ACEIs used
9) possibly help hyperglycemia in DM2 (ramipril study)

68
Q

contraindications for ALL RAS blockade drugs

A

a) no in PREG or nursing women or might become PREG
b) anyone with reduced renal perfusion (hypotension, dehyd, sepsis)
c) anyone with solitary kidney (one kidney)

OTHER STUFF

1) ACEIs and DRIs: can cause coughing and edema; cough may be worse in pateints with lung disease
2) RAS blockad drugs: poss harmful in renal disease, weird b/c has protective function sometimes
3) hyperkalemia, all (poss worse if with K+ sparing DIUR or K+ supplements)
4) none with NSAID drugs due to increase renal damage

69
Q

Implications for RAS blockade drugs

A

1) ensure adequate hydration
2) no if solitary kidney, dehydration, sepsis, preg,
3) stop NSAIDs
4) no K+ supplements
5) no K+-sparing DIUR
6) consider discontinuing any DIUR
7) lowest available dose in renal failure patients
8) check RFT within 7-14 days of first dose
9) don’t combine ACEI/ARB/DRI drugs, use only one

70
Q

main points for safety using RAS blackade drugs

A

1) do NOT combo with K+sparing DIUR due to risk of SEVERE hyperkalemia
2) do NOT combine with longterm nonselective NSAIDs
3) don’t COMBO with K+ supplements
4) preg cat D all trimester, don’t use if preg!
5) can cause hyperkalemia
6) can cause angioedema (severe swelling and upper airway swelling) and cough in some patients

71
Q

older drugs for HTN

A

1) adrenergic outflow blockade
MOA: deplete norepi stores or stop release
utility: too many side effects, don’t use
AEs: drug-drugs, diet with tyramine, HTN in pheochromocytoma, depression
(reserpine/Serpasil,Serapes, guianethidine/Esimel, guanadrel/Hylorel, pargyline/Eutonyl

2) Ganglion blockers: prevent autonomic outflow, only trimethaphan (Arfonad) used for HTNcrisis rarely and for controlled hypotension in neurosurgery
- severe toxicity (sympathoplegia/para””)

3) central alpha-adrenergic agonists
MOA: work in CNS
methyldopa/Aldomet,clonidine/Catapres, guanabenz/Wytensin, guanfacine/Tenex

Toxicity
General: bradycardia, ortho hypo, glactorrhea, sex dysfunct, HF; abrupt stop may cause acute withdrawal syndrome (HTN, tachycar,diapho)
Special: methyldopa -> positive Coomb’s test and hemolytic anemia (lethal antibodies)
- pos ANA test that may cause potentially lethal hepatiti
- guanabenz/guanfacine: beneficial effect of lowered total cholest triglyceride levels

Other clinical uses

1) ADHD: ER guanfacine (Intuniv) 6-17 yo
2) alcohol/drug detox: clonidine
3) hot flashes

most important: clonidine will see again, REMEMBER don’t stop abruptly but taper down

72
Q

what is PIH

A

pregnancy-induced hypertension, HTN in pregnancy

- most common disorder of preg

73
Q

what is the cap for BP in pregnancy

A

140/90 mmHg
mild HTN: 140-159/90-109
remember distinguish between chronic and preg induced

74
Q

what are the four types of HTN in pregnancy?

A

1) chronic: predate preg or develops before 20 weeks GA (3% all pregnancies)
2) preeclampsia-eclampsia: high BP and proteinuria after 20 weeks GA (5-8%)
- often closer to term, underperfusion of placenta
- goal to prevent sudden BP rise cause of CV problems
3) superimposed preeclampsia on gestational (25% of pregs with chronic HTN)
4) gestational HTN (PIH)
- develops in last half of preg

75
Q

risk for high BP in preg

A

mom: placental abruption, target organ damage
fetus: growth restriction, prematurity

