anti HTN drugs (part 2-guest lecturer) Flashcards
(82 cards)
1
Q
womens heart health facts:
A
- one in 4 women die from heart disease
2. 23% of women die within 1 year of having an MI
2
Q
hypertension
- how does htn rank in causes of cardiac disease?
- what is considered hypertension
- what is HTN when no cause is apparent?
- what is HTN caused by another disease?
A
- number 1 cause of CV disease
- HTN is 140/90
- primary or essential hypertension
- secondary hypertension
3
Q
- how many millions suffer from chronic hypertension?
- what percent are underdiagnosed?
- what percent are untreated?
- what percent are undertreated?
A
- 73 million
- 16%
- 27%
- 45%
4
Q
what are the major cardiovascular risk factors (9 things)?
A
- hypertension
- cigarette smoking
- obesity (BMI>30 kg/m2)
- sedentary lifestyle
- dyslipidemia
- diabetes
- microabluminemia or GFR < 60mL/min
- age (men <65)
- family history of premature CV disease
5
Q
diseases, conditions or “activities” that cause hypertension (9 things):
A
- sleep apnea
- drugs
- chronic kidney disease
- primary aldosteronism
- renal-vascular disease
- chronic steroid therapy/cushings syndrome
- pheochromocytoma
- coarctation (dissection) of aorta
- thyroid/parathyroid disease
6
Q
what is involved with a hypertensive crisis (5 things)?
A
- acute elevation of BP associated with end organ damage (kidneys (renal arteries), liver, eye (retinal arteries)& mural cardiac muscle
- BP 190/100 x2 consectutive readings
- hypertensive crisis, hypertensive emergency, malignant hypertension
- potentially fatal
- 4-35% of patients suffer from post op hypertension (2-4% of this group is hypertensive crisis)
7
Q
- when will symptoms be seen in hypertensive crisis?
- which persons have less of a chance of developing symptoms?
- which have greater chance of developing symptoms?
A
- when diastolic >130 mmhg
- persons with longstanding hypertension
- children and pregnant women
8
Q
what are symptoms of hypertensive crisis (6 things)?
A
- hypertensive encephalopathy
- acute aortic dissection
- acute MI
- acute CVI
- acute renal failure
- acute CHF
9
Q
what are the common causes of hypertensive crisis?
- med changes such as…
- _____ hyperactivity
- diseases such as______
- _____ artery ______
- _____ trauma that causes _____?
- what type of cancer?
- what pregnancy condition?
- what recreational drugs?
A
- abrupt withdrawl of clonidine (or even propanolol)
- sympathetic (autonomic) hyperactivity
- collagen vascular disease such as scleroderma
- renal artery stenosis
- head trauma that causes loss of consciousness >30 min
- renal neoplasm
- pre eclampsia leading to seizures
- recreational drugs like cocaine
10
Q
evaluation of hypertensive crisis patient:
- what histories should be explored?
- what should be assessed (physically palpated)?
- what diagnostics?
- what meds to treat it?
- what is goal with these patients?
A
- medical history (renal, cardiac, medication), rec. drugs
- pulses x4 (differences in pulses may be coarctation of aorta)
- cbc, lytes, bun,creat, UA, cxr, head ct, EKG
- Meds:
- Nipride (direct acting arterial vasodilator)
- nifedipine (ca++ channel blocker)
- labetolol (Beta blocker (some alpha blocker activity)
- esmolol (beta blocker)
- diazoxide (potassium channel ACTIVATOR)
- minoxidil- vasodlator
- prompt recognition and immediate treatment to halt vascular damage
11
Q
hypertension: effects on body:
1. increased risk of what? also causes what related conditions?
2. damage to what organ accelerates with HTN?
3. what does HTN do to cause stroke and heart attack?
4. why is HTN called the silent killer?
A
- stroke and heart attack risk increases dramatically with blood pressure increases, also causes TIAs, PEs, CAD.
- kidneys
- plaque in vessel walls ruptures more easily with increased BP
- HTN silently causes all these conditions which all have high mortality rates.
12
Q
how do you calculate blood pressure?
A
cardiac output x peripheral vascular resistance
13
Q
what are the classes of antihypertensive drugs (7 types)?
