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Summary for Treatments for CVD

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Clinical Pharmacy: Cardiovascular Diseases Treatment Summary

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Disease Therapeutic Treatment (Tx) Secondary prevention/ Non-pharmacological Monitoring
Goal Primary prevention Tx / side notes parameters/
Evaluation of
outcomes
L9 AKI Short term Severe AKI: Primary prevention AKI o Receive no more IP: hydration,
goals: RRT (intermittently/ ▪ Avoid nephrotoxic than 3g of Na per maintenance of target
-Minimizing continuously) drugs day from all mean arterial pressure
the degree of → Intermittent: ▪ Adequate sources, incld IV (MAP) of
insult to 3-4hrs, 200-400mL/min hydration (2L/day) antibiotics to 70-105mmHg in the
kidney [rapid correction of most (OP) prevent diuretic critically ill, avoid
-Reducing of electrolyte ▪ IV: 0.9% NaCl therapy fails nephrotoxic drugs
extrarenal abnormalities] [can be preferred o Enteral nutrition 3g
complication scheduled at times which ▪ Patient education per day potassium Monitor serum K daily
s maximize staffing ▪ Drug therapies to Electrolyte disorder: for those who have
-Expediting availability and decrease hyperkalemia AKI, and those who
patient’s treatments per day per incidence of (Thus limiting receive RRT, twice
recovery of machine] contrast induced Potassium is important, daily for those who are
renal → Continuous: over 24 hrs nephropathy (after life threatening cardiac seriously ill.
function (for hemodynamically admin of iodine arrhythmias occur when
unstable patients with contrast for CT serum K+ is over 6 Also monitor:
Ultimate AKI), improved outcomes scans mainly) mmol/L) Phosphorus and
goal: - in critically ill patients ▪ Aggressive o Avoid calcium- magnesium
Restore Continuous infusion of loop hydration can containing antacids (eliminated by
patient’s diuretics is able to prevent prevent additive **calcium balance kidneys, not removed
renal myalgia and hearing loss due to insults usually not an issue for efficiently by dialysis)
function to avoiding high serum Prevention of CIN AKI patient
pre-AKI concentrations –preferred Contrast Induced Established AKI:
baseline Nephrotoxicity Side notes: Measure daily:
Fluid overloaded: ▪ IV isotonic saline/ Causes of diuretic Urine output, fluid
IV Loop diuretics [Frusemide, sodium resistance: intake, weight
Bumetanide -- better oral F, bicarbonate  Excessive
Torsemide] ▪ Beginning 6-12hrs sodium intake Routine for
IV mannitol (must carefully before procedure (reduce Na intake) hospitalized patients:
▪ Use alternate Daily blood test for
imaging if possible electroytes, BUN,

,monitor urine output, serum ▪ Discontinue  Inadequate complete blood cell
electrolytes, osmolality) nephrotoxic agents diuretic dose count
▪ Loop diuretics + thiazide ▪ Use low-osmolar/ (use cont. Infusion/ Contrast induced
▪ Oral Metolazone 5mg iso-osmolar combination therapy) nephrotoxicity:
(administered 30 minutes contrast agents  Reduced oral F Maintain urine output
before) + IV Frusemide ▪ Ascorbic acid 3g (use torsemide, > 150 mL/hr
orally before bumetanide or
Indications for RRT procedures , 2g parenteral)
AEIOU orally 2 times a day  Nephrotic
Acid-base abnormalities x 2 doses after syndrome
-metabolic acidosis procedures (loop diuretic binding
▪ Acetylcysteine in tubule lumen) --
Electrolyte imbalance 600-1200 mg (increase dose, switch
-hyperkalemia, q12hr (before/after diuretics, combination
hypermagnesemia exposure) therapy)
(NAC helps to make  Reduced renal
Intoxications glutathione under blood flow
-salicylates, litium, methanol, oxidative stress) (NSAIDs, ACEIs,
ethylene, glycol, theophylline, (antioxidant, vasodilatory) vasodilators—
phenobarbital -conflicting evidence/ discontinue
heterogeneity// but , hypotension or
O- fluid overload considered safe intravascular volume
Postoperative fluid gain depletion ------------
intravascular volume
Uremia expansion
-high catabolism of acute renal  Increased
failure sodium
resorption:
--- combination
therapy, sodium
restriction, discont
NSAID, treat HF, high
volume paracentesis
(draining fluid from
belly)
for cirrhosis

, Disease Therapeutic Treatment (Tx) for Acute Primary Prevention/ Secondary Non-pharmacological Monitoring
Goal Management Prevention Tx / side notes parameters/
Evaluation of
outcomes
L8 Acute Management Primary prevention Contraindications for Rt-PA
Stroke 1. Blood Pressure Aspirin 100mg E.O.D IV thrombolytic (for rt- • Perform
Do not treat if HTN <220mmHg SBP – women above 65 y/o PA) neurological
Or ◼ Current use of oral assessments
<120 mmHg DBP HTN issues anticoagulant or a every 15 mins
Desirable: • Isolated SBP (>140/<90mmHg) prothrombin time (PT) during rt-PA
160-180/90-100mmHg - risk factor > 15 seconds (INR infusion
• Lowering SBP by 10 mmHg >1.7) • Every 30 mins
BP reduction: no more than 10-20% reduce risk of stroke ◼ Use of heparin in for next 6 hrs
from baseline over 24 hrs • Long acting CCB preferred for the previous 48 hours • Then, Every
-- do not use calcium antagonist due Asian populations and a prolonged hr until 24 hrs
to rapid decline →Amlodipine, Felodipine 5- partial from Tx
10mg OD thromboplastin time • If pt develop
Labetolol 10-20 mg Secondary Prevention (PTT) severe
IV bolus at 10 minutes interval (up Anti-platelet therapy ◼ A platelet count headache,
to 150-300mg) (means 20mg x15 Aspirin- 25% risk reduction, if < 100,000/mm3 N,V,
times 10 mins interval max) given within 48 hrs, shown to ◼ Another stroke or discontinue
reduce recurrent stroke and any serious head infusion,
Labetolol 1-3mg/mL infusion death injury in the previous obtain CT
Rate: 1-3mg/min Post-stroke 3 months scan
◼ Major surgery Increase BP
Captopril 6.25-12.5mg oral (short Aspirin 75-325mg orally OD within the preceding measurements
half-life, fast onset) 14 days if BP=
Aspirin + dipyridamole Slow ◼ Arterial puncture at >180/105
Don’t rush to lower BP in acute release noncompressible site mmHg
Ischemic stroke (50mg + 400mg) within the last 21 days
UNLESS Not available in Msia ◼ Pre-treatment
systolic blood Ticlopidine /
▫ Hypertensive encephalopathy Alternatives: pressure >185mmHg Cilostazol
▫ Severe left ventricular failure
▫ Acute renal failure

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