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Transcript of Ht Emergency and Urgency - Slides Org
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HYPERTENSIVE RISIS
RUDI MAHMUD
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DefinitionsHypertensive Emergency.Acute elevation of blood pressure is associated
with acute and ongoing organ damage in the kidneys, brain, heart,
eyes or vascular system
Hypertensive Urgency. Acute or chronic blood pressure elevation not
associated with any observable acute organ damage
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Epidemiology of Hypertensive Emergencies
Less than 1 to 2 of hypertensive population
More common among black and older patients
Majority of patients know that they are hypertensive and are receiving treatment
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Comparison of Hypertensive
Emergencies and UrgenciesVariable Hypertensive
Emergency
Hypertensive
Urgency
SymptomsAcute BP elevation
Acute organ damage
Hospitalizazion
Intensive care
Route of therapy
Arterial line
Rate of BP lowering
Evaluate for secondary hypertension
YesYes
Yes
Yes
Yes
Intravenous
Yes
Minute to hours
Yes
NonminimalYes
No
No
No
Oral
No
Hours to days
Yes
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Most common types of hypertensive emergencies
Hypertensive encephalopathy
Hypertension with acute cerebrovascular syndromes
Hypertension with acute coronary syndromes, heart failure, or pulmonary edema
Hypertension with aortic dissection
Hypertension with severe hypertensive retinopathy
Hypertension with eclampsia
Pheochromocytoma
Hypertension with acute renal insuficiency
Antihypertension withdrawal syndrome
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Pathophysiology abnormality in HE
Normotensive :arteries dilate or constrict in respons to changes in blood
pressure to maintain a constant flow to the stissue bed.
Chronic hypertension :functional and structural changes in the arterial tree
that shift autoregulatory curve to the right, to maintain normal perfusion
in important organs and avoid an increase in local blood flow at the
higher blood pressures.
Hypertensive emergency :blood pressure increased above the capacity of
the autoregulatory mechanisms to compensate by vasoconstriction ---
tissue damage,ischemia or loss of vascular integrity.
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Lancet 2000; 356: 411
17
Autoregulation of Cerebral Blood Flow
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Idealized curves of CBF at varying levels of systemic blood pressure in normotensive and
hypertensive subjects. Rightward shift is shown in auto regulation with chronic hypertension.
Adapted from Kaplan NM. Kaplans Clinical Hypertension. 8thed. 2002; p345
Cerebral Autoregulation in Normal & Hypertensive Pts
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Implications of Treatment
1. The goal of treatment in a hypertensive emergencies is to
restore blood pressure to a range in which autoregulatory forces
may be re-established.
2. The treatment target is often not a normal blood pressure, but
instead one that is only moderately lower, just sufficient to
allow autoregulation to be restored.
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Lancet 2000; 356: 41117
Putative Vascular Pathophysiology of Hypertensive Emergencies
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Initial Evaluation of Patients with a
Hypertensive Emergencies (1)
M. Kaplan, Clinical Hypertension, 8thed, : 2002
HISTORY
Prior diagnosis and treatment of hypertension.
Intake of pressor agent : street drugs,sympathomimetics.
Symptom of cerebral, cardiac, and visual dysfunction.
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Initial Evaluation of Patients with a
Hypertensive Emergencies (2)
PHYSICAL EXAMINATION
Blood Pressure Funduscopy
Neurologycal Status
Cardiopulmonary status
Body fluid volume assessment
Peripheral pulses
M. Kaplan, Clinical Hypertension, 8thed, : 2002
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Initial Evaluation of Patients with a
Hypertensive Emergencies (3)
LABORATORY EVALUATION
Urine analysis
Chemistry : creatinine, glucose, electrolytes
Electrocardiogram
Chest radiograph (if heart failure or aortic dissection issuspected)
PRA and aldosterone (if primary aldosteronism is
suspected)
PRA before and 1 hour after 25 mg Captopril (if
renovascular hypertension is suspected).
Spot urine for metanephrine (if pheochromocytoma is
suspected)
M. Kaplan, Clinical Hypertension, 8thed, : 2002
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Management of Hypertensive Urgencies
Absence of Comp licat ion . No end -organ injury
Reduction of BP is needed within a few hours (e.g : level
stage 3 hypertension, hypertension with optic disc edema,
severe perioperative hypertension, progressive targetorgan complication).