A
- diuretics
- ACE inhibitors
- ARBs
- Ca++ channel blockers
- Beta blockers
- Alpha blockers
- centrally acting antihypertensives
14
Q
what 2 things regulate blood pressure & how?
A
- baroreceptors-modulate sympathetic stimulation of cardiac output and HR and adjust the BP in response to postural changes and altered physical activity (short term regulation of BP via sympathetic nervous system)
- kidneys-regulate plasma volumes and renin-angiotensin II and aldosterone
- keep blood pressure within narrow range (homeostasis)
15
Q
diuretics:
1. what do diuretics do?
2. how do they work?
A
- work at varius sites in nephron to increase urine output
2. use changes in osmotic gradients to eliminate water (blocks sodium reabsorption; where sodium goes, water goes).
16
Q
clinical uses for diuretics (7 things)
treatment of:
A
- cardiovascular disease
- HTN
- renal disease
- endocrine abnormalities
- glaucoma
- increased ICP
- treat metabolic alkalosis or to alkalyze urine
17
Q
Diuretics:classification
4 types, give examples
A
- high ceiling or LOOP diuretics (LASIX)
- thiazide diuretics (HCTZ)
- Potassium sparing diuretics
- aldosterone (ALDACTONE)
- non-aldosterone (TRIAMTERENE)
- Others:
- carbonic anhydrase inhibitors (DIAMOX)
- osmotic diuretics (MANNITOL)
18
Q
what does high ceiling diuretic mean?
A
it has a high theraputic index
ex: lasix does is 20 mg to 200 mg
19
Q
Diuretics: LOOP:
I. name 4 different loop diuretics:
II. how effecient are loop diuretics?
III. how do they work?
A
I. 1. lasix 2. bumex 3. torsemide 4. ethacrynic acid II. the most effecient diuretic III. act at ascending loop of Henle to inhibit sodium, potassium and chloride reabsorption= more water loss.
20
Q
diuretics: loop:
1. Furosimide (aka)
2. how does it work
A
- lasix
- potent naturetic
- -works in the ascending loop of henle to block reabsorption of Na+, K+, Cl-
- -produces kaliuresis (excretion of K+ in urine as) by increasing sodium-potassium exchange (sodium is reabsorbed) in the late distal tubule and collecting duct
- -also increases magnesium and calcium excretion.
21
Q
Loop diuretics: adverse effects
- what lyte imbalance is seen? what are the side effects?
- what organ toxicity is seen?
- what is a side effect of its main purpose?
- what does this side effect cause in the patient?
A
- hypokalemia (d/t increased exchanged with sodium in late distal and collecting ducts) -causes dysrhythmias (irritablilty)
- ototoxicity (reversible); tinnitus, ear pain, vertigo, balance issues, hearing impairment
- dehydration -dry mouth, unusual thirst, decreased urine output
- hypotension-dizziness and light headedness
22
Q
Usually sodium and potassium are exchanged for each other but what is different about the proportion of NA+ to K+ in the collecting duct (d/t exchange in the late DCT and early collecting ducts)?
A
NA+ & K+ are inversely proportional
23
Q
Diuretics: Lasix interactions:
- what drug interacts with lasix with lyte imbalances are present? what is the reaction? what is the lyte?
- what other drugs would cause the “organ toxicity” worsening the problem?
- what drug is held on to due to the action of what lasix does?
- what drug would counteract the effect of lasix and therefore should not be used with it?
A
- Digoxin; hypokalemia potentiates dig toxicity; predisposes patient to ventricular arrhythmias
- aminoglycosices (gent, tobra, strepto, neomycin, amikacin) all cause ototoxicity
- lithium excretion is reduced; lithium is a salt and lasix increases salt/K+ exchange; pulls salt in and pushes K out
- potassium sparing diuretics keep K+ in, so it would decrease action of lasix.
24
Q
what diuretics are considered low ceiling?
A
thiazide diuretics
25
what does "thio-" mean in chemistry?
sulfur
26
diuretics: thiazide and related:
1. how often used?
2. how do they work?
3. what type of ceiling?
4. are they effective if your patient is in pulmonary edema?
5. what allergy should you use caution with this drug?
1. very frequently used diuretics
2. block reabsorption of sodium and chloride in the DCT therefore increasing renal excretion of sodium, chloride, water & potassium.