76
Q

pharmacotherapy for mild/moderate HTN in preg

A

preferred: methyldopa (cat B)

2nd line
labetolol, nifedipine, hydralazine, BBs, hydrochlorthiazide (preg cat C)

contrainidcated
DON’T USE RAS BLOCKERS DRUGS (cat D but really think of them as Cat X)
- cause intra-uterine growth retardation, oligohydraminos, fetal RF, fetal death

77
Q

pharmacotherapy for severe HTN

A

preferred

first: IV labetolol or IM/IV hydralazine
second: oral long-acting nifedipine, IV diazoxide
last: IV nitroprusside

Contraindicated: RAS blocker drugs

78
Q

pre-eclampsia vs eclampsia/toxemia vs HELLP

A
  • often used as same
    1) pre-eclampsia: fluid retention and edema, proteinuria, HTN,
    2) eclamp/toxemia: pre-eclamp with seizures or other CNS stuff
    3) HELLP: Hemolysis, Elevated Liver Enzyme Tests, Low Platelet count, may progress to complciation of DIC

ris factors
pre-eclamp: nulliparity, age 45yo, +FH of preeclamp, DM, HTN, multiple gestation
HELLP: multiparity, age >25yo, caucasian, h/o prior poor preg outcome
HTN/proteinuria: levels of these can’t predict progression to eclampsia, without proteinuria can still have seizures

other symptoms suggestive of these complications
- edemia, proteinuria, HTN

79
Q

progression of symptoms in HeLLP syndrome/eclamp etc

A

1) CNS incolcement
2) placental involvement
3) coagulation dysfunction
4) cardiovasc dysfunction: pulmonary edema
5) HELLP syndrome: liver failure, bleeding, death
6) renal failure

80
Q

Nursing care for HELLP/eclamp

A
  • monitoring weight, BP, platelets, proteinuria, fetal satus

- may get early induciton for labor

81
Q

drugs for HELLP/eclamp

A

1) steroids
2) AEDs like IV magnesium sulfate (MgSO4) or IV phenytoin
3) parenteral anti-HTNs like hydralazine or nifedipine (Procardia)
4) maybe transfusion

82
Q

Terminology for myocardial ischemia syndromes

A

1) CAD: coronary artery disease, atherosclerosis (ASHD) from buildup of plaque
2) coronary heart disease (CHD): synonym for CAD
3) myocardial ischemia and angina syndrome: insufficient blod delivery to heart muscle due to arterial blockage from atherosclerosis
- stable angina: only occurs with exertion and relieved by meds
- idiopathic coronary spasm (variant, Prinzmetal, atypical, and rest angina) where even at rest can have ischemia due to temporary spasm
- angina symptoms include substernal chest paint or to jaw/left arm, in women can include fatigue
4) acute coronary syndrome (ACS) including unstable angina and myocardial infarction
1) unstable angina pectoris (UAP): results from partial occlusion of coronary artery, providing insufficient blood (oxygen) to cardiac myocytes
2) myocardial infarction: includes non-ST elevation MI (STEMI) and ST-elevation MI (STEMI) and in both there is a complete occlusion of coronary artery, thus completely preventing delivery of blood to myocardium resulting in death of cardiac myocytes

83
Q

major cardiac risk factors in development of CAD

A

1) elevated LDL-C (this is the bad cholesterol)
2) HTN
3) fam hx of premature CAD
4) male >45, female >55
5) smoker
6) low HDL-C (60mg/dl protective

84
Q

Acute Coronary Syndromes

A
  • most occur in morning
  • also called heart attacks
    1) Sudden cardiac death: death due to undiagnosed CHD, usually vent arrhythmias