Treat with oral drugs with rapid onset of action.
Repeat BP measurement after 30 minutes of bed rest.
Reduce BP 25 % over 24-48 hours. The use of SL fast acting nifedipine is no longer
recommended. It can result in uncontrolled drop in BP
leading to stroke, MI or death.
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Oral Antihypertensive Drugs for
Treating Hypertensive Urgencies
Drug Dose(mg)
Onset of Effect(min)
Duration(h)
Captopril 25 15-30 4-6
Clonidine 0.1-0.2 30-60 4-6
Nifedipine 10-20 15-30 3-6
Prazosin 1-2 30-60 4-6
Labetalol 100-400 30-120 3-6
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1. The approach is to initially reduce mean arterial pressure
by about 25 %with further reductions accomplished more
gradually.
2. In general the initial reduction should be achieved over a
period of 1 to 2 hours with less rapid reduction over the
ensuring 6 hours to a DBP of + 100 mm Hg.
3. With the exception of patients with aortic dissection, the
BP should not be reduce to normotensive and especiallyhypotensive levels, as target organ hypoperfusion may
results.
Management of Hypertensive Emergencies
With com pl icat ion / end-organ injury
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COMMONLY USED DRUG IN
HYPERTENSIVE EMERGENCY
CLONIDINE I.V.
W.H. Frishman, et al., Cardiovascular Pharmacotherapy, 1996
NITROGLISERIN I.V.
DILTIAZEM I.V.
NICARDIPINE I.V.
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Target MBP
Level
Bolus I.v.
0.2 mg/kg
Drip infusion
50 mg/hour
Drip infusion30 mg/hour
Drip infusion
5-10 mg/hour
10% MBP reduction
From Baseline
20% MBP reduction
From Baseline
10
20
30
Switch to Oral
DILTIAZEM 180SR
Every 30-60 minutes observation
DILTIAZEM-Injection
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ACUTE RENAL FAILURE
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Definitions
Renal Failure
, A lost of renal function leading to a fall of GFR to below 80 ml/min1 andto an accumulation of creatinine, urea and other nitrogenous wastes.
Acute Renal Failure, a rapid loss of renal function reduces waste excretion rate well
below production rate so that a daily rise in Scr and blood urea nitrogen level (BUN) results.
Chronic Renal Failure, Chronic loss of renal function. Usually irreversible.
Subacute or Rapidly Progressive Renal Failure, renal failure with a loss of
renal function that is occuring at a tempo intermediate between that of acute and
chronic renal failure.
Acute-on-Chronic Renal Failure, An intercurrent process such as volume
depletion may produce a rapid worsening of renal failure with a daily rise in BUN and Scr
in individuals with chronic renal failure. Thus acute deteration is often reversible if
the underlying cause resolves.
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Oligouric Renal Failure, Renal failure accompanied by a fall in urine output
to less than 500 ml/day.
Nonoligouric Renal Failure, Renal failure with a urine output greater than 500 ml/day.
Azotemia
, Accumulation of nitrogenous wastes in the blood, when the renal excretionof these products of protein and nucleic acid metabolism is impaired. It is reflected by
an increase in BUN and Scr.
Uremia. The complex of symptoms produced by severe renal failure.
Definitions
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Epidemiology of Acute Renal Failure
ARF is caused by ischemic (50%), nephrotoxic (35%), and acute tubular
interstitial nephritis (15%).
ARF occurs in approximately 1% of hospitalized patients, 20% of patients
treated in ICU, and 4% to 15% of patients after cardiovascular surgery.
30% of patients who experience ARF will require renal replacement therapy.
Every patient with ARF who requires dialysis, 10 to 12 patients with milder forms
of renal insufficiency are manageble by consevative treatment.
