Download - Hypertension in icu ppt
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.
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