Arterial Hypertension (HTN)

Definition ​= 140/90
We speak of HTN if:
● Systolic arterial pressure equal to or more than 140 mmHg, and/or
● Diastolic arterial pressure equal to or more than 90 mmHg
WHO Classification ​(systolic/diastolic)
● Optimal = less than 120/80
● Normal = 120-129/80-84
● High normal = 130-139/85-89
● Grade I HTN (mild) = 140-159/90-99
● Grade II HTN = 160-179/100-109
● Grade III HTN (severe) = 180+/110+ (+ = equal or more than)
● Isolated systolic htn = 140+ systolic, but <90 diastolic
Global cardiovascular (CV) risk
What does it mean? The probability of developing a CV disease in a defined time frame,
while taking into account multiple risk factors.
Risk stratification
Global CV risk in HTN patients can be assessed by plotting the severity grade of HTN
against risk factors:

CV risk factors = atherosclerosis risk factors:

● HTN
● Male sex
● Age: men 55+, women 65+
● Family history (premature CV death; premature = before age mentioned above)
● Smoking
● Dyslipidemia
o Total cholesterol > 190 mg/dl
o LDL > 115 mg/dl
o HDL < 40 mg/dl for men; <46 mg/dl for women
o Triglycerides > 150 mg/dl
● Abdominal obesity
o 102 cm or more for men
o 88 cm or more for women
● General obesity (BMI of 30kg/m​2 ​or more)
● Glycemia (102-125 mg/dl)
● Abnormal glucose tolerance test

Subclinical organ damage ​(subclinical = asymptomatic)

● Increased pulse pressure (elderly) 60+ mmHg
● LV hypertrophy
● Echographic evidence of vascular wall thickening or damage (plaque)
 ● Pulse velocity increased (carotid – femoral) > 10 m/s
● Ankle-brachial index < 0,9
● CKD with low eGFR (30-60 mL/min/1.73m​2​)
● Microalbuminuria
Diabetes
Fasting plasma glucose 126+ mg/dl; postprandial 198+ mg/dl
Other
Cerebrovascular, coronarian, peripheral artery diseases, cardiac failure, CKD, retinopathy
Prevalence
Blood pressure in childhood and adolescence increases mostly in boys. In adulthood, it rises
in both sexes, but predominantly in women. Around 60 years, BP tends to equalize between
the sexes, but after 60 years it increases more in women. Interestingly, systolic BP will
continue to rise over time after that age, but diastolic BP stays the same (or may even
decrease slightly).

Blood pressure regulation

BP= cardiac output x peripheral vascular resistance
Cardiac output = HR x stroke volume
Stroke volume depends on LV contractility, preload (venous return) and afterload.
Regulatory mechanisms of BP:
● Heart (pump function)
● Vascular tone (peripheral resistance)
● Kidney (volume regulation, absolutely vital for BP maintenance!)
● Neurohormonal mechanisms involved with aforementioned organs
Etiology
90% of HTN is idiopathic – this is primary HTN
The rest, or secondary HTN, may have the following causes:
● Renal (vascular: stenosis of renal a., vasculitis; or parenchymal disease)
● Endocrine (hypo-/hyperthyr., Cushing, hyperaldosteronism, etc)
● Cardiac (coarctation of ao., ao. regurgitation, hyperkinesia)
● Neurological
● Durg induced (oral contraceptive, corticoids, EPO)
● Pregnancy
● Acute trauma (burns, pancreatitis, surgical interventions)
Pathogenesis of primary HTN
● Genetic (renal sodium channel or angiotensinogen gene defects)
● Neural (increase in sympathetic activity)
● Renal (impaired elimination of salt)
● Vascular (remodeling, endothelial dysfunction, arterial rigidity)
● Hormonal (RAAS)
Renin-Angiotensin-Aldosterone System (RAAS)