Community-acquired ARF occurs in approximately 209 patients per 1 million
population
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Useful Features to Suggest
Chronic vs Acute Renal Failure
Chronic history ofNocturia, polyuria, edema, or hematuria
Pruritus or other uremic symptomatology (e.g. neuropathy)Underlying predispoising illness (hypertension, diabetes mellitus)
Objective findingsRenal osteodystrophy
Band keratopathy or conjungtival calcificationBilateral small kidneys
Carbamylated hemoglobin
Less riable because they develop repidly in ARFHypocalcemia
Hyperphosphatemia
Anemia
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Hypovolemia, Cardiac failure,
Systemic vasodilatation
Renal artery occlusion
Renal vein occlusion
Glomerulonephritis
Ischemic acute tubular necrosis ATN)
Toxic ATN
Interstitial nephritis
Intrarenal obstrcution
Intrarenal occlution
Urinary tract obstruction
Renal parenchymal
Prerenal
Renal
Postrenal
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Clinical Clues to Prerenal Renal Failure
Recent volume loss
Recent cardiac insults
Fever or other signs of sepsis
Orthostatic symptoms
Blood pressure < usual level
BUN/Scr > 20 : 1 (< 0.08 SI)
Urine spesific gravity > 1.020
Albumin < 3 g/dl, without edema
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Clinical Clues to Postrenal Renal Failure
Bladder symptoms
Old age in men
Solitary kidney
Urinary tract pain
Anticholinergic drugs
History of pelvic or urologic malignancy
Prostatic hypertrophy
Gross hematuria
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Urine Chemistry in Acute Renal Failure
Urine chemistry Prerenal
a
Acute tubular
necrosis
b
Urine osmolality, Uosm (mosmol/kg)
Urine-to-plasma osmolality
Spesific gravity
Urine-to-plasma urea
Urine Na+ (mmol/L)
Fraction Na+ excretion
Renal failure index
> 500
> 1.5
>1.018
> 8
< 10
< 1
< 1
< 300
< 1.1
< 1.015
< 3
> 40
> 2
> 1
Parameters suggesting prerenal failure are sometimes seen with nonoligouric ATN and
in acute glomerulonephritis and early obstruction
Parameters suggesting ATN may be misleading and occur in prerenal failure in the elderly,
in those with pre-existing renal impairment, and following diuretic administration
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Urine Sediment in Acute Renal Failure
Condition Proteinuria Hematuria Microscopy
Prerenal azotemia
- -
Normal
Vascular occlusion
- -
Normal
Glomerulonephritis
+++ +++
Dysmorphic red cells, red
cell casts, granular casts
Acute interstitial nephritis
++ +
White cells (pyuria) and
accasionally white cell casts
Hemolytic uremi syndrome /
thrombotic
thrombocytopenic purpura
+ / - +
Normal
Acute tubular necrosis
(ATN)
- -
Muddy brown granulat
ATN casts tubular
epithelial cell casts ( fewer
casts, sometimes none in
nonoligouric ATN)
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Blood urea nitrogen BUN) :
creatinine ratio in acute renal failure
BUN : creatinine ratio Cause
High : > 20:1
(> 80:1 SI units) aPrerenal failure
Urinary tract obstruction
Increased urea production : catabolic states, gastrointestinalbleeding, increased protein intake, infusion of amino acids,corticosteroid, tetracyclines.
Low : < 5-10:1
(< 20-40:1 SI units)aReduced urea production : severe liver disease, malnutrition.
Increased release of creatinine : cimetidine, trimethoprim.
Interference with creatinine assay : ketones (acetoacetic acid),cephalosporins.
aUrea (mmol/L) : creatinine (mmol/L) ratio = 3.8 BUN (mg/dl) : creatinine (mg/dl) ratio
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Renal ultrasound in acute renal failure
Observation Indication
Pelvicayceal dilatation a Obstructive nephropathy
Shrunken kidney Chronic intrinsic renal disease
Normal size kidneys
Echogenic
Normal echo pattern
Acute glomerulonephritis, acute tubular necrosis
Prerenal azotemia, renal artery occlusion
Enlarged kidneys Malignant infiltration, renal vein thrombosis, HIV-associated nephropathy, amyloid
PC dilatation is usual but not universal in the presence of obstruction
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Clinical assessment of patients with acute renal failure
Search for reversible factors that may be exacerbating acute renal failure,e.g. hypovolemia, ongoing administration of nephrotoxins.
Examine for clinical evidence of uremic syndrome,e.g.confusion, hiccups, nausea, vomiting, pericarditis, convulsions.
Clinical assessment of intravascular volume.
Review most recent laboratory results for metabolic complications :hyperkalemia, acidosis, hyperphosphatemia.
Review drug prescribtion : discontinue all non-essential drugs and adjust doseor dose internal of drugs eliminated by kidney.
