From simple to
complex
reaction
in hypertension
emergency
Jana Brguljan, MD, PhD, FESC
University Medical Centre Ljubljana
Hypertension Department
Medical University Ljubljana
Slovenia
Disclosure
Nothing to disclose
M/28 y – CVI, disection a. vert.
Different BP levels! 160/100 mmHg
Her usuall BP 138/85 mmHg
M/52 y – kidney failure,
F/37 y – aortic dissection TIA
270/130 mmHg 190/110 mmHg
Her usuall BP 160/100 mmHg His usuall BP 150/90 mmHg
F/93 y – NSTEMI,
Pulomonray oedema
175/75 mmHg
His usuall BP 130/60 mmHg
Case 1: Outpatient clinic
• 28yrs old woman
With..
• In several ocasions at clinical visit with family doctor BP
142/86mmHg
• Shortness of breath on severe exertion for 2 months
• Diabetes for 1 year, on diet
• No other symptoms
Patient history
• Family history:
➢ Father: hypertension, hyperlipidemia, CVI at the age
of 54
➢ Mother: myocarditis at the age of 32
➢ Grandmother: diabetes mellitus type 2, carcinoma
uteri
• Past history:
➢ Op. due to apendicitis 5y ago
• Allergies: amoxicillin with clavulanic acid
• Social history: not smoking, denies alcohol abuse
Evaluation of patient with
hypertension:
Assess CV risk,
Confirm the Detect causes of
OD and
diagnosis of secondary
concomitant
hypertension hypertension
clinical conditions
Physical examination Treatment??
BMI=29 kg/m2
BP left arm:
BP right arm: 144/92 142/93mmH
mmHg, pulse 76/min g,
pulse 71 bpm
Neck: no bruits BP on standing:
144/90 mmHg,
pulse 89/min
Heart: no murmur
Extremities: no edema, Abdomen:
normaly palpable no abdominal
peripheral pulses bruit
Complex reaction in hypertension emergency
➢ Many of patients who present to the Emergency Department (ED) may have
elevated blood pressures recorded during their visit. This can be due to a
number of reasons including pain, anxiety, missing their normal anti-
hypertensive medications and "white coat hypertension".
➢ No current evidence based or guideline recommendations exist for a blood
pressure cut-off at which point an asymptomatic patient must be acutely
treated.
➢ So who can we safely send home and who needs more urgent treatment?
The concern is not so much with the absolute numbers of the blood pressure
readings but the effects of severe hypertension on the rest of the body.
Patients with severe hypertension but no organ damage are often considered
to be hypertensive urgencies rather than emergencies. They will require
commencement of oral anti-hypertensive agents or alteration of existing
regimen but can usually be discharged home with appropriate follow-up.
➢ Hypertensive emergencies will usually require intravenous anti-
hypertensive therapy aiming for a 25% reduction in blood pressure over 1-
4 hours.
.
doi:10.1093/ehjcvp/pvy032
Definition of Hypertensive Emergencies
➢ Very high BP values associated with acute hypertension-
mediated organ damage
➢ Key target organs: heart, retina, brain, kidneys, and large
arteries
➢ Immediate BP reduction required to limit extension or
promote regression of target organ damage
➢ The type of target organ damage is the principal determinant
of the choice of treatment, target BP, and timeframe by
which BP should be lowered
Stratification of hypertensive emergencies
according to the condition or target organ involved
P van den Born ,G Lip, J Brguljan-Hitij, et al. Management of hypertensive emergencies
European Heart Journal - Cardiovascular Pharmacotherapy 2018
Important !
➢ Patients with a hypertensive emergency should be
admitted for close monitoring and, in most cases,
treated with intravenous BP-lowering agents to
reach the recommended BP target in the designated
time-frame.
➢ Patients that have no hypertensive emergency can
usually be treated with oral BP-lowering agents and
usually discharged after a brief period of
observation.
Epidemiology
➢ Coding differences among institutions
➢ One in every 200 patients presents at the emergency department with
a suspected hypertensive emergency
➢ Despite improved treatment for hypertension in the past decades, the
incidence of hypertensive emergencies has not declined
➢ Acute pulmonary oedema, stroke, myocardial infarction, heart failure,
acute aortic dissection, acute renal failure and hypertensive
encephalopathy.
Pathophysiology
➢ Many pathophysiological mechanisms are involved in the
development of hypertension emergencies, but the initiating
events for the sudden escalation in BP are not completely
understood.
➢ Among patients presenting at the Emergency Dept. with
malignant hypertension, secondary causes can be found in 20-
40% and most often consist of renal parenchymal disease and
renal artery stenosis, whereas endocrine causes appear to be
rare.
➢ The majority of patients with malignant hypertension have
unrecognized or uncontrolled essential hypertension.
Acute HT mediated organ
damage
Aorta – dissection, aneurysm
Heart – MACE, acute pulmonary
oedema
Brain – stroke, hypertensive
encephalopathy
Retina & Kidneys – malignant
hypertension
Case 2
➢ 39 y old lady admitted to the emergency department due to
chest pain which started in late afternoon and escalated till
evening so relatives called an ambulance.