2) ACS: unstable angina and MI
a) unstable angina pectoris UAP or crescendo angina
= more severe than normal, last longer, no angina drugs work
b) non-ST-elevation MI (NSTEMI or NSTEACS)
- outrigh cardiac necrosis
- was non-Q-wave myocardial infarction (NQWMI) b/c EKF changes usually don’t progress to a Q-wave
- damage not transmural (entire wall) and was called subendocardial MI
c) ST-elevation MI (STEMI or STEACS)
- ouright cardiac necrosis
- usually progresses to Q-wave on EKG and was Q-wave myocardial infarction (QWMI)
- was transmural MI

85
Q

what to do if patient comes in with chest pain, determining ACS type

A

1) take an EKG (if ST elevation then STEMI)

2) do labs and look for cardiac markers like troponin (if positive then NSTEMI or STEMI)

86
Q

Lab test to make diagnosis using cardiac enzymes

A

early markers

1) myoglobin
2) cardiac troponin T (cTnT) and cardiac troponin I (cTnI): THE GOLD STANDARD
3) creatine kinase (CK) - measure cardiac isoenzyme (CKMB): older test

Intermediate markers
1) AST (formerly SGOT), need to measure cardiac isoform, rarely used

Late marker: LDH

1) thrombolytic therapy may result in earlier/higher lab enzyme results
2) combo of EKG and these lab cardiac panels

87
Q

CAM for CV ilnesses

A

DIETARY PHYTOCHEMICALS

  • plant chemicals that are cardioprotective b/c anti-thrombotic, anti-platelet, anti-oxidant, improve lipid profile, lower BP, reduce/maintain normal weight
  • benefits seems to exist only when used as replacement foods in diet and NOT as add ons/supplements (ex: Mediterranean Diet)
  • thus NOT recommended as supplements, actually have AEs

Examples

1) beta-carotene: vitamin A precursor, may increase risk of lung cancer in smokers and possible increase in angina symptoms, get in food not supplement
2) allicin: get it from garlic, may lower cholesterol
3) olive oil: 2 TBSPNs daily to replace animal fat
4) barley: in food claims to reduced CHD
5) red wine alcohol/grapes: prob due to polyphenol flavonoids and a substance called resveratrol in red-wine
6) other plans: nuts/seeds with lipid lowering ability
7) black/green tee: polyphenolic compounds lower TC

88
Q

Exercise for heart

A

healthy: either moderate for 30min/day 5 days/week (10 minute intervals 150 min per week) OR vigorous 20min/day 3 days/week
- resistance and flex training

89
Q

what important compound for the heart is found in fish

A

omega-3 fatty acids (polyunsat fatty acids, PUFAs)
- LvazaL for high TG, drug at 4gm.day

types of PUFA: EPA (eicosapentaenoic acid) and DHS (docosahexaenoic acid)

90
Q

diets for cardioprotection

A
91
Q

CAM products often discussed for cardiac health

A

1) Choline
- found in organ meat and other phospholipid-rich foods like eggs/meats) and as supplement lecithin
- upper range of safetyL 1gram children, 3.5 grams adults
- low-cholest diet may choline deficiency
2) plant sterols and plant stanol esters
- plant cholesterols are similar to our own
- Benecol: based on canola oil with sitosterol and stanosterol added

3) cholestin in Chinese Red Yeat
- NOT RECOMMENDED, TOXIC

4) dietary fiber
soluble: forms gel when added to water and lowers cholesterol (psyllium/Metamucil; methylcellulose/Citrucel; pectin, oats apples beans fruits corn peas and rice
insoluble: stool bulking, no benefit, wheat bran

5) trans-fatty acids
- NOT HEALTHY

6) coenzyme-Q-10
- called ubiquinol, ubiquinone, and doquinol
- helps our mitochon get energy from food
- some say stain drugs deplete this
- no serious AEs except those on insulin

7) B vitamins
- not recommended for cardiac protection; infact high-risk cardiac clients get WORSE

8) anti-oxidant citamins like selenium, E, C
- NOT RECOMMENDED same as B

92
Q

What are the classes of drugs used in angina and ACS management?

