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HTN EMERGENCIES AND URGENCIES

Hypertensive emergencies require immediate blood pressure reduction to prevent end organ damage. They are characterized by severely elevated blood pressure and signs of acute target organ injury. The goal is to lower mean arterial pressure by 20-25% within minutes to hours using intravenous antihypertensive drugs like sodium nitroprusside. Hypertensive urgencies also involve severely high blood pressure but without acute organ injury, allowing for oral drugs to safely lower blood pressure within 24 hours. Rapid blood pressure reduction is avoided to prevent hypotension in both conditions.

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HYPERTENSION EMERGENCIES and HYPERTENSION URGENCIES Case based approach and management
Introduction • Hypertension is the most common modifiable risk factor for cardiovascular diseases. • Most common indication for adults to visit a physician. • Its prevalence will continue to increase,both among the young because of increasing obesity and in older adults because of longer life expectancy. • Despite being common, it is inadequately treated.
Epidemiology • Approximately 1% hypertension pts may develop hypertensive crises during their lifetime. • Annual incidence of hypertensive emergencies being 1-2 cases/1,00,000 pts. • Higher rates have been reported in African Americans, low socioeconomic people, in developing countries. • Incidence in men 2 times higher than in women Curr Opin Cardiol 2006; Curr Hypertens Rep 2003;
Joseph varon et al.Critical care 2008
Hypertensive Crises • More generalised term . • Not defined by a specific blood pressure reading, rather it is a clinical syndrome that is associated with acute elevation of blood pressure. • It includes – Hypertensive Emergency – Hypertensive Urgency
• Characterised by severe increase in systolic and/or diastolic blood pressure assosciated with signs or symptoms of acute end-organ damage.  No blood pressure threshold for diagnosis. • Usually, – SBP > 180-220 mm Hg – DBP > 120-130mm Hg – MAP > 180 mm Hg • Requires an immediate BP reduction in few minutes –hours. • Requires an ICU care. • IV drugs Hypertensive Emergency
Hypertensive Emergencies Hypertensive encephalopathy Hypertension assosciated with acute cerebrovascular disease Hypertension assosciated with pulmonary edema Hypertension assosciated with acute coronary syndromes Hypertension assosciated with dissecting aortic aneurysm Pheochromocytoma Hypertension associated with acute renal failure Eclampsia Microangiopathic anemia
What is the primary reason for hypertensive emergencies ? 1. Renovascular Disease 2. Pheochromocytoma 3. Non-adherence to anti-hypertensive medication 4. Hyperaldosteronism 5. Erythropoeitin
Hypertensive Urgency • Severe elevation in BP >180/120 mm Hg without symptoms or signs of acute target organ involvement. • Adequate treatment of these conditions, a BP lowering within 24 hrs by administration of oral drugs. • ICU admission is usually not required.
Hypertensive Urgency Severe uncomplicated essential hypertension Severe uncomplicated secondary hypertension Postoperative hypertension Hypertension assosciated with severe epistaxis Drug induced hypertension Rebound hypertension (i.e sudden withdrawal of clonidine) Cessation of prior antihypertensive therapy Anxiety ,panic attacks or pain
Why rapid reduction of BP not recommended in absence of end organ damage?? An aggressive approach. A precipitous and unpredictable BP fall Harmful (esp . In pts with multiple risk factors) Cardiol clinics 2006;24:135-46.
Accelerated - Malignant Hypertension • Severe hypertension and presence of retinopathy . • Exudates,hemorrhages – Accelerated hypertension. • Papilledema – Malignant hypertension.
Acute target organ damage in hypertension Target organ Complications Brain Hypertensive encephalopathy Cerebral infarction Cerebral hemorrhage Advanced retinopathy Heart Acute coronary syndrome Acute heart failure Aorta Aortic dissection Kidney Acute renal failure Placenta Eclampsia
• Single organ inv. in approximately 83%. • Two organ inv. found in 14%,multiorgan inv. in 3 % pts. Most common clinical presentations - cerebral infarction (24%) - pulmonary oedema (22%) - HTN encephalopathy (16%) - Cong. HF (12%) •Less common presentations – IC hemorrhage, Aortic dissection and Eclampsia ESC/ESH 2013
Joseph varon et al.Critical care 2008
Etiology • Essential hypertension : Inadequate blood pressure control and noncompliance are common precipitants (MOST COMMON) • Renovascular • Eclampsia/pre-eclampsia • Acute glomerulonephritis • Pheochromocytoma • Anti-hypertensive withdrawal syndromes • Head injuries and CNS trauma • Renin-secreting tumors • Drug-induced hypertension • Burns • Vasculitis • Post-op hypertension • Coarctation of aorta (very rare) 2nd common