3. low ceiling, small theraputic index
4. not effective for immediate diuresis (slow acting)-considered a maintainance diuretic
5. caution with sulfa allergies (same as sulfites)
27
diuretics: thiazide and related diuretics
1. how effective orally and how severe is naturetic effect?
2. how severe are side effects?
3. what patients may have undesirable side effects; what are these?
1. very effective orally with moderate naturetic effect
2. very few adverse side effects
3. diabetics (increased serum glucose); gout (increased levels of uric acid)
28
diuretics: thiazide
1. action? where?
2. diuresis in comparison to lasix?
3. efficacy is dependent on what? what patient wont get thiazide?
1. blocks reabsorption of sodium and chloride in early segment of DCT
2. increased urine flow not as much as lasix
3. efficacy depends of kidney function ;do not give in renal failure (it won't work??).
29
diuretics: thiazide
1. what does diuresis do to perfusion?
2. what happens to the ECG?
3. what happens to catecholamine response? why?
4. how can this effect be counteracted?
1. excretion of water volume decreases cardiac output
2. decreased SVR with decreased sodium
3. low sodium blunts response to catecholamines (or vasopressors : epi, NE) d/t decreased ability to generate action potentials
4. effect counteracted by increased intake of dietary sodium
30
```
diuretics: thiazides:
Hydrochlorothiazide: Clinical uses
1. number one use:
2. obvious but secondary use:
3. unconventional use:
4. safe to use for fluid overload in what condition?
```
1. used to treat essential hypertension by:
- decreasing blood volume; immediate antihpertensive effect
- reduces arterial resistance (develops over time and action is unknown - ??may have to do with sodium action potentials??)
2. treatment of edema in:
- heart failure patients (mild to moderate)
- mild renal or hapatic disease (remember, not for use in renal failure--will not work).
3. treatment of Diabetes Insipidus:
- paradoxical effect, mechanism unknown
4. pregancy (category B)
31
diuretics:
1. 2 main types of thyazide (A,B)
2. combinations of A?
3. combinations of B?
1. A.Hydrochlorothiazide (HCTZ)
B. Chlorothiazide (diuril)
2. A. HCTZ can be used alone as (Apo-Hydro) or in combination:
-HCTZ with propanolol=INDIRIL
-HCTZ with ARB (olmesartan)= benicar; (losartan)=cozaar
3. B. Diuril can be used alone or in combination:
-diuril (chlorothiazine) and reserpine=Diupres 20
32
diuretics: thiazide LIKE diuretics:
1. thyazide-LIKE diuretic
2. what is it used for?
3. what condition is it contraindicated in?
1. Indapamide (Lozide)
2. used for long term management of heart failure, hypertension.
3. contraindicated in pregnancy (teratogenic effect).
33
diuretics: hydrochlorothiazide:
contraindications:
contraindicated in sulfa allergy
34
diuretics: hydrochlorothiazides
Adverse reactions:
1. ____e imbalance; which one? why? signs and symptoms?
2. increased __ A___levels? why?
3. altered serum L____ levels? which ones?
4. increased ____ G____ ? what is the cause?
1. electrolyte imbalance;
- -potassium;
- -d/t excessive loss especially with inadequate K+ intake
- -s/s: dry mouth, thirst, irregular heart beat, mood and mental changes, muscle cramps, n/v, weak pulse
2. increased Uric acid levels
- -d/t inhibited uric acid secretion from PCT (accumulates in joints)
3. increased Serum Lipid levels (hyperlipidemia)
- -increased HDL, LDL
4. elevated blood glucose
- -in part due to hypokalemia which REDUCES insulin secretion by pancreatic beta cells
35
Potassium sparing diuretics:
1. action: where do they work? how?
2. what are these good for counteracting? what patient is it good for?
3. how effective is it?
1. act in DCT where sodium is usually reabsorbed and exchanged for potassium; blocks Na+ reabsorption (leaving more in the lumen) and therefore retains the K+, "sparing" the K+.
2. useful in counteracting postasium loss induced by thiazide and loop diuretics. Good for hypokalemic patients.
3. produces only modest increase in urine output, not potent as a stand alone drug.
36
```
diuretics: potassium sparing:
2 types;
1. A
2. B
3. what is the action of aldosterone?