Other factors associated with primary HTN

● Smoking
● Excess alcohol consumption
● Drugs (estrogens, steroids, sympathomimetics)
● Obesity (due to: angiotensinogen from adipocytes (!), increased blood volume (to
supply increased body mass) and increased blood viscosity!)
● OSAS
● Polycythemia Vera (increased viscosity)
● Hyperuricemia
HTN risk
HTN itself is not the killer, but high BP levels are correlated with increased risk of
● Stroke
● CHD
● Heart failure
● Kidney failure
● Recurrent CV events
HTN consequences
Increased risks mentioned above may be explained by looking at the consequences of HTN.
● Cardiac
o LVH (hypertrophy is an important predictor of CV events and mortality!)
o LV dysfunction, failure
o Ischemic heart disease (coronary atheroscl + increased O2 demand)
● Ocular (retinopathy)
● Neurological (stroke! Ischemic, hemorrhagic or lacunar (small arteries))
● Renal (failure, sclerosis)
● Peripheral vascular disease
● Aortic aneurysm / dissection
Diagnosis & evaluation
● Measuring blood pressure: by doctor in hospital/practice - repeatedly; 24hr
ambulatory monitoring and/or self-monitoring at home (lower threshold for
self-monitoring; HTN assumed at 130+ mmHg)
● Evaluation of patient through anamnesis, physical, paraclinical investigations
BP measurement by doctor:
Other modalities:

White coat HTN

HTN only while in hospital / at doctor's office
Prevalence: approx 13% in general pop; 34% of HTN patients
Usually women, non-smoker. Lower prevalence of organ damage compared to sustained
HTN. May seem HTN patient when examined but in reality is not.
Masked HTN
Prevalence: approx 13%
In some ways the opposite of white coat HTN: the patient is hypertensive only when out of
hospital / doctor's office – so HTN is not seen by doctor
Typically young males. Rf: drinkers, smokers, obese, stress, anxious, diabetic, kidney
disease, known HTN cases in family. CV risk similar to sustained HTN patients.
Indications for self-monitoring (HBPM) or ambulatory monitoring of BP (ABPM)
● Suspicion of white coat HTN in office, with
o Grade I HTN when measured
o High BP levels in office in patients without organ damage and risk factors
● Suspicion of masked HTN
 o High or normal BP when measured in office
o Normal BP but with (subclinical) organ damage or CV risk factors
● Identification of white coat effect in HTN patients
● Considerable variability in measured BP at same / repeated visits
● Hypotension: autonomous, postural, post-prandial, post-siesta, drug induced
● Elevated office BP or pre-eclampsia in pregnant w
● ID of true and false resistant HTN
Specific indications for ambulatory monitoring (ABPM):
● Marked difference between office BP and home BP
● Assessment of dipper status (see table above)
● Suspicion of nocturnal HTN
● BP variability

Effort HTN (exercise htn)

● Systolic BP increases during dynamic/static effort, but diastolic BP does not
● Effort HTN definition: 210+ mmHg in men, 190+ in women
● In normotensive patients, increased effort BP predicts HTN onset
● Indication for ABPM!
● Prognostic value uncertain

The importance of good history:

Physical examination:

Paraclinical investigations:
+ Brain: CT, MRI – to document lacunar stroke, white matter lesions, microhemorr.

Secondary HTN
Why is it important to differentiate between primary and secondary HTN?
● Secondary may have a curable cause!
● Treatment may differ
● Left untreated, secondary HTN leads to the same consequences as primary
When to suspect secondary HTN?
● Age: (sudden) onset either before 20 years or after 50 years of age
● Severe from the beginning and hard to control
● Sudden onset in previously normal person
● Signs and symptoms suggesting underlying disease: needs good anamnesis and
examination
● Family history: absence of familial HTN (1​st​ degree relatives)
Attitude to patient:
● Think of what could cause secondary HTN – see etiology paragraph – and examine
patient with that in mind:
● Auscultation of renal arteries, checking for weight changes, hirsutism (thyroid issues,
Cushing), drugs (medical and otherwise)
● Workup:
o Urinalysis, serum creatinine & urea
o Potassemia, glycemia (if diabetes: often associated with renal disease)
o Lipid profile
o ECG
Clues for secondary HTN in investigations:
The most common cause of secondary HTN is ​renal parenchymal hypertension. ​This is the
result of impaired Na and RAAS mechanisms. Other common causes can be:
Take home messages
Threshold value for HTN should be thought of as flexible, greatly depending on grading and
CV risk of patient. The same goes for treatment choice
HTN Grading not only based on BP values alone, but also considering global CV risk of
patient
HTN by itself is (almost) asymptomatic, yet its consequences can be lethal