• Unclear, but some candidates – ACE DD genotype – Absence of the β and γ subunit of ENaC – Elevated adrenomedullin levels – Elevated natriuretic peptide level – Abnormalities in oxidative stress markers and endothelial dysfunction Vaughan and Delanty Lancet 2000; 356:411 Why only some are affected?
Pathophysiology Increase in BP Mechanical stress Endothelial injury Increased permeability ischemia RAAS Activation of coagulation cascade,platelets Deposition of fibrin IL-6 PRESSURE NATRIURESIS End organ hypoperfusion, ischemia, dysfunction Increase in SVR Humoral factors Vaughan and Delanty Lancet 2000; 356:411 Fibrinoid necrosis
Vaughan and Delanty Lancet 2000; 356:411
CASE 1 • A 65 yr old male, hypertensive, chronic smoker, driver by occupation admitted in ED with c/o headache since 3 days,increased in severity over the past one day, associated with vomitings and altered sensorium. • He has been noncompliant to drugs since 15 days. • At presentation his pulse rate was 70/min,regular, BP recording was 240/140 mm Hg, CVS- being normal on auscultation, lungs b/l basal crepts. • What is the diagnosis ?What would you do ? • Admit ? What would be BP goal in this patient?
CASE 2 • A 38 yr old male,daily labourer, hypertensive since past 6yrs,came for follow up at OPD. • His BP was 180/100 mm Hg . • ECG showed LV strain. • No symptoms of SOB on exertion,angina. • Admit ?/ OPD Rx ? • IV drugs / oral?
CASE 3 • A 28 yr old female, primi (6 months amenorrhea) was referred to physician with c/o headache,vomitings,decreased urine output. her BP was recorded to be 170/100 mm Hg • CBP –leucocytosis,low platelets. • CUE –pus cells,RBC • LFT – mildly raised aminases,bilirubin being 2.8mg/dl • ECG –sinus tachycardia ,LVH with strain. • 2Decho – concentric LVH. • What to do ? • Admit ? • Normalize BP ?
CASE 4 • A 54 yr old male was admitted in ED with c/o weakness of right upper limb and lower limb since morning, • Known hypertensive,diabetic. • Alcoholic • Was unconscious, BP was 190/100 mm Hg • CT brain – large MCA territory ischemic infarct • What to do ? • Normalize BP?
CASE 5 • A 45 yr old male ,K/C/O CAD, hypertensive,diabetic, smoker came with sudden onset of ripping pain, sharp sensation in the back, along with SOB class IV. • At presentation BP was 240/140 mm Hg • Pulses discreprenancy on palpation. • What to do ? • Normalize BP ?
CASE 6 • A 23 yr old male,degree student, was brought to casualty with sudden onset of SOB since 2 hours,saturations at room air were normal. • BP – 180/100 mm Hg • CVS/RS –NAD • What to do ? • IV/oral/reassurance
Clinical assessment • Complete history collection • Detailed physical examination • Duration and degree of pre existing hypertension • Evidence of target organ damage • Details of antihypertensive therapy • Compliance with medications • Use of the over counter drugs • Illicit drugs usage
Symptom End organ damage
Examination of pt • BP sitting and standing position (if possible) with an appropriate size cuff in both arms(difference - aortic dissection). • If peripheral pulses are markedly reduced (lower limb BP required). • RR,HR • O2 saturation • Fundoscopic examination. • CVS – murmurs (aortic insufficiency, ischemic MR) • S3,gallop,crackles in lung fields, raised JVP (signs of HF) • Renal bruit (renovascular HTN) • Abdominal mass (PCKD) • Level of consciousness ,focal signs of ischemia
Joseph varon et al.Critical care 2008
ESC/ESH,2013
Keith-Wagener-Barker Classification • Grade 1 – Mild narrowing of the arterioles – “Copper Wire” • Grade 2 – Moderate narrowing – – Copper wire and AV nicking • Changes associated with long standing essential hypertension Grade 3 Severe Narrowing - Silver wire changes, hemorrhage, cotton wool spots, hard exudates Grade 4 Grade 3 + Papilledema Grade 3 and 4 highly correlated with progression to end organ damage and decreased survival
Normal
Grade 1
Grade 2
Grade 3 KWB Retinopathy
Investigations • Blood electrolytes • Creatinine • Urea nitrogen • Cell count • Smear (microangiopathic hemolysis) • ECG • CXR • CT Brain • CT chest/MRI
Management
Normalisation of BP is usually not recommended* How fast and how much BP to be lowered to be given importance.
Why ?? • Sudden fall in BP may cause acute hypoperfusion of vital organs and results in myocardial ischemia or infarction, hemiplegia,or acute renal failure. • Older patients with long lasting hypertension and preclinical organ involvement (LVH, atherosclerosis and arteriolar remodelling) are at risk of these complications as the lower limit of autoregulation shifted to right.
Appropriate treatment is dictated more by the features of the acute syndrome and by the patient’s characteristics than by a body of scientific evidence. • Controlled trials not available (extremely heterogenous population) • Tailored on individual patient – Organ at risk. Varon J et al ;Crtical care 2003 ESC/ESH manual of Hypertension 2009
HYPERTENSIVE EMERGENCIES
