DR IMRAN GAFOORDR ASHOK ANANDDEPTT OF CCEM ,

SIR GANGARAM HOSPITAL,N.DELHI

DEFINITIONS HYPERTENSIVE EMERGENCY BP elevation is associated with ongoing

neurological, myocardial, hematological or renal TARGET ORGAN DISEASE (TOD)

HYPERTENSIVE URGENCY - potential for TOD is great & likely to occur if BP is not controlled. - occurs on chronic stable complication . Stable angina . Old MI . CCF,CRF . TIA,old CVA

DEFINITIONS ACCELERATED HYPERTENSION

- keith wagener barker retinopathy grade 3

(constriction,sclerosis+hemorrhages,exudates)

- may be urgency or emergency - presence of exudate more worrisome

DEFINITIONS • MALIGNANT HYPERTENSION

- KWB grade 4 retino + papilledema

(neuroretinopathy) - Always an emergency

MALIGNANT HYPERTENSION….MALIGNANT HYPERTENSION - Increased BP + neuroretinopathy - Fundus : flame shaped hemmorhags, cotton wool spots, papilledma - Assoc with : encephalopathy, LV failure, micro angio hemolytic anemia, renal fibrinoid necrosis with

endarteritis. Risk factors : 30-50ys, male, smoking

MALIGNANT HYPERTENSION….Renal failure is most common cause of

death(fibrinoid necrosis+prolif endarteritis) espc if assoc with glomerulonephritis.

Recovery predicted if combined length of both kidneys >20.2cm & highly unlikely if <14.2 cm.

Presenting creatinine >4.5 - dialysisTreatment-sod nitroprusside

(0.3microg/kg/min) also-labetolol, nicardipine,fenoldopam

BP CLASSIFICATION(Chobanian et al/JNC 7)

sys(mm Hg) dias(mm Hg)

NORMAL <120 & <80

Pre Htn 120-139 or 80-89

Stage I Htn 140-159 or 90-99

Stage II Htn ≥160 or ≥100

Iso sys Htn ≥140 &<90

MANIFESTATIONS OF TARGET ORGAN DISEASELARGE VESSELS Aneurysmal dilations , Acc

atheroscl., Aortic dissection

CARDIAC Acute - pulm edema , MI Chronic - LVH , CAD

CEREBROVASCULAR Intracereb bleed, TIA, seizures, mental status change, stroke

RENAL Hematuria, azotemia, Cr>1.5, proteinuria>1+

RETINOPATHY Papilledema, Hemorrhages, Exudates, Arterial nicking

PATHOPHYSIOLOGY Increased SVR Damage to endothelial lining Leakage of plasma Fibrinoid necrosis of arterioles(histo hallmark) Local edema & sclerosis Ischemia of brain ,heart, kidneys

PATHOPHYSIOLOGYPatients with antecedent Htn can tolerate

higher fluctuations due to shift of autoreg

threshold.

Patients with no antecedent Htn – organ

specific changes occur with DBP>100.

Most sensitive vascular bed is CEREBRAL.

INITIAL EVALUATIONCardinal points in history- - TOD symptoms (most imp) - prior Htn - Medical Renal Disease - medicine with compliance - cocaine, amphetamine -Htn from any cause may enter emergent phase. -Usually occurs on background of essential hypertn. - Imp secondary causes- renovascular(fibromuscular dys- plasia/atheresclerosis) - chronic GN - reflux nephropathy - analgesic nephropathy

SYMPTOMS OF HYPERTENSIVE CRISIS

MC is - headache (usually worse in morning) - visual (scotoma, diplopia, hemianopia, blindness)

- neuro (focal deficits, stroke, TIA, somnolence) - ischemic chest pain - renal (polyuria, nocturia, hematuria) - back pain (aortic aneurysm) - nausea ,vomiting - wt loss.

PATIENTS OFTEN HAVE INTRAVASCULAR VOLUME DEPLETION.

EXAMINATION• Verify BP recordings in diffn position(if possible)

• Fundus exam – arterio thickng, Incr light reflex, vascular

tortuosity, AV nicking retinal hemmorhages, lipid leakage (hard

exudates) nerve ischemia, papilledema (cotton wool spots)• ABDOMEN

masses(PCKD),bruits(aneuyrsm)

ANCILLARY TESTSSr Na, K, bicarb, BUN, Cr, CBC (with P/S for

schitocytes) PT/aPTT, tox screen, pregnancy test, ECG,

urinanalysis

USUALLY - hypoNa and matabolic alkalosis - incr BUN, Cr - proteinuria, hematuria - marked proteinuria suggets GN

PSUDOHYPERTENSIONOverestimation of true BP due to stiff artery

OSLERS MANOEUVRE. : inflate BP cuff to greater than brachial systolic, a palpable radial artery but pulseless.

