Blood Pressure =

Cardiac Output x Peripheral Resistance

1

Blood Pressure =

[Stroke Volume x Heart Rate] x Peripheral Resistance

2

Blood pressure gets elevated if either, or more of the following increases

• Stroke volume
• EDV – ESV.
• Dependent on cardiac contractility, preload, afterload
• Heart rate
• Peripheral resistance

3

• Occurrence of lower BP levels with repeated measurements in clinical settings because of;
• inherent BP variability as well as
• an adjustment to the experience of having BP measured.

Accommodation effect

• When BP readings in clinical settings > outside clinical settings. Anxiety related.
• Not as benign as once thought- considered “elevated BP”
• Requires follow-up! eg school nurse takes daily BP for 3-4 weeks. OR
• Average of 2 or 3 BP readings taken morning and night for 1 week OR
• 24-hour ABPM

White-coat phenomenon

Upper arm auscultation- bases for reference

• Concept of peripheral amplification of systolic BP; Radial BP>arm BP in children

Wrist BP measurement

• More accurate for HTN diagnosis than clinic-measured BP
• For confirmation of HTN in children >5yrs.
• LVH correlates more strongly with ABPM than casual BP measurement

Ambulatory BP measurement

The bladder length at least 80% to 100% of the arm circumference

The bladder width at least 40-50% of arm circumference

Begin at 3 years of age

• For otherwise healthy children, measure annually thereafter
• For obese children (BMI ≥95 centile), renal disease, DM, coactation of aorta, those on meds known to ↑BP, measure at every health encounter

@ <3yrs, meaure BP at well-child care visits if they are at ↑risk for developing HTN eg

• Prematurity GA<32 weeks or SGA, VLBW, umbilical arterial line insertion history
• Congenital heart defects (repaired or not)
• Recurrent UTI, haematuria, proteinuria, known renal diesease or family hx
• Systemic illnesses eg SCD, tuberous sclerosis
• Evidence of ↑intracranial pressure

• Specific cause not identifiable

Essential (or primary)

• Specific cause can be identified
• Renal- glomerulonephritis, pyelonephritis, obstructive uropathy, renovascular, RVT
• Cardiovascular- CoA, PDA, aortic insufficiency
• Endocrine- hyperthyroidism, catecholamine (pheochromocytoma, neuroblastoma)
• Neurogenic- ↑ICP, GBS, poliomyelitis
• Drugs- NSAIDS, Corticosteroids, sympathomimetic drugs (nose drops, cough meds, theophylline)

Secondary

Distinguish between primary and secondary hypertension

Identify any treatable conditions that may be causing or contributing to hypertension

Identify comorbidities or risk factors for early CVD

• Obesity, dyslipidemia, DM

Identify patients for whom antihypertensive drug therapy is warranted

• Secondary or symptomatic hypertension without an associated risk factor amenable to treatment eg obesity
• Any stage of HTN with comorbid CKD or DM
• Those failing a trial of lifestyle change

• Highlighting importance of accurate measurement of BP

Mild HTN- usually asymptomatic

• Acute glomerulonephritis- headache, dizziness, nausea/vomiting, irritability
• ±neurological manifestations (eg stroke), congestive heart failure, renal dysfunction, etc

Acute severe HTN- may be symptomatic in presentation;

• CVS
• Of CoA or surgery for it
• Renal
• History of obstructive uropathies, UTI, renal surgery

Review of systems

• Corticosteroids, antiasthmatic drugs, cold medications, aminoglycosides, cocaine use

Medications history

• Smoking or consumption of excessive amount of coffee or tea

Social history

• Essential HTN, atherosclerotic heart disease and stroke

Family history

• Obesity common cause of essential HTN, and HTN from adrenocortical disorders
• Children with secondary HTN from renal disease are rarely obese

General examination; BMI

• Bounding peripheral pulse- in PDA or aortic regurgitation
• Weak or absent femoral pulses + BP differential between the arms and legs (CoA)
• In normal children, SBP in LL is > 5-10mmHg higher than in UL

Pulse analysis

Imaging for renovascular disease- detection of renal artery stenosis

• Doppler renal ultrasonography in normal weight children >8 yrs
• Computered Tomography Angiography
• Magnetic Resonance Angiography

Specialized chemistries

• Peripheral Plasma Renin Activity
• ↑(high-renin HTN)⇒renal parenchymal or renovascular disease
• ↓(low-renin HTN)⇒excess mineralocorticoid effects eg hyperaldosteronism

Started as an initial treatment

• Weight reduction if overweight or obese
• Healthy diet
• Regular aerobic exercise
• Avoidance of smoking and oral contraceptives

Counselling on-

Used when nonpharmacological approaches are ineffective

Indications for drug therapy

• Severe symptomatic HTN- use IV antihypertensives initially
• Persistent HTN despite a trial of lifestyle modification
• Symptomatic HTN
• Stage 2 HTN without clearly modifiable factor (like obesity)
• Any stage of HTN associated with renovascular & renoparenchymal disease or DM
• Hypertensive target-organ damage: LVH, ↑LV mass
• Family history of early complications of HTN
• Child who has dyslipidemia

Initiation drugs-

• ACE inhibitors, ARB, long-acting calcium channel blocker, or thaizide diuretic
• NB; African American children do not show as robust response to ACE inhibitors, so CCBs appear better for them

In children with HTN & CKD, proteinuria, or DM

• ACE inhibitor or ARB as initial drugs as these are renoprotective

Overweight children at risk of developing DM

• ACE inhibitor, ARB, & CCBs. Avoid diuretics & beta-blockers as they raise blood glucose levels

For uncomplicated primary HTN without hypertensive end-organ damage

• Reduce BP to <95^th centile

For children with CKD, DM or hypertensive end-organ damage

• Reduce BP to <90^th centile

Step-down or cessation of therapy

• In selected patients (overweight children with successful weight loss) with uncomplicated primary HTN.

Ballon angioplasty

Endovascular stenting

Surgery; extended resection and end-to-end anastomosis is preferred

Patients with stage 1 HTN should complete a full evaluation for causes and end-organ damage (primarily LVH).

If there is no evidence of end-organ damage, they may participate in competitive sports without restrictions

Patients with stage 2 HTN should initially be restricted from high-static sports even if there is no evidence of end-organ injury.

High-static sports are defined as classes IIIA to IIIC in a system that classifies sports based on their cardiovascular demands