Hypertensive Emergency • Damage Heart - CHF, MI, angina Kidneys - acute kidney injury, microscopic hematuria CNS - encephalopathy, intracranial hemorrhage, Grade 3-4 retinopathy Vasculature - aortic dissection, eclampsia
• GOAL reduce MAP by no more than 20-25%, DBP to 100-110mm Hg within few minutes to 2 hours. • More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) • More slowly for acute cerebrovascular damages with monitoring of neurological status. • Constant infusion of intravenous agents required (no intermittent IV boluses/oral/sublingual drugs- drastic BP fall).
Ideal drug  Fast acting  Easily titratable  Rapidly reversible and safe  No single agent has these characteristics
Sodium nitroprusside • Potent short acting arterial and venous dilator (reduces pre- and after- load) • Rapid onset of action.(seconds) • Continuous intra-arterial BP monitoring required. • Infusion chamber and tubing to be covered. •  intracranial pressure (caution in intracerebral hemorrhage) • Induces coronary steal (non selective coronary vasodilation) • Increases mortality in pts with acute MI. (NEJM,1982) • Thiocyanate toxicity (nausea,vomiting,lactic acidosis and altered mental status) – Usually rare, seen in pts with renal ,hepatic dysfunction. Freiderich et al, Anesth Analo 1995:81:152-162
Fenoldopam • A peripheral dopamine-1 receptor antagonist (DA1). {highly specific} • 10 –fold more potent than dopamine as a renal vasodilator. • Antihypertensive effect by combined natriuretic and vasodilatory effect (esp. intrarenal arteries) • Not to be used as prophylactic agent for preventing CIN (CAFCIN Trial) • Agent of choice in hypertensive emergencies assosciated with renal dysfunction. • Adv effects – hypotension ,hypokalemia Clin Invest 1993;72:60-64
Nicardipine • Second generation DHP CCB. • Strong cerebral and coronary vasodilation. • Onset of action 5-15 min, Duration being 2-6 hrs. • Increases both stroke volume and coronary blood flow with a favourable effect on myocardial oxygen balance. • CAD with Systolic HF. C/I in Aortic stenosis. • Dosage independent of weight. • Infusion rate of 5mg/h – 2.5 mg/h increments every 5 min –max being 15 mg/h. • IV Nicardipine maintained BP in Treatment range > IV Labetalol (CLUE trial) BMJ,2013 J Emerg Med 1987:5:463-473
Clevidipine • Third generation, intravenous, dihydropyridine caclium channel antagonist. • FDA approval (2008) • Ultra short half life of about 1 min. • Potent arterial vasodilation (no effect on venous capacitance, myocardial contractility)* • No significant adverse effect on heart rate’. • Injectable emulsion. • 99.9% bound to protein. • Safe in pts with renal,hepatic dysfunction. • C/I –allergies to soy products,eggs and egg products,defective lipid metabolism. *Rivera et al .,2010,Polly et al 2011. 50mg/100ml
Dosage •An IV infusion at 1–2 mg/hour is recommended for initiation and should be titrated by doubling the dose every 90 seconds. • As the blood pressure approaches goal, the infusion rate should be increased in smaller increments and titrated less frequently. •The maximum infusion rate for Cleviprex is 32 mg/hour. •Most patients in clinical trials were treated with doses of 16 mg/hour or less. No more than 1000 mL (or an average of 21 mg/hour) of Cleviprex infusion is recommended per 24 hours.. Am J Cardiovascular Drugs 2009;9;117-134
Clevidipine • ESCAPE1(pre op),ESCAPE 2(post op) plaebo controlled trials – 15% reduction in SBP within 6 min post infusion. Rivera et al.,2010. Levy et al .,2007. • ECLIPSE – Clevidipine maintained BP within target range with minimal excursions. Singla et al .,2008 • VELOCITY study for hypertensive crises. Pollack et al .,2009 • ACCELERATE trial –management of severe HTN with ICH Graffagnino et al., 2009
Labetalol • Combined selective 1 adrenergic and non selective β adrenergic receptor blocker (1:7). • Hypotensive effect – in 2-5 min after IV admin. • Maintains cardiac output (unlike other BB). • Reduces SVR, but does not decrease PBF. • Cerebral,renal,coronary blood flow maintained. • Less placental transfer can be used in pregnancy induced HTN emergency. • Metabolised by liver. • Oral/IV. Drugs 1984,Suppl 2 :35-50.
Esmolol • Ultrashort acting cardioselective β adrenergic blocking agent. • Ideal β blocker in critical cases. • Useful in severe postoperative HTN. • Onset of action is within 60 sec • Duration of action being 10-20min. • Rapid hydrolysis of ester linkages by RBC esterases(metabolism), not dependent on renal or hepatic function. • 0.5 to 1mg/kg loading dose over 1min,followed by an infusion - 50ug/kg/min.(max 300ug/kg/min) Chest 1988;93:398-403
Not to use Sublingual Nifedipine • Drug is poorly soluble, not absorbed through buccal mucosa • Sudden uncontrolled and severe reductions in BP,may precipitate cerebral,renal and myocardial ischemic events. • Lack of clinical documentation attesting to a benefit from its use. • The Cardiorenal Advisory Committee of the FDA has concluded “that the practice of administering SL/oral nifedipine should be abandoned because this agent is not safe nor efficacious”. Anaesth Clin North Am.1999.