A

1) nitrates (vasodilators!!!)
2) BBs
3) CCbs
4) Partial Fatty acid oxidase inhibitors (pFOX inhibitors): for chronic stable angina
5) antiplatelet/anti-thrombotic drugs (ASA, clopidogel)
6) anticoagulants or antiplatelet agentsL part of afib management

93
Q

Nitrates Info

A

VASODILATORS
MOA: release nitric oxide to vasodilate periph vasodilation ancoronary arteries

Meds

1) nitroglycerin (NTG)
- many forms: sublingual dissolving tablets, topical ointments like Nitrobid, transderm like Depnit&Nitrodur, IV preps, oral aerosol like NitroMist
* ***- NTG tabs and oral mist sprays used PRN Q5min, max 3 sprays over 15 min
2) long-actingL long-acting nitro; isosorbide dinitrate (Isordil), isosorbide mononitrate (Imdur, Ismo)
3) amyl nitrate????: rarely used, crushed capsule inhaled, HIGH abuse potential espec as isobutyl nitrite (really a drug of abuse); not thought of as cardiac drug

TOXICITY/AEs
- hypotension, bradycardia, cerebral ischemia, edema, headache

DRUG-DRUGS

1) alcohol, BP drugs, other vasodilator
2) WARNING: do NOT USE with erectile dysfunction drugs (sildenafil/Viagra, tadalafil/Cialis, vardenafil/Levitra)

topical delivery: 12 hours on, 12 hours off or drug stops working

How to take….

a) 5-10 min prior to exertion prophylaxis
b) Q5min, call 911 if no relief after 3 doses (15 min)
c) some believe 911 if no relief after one dose

94
Q

drugs for angina other than nitrates

A

1) BBs: prevention, preop cardioprotective
2) CCBs: prevention daily, long-acting used
- rest angina (vasospastic Prinzmetal angina)
3) pFOX inhibitors: chronic stable angina
- newer, 3rd line after BB, nitrates and CCBS
- prevention
drug = ranolazine (Ranexa), 2x daily, AEs of headache, weakness, constipation, nausea, used in combo with BB CCB (amlodipine) or nitrates, cannot be used with diltiazem CCB due to drug-drug
4) antiplatelet/anti-thrombotic: ASA, clopidogel
5) anticoag or antiplatelet agents: afib management
- thrombo-embolic stroke prevention
- anticoags: vitamin K antagonists (warfarin), direct thrombin inhibitors (dabigatran/Pradaxa), direct factor Xa inhibitor (rivaroxaban/Xarelto)
- aspirin is an antiplatelet agent

95
Q

decision on angina treatment

A

CHA2DS2-VASC scoring

96
Q

OVERVIEW: current guidelines for management of chronic stable angina (CSA) from AHA

A

1) manage HTN, cholesteral, diabetes
2) stop smoking, diet, weight
3) physical activity and cardiac rehab
4) anti-platelet like aspiring
5) RAS bloackade if hx of HF, MI
6) BB therapy in patients with MI, unstable angina
7) annual flue vaccine
8) angina preventionL first BB, nitrates, ACEI, aspring; second are CCBs (CCBS are first-line for rest/vasospastic angina)
9) NTG for acute chest pain; long-acting NTG poss
10: surgical revascularization (coronary artery bypass surgery, CABG) for multiple vessel disease
11) screan for depression/treat
12) do NOT recommend vitamin supplements
13) TLC diet for cholesterol management, DASH for hypertension
14) increase fruits/veggies or condiser using soy protein to replace animal
15) if afib develops TREAT WITH anticoagulant therapy

97
Q

look at chart

A

for determining with chest pain is UA or MI, ACS

lots of charts pg 44

98
Q

what is the main thing to remember when treating a STEMI (S-T elevated myocardial infarction)?