```
1. A. epithelial sodium channel blockers (amiloride; triamterene)
2. B. aldosterone receptor antagonist (spironolactone (aldactone)), which blocks action of aldostorone.
3. aldosterone promotes sodium retention and potassium excretion; by blocking aldosterone, more sodium is excreted and potassium is spared.
37
diuretics: potassium sparing
Aldactone: side effects:
1. electrolyte imbalance; which one?
2. endocrine effects; since it blocks aldosterone, what else will it block? how does it affect men and women differently?
1. hyperkalemia (d/t potassium sparing)
2. blocks aldosterone (a steroid) and thus blocks sex steroids (men become more like women, women become more like men)
- men: gynecomastia, impotence
- women: menstrual irregularities, hirsuitism, deepening voice
38
diuretics:potassium sparing
aldactone
uses: (4 things)
1. prevention and treatment of hypokalemia
2. treatment of primary aldosteronemia
3. anti-androgen effect for *polycystic ovary disease (*polycystic ov. disease usually occurs in obese)
4. treatment of hirsutism & seborrheaic acne
39
diuretics: potassium sparing: Epithelial sodium channel blocker:
1. name 2 name brands?
2. brand names when mixed with HCTZ
2. adverse side effects:
1. Triamterene, Amiloride
2. maxzide, dyazide
3. hyperkalemia, n/v, diziness, peaked T wave, blood dyscrasias (rare).
40
potassium sparing: triamterine/ amiloride
drug interactions:
1. what drugs should be avoided?
2. what supplements should be avoided?
1. drugs that increase potassium, ACE inhibitors
| 2. potassium supplements
41
osmotic diuretics:
1. name 4 of them
2. how do they work?
1. mannitol, isosorbide, urea, glycol
2. no specific receptor or molecular target
- freely filtered at glumerulus and undergo minimal absorption
- increase osmotic pressure of tubular fluid, reducing bodies reabsorption of water
- act via physiochemical properties
42
```
osmotic diuretics:
mannitol:
1. what is it?
2. how does it work?
3. clinical uses:
```
1. a sugar alcohol
2. given IV, it is filtered by glumerulus but NOT REABSORBED (passes thru), creating an osmotic gradient in the lumen of the nephrom causing water to move into lumen, sodium is also retained in the lumen.
3. used in:
- oliguria
- acute renal failure
- promote excretion of toxic substances (administered with cisplatin to help secrete antineoplastic platinum compounds)
- help alzheimers meds get to brain(shrinks endothelial cells increasing gap size in BBB)
- increased ICP
43
diuretics: carbonic anhydrase inhibitors:
1. what is it?
2. what does it do?
1. a naturally occuring enzyme present in :
- nephron basolateral and luminal membranes
- cytoplasm of epithelial cells
- RBCs
2. Blocks sodium bicarbonate reabsorption causing sodium bicarb diuresis and a reduction in bicarbonate stores (increased secretion of HCO3-)
44
```
diuretics: carbonic anhydrase inhibitor:
clinical uses (4 things)
```
1. treatment of glaucoma: Brizolamide or Dorzolamide reduces IOP
2. urine alkalynization: Acetazolamide increases urinary Ph which enhances excretion of uric acid and ASA
3. treatment of metabolic alkalosis: acetazolamide helps to excrete bicarb causing nomalization of Ph and increases carboxic drive
4. acute mountain sickness: acetazolamide: see next note:
45
acute mountain sickness:
1. how does it occur?
2. what are symptoms (mild)?
3. what are severe symptoms?
4. what else will the patient be on?
1. occurs with rapid ascent above 10,000 feet (3000 meters)
2. mild symptoms include dizziness, insomnia, headache, nausea lasting days
3. serious cases cause rapidly progressing pulmonary or cerebral edema (this relieves hypoxia)
4. patient will also be on oxygen and steroids
46
diuretics: clinical indications for anesthesia:
1. what factors caused by diuretics can cause problems with anesthesia?
2. hyperkalemia causes what affect that interferes with what anesthesia drug?
3. what does hypokalemia cause in anesthesia?
4. what does high dose lasix block and what does it cause? what anesthesia drug does it go against?
5. giving diuretics to ICH patients; what must they be monitored for?