SPECIAL SCENARIOS
Myocardial ischemia/infarction • may be assosciated with HTN at presentation (usually in a previously HTN pt). • High BP exacerbated by pain and agitation. • IV Nitrates reducing systemic vascular resistances,LVpreload, improves coronary perfusion. • B blockers may contribute to a fall in BP (reduces myocardial O2 consumption) • BP control mandatory before thrombolysis (BP<180/100 mmHg). Vaughan et al Lancet 2000;356:411-7
Acute Cardiogenic Pulmonary Edema • Ventilation • Reduction of LV preload and afterload. • IV nitrate, loop diuretics. • Others – urapidil, nicardipine,sodium nitroprusside. • {Urapidil is a sympatholytic antihypertensive drug. Peripheral α1- adrenoceptor antagonist and a central 5-HT receptor agonist, does not elicit reflex tachycardia(weak β1adrenoceptor antagonist activity, effect on cardiac vagal drive). Not approved by the USFDA, but it is available in Europe}. • Bolus 12.5-25 mg (50 mg),infusion 5-40mg/h,onset 3-6 min,duration 4-6 hr . Salgado et al.Annals of intensive care 2013;3:17
Aortic Dissection • Most dramatic and rapid fatal complication in HTN emergencies. • Acute BP reduction reduces shear forces on damaged aorta. • Aim of treatment to reduce SBP as rapidly as possible down to 100-110 mmHg, simultaneously control tachycardia resulting form the sympathetic activation. • B blocker + vasodilator to be given • Esmolol + nitroprusside would be a better combination. • Hydralazine is C/I Circulation 2006;114:1384-89
Ischemic stroke • BP elevations can occur in previously hypertensive and in normotensive pts. • BP declines to pre stroke values within 3-4 days after an ischemic stroke. • Severe HTN Rx controversial issue. Lesions in cerebral area Impaired neurogenic control of CVS HIGH BP Arch Intern Medicine 2003;163:211-216
Shift to right in case of chronic HTN
AHA recommendation • Threshold for treatment BP > 220/120 mmHg • Target BP should be a 10-15% lowering of BP. • Raised ICP – MAP<130 (1st 24hrs) • No raised ICP – MAP<110 • IV Labetalol or Nicardipine . • IV tPA (if to be given) BP <185/110mm Hg. Stroke 2003;34:1056-83
IC bleed • To prevent rebleeding and reduce edema formation. • BP >180/105 mmHg ,may benefit from gradual 20-25% reduction in BP. Nimodipine, a dihydropyridine calcium blocker,is effective (antagonist effects on cerebro vasospasm). AHAguidelines;Critical care Med 2006;34:1975-1980
Hypertensive Encephalopathy • Potential lethal complication of severe or abrupt BP elevation. • Previously HTN/normotensive pts. • Acute glomerular nephropathy, Eclampsia, TTP, Pheochormocytoma, Erythropoietin administration, immunosupressive drugs HIGH BLOOD PRESSURE Excessive increase in cerebral blood flow HYPERFILTRATION LOCALISED OR WIDESPREAD EDEMA Hinchey J et al,NEJM 1996;334:494-500
• Cerebral ischemia resulting from arteriolar spasm*. • Severe headache,vomitings,visual disturbances,confusion, focal or generalized seizures. • Fundoscopic examination(key role) • Mean BP should be reduced by 20% within first hour. • IV sodium nitroprusside is DOC (rapid onset of action) ESC/ESH 2003 • IV labetalol,nicardipine,hydralazine . Circulation,2004;110:2241-5
Eclampsia • Hypertension complicates 12% pregnancies, 18% maternal deaths. • Volume expansion,MgSo4 for seizure prophylaxis. • MgSo4 4-6 g in 100ml 5%D over 15- 20 min - 1-2g/h infusion (hourly DTR,urine output). • Antihypertensive therapy (to prevent complications in mother). • SBP :155-160 mmHg,DBP>105mm Hg.(initiation of Rx) • ICH is a devastating complication. • Methyl dopa,Hydralazine DOC, • Others being IV labetalol,nicardipine. • Avoid sublingual or oral nifedipine. • Nitroprusside,ACEI – C/I Am J Obst 2000:183:S1-S22
HTN emergencies due to catecholamine excess Abrupt increase in alpha adrenergic tone. • IV labetalol • Pheochromocytoma crisis (IV alpha blocker phentolamine) followed by B blocker(for tachycardia or VPCs). Withdrawal of centrally acting anti HTN drugs (clonidine) Pheochromocytoma Cocaine intoxication Abuse of sympathomimetics Post operative Hypertension
ORAL DRUGS FOR HTN URGENCIES Drug Initial dose Onset duration Adverse effects
Acute and transient BP elevations • Anxiety • Panic attacks • Pain Rx - Administration of anxiolytic or analgesic drugs. • Refractory nose bleeding – IV drugs to be used sometimes
TAKE HOME MESSAGE • Most common cause for HTN crises is UNDIAGNOSED/UNTREATED/ INADEQUATELY TREATED HYPERTENSION • Differentiation of emergency from urgency is absence of target organ damage in the later. • Clevidipine is the new drug approved for hypertensive emergencies. • IV Nicardipine , IV Labetalol are preferred for most of emergency situations. • SL/oral nifedipine not to be used..
THANK YOU