A

MONA
Morphine: 2-4 mg IV with increments of 2-8 mg IV Q 5 to 15-minute intervals; stop NSAIDs
Oxygen: if SaO2

99
Q

treatment for STEMI

A

1) Initial management: MONA
2) evaluate for reperfusion and percutaneous coronary angioplasty (PCI)
- if PCI can’t happen w/in 90 mins give thrombolytics within 30 min
- thrombolytics can be given within 12 hours of symptom onset (not more than 24 hours after)
3) adjunctiver therapy
a) anticoagulation: heparin (UHF) or LMWH (enoxaparin) or direct factor X inhibitor (fondaparinux)
b) RAS blockade: start ACEI or ARB if ACEI intolerant
c) glucose control: insulin infusion for strict glucose control
d) aspiring
e) thienopyridines: clopidogrel
f) beta-blockers
g) prep for PCI or CABG
h) arrhythmia mangament/possible pacemaker
4) convalescent and followup: secondary prevention
- continue statins, BBs, RAS-blockade drugs
- continue aspirin cardioprophylaxis with maybe addition of clopidogrel (Plavix) if stent placed as part of angioplasty

100
Q

what does heart failure mean?

A

the heart can’t get enough blood to the body to meet its metabolic needs

101
Q

what are the types of heart failure?

A
  1. Most HF = low ouput or systolic HF
    - LV not pumping enough due to LV disease
    - not enough blood leaves LV (ejection fraction or EF is low, also called heart failure with reduced ejection fraction HFrEF)

2) high ouput HG
- huge metabolic need that normal heart can’t meet
ex: beriberi, hyperthyroidism, anemia, AV shunts

3) diastolic HF
- EF (amount of blood pumped) normal but abnormal pressures in LV that causes mycardium disease; somtimes called HF with preserved ejection fraction or HFpEF
- contractility OK but myocytes sick - gets worth over time

4) congestive heart failure CHF, older term
- past diagnosis based on fluid retention symptoms like edema and lungs with fluid
- now call anyone with pulmonary fluid congestion or peripheral edema from fluid retention a decompensated HF

102
Q

what are usual causes of HF

A 
chronic/untreated HTN
obesity
DM
smoking
hyperlipidemia
hx of MI
103
Q

what are signs and symptoms of HF?

A

edema: kidney underperfused and activates RAS resulting in fluid/salt retention then edema
LVH: left ventricular hypertrophy due to RAS activation and cardiomegaly

104
Q

classification of HF

A

NY heart associaition: functional classification

AHA: stages, development over time and suggests best intervention

Stage A) AT RISK at high risk for HF without structural disease or symptoms of HF
-> treat HTN, lipids (cholesterol), prescribe ACEI or ARB

Stage B) ASYMPTOMATIC: structural disease without sx
-> ACEI or ARB and BB (in those with decreased LF EF or hx of MI)

Stage C) SYMPTOMATIC: structural with prior or current sx

  • > routine: ACEI, BB, loop DIUR for fluid retention
    selected: vasodilators (hydralazine, isosorbide) in those with persistent sx despite ACEI/ARB and BB, pacing, implantable defivs, AA drugs

Stage D) REFRACTORY, requires special interventions
-> end-of-life care; heart transplant, permanent mechanical support, experimental surgery/drugs

105
Q

what are the drugs to treat HF

A

1) cardiac glycosides
2) ACEIs/ARBs
3) BBs
4) DIUR
5) direct vasodilators
6) synthetic ANP
7) others approaches: surgically implanted cardiac pacemaker for HF and recurrent arrhythmias; continuous poitive airway pressures or CPAP to improve O2

106
Q

First three drugs to treat HF (detail)

A

1) cardiac glycosides: OLDER DRUGS, NO LONGER ROUTINELY USED
“cardiotonics”
“cardiac stimulants”

