Ht Emergency and Urgency - Slides Org

8/10/2019 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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PHYSICAL EXAMINATION

Blood Pressure Funduscopy

Neurologycal Status

Cardiopulmonary status

Body fluid volume assessment

Peripheral pulses



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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)



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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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Th nK YoU

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