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In this document
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Introduction to hypertension as a key cardiovascular risk factor, its rising prevalence, and the epidemiology of hypertensive crises.

Hypertensive crises encompass emergencies and urgencies, with emergencies requiring immediate BP reduction and ICU care. Key reasons for hypertensive emergencies, including non-compliance and specific diseases like pheochromocytoma.

Risks associated with aggressive BP drops and specifics of accelerated vs malignant hypertension.

Impact of high BP on organs such as brain and kidneys, detailing common presentations of organ damage.

Various causes of hypertension, highlighting inadequacies in treatment and mechanisms of end-organ injuries.

Real-life scenarios for managing hypertensive crises, emphasizing diagnosis and treatment strategies.

Keith-Wagener-Barker classification levels of retinal changes tied to hypertension severity and risk.

Essential tests for diagnosing hypertension-related crises and overall management strategies.

Emphasis on controlled BP reduction and individual patient treatment tailored to acute presentations.

Detailed treatment options for hypertensive emergencies, stressing ideal drug selections and infusion protocols.

Specific cases such as myocardial ischemia, aortic dissection, and their unique treatment requirements.

Key takeaway messages emphasizing treatment priorities and advisories against certain BP medications.

HTN EMERGENCIES AND URGENCIES

  • 1.
  • 2.
    Introduction • Hypertension isthe most common modifiable risk factor for cardiovascular diseases. • Most common indication for adults to visit a physician. • Its prevalence will continue to increase,both among the young because of increasing obesity and in older adults because of longer life expectancy. • Despite being common, it is inadequately treated.
  • 3.
    Epidemiology • Approximately 1%hypertension pts may develop hypertensive crises during their lifetime. • Annual incidence of hypertensive emergencies being 1-2 cases/1,00,000 pts. • Higher rates have been reported in African Americans, low socioeconomic people, in developing countries. • Incidence in men 2 times higher than in women Curr Opin Cardiol 2006; Curr Hypertens Rep 2003;
  • 4.
    Joseph varon etal.Critical care 2008
  • 5.
    Hypertensive Crises • Moregeneralised term . • Not defined by a specific blood pressure reading, rather it is a clinical syndrome that is associated with acute elevation of blood pressure. • It includes – Hypertensive Emergency – Hypertensive Urgency
  • 6.
    • Characterised bysevere increase in systolic and/or diastolic blood pressure assosciated with signs or symptoms of acute end-organ damage.  No blood pressure threshold for diagnosis. • Usually, – SBP > 180-220 mm Hg – DBP > 120-130mm Hg – MAP > 180 mm Hg • Requires an immediate BP reduction in few minutes –hours. • Requires an ICU care. • IV drugs Hypertensive Emergency
  • 7.
    Hypertensive Emergencies Hypertensive encephalopathy Hypertensionassosciated with acute cerebrovascular disease Hypertension assosciated with pulmonary edema Hypertension assosciated with acute coronary syndromes Hypertension assosciated with dissecting aortic aneurysm Pheochromocytoma Hypertension associated with acute renal failure Eclampsia Microangiopathic anemia
  • 8.
    What is theprimary reason for hypertensive emergencies ? 1. Renovascular Disease 2. Pheochromocytoma 3. Non-adherence to anti-hypertensive medication 4. Hyperaldosteronism 5. Erythropoeitin
  • 9.
    Hypertensive Urgency • Severeelevation in BP >180/120 mm Hg without symptoms or signs of acute target organ involvement. • Adequate treatment of these conditions, a BP lowering within 24 hrs by administration of oral drugs. • ICU admission is usually not required.
  • 10.
    Hypertensive Urgency Severe uncomplicatedessential hypertension Severe uncomplicated secondary hypertension Postoperative hypertension Hypertension assosciated with severe epistaxis Drug induced hypertension Rebound hypertension (i.e sudden withdrawal of clonidine) Cessation of prior antihypertensive therapy Anxiety ,panic attacks or pain
  • 11.
    Why rapid reductionof BP not recommended in absence of end organ damage?? An aggressive approach. A precipitous and unpredictable BP fall Harmful (esp . In pts with multiple risk factors) Cardiol clinics 2006;24:135-46.
  • 12.
    Accelerated - MalignantHypertension • Severe hypertension and presence of retinopathy . • Exudates,hemorrhages – Accelerated hypertension. • Papilledema – Malignant hypertension.
  • 13.
    Acute target organdamage in hypertension Target organ Complications Brain Hypertensive encephalopathy Cerebral infarction Cerebral hemorrhage Advanced retinopathy Heart Acute coronary syndrome Acute heart failure Aorta Aortic dissection Kidney Acute renal failure Placenta Eclampsia
  • 14.
    • Single organinv. in approximately 83%. • Two organ inv. found in 14%,multiorgan inv. in 3 % pts. Most common clinical presentations - cerebral infarction (24%) - pulmonary oedema (22%) - HTN encephalopathy (16%) - Cong. HF (12%) •Less common presentations – IC hemorrhage, Aortic dissection and Eclampsia ESC/ESH 2013