Seen in - atherosclerosis, - monckebergs medial calcification, - metastatic calcification(ESRD)

TREATMENTInitial therapy should terminate ongoing TOD, not

return of BP to normal. Generalized goal : decrease MAP by 20-25% within

one hour f/b decr to ~160/100 by 2-6 hrs and towards normal over 1-2 days EXCPTNS : . ischemic stroke . aortic dissection . active unstable angina or CCF

• More gradual reduction in elderly with carotid stenosis .

SPECIFIC HYPERTENSIVE CRISIS 1 . PULMONARY EDEMA a) with preserved systolic function(LVH)- - abrupt increase in afterload with poor

diastolic relaxation leads to pulmn HTN and

edema. - Treatment is with Na-nitropru (it

prefrnn dilates resistance vessels) - less emergnt condn – ACEI/CCB

PULMONARY EDEMA…B) with poor systolic functionMYOCARDIAL ISCHAEMIA -nitroglycerine is preferred(dilates

collaterals)

MYOCARDIAL INFARCTION - sedn/pain control - DBP>100 - nitroglycr - early β-blockade

SPECIFIC HYPERTENSIVE CRISIS2) AORTIC DISSECTION

BP lowered rapidly to lowest clinically acceptable level

Agents used lobet or esmolol, later on

nitropru added Alternative agent-trimetaphan

SPECIFIC HYPERTENSIVE CRISIS3) HYPERTENSIVE ENCEPHALOPATHYWhen high perfusion pressure overwhelms

cerebral autoregulation. Can lead to blindness, seizures, coma, gradually

worsening headache. Pathologically-cerebral edema, petechial

hemorrhg, microinfarcts. Immed Neuroimagng - to rule out ischemic

stroke/hemorrhage Hallmark is improvement in 12-24 hrs of BP redn.

HTN ENCEPH…Treatment short acting parenteral agents used. MAP should decrease by 15-20% over 2-3 hrs. D/d : cerebral infarct, ICH/SAH, subdural hematoma, brain tumor, seizures, vasculitis/meningoenceph.

HTN ENCEPH…DIFFN POINTS : 1) Focal neurological deficit is unusual

without cerebral bleed 2) Papilledema is almost always assoc with

Htn enceph 3) Mental staus improves by 24-48hrs-delayed

in CNS bleed 4) Brain dysfunction develops by 12-24 hrs in

Htn but more acutely with ischemic stroke/bleed.

HTN ENCEPHAL..Posterior leukencephalopathy syn.- reversible vasogenic subcortical edema

without infarct

MRI – white matter edema in post cerebral hemispheres

ISCHEMIC STROKEFor every 10 mmHg incr in pressure >180 a 40%

incr in worsening neurological status. Area of stunned but viable tissue(ischemic

penumbra)may need higher perfusion pressures, so

ASA/AHA-recommends (after excluding pain, nausea, full bladder, hypoxia, incr ICP)

BP redn. If sys>220 or dias > 120Also, for thrombolysis BP<185/110. And post reperfusion use lobet or nicardipine for

sys>180 or dias>105 & Na nitro for sys >230

ISCHEMIC STROKELatest studies recommend modest reduction

of BP

(10-27mmHg) improved outcomes but effect

waned with increasing age ,so,avoid >10%

sudden drop

SUBARACHNOID HEMORRHAGESAH incr ICP & decr cerebral perfusion causing

global ischemia Induces intense vasospasm in neighbouring

vessels (4- 12 days) after initial bleed. Goal-dec 20-25% of MAP over 6-12 hrs but

not <160/100. If vasospasm occurs later-inc BP with 3H(not

proven) Preffred - lobet Avoid- nitrodilators No data to support oral nimodip dec vasospasm.

INTRACRANIAL HEMORRHAGEMajor risk factor is Htn. Most rapid decline in BP occurs in first 24 hrs but

may remain elavated for 7-10 days (while in ischemic stroke BP dec to normal in 24-48 hrs)

AHA/ASA recommends…decrease BP if- Sys>200 or MAP>150, ICP incr suspected –sys>180 or map>130 ICP incr not suspec-target MAP~100 or

BP~160/90 Preffred agent : lobet

HEAD TRAUMAWith trauma comes edema

With ICP monitoring –target MAP ≥90

Prefferd- lobet or nicardipine

POST OP PAINEarly-(0-2hrs) : pain, hypoxemia, hypercabia,

shivering.