➢ At the admission she described her pain as sharp abrupt
onset in her chest, tearing character radiating towards back
➢ Few days before her blood pressure was not well controlled
and she measured SBP around 200mmHg
Examination list:
➢ History
➢ Physical examination
➢ Haemoglobin, platelet count
➢ Creatinine, GFR, sodium, potassium, lactic
dehydrogenase (LDH), haptoglobin
➢ Quantitative urinalysis for protein, urine sediment
for erythrocytes, leukocytes, cylinders and casts
➢ ECG
➢ Chest X Ray
➢ Family history: Grandfather died because of CVI, father survived CVI and is
treated for AH, grandmother is treated for DM and AH
➢ Past history: DM for few years on diet, chronic kidney disease stg 4 for 3 y,
extreme obesity, hypertensive retinopathy
➢ Present history: Treated for hypertension for 4 years, she delivered 3
times, 2 times normal pregnancy, 1 spontaneous abortion and 1 on
hypertensive therapy
➢ She was obese since her childhood, BMI in y2017 was 50.1 (163cm, 133kg)
➢ She was tested for secondary hypertension but was not discovered. Was
hospitalised many times and often her SBP was measured even 280mmHg
➢ On medications: bisoprolol 10mg in the evening, furosemide 40mg ,
amlodipine 5mg, perindopril 4mg, moxonidine 0.3mg
➢ Smoker 10y 30 cig/day, now 10 cig/day
Physical examination
➢ Extreme obesity, BMI 43
➢ On admission, her oxygen saturation was 92%
➢ BP 250/130mmHg D arm, 220/112mmHg L arm, HR 74/min
➢ Jugular venous pressure was normal
➢ Lungs: some inspiratory crackles were heard at pulmonary basis
➢ Heart: rhythmic action fr 74/min, no murmurs
➢ No abnormalities in abdomen
➢ No peripheral oedema
variable result variable result
RBC 4.2 (1012/L)
WBC 9.7 (109/L) pH 7.39
Hb 120 g/L pO2 11.1 kPa
Creatinine 308 μmol/L pCO2 5.2 kPa
(3.5 mg/dL)
GFR 16 (CKD-EPI)/1.73m2 HbO2 0.94
K 3.6 mmol/L
Na 141 mmol/L urine Proteinuria 2
LDH 4.68 μkat/L
CRP 109 mg/L
Trop I ultra 0.02 μg/L
NT-pro BNP 2878.5 ng/L
Enlarged heart, mild interstitial oedema
Differential diagnosis of acute chest pain
➢Nonvascular pathology: pulmonary embolus, spontaneous
pneumothorax, aortic regurgitation without dissection,
esophageal rupture, pericarditis and pleuritis
➢Vascular pathology: acute coronary syndrome, acute aortic
dissection, other acute aortic pathologies as intramural
hematoma without dissection, aortic aneurysm, aortic injury
without dissection, peripheral artery dieses, chronic aortic
dissection
Up to Date 2019
Acute aortic dissection
➢ Relatively uncommon, estimated 2.6 to 3.5 per 100.000
person-years, 66% men
➢ Hypertension is the most important predisposing factor,
more common in distal aortic dissection
➢ Important to define ascending vs descending aortic
involvement (surgical vs medical management)
Drug choice according the cause and mechanism of the HTN Emergency
Case-Treatment
➢ Continuous perfusion of anti-hypertensive is mandatory, our case urapidil i.v.
(25mg till 75mg i.v.) and gliceriltrinitrat infussion, furosemid 40mgi.v.
➢ Pain control - analgesia
Admission to the ward
➢ Intensive care unit, regulating BP, ACE
inhibitor creat 455
➢ Doppler of renal arteries: bad visibility,
no obvious stenosis, RK: 10.3cm, RI 0.78,
LK 10.4cm, RI 0.8,
➢ Echocardiography
LV EDD 5.1cm, ESD 3.3cm, IVS 1.8cm, INF LAT 1.6cm, LVMI (ASE) 201g/m², LVMI (Ht) 115g/m, RWT 0.60,
EDV 116ml, EDVI 53ml/m², SV 2D 77ml, EF 2D 66%. LVOT premer 2.5cm. LA premer (PLAX) 4.9cm,
Discharge from the ward
➢Her th. on discharge was: amlodipine 10mg/24h,
furosemide 40mg 2 times daily, minoxidil
2.5mg/12h, bisoprolol 10mg, doxazosin 4mg/12h,
moxonidine 0.3mg/12h, rosuvastatin 10mg, aspirin
100mg, sodium bicarbonate 2x1g, CaCo3 3x 1g
➢ Advised to continue loosing weight
Case 3
➢ 59 y old lady admitted to the emergency department due
to heavy breathing which started in late afternoon and
escalated till late evening so relatives called an
ambulance.
➢ Rescue team measured blood pressure 240/100mmHg
oxygen saturation 70% and put her on OHIO mask where
oxygen saturation elevated to 90%, administered
furosemide 40mg i.v., Morphin 2mg plus 2mg i.v.,
metoclopramide i.v. and fenoterol and ipratropium
bromide in inhalation.