1. hypotension and electrolyte imbalances
2. hyperkalemia produces metabolic acidosis that may affect duration of NMBs like nimbex
3. hypokalemia can cause decreased pancuronium levels
4. high dose lasix can inhibit phosphodiesterase which increases cAMP and increases muscle contraction which antagonizes NMBs.
5. must monitor patients with ICH for anuria and dehydration
47
antihypertensives: ace inhibitors
1. uses:
2. where is renin stored?
3. what causes its release?
1. HTN, heart failure, post MI
2. stored in afferent and efferent vessels
3. released with adrenergic stimulation (beta 1 stimulation), reduction of wall tension in afferent receptors (low pressure), reduction in sodium levels at macula densa
48
antihypertensives: ACE
angiotensin:
1. how many types of angiotensin
2. what does the release of AT cause (7 things)?
1. 3 types (but only 2 have actions): AT1, AT2 (AT3 no known axn)
2. -increase in inositol phosphate (IP3) which causes increased intercellular calcium
- increase in arachidonic acid metabolites
- decrease in cAMP
- adrenal cortex activation increases release of aldosterone
- causes vasocostriction of arterioles (local and systemic)
- causes release of aldostorone
- alteration of cardiac and vascular structures (causes remodeling of heart)
49
1. remodeling of the heart means what?
| 2. what medication prevents this?
1. increased thickness of the heart and blood vessel walls after damage (post MI)
2. ACE inhibitors
50
1. what are ' prils' used for?
| 2. what vessels does it work on?
1. hypertension, cardiac failure, diabetic nephropathy, post MI
2. works mainly on arterioles (less on veins) so less chance of postural hypotension, but decreases both preload and afterload
51
anesthetic aspects of "prils"
1. blood pressure effects with diuretics
2. nsaid interaction (after how many days)
3. blood pressure with anesthesia is...
4. lisinopril increases action what MRs?
5. what do antacids do to what___ pril?
1. hypotension increased when on pril + diuretic
2. nsaids used more than 7 days decrease antihypertensive effect
3. hard to control hypotension with anesthesia from ACEs
4. lisinopril increases of "curarie like" MRs
5. antacids block captoril d/t chelating (binding) action of the calcium carbonate
52
name some "prils" (5)
lisinopril, captoril, enalapril, fosinopril, ramipril
53
drug interactions of prils:
| what medications should be used with caution (4) and reasons?
1. loop and thiazide diuretics (increase hypotension and renal insuffeciency)--- but good for CHF patients
2. some antihypertensives (too strong)
3. drugs that increase K+ levels
4. lithium drugs (levels will increase).
54
ACE inhibitor s/e
1. how do prils cause cough? whats the chance (%)?
2. what cutaneous side effect is common?
3. what patient is it contraindicated with?
1. comes from bradykinin release; chance: 5%
2. rash: 5-10% risk
3. --pregnancy (teratogen)
- -renal failure: this patient is dependent on angiotensin II to maintain renal blood flow and glumerular filtratin
55
ARBS:
1. How do they work?
2. what was the first ARB?
3. if combined with HCTZ, what is name?
1. competatively prevent angiotensin II from attaching to ARB receptors to prevent hypertension
2. Losartan (cozaar) was 1st;
3. combined with HCTZ is Hyzaar
56
1. what sites do ARBS work at?
| 2. side effects
1. vascular smooth muscle, adrenal glands (decrease aldosterone secretion-which increases water and salt excretion),
2. no MAJOR adverse side effects (no effect on calcium, , no effect on arachadonic acid so no cough, no effect on K+,
- headache
- flushing
- dizziness
- cough
- sinusitis
- fatigue
- chest pain
- benign ST changes on ECG
- muscle cramps/ arthalgia
57
ARBS
1. contraindications:
2. anesthesia implications:
1. pregnancy (2nd and 3rd trimester, renal artery stenosis (needs angiotensin II to maintain perfusion).
2. marked hypotension with anesthesia, increased NM action with curarae like MRs.