Intermed(12-36hrs) : fluid overload, reaction

to ET/FOLEYS.

PheochromocytomaVery rare cause of hypertension Headache,palpitations,Htn,anxiety,abd pain

diaphoresis Orthostatic changes in BP Paroxsysmal symptoms T/t : i/v phentolamine f/b b-blockade

GESTATIONAL HYPERTENSIONAfter 20 wks in normotensive. SBP>140 & DBP>90 on two separate

occasions 6 hrs apart. Pre-eclampsia – gestn htn + 300 mg in 24 hrs

proteinuria Eclampsia- +seizures T/t – bed rest & parenteral Mg Use (lobet,hydralazine) if SBP>160 or

DBP>100

ANTIPHOSPHOLIPID Ab SYNDROMEMicrovasculopathy & emboli to renal artery T/t – Na nitropru/lobet & anticoagn.

GBSDysreflexia (bladder/bowel distension below

level of lesion trigger massive sympatc discharge)

Symptoms – Htn,bradycardia, diaphoresis,headache.

T/t – Na nitroprus., phentolamine,lobet

RENAL TRANSPLANT RECEPIENTAcute rejection Obstructive uropathy Cyclosporine/steroid. T/t oral CCB

NEW ONSET HYPERTENSION IN ICUPain Anxiety Hypoxemia Hpercarbia Shivering Vol overload Discontinuation syndrome

INTRAVENOUS MEDICATIONSSodium nitoprusside : nitric oxide compound -arterio-veno dilator -useful in most Htn crisis dose 0.25mic/kg/min(max 8) C/I – high output cardiac failure, cong optic atrophy. Cyanide toxicity – anemia & liver d/e -acidosis, tachycardia, almond smell, change in mental status. Thiocyanate tox. – renal d/e -psychosis,

hypereflexia,seizure,tinnitus -thiocyanate>10 should be avoided. Avoiod infusion>48 hrs.

INTRAVENOUS MEDICATIONSNITROGLYCERINE- predom. Veno dilator,

decreases preload.

Use : cardiac ischemia

Dose : 5mic/min(max 100)

C/I : incresed ICP, angle closure glaucoma

Most useful in cadiac compromise(MI,LV

failure,pulm edema),,not recommnded > 48 hrs.

INTRAVENOUS MEDICATIONSLABETOLOL : β > α (7 : 1) adrenergic blockade

Onset 2-5 min, durn 3-6 hrs

Bolus 20 mg (max 300 mg)

Infusion 0.5-2mg/min ,used in pregnancy along

with hydralazine.

Avoid in bronchospasm, bradycardia, CCF,

>first degree heart block,

INTRAVENOUS MEDICATIONSESMOLOL: cardioselective β1 blocker

Used in aortic dissection

Onset 60 seconds, duration 10-20 min.

Infusion 50-300 mic/kg/min.

Not dependant on hepatic/renal function

INTRAVENOUS MEDICATIONSFENOLDOPAM : post synaptic dopamine agonist.

-primarily arterial dilator,rapid

onset/offset of effect.

Advantageous in kidney d/e, increases renal blood

flow,natriuresis.

Dose : 0.1 mic/kg/min.

C/I : glaucoma,hypotension,,check K+ every 6 hrs

INTRAVENOUS MEDICATIONSHYDRALAZINE : direct arteriolar dilator.

Used in pregnancy/eclampsia

Dose 10 mg every 60 min (max 20 mg)

Duration of action 2-4 hrs

Reflex tachycardia, exacerbates angina,BP

lowering response is less predictable(depends

on renin&volume status)

INTRAVENOUS MEDICATIONSPHENTOLAMINE: α – blockade

Used primarily in pheochromocytoma

Dose 5-15 mg

Always f/b β-blockade

INTRAVENOUS MEDICATIONSNICARDIPINE : dihydropyridine CCB Onset 10-20 min,duration 1-4 hr Dose 5 mg/hr (max 15 mg/hr) Avoid in CCF,cardiac ischemia.

CLEVIDIPINE : short acting dihydropyridine CCB.

Reduces BP without affecting cardiac filling pressures or reflex tachycardia

INTRAVENOUS MEDICATIONSENALAPRILAT : only parenteral ACE-I.Dose 1.25-5 mg every 6 hr. Response not predictable, hyperkalemia in

reduced GFR.

TRIMETHAPHAN : nondepolarizer ganglionic blocker. Dose : 0.5-5mg/min Used in aortic dissection Disadvntges : paralytic ileus, bladder atony,

tachyphyl.

Thank you