-> mainly used today to manage a fib

a) digitalis glycosides
ex: digoxin (Lanoxin): improves myocardial contractility aka positive inotropy by enhancing inflow of Ca+
- also effect on rhythm like slower vent rate in afib/flutter (increased sensitivity of AV nodes to vagal inhibition)

b) TOXICITY/AEs
- arrhythmias eg heart block/bradycardia
- NVD, headache, fatigue, malaise, visual stuff, gynecomastia
- toxicity digoxin due to narrow therapeutic window with possibly fatal results
- renally excreted

c) drug-drugs
- cardiac drugs, BBs, thiazide, loop DIUR, quinidine, amiodarone, CCBs

d) current use: if already on drug continue, a fib management, not really used as much

2) ACEIs, ARBs
* * DoC! for HF
- start with ACEI if no then ARB, some start with ARB b/c less AEs
- CANNOT BE USED IN PREG

a) benefits: improved survival, reduction of CV mortality, stroke prevention, better LV dysfunction and regression of LVH

3) BBs
- routine add-on
exs:
a) carvedilol (Coreg),
b) metoprolol (Toprol XL, Lopressor)
c) bisoprolol (Zebeta, with thiazide called Ziac)

USING BB in HF: patient must be in compensated HF (hemodynamically stable); low doses to start then titrate
REMEMBER: may be prob with diabetics, hypoglycemia

107
Q

Last 3 drugs for HF

A

4) Diuretics
- beneficial when symptoms of congestion (edema, pulmonary fluid)

a) typical is loop DIUR
- PRN of fluid retention if creatinine is 1.5 or greater
- pt to adjust dose PRN
- K+ supplementation may not be needed b/c will be on ?ACEI or ARB which hold K+
b) special situation, aldosterone antagonist DIUR
- eplerenone (Inspra): management of post-MI pts in HF due to reduced LV function
- concern with with FATAL hyperkalemia, esp in combo with ACEI or ARB

5) Direct vasodilators
* ** used in Stage C (symptomatic congestive) HF

a) drugs
- nitroglycerin
- long acting nitrates - isosorbide dinitrate (Isordil)
- hydralazine (Apresoline)

b) FDA approved for AfAm pts only
- combo of isosorbide + hydralazine called BiDil
- or rx 2drugs as generics

c) Rx notes
- isosorbide is nitrate and should NOT BE USED with ED drugs (Viagra/Revatio, Levitra, Cialis) can cause hypotension
- hydralazine can cause lupus-like syndrome (fever, malaise, joint pain)
- direct-acting vasos can cause tachy - use BB
- direct-acting basos cause fluid retention - more DIUR

6) synthetic atrial natriuretic peptide (ANP)
- for acute decompensated HF (ADHF)

ex: nesitiride (Natrecor IV)

a) used 2 days as IV bolus and infusion for vaso and natriuresis
b) AEs: hypo, up serum creatinine and poss increased mortality

108
Q

what is acute pulmonary edema?

A

complication of ADHF (acute decompensated HF)
*** MEDICAL EMERGENCY!, life-threatening

a) DIUR to remove fluid: loops parenterally, furosemide, bumetanide
b) morphine
- venous dilator decreased preload
- reduce anxiety, diminishes sympathetic outflow
c) nitrates to vasodilate coronary arteries: trans patch/past and IV
d) inotropic agents to improve cardiac contractility
- short term via IV
- inamrinone (Inocor, new name used to be amrinone) and milrinone (Primacor) which are PDEIs that increase cellular cAMP to improve Ca+ iuptake in heart muscle
- dobutamine (Dobutrex) beta1 agonist for myocardial contractility
e) vasopressors to maintain BP
- vasoconstrict periph vessels and shunt blood to heart/lungs
- pressor amine drugs
- norepi (Levophed)
- dopamine (Intropin) adrenergic and dopamine agonist (dopamine preferred since renal protective b/c vasodilates renal vessels)
- aren’t helping to perfuse tissues so acidosis continues if mycardium continues low output

Pharmacology (7 decks)

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