58
BETA BLOCKERS:
1. uses:
2. side effects:
1. -inexpensive, can be beta 1&2 or just beta 1
- decrease pulse and oxygen demand
- block inotropic, dromotropic and chronotropic effects
2. -blocks glycogenolysis that occurs with catecholamines, -blocks symptoms of hypoglycemia and recovery may be delayed
- may cause life threatening bronchospasm
59
beta blockers:
1. timolol:
2. pindolol:
3. nadolol:
4. propanolol:
1. timolol blocks beta receptors on cilliary blood vessels (decreases aqueous humor in glaucoma)
2. pindolol-has intrinsic beta activity; used for chronic hypertension
3. nadolol is non selective-may cause bronchospasm
4. propanolol (inderal): good for angina, migraines, SVT, tremors, social phobia, general anxiety disorder, hypertension
60
propanolol:
1. uses:
2. how does it work?
3. contraindicated in...
1. mild to moderate HTN; used with vasodilators for severe HTN, arrhythmias
2. blocks B1 & B2, inhibits stimulation of Renin production
3. contraindicated in 1st degree heart block, CHF, cardiogenic shock, COPD & asthma
61
METOPROLOL:(lopressor/toprol)
1. Action:
2. good for what patients?
3. uses:
4. anesthesia side effects:
1. cardioselective: blocks B1 (spares B2), blocks Renin production
2. can be used on asthmatics, diabetics and pvd patients
3. used for HTN, angina, MI, CHF
4. enhances CNS depression with benzos, causes marked bradycardia when used with Neostigmine reversal, masks signs of hypoglycemia and hyperthyroidism
62
LABETOLOL (trandate/normodyne)
1. action (receptors and effects)
2. uses (intra op, post op etc.)
1. alpha 1, beta 1 beta 2 blocker (directly blocks SA node impulse generation, vasodilates
2. used intra op on cardiac, vascular, general and intracranial surgeries; used to treat pheocrhromcytoma and clonidie withdrawl, attenuates post op HTN and tachycardia
63
beta blocker anesthetic considerations:
| 6 things:
- should not be stopped abruptly d/t rebound HTN and tachy
- discontinuing pre-op increases chance for post op MI
- anesthetic agents increase cardiac depression effects
- hypoglycemia and hyperthyroid symptoms masked (harder to dx)
- tachycardia d/t intra op bleeding is blunted (harder to dx)
- reversal agents will cause marked bradycardia with BBs
64
calcium channel blockers:
1. ACTION:
2. clevidipine is used for...
3. verapamil does what? what part of heart?
1. blocks calcium entry into cells decreasing contraction; causes vasodilation of arterioles and is negative inotropic and chronotropic to heart
2. used for periopertive HTN
3. slows SA and AV conduction TRANSMURALLY
65
CALCIUM CHANNEL BLOCKERS:
1. name 4 major ccbs:
2. potency:
3. action
4. Adalat (aka) used when?
1. amlodipine, nifedipine, diltiazem, verapamil
2. very potent
3. directly act on smooth muscle of arterioles to cause relaxation; also decreases heart rate and force of contraction (minimally)
4. aka nifedipine; used in acute situations
66
1. what Calcium channel blocker group causes a strange oral disorder?
2. what is the disorder?
3. what is the other CCB group (class)
1. Dihydropyradines (amlodipine, nifedipine)
2. gingival hypertrophy
3. non-dihydroperidine (diltiazem)
67
anesthetic considerations of CCBs:
1. CCBs interact how with anesthesia
2. what decreases these effects? who is most at risk?
3. what defeciency will have prolonged recovery with (what?) CCB?
4. what CCB has increased sedation with ____?
5. increased risk of ___ and ___ if used with what other antihypertensive
1. CCBs increase hypotensive and cardiodepressive effects of anesthesia
2. adequate hydration; elderly persons
3. patients with pseudocholinesterase deficiency have reduced clearance and prolonged recovery with Clevidipine
4. Diltiazem increases sedative effects of benzos
5. if used with beta blockers, increased chance of hypotension and bradyarrhythmias
68
what drugs are used for heart failure (5)?
1. cardiac glycosides (dig)
2. prils
3. diuretics
4. beta blockers
5. ace inhibitors
69
1. what is a good drug therapy combination for CHF?
2. why?
3. what group is it bad for?
4. why?
1. ace inhibitors mixed with diuretics
2. decreases mortality rates
3. renal failure patients
4. they need angiotensin II to maintain GFR and renal artery blood flow
70
cardiac glycosides:
1. brand name?
2. theraputic window?