  • 15.
    Joseph varon etal.Critical care 2008
  • 16.
    Etiology • Essential hypertension: Inadequate blood pressure control and noncompliance are common precipitants (MOST COMMON) • Renovascular • Eclampsia/pre-eclampsia • Acute glomerulonephritis • Pheochromocytoma • Anti-hypertensive withdrawal syndromes • Head injuries and CNS trauma • Renin-secreting tumors • Drug-induced hypertension • Burns • Vasculitis • Post-op hypertension • Coarctation of aorta (very rare) 2nd common
  • 17.
    • Unclear, butsome candidates – ACE DD genotype – Absence of the β and γ subunit of ENaC – Elevated adrenomedullin levels – Elevated natriuretic peptide level – Abnormalities in oxidative stress markers and endothelial dysfunction Vaughan and Delanty Lancet 2000; 356:411 Why only some are affected?
  • 18.
    Pathophysiology Increase in BP Mechanical stress Endothelialinjury Increased permeability ischemia RAAS Activation of coagulation cascade,platelets Deposition of fibrin IL-6 PRESSURE NATRIURESIS End organ hypoperfusion, ischemia, dysfunction Increase in SVR Humoral factors Vaughan and Delanty Lancet 2000; 356:411 Fibrinoid necrosis
  • 19.
    Vaughan and DelantyLancet 2000; 356:411
  • 20.
    CASE 1 • A65 yr old male, hypertensive, chronic smoker, driver by occupation admitted in ED with c/o headache since 3 days,increased in severity over the past one day, associated with vomitings and altered sensorium. • He has been noncompliant to drugs since 15 days. • At presentation his pulse rate was 70/min,regular, BP recording was 240/140 mm Hg, CVS- being normal on auscultation, lungs b/l basal crepts. • What is the diagnosis ?What would you do ? • Admit ? What would be BP goal in this patient?
  • 21.
    CASE 2 • A38 yr old male,daily labourer, hypertensive since past 6yrs,came for follow up at OPD. • His BP was 180/100 mm Hg . • ECG showed LV strain. • No symptoms of SOB on exertion,angina. • Admit ?/ OPD Rx ? • IV drugs / oral?
  • 22.
    CASE 3 • A28 yr old female, primi (6 months amenorrhea) was referred to physician with c/o headache,vomitings,decreased urine output. her BP was recorded to be 170/100 mm Hg • CBP –leucocytosis,low platelets. • CUE –pus cells,RBC • LFT – mildly raised aminases,bilirubin being 2.8mg/dl • ECG –sinus tachycardia ,LVH with strain. • 2Decho – concentric LVH. • What to do ? • Admit ? • Normalize BP ?
  • 23.
    CASE 4 • A54 yr old male was admitted in ED with c/o weakness of right upper limb and lower limb since morning, • Known hypertensive,diabetic. • Alcoholic • Was unconscious, BP was 190/100 mm Hg • CT brain – large MCA territory ischemic infarct • What to do ? • Normalize BP?
  • 24.
    CASE 5 • A45 yr old male ,K/C/O CAD, hypertensive,diabetic, smoker came with sudden onset of ripping pain, sharp sensation in the back, along with SOB class IV. • At presentation BP was 240/140 mm Hg • Pulses discreprenancy on palpation. • What to do ? • Normalize BP ?
  • 25.
    CASE 6 • A23 yr old male,degree student, was brought to casualty with sudden onset of SOB since 2 hours,saturations at room air were normal. • BP – 180/100 mm Hg • CVS/RS –NAD • What to do ? • IV/oral/reassurance
  • 26.
    Clinical assessment • Completehistory collection • Detailed physical examination • Duration and degree of pre existing hypertension • Evidence of target organ damage • Details of antihypertensive therapy • Compliance with medications • Use of the over counter drugs • Illicit drugs usage
  • 27.
  • 28.
    Examination of pt •BP sitting and standing position (if possible) with an appropriate size cuff in both arms(difference - aortic dissection). • If peripheral pulses are markedly reduced (lower limb BP required). • RR,HR • O2 saturation • Fundoscopic examination. • CVS – murmurs (aortic insufficiency, ischemic MR) • S3,gallop,crackles in lung fields, raised JVP (signs of HF) • Renal bruit (renovascular HTN) • Abdominal mass (PCKD) • Level of consciousness ,focal signs of ischemia
  • 29.
    Joseph varon etal.Critical care 2008
  • 30.
  • 31.
    Keith-Wagener-Barker Classification • Grade1 – Mild narrowing of the arterioles – “Copper Wire” • Grade 2 – Moderate narrowing – – Copper wire and AV nicking • Changes associated with long standing essential hypertension Grade 3 Severe Narrowing - Silver wire changes, hemorrhage, cotton wool spots, hard exudates Grade 4 Grade 3 + Papilledema Grade 3 and 4 highly correlated with progression to end organ damage and decreased survival
  • 32.
  • 33.
  • 34.
  • 35.
    Grade 3 KWBRetinopathy
  • 37.
    Investigations • Blood electrolytes •Creatinine • Urea nitrogen • Cell count • Smear (microangiopathic hemolysis) • ECG • CXR • CT Brain • CT chest/MRI
  • 38.
  • 39.
    Normalisation of BPis usually not recommended* How fast and how much BP to be lowered to be given importance.
  • 40.
    Why ?? • Suddenfall in BP may cause acute hypoperfusion of vital organs and results in myocardial ischemia or infarction, hemiplegia,or acute renal failure. • Older patients with long lasting hypertension and preclinical organ involvement (LVH, atherosclerosis and arteriolar remodelling) are at risk of these complications as the lower limit of autoregulation shifted to right.