➢ They transferred her to emergency department of our
university hospital.
Diagnostic examination:
➢ Detail history and physical examination with BP meassured
on both arms
➢ ECG (ischemia, arrhythmias, left ventricular hypertrophy)
On indication:
➢ Troponin-T, CK, CK-MB
➢ Chest X-ray (fluid overload)
➢ Fundoscopy
➢ Transthoracic echocardiography (cardiac structure and function) or
➢ point of care cardiac and lung ultrasound (cardiac pulmonary
oedema)
➢ CT (or MRI)-brain (intracranial haemorrhage)
➢ CT-angiography of thorax and abdomen (acute aortic disease)
➢ Renal ultrasound (postrenal obstruction, kidney size, left to right
difference)
Case 3
➢ Family history: Father CVI, mother operated on heart but
no details known
➢ Past history: Hypothyreosis from 2001 on therapy,
➢ PTA AIC bilateral with stenting in year 2013,
➢ Known three vessel coronary disease. CABG on February
2018 (LIMA-LAD, SVG-OMV, RCA off pump)
➢ Aorto-bifemoral bypass and TEA AFC sin on May 2018
➢ Present history: Treated for hypertension for 15 years,
two days before admission she had breathing problems
which worsened the night of admission
➢ On medications: bisoprolol 2x5mg, Aspirin 100mg,
perindopril/indapamide/amlodipine 10/2.5/10mg,
rosuvastatin 40mg, levothyroxine 50microg
➢ Smoker 30y 15 cig/day, now 6 cig/day
Case 3
➢ On admission, her oxygen saturation on OHIO
oxygen mask was 94%
➢ BP 233/125mmHg, HR 141/min
➢ Jugular venous pressure was measured as 20 cm
➢ Lungs: diffuse inspiratory crackles and expiratory
wheezing were heard
➢ Heart: rhythmic action fr 130/min, no murmurs
➢ No abnormalities in abdomen
➢ Moderate peripheral oedema
variable result variable result
Lab. test RBC 5.22 (1012/L) OHIO
mask
WBC 20.1 (109/L) pH 7.29
Hb 143 g/L pO2 9.1 kPa
Creatinine 120 μmol/L pCO2 6.0 kPa
(1.36 mg/dL)
GFR 43 (CKD- HbO2 0.91
EPI)/1.73m2
K 4.1 mmol/L
Na 141 mmol/L
LDH 4.68 μkat/L
CRP 117 mg/L
Trop I ultra 0.289 μg/L
NT-pro BNP 26926 ng/L
Case 1: admission
Case 3: treatment
➢ OHIO oxygen mask
➢ NTG 2x subl, Nitroglycerine infusion, furosemide
40mg iv, MO 3mg,
➢ Beside cefotaxime, azithromycin were suggested
from our infectologists
➢ BP dropped to 150/82, HR 120/min
➢ She was feeling better and admitted to our
department
➢ During hospitalization we noticed, murmur in
abodmen,transitional decline in renal function,
SBP was 100-110 mmHg
➢ Abdomen US and renal doppler was performed
Case 3: hospitalization
➢ Sizes: right kidney 11.6 cm,
left kidney 9 cm
➢ Resistence indexes: right 0.61
left 0.55
➢ Stenosis of left renal artery
➢ ECHO: normal EF,
contractility abnormalities,
elevated LVMI
Dg.:Pulmonary oedema
Acute respiratory infection
Renovascular hypertension
CABG 2018
Peripheral Arterial Disease
Hypothyreosis on th.
Woman, 59 y Succ. 95%
Hypertension 24-h average: 139 / 69 mmHg
SD (weighted): 17 / 9 mmHg
Therapy: Awake: 133 / 69 mmHg ARVd = 15/7 mmHg
ARV24 = 13/7 mmHg
bisoprolol 2x5mg, Aspirin 100mg, Sleeping: 148 / 69 mmHg
amlodipine 10mg, BP dipping: +11 / 0 %
rosuvastatin 40mg, Max. (last hour): 169/81 mmHg
levothyroxine 50microg HR (24 h/awake/sleep): 85 / 84 / 87 min-1 (+4%)
24-hour
Ambulatory
Blood
Pressure
Monitoring
2019-03-13
KOHip 2019
Drug choice according the cause and mechanism of the HTN Emergency
https://epmonthly.com/article/dont-let-hypertens
https://epmonthly.com/article/dont-let-hypertens
Final take home messages
Definition Important points
➢ We should abandon the term ‘hypertensive ➢ HT emergencies 1 in 200 pts at the
crises’, which may not precisely characterize emergency department
the clinical picture. ➢ A correct diagnosis and appropriate
➢ We should use the terms: treatment are critical.
➢ Blood pressure should be reduced:
➢ Hypertensive emergencies,
➢ within minutes to hours (target BP
or depending on the clinical diagnosis)
➢ Uncontrolled hypertension in patients with hypertensive
➢ depending on the presence (emergencies) or emergencies
absence of acute and rapidly progressing ➢ within 24 to 48 hours in patients
end-organ dysfunction/damage with hypertensive urgencies.