Review nutritional status : consider protein, salt, potassium, and phosphaterestriction ; consider need for enteral nutrition or hyperalimentation.
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Treatment of ARF
Prevent or ameliorate ARF
Treat established ARF
Treat systemic diseases which result in ARF or specific form of ARF
Treat patients recovering from ARF
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Prevention of ARF
Diuretics : loop diuretic, manitol
Vasoactive agents : calcium channel blockers
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Management Priorities in Acute Renal Failure
Initiation Phase
Search for and correct prerenal & postrenal
factors.
Search for and treat acute complications of
renal failure e.g.
Hyperkalemia
Hyponatremia
Acidosis
Pulmonary edema
Optimize cardiac output and renal blood
flow.
Discontinue nephrotoxic medications and
agents which may hemodynamically
decrease GFR e.g
ACE inhibitors
NSAIDs
Establish diagnosis and initiate spesific
treatment.
Maintenance Phase
Monitor blood chemistries, fluid intake
and output, daily weight.
Match fluid intake to output plus
insensible losses.
Limit potassium, sodium, and phosphorus
intakes, as guided by laboratory.
Correct acidosis.
Provide phosphorus binders for
phosphorus > 6 mg/dl (1.9 mmol/L).
Initiate nutritional support early.
Initiate dialysis before uremic
complications emerge.
Dose drugs appropriate for their clearance.
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Treatment of patient with established ARF
Control of :
Salt and water
Potassium
Acid base
Calcium and phosphor
Management of complication :
Cardiovascular
Hematologic
Gastrointestinal
Neurologic
Infection
Dialysis
Hyperalimentation
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Treatment of specific form of ARF
Steroid therapy
Immunosuppressive agentPlasmapheresis
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Complications of Acute Renal Failure
Clinical Problem Etiology
Hypertension
Encephalopathy
Convulsions
Cardiac failure
Cardiac arrhythmias
Pericarditis
Bleeding
Infection
Malnutrition
Na & H2O overload
Uremia, hyponatremia
Uremia, hyponatremia, hypocalcemia
Na & H2O overload, acidosis, uremia
Hyperkalemia, hypocalcemia, acidosis
Uremic serositis
Uremic platelet dysfunction, acidosis
Uremic leukocyte dysfunction, acidosis
Uremic catabolic state, uremic anorexia
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Nondialytic Management of Acute Tubular Necrosis 1)
Complication Treatment
Intravaskulervolume overload Restrict salt (1-2 g/day) and water (usually < 1 L/day)Diuretics (usually loop diuretics thiazide)
Hyponatremia Restrict enteral water intake (1 L/day)
Avoid hypotonic intravenous solutions
Hyperkalemia Restrict dietary K+ intake (usually < 40 mmol/day)
Eliminate K+ suppl and K+-sparing diuretics.
Pottasium-binding ion-exchange resins, e.g. sodium polystyrenesulfonate.
Glucose (50 ml of 50% dextrose) and insulin (10 units regular).Sodium bicarbonat (usually 50-100 mmol)
2-agonist (e.g. albuterol 10-20 mg inhaled or 0.5-1 mg i.v).
Calcium gluconate (10 ml of 10% sodium over 2-5 minutes)
Hypermagnesemia Discontinue Mg2+- containg antacids
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Complication Treatment
Metabolic acidosis Restrict dietary protein (usually 0.6 g/kg per day of high biologicvalue).
Sodium bicarbonate (maintain serum bicarbonate >15 mmol/L andarterial pH >7.2).
Hyperphosphatemia Restrict dietary phosphate intake (usually
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Indication of Dialysis
Fluid overload
Hyperkalemia
Acidosis
Profound hyponatremia
Overt uremic complication, e.g.
Pericarditis
Encephalopathy
ConvulsionsBleeding
To provide for hyperalimentation
To remove toxins
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Dialytic Therapy of Acute Renal Failure
Favor hemodialysis
Catabolic patients
Hemodynamically stable,
non hypotensive patients
Undiagnosed intraabdominal
disease
Recent abdominal or
retroperitoneal surgery (avoid
peritoneal dialysate leaks)
Favor peritoneal dialysis
Noncatabolic patients
Hemodynamically unstable patient
Poor vascular access
Active hemorrhage (avoids
anticoagulation)
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