  • 41.
    Appropriate treatment isdictated more by the features of the acute syndrome and by the patient’s characteristics than by a body of scientific evidence. • Controlled trials not available (extremely heterogenous population) • Tailored on individual patient – Organ at risk. Varon J et al ;Crtical care 2003 ESC/ESH manual of Hypertension 2009
  • 42.
  • 43.
    Hypertensive Emergency • DamageHeart - CHF, MI, angina Kidneys - acute kidney injury, microscopic hematuria CNS - encephalopathy, intracranial hemorrhage, Grade 3-4 retinopathy Vasculature - aortic dissection, eclampsia
  • 44.
    • GOAL reduceMAP by no more than 20-25%, DBP to 100-110mm Hg within few minutes to 2 hours. • More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) • More slowly for acute cerebrovascular damages with monitoring of neurological status. • Constant infusion of intravenous agents required (no intermittent IV boluses/oral/sublingual drugs- drastic BP fall).
  • 45.
    Ideal drug  Fastacting  Easily titratable  Rapidly reversible and safe  No single agent has these characteristics
  • 46.
    Sodium nitroprusside • Potentshort acting arterial and venous dilator (reduces pre- and after- load) • Rapid onset of action.(seconds) • Continuous intra-arterial BP monitoring required. • Infusion chamber and tubing to be covered. •  intracranial pressure (caution in intracerebral hemorrhage) • Induces coronary steal (non selective coronary vasodilation) • Increases mortality in pts with acute MI. (NEJM,1982) • Thiocyanate toxicity (nausea,vomiting,lactic acidosis and altered mental status) – Usually rare, seen in pts with renal ,hepatic dysfunction. Freiderich et al, Anesth Analo 1995:81:152-162
  • 47.
    Fenoldopam • A peripheraldopamine-1 receptor antagonist (DA1). {highly specific} • 10 –fold more potent than dopamine as a renal vasodilator. • Antihypertensive effect by combined natriuretic and vasodilatory effect (esp. intrarenal arteries) • Not to be used as prophylactic agent for preventing CIN (CAFCIN Trial) • Agent of choice in hypertensive emergencies assosciated with renal dysfunction. • Adv effects – hypotension ,hypokalemia Clin Invest 1993;72:60-64
  • 48.
    Nicardipine • Second generationDHP CCB. • Strong cerebral and coronary vasodilation. • Onset of action 5-15 min, Duration being 2-6 hrs. • Increases both stroke volume and coronary blood flow with a favourable effect on myocardial oxygen balance. • CAD with Systolic HF. C/I in Aortic stenosis. • Dosage independent of weight. • Infusion rate of 5mg/h – 2.5 mg/h increments every 5 min –max being 15 mg/h. • IV Nicardipine maintained BP in Treatment range > IV Labetalol (CLUE trial) BMJ,2013 J Emerg Med 1987:5:463-473
  • 49.
    Clevidipine • Third generation,intravenous, dihydropyridine caclium channel antagonist. • FDA approval (2008) • Ultra short half life of about 1 min. • Potent arterial vasodilation (no effect on venous capacitance, myocardial contractility)* • No significant adverse effect on heart rate’. • Injectable emulsion. • 99.9% bound to protein. • Safe in pts with renal,hepatic dysfunction. • C/I –allergies to soy products,eggs and egg products,defective lipid metabolism. *Rivera et al .,2010,Polly et al 2011. 50mg/100ml
  • 50.
    Dosage •An IV infusionat 1–2 mg/hour is recommended for initiation and should be titrated by doubling the dose every 90 seconds. • As the blood pressure approaches goal, the infusion rate should be increased in smaller increments and titrated less frequently. •The maximum infusion rate for Cleviprex is 32 mg/hour. •Most patients in clinical trials were treated with doses of 16 mg/hour or less. No more than 1000 mL (or an average of 21 mg/hour) of Cleviprex infusion is recommended per 24 hours.. Am J Cardiovascular Drugs 2009;9;117-134
  • 51.
    Clevidipine • ESCAPE1(pre op),ESCAPE2(post op) plaebo controlled trials – 15% reduction in SBP within 6 min post infusion. Rivera et al.,2010. Levy et al .,2007. • ECLIPSE – Clevidipine maintained BP within target range with minimal excursions. Singla et al .,2008 • VELOCITY study for hypertensive crises. Pollack et al .,2009 • ACCELERATE trial –management of severe HTN with ICH Graffagnino et al., 2009
  • 52.
    Labetalol • Combined selective1 adrenergic and non selective β adrenergic receptor blocker (1:7). • Hypotensive effect – in 2-5 min after IV admin. • Maintains cardiac output (unlike other BB). • Reduces SVR, but does not decrease PBF. • Cerebral,renal,coronary blood flow maintained. • Less placental transfer can be used in pregnancy induced HTN emergency. • Metabolised by liver. • Oral/IV. Drugs 1984,Suppl 2 :35-50.
  • 53.
    Esmolol • Ultrashort actingcardioselective β adrenergic blocking agent. • Ideal β blocker in critical cases. • Useful in severe postoperative HTN. • Onset of action is within 60 sec • Duration of action being 10-20min. • Rapid hydrolysis of ester linkages by RBC esterases(metabolism), not dependent on renal or hepatic function. • 0.5 to 1mg/kg loading dose over 1min,followed by an infusion - 50ug/kg/min.(max 300ug/kg/min) Chest 1988;93:398-403
  • 54.