3. action:
1. digoxin, digitek
2. small (1.5-2)
3. positive inotrope with negative chronotropic action
4. inhibits Na+/K+-ATPase enzyme (this enzyme decreases movement of calcium into cell and sodium out)which allows for more calcium to stay in the cell increasing strength of contraction and decreasing rate.
71
dig toxicity:
| s/s
1/ s/s:
- fatigue
- confusion
- delirium
- psychosis
- gi distress
- halos /photophobia
- color disturbances
- arrhythmias
72
how does dig cause color disturbances, photophobia and halos in eyes?
dig is rapidly taken into rods and cones of eyes
73
dig: caution in surgery:
| what can happen intra-op?
- electrolyte imbalances
- hypokalemia
- v-fib
- AV block
- sinus brady
74
1. what skin side effect can dig cause?
| 2. what patients is dig reserved for?
1. digitalis purpura
| 2. systolic dysfunction (increases contractile force)
75
cardiostimulatory drugs:
1. what are they?
2. how do they work?
3. what are they (3 of them) and what do they do?
1. drugs that have inotropic, chronotropic and dromotropic effects
2. may reduce afterload or enhance myocardial contractions
3. -dobutamine: synthetic beta agonist; causes mild vasodilation and decreases pre and after load while increasing contractility
- nitrates: vasodilator acts on venous capitance vessels decreasing preload to failing heart while vasodilating arteries to decrease afterload
- dopamine: natural catecholamine which increases cAMP production in myocardium to increase contractility at moderate dose (vasodilates renal at low dose, vasoconstricts vessels at high dose).
76
Endothelin Receptor Antagonist:
1. what is it?
2. how does it work?
3. uses:
4. chemical and brand name:
5. contraindications:
6. side effects:
1. competetive antagonist of Endothelin 1 which is produced excessively in CHF (endothelin 1 causes pulmonary vasoconstriction (increases pulm vasc resistance)).
2. inhibits Endothelin 1 causing vasodilation
3. pulmonary artery hypertension
4. Bosentan (Tracleer)
5. contraindicated in pregnancy (teratogen)
6. liver damage
77
angina:
1. cause:
2. symptoms:
3. at what point of blockage will a patient have angina symptoms?
4. management of angina:
1. narrowing of coronary vessels d/t plaque, vasospasm, increased cardiac workload (or combination of these).
2. can be symptom free (especially diabetics), n/v, feelings of impending doom, dizziness, shoulder pain radiating down top of arm, women may have jaw pain; men have classic substernal crushing pain.
3. 90% occlusion
4. nitrates, CCBs, BBs, control weight, stop smoking, reduce blood pressure, exercise, surgical revascularization, stents or laser therapy.
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Nitrates:
1. what can increase effects of nitrates?
2. what is the sub lingual version called?
3. what is the onset and duration
4. what is the time released (prophylactic) version called? what is it made from?
1. alcohol
2. isorbide di-nitrate
3. 2 min onset/ 3 hour duration
4. Isorbide mono-nitrate (imdur); a metabolite of isorbide di-nitrate
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Heart failure: 10 causes:
1. dilated cardiomyopathy=5-10%
2. CAD & HTN=5-10%
3. alcoholic, viral or hypertrophic cardiomyopathy
4. IHD (ischemic heart disease)
5. mitral valve regurg
6. septicemia
7. alcohol intoxication
8. cocaine
9. drug induced (cyclophosphamide chemotherapy)
10. excess thyroxin ingestion
80
heart failure:
| s/s
1. cough
2. change in breathing
3. dyspnea
4. palpitations
5. swelling/ ankle edema
6. abdominal swelling
7. anorexia and bloating
8. fatigue/ weakness
9. excercise intolerance
81
goals of managing heart failure:
| 8 things
1. NUMBER 1: delay onset of symptoms
2. improve quality of life
3. reduce hospitalizations
4. treat underlying diseases
5. decrease sodium to 1-2 g/day
6. reduce fluids to <2L/day
7. walk 20-30 min/day
8. lifestyle changes (low fat, smoking cessation, decrease stress).
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antiarrhythmics:
Lidocaine:
1.class
2. s/s toxicity
1. class 1B
2. s/s of toxicity:
- tinnitus
- metalic taste
- slurred speech
- paresthesias
- tremors
- seizures to coma
3. patients with liver impairments