    Not to use SublingualNifedipine • Drug is poorly soluble, not absorbed through buccal mucosa • Sudden uncontrolled and severe reductions in BP,may precipitate cerebral,renal and myocardial ischemic events. • Lack of clinical documentation attesting to a benefit from its use. • The Cardiorenal Advisory Committee of the FDA has concluded “that the practice of administering SL/oral nifedipine should be abandoned because this agent is not safe nor efficacious”. Anaesth Clin North Am.1999.
  • 55.
  • 56.
    Myocardial ischemia/infarction • maybe assosciated with HTN at presentation (usually in a previously HTN pt). • High BP exacerbated by pain and agitation. • IV Nitrates reducing systemic vascular resistances,LVpreload, improves coronary perfusion. • B blockers may contribute to a fall in BP (reduces myocardial O2 consumption) • BP control mandatory before thrombolysis (BP<180/100 mmHg). Vaughan et al Lancet 2000;356:411-7
  • 57.
    Acute Cardiogenic PulmonaryEdema • Ventilation • Reduction of LV preload and afterload. • IV nitrate, loop diuretics. • Others – urapidil, nicardipine,sodium nitroprusside. • {Urapidil is a sympatholytic antihypertensive drug. Peripheral α1- adrenoceptor antagonist and a central 5-HT receptor agonist, does not elicit reflex tachycardia(weak β1adrenoceptor antagonist activity, effect on cardiac vagal drive). Not approved by the USFDA, but it is available in Europe}. • Bolus 12.5-25 mg (50 mg),infusion 5-40mg/h,onset 3-6 min,duration 4-6 hr . Salgado et al.Annals of intensive care 2013;3:17
  • 58.
    Aortic Dissection • Mostdramatic and rapid fatal complication in HTN emergencies. • Acute BP reduction reduces shear forces on damaged aorta. • Aim of treatment to reduce SBP as rapidly as possible down to 100-110 mmHg, simultaneously control tachycardia resulting form the sympathetic activation. • B blocker + vasodilator to be given • Esmolol + nitroprusside would be a better combination. • Hydralazine is C/I Circulation 2006;114:1384-89
  • 59.
    Ischemic stroke • BPelevations can occur in previously hypertensive and in normotensive pts. • BP declines to pre stroke values within 3-4 days after an ischemic stroke. • Severe HTN Rx controversial issue. Lesions in cerebral area Impaired neurogenic control of CVS HIGH BP Arch Intern Medicine 2003;163:211-216
  • 60.
    Shift to rightin case of chronic HTN
  • 61.
    AHA recommendation • Thresholdfor treatment BP > 220/120 mmHg • Target BP should be a 10-15% lowering of BP. • Raised ICP – MAP<130 (1st 24hrs) • No raised ICP – MAP<110 • IV Labetalol or Nicardipine . • IV tPA (if to be given) BP <185/110mm Hg. Stroke 2003;34:1056-83
  • 62.
    IC bleed • Toprevent rebleeding and reduce edema formation. • BP >180/105 mmHg ,may benefit from gradual 20-25% reduction in BP. Nimodipine, a dihydropyridine calcium blocker,is effective (antagonist effects on cerebro vasospasm). AHAguidelines;Critical care Med 2006;34:1975-1980
  • 63.
    Hypertensive Encephalopathy • Potentiallethal complication of severe or abrupt BP elevation. • Previously HTN/normotensive pts. • Acute glomerular nephropathy, Eclampsia, TTP, Pheochormocytoma, Erythropoietin administration, immunosupressive drugs HIGH BLOOD PRESSURE Excessive increase in cerebral blood flow HYPERFILTRATION LOCALISED OR WIDESPREAD EDEMA Hinchey J et al,NEJM 1996;334:494-500
  • 64.
    • Cerebral ischemiaresulting from arteriolar spasm*. • Severe headache,vomitings,visual disturbances,confusion, focal or generalized seizures. • Fundoscopic examination(key role) • Mean BP should be reduced by 20% within first hour. • IV sodium nitroprusside is DOC (rapid onset of action) ESC/ESH 2003 • IV labetalol,nicardipine,hydralazine . Circulation,2004;110:2241-5
  • 65.
    Eclampsia • Hypertension complicates12% pregnancies, 18% maternal deaths. • Volume expansion,MgSo4 for seizure prophylaxis. • MgSo4 4-6 g in 100ml 5%D over 15- 20 min - 1-2g/h infusion (hourly DTR,urine output). • Antihypertensive therapy (to prevent complications in mother). • SBP :155-160 mmHg,DBP>105mm Hg.(initiation of Rx) • ICH is a devastating complication. • Methyl dopa,Hydralazine DOC, • Others being IV labetalol,nicardipine. • Avoid sublingual or oral nifedipine. • Nitroprusside,ACEI – C/I Am J Obst 2000:183:S1-S22
  • 66.
    HTN emergencies dueto catecholamine excess Abrupt increase in alpha adrenergic tone. • IV labetalol • Pheochromocytoma crisis (IV alpha blocker phentolamine) followed by B blocker(for tachycardia or VPCs). Withdrawal of centrally acting anti HTN drugs (clonidine) Pheochromocytoma Cocaine intoxication Abuse of sympathomimetics Post operative Hypertension
  • 72.
    ORAL DRUGS FORHTN URGENCIES Drug Initial dose Onset duration Adverse effects
  • 73.
    Acute and transientBP elevations • Anxiety • Panic attacks • Pain Rx - Administration of anxiolytic or analgesic drugs. • Refractory nose bleeding – IV drugs to be used sometimes
  • 74.
    TAKE HOME MESSAGE •Most common cause for HTN crises is UNDIAGNOSED/UNTREATED/ INADEQUATELY TREATED HYPERTENSION • Differentiation of emergency from urgency is absence of target organ damage in the later. • Clevidipine is the new drug approved for hypertensive emergencies. • IV Nicardipine , IV Labetalol are preferred for most of emergency situations. • SL/oral nifedipine not to be used..
  • 75.