Hypertension: Symptoms, Causes and Treatment

Hypertension is one of the most common conditions in which the force of the blood against the artery walls is too high (140/90 mmHg or higher). While it is quite common, it can be serious if not treated. Usually patients are unable to feel that they are suffering from hypertension. The only way to know is to get the blood pressure checked. 

Hypertension is one of the most common topics for Medicine. Read this blog post thoroughly to learn everything about Hypertension and elevate your NEET PG preparation. 

Introduction

• Normally nocturnal dip around 4-6 am with approximately 10% of fall in blood pressure
• Early feature: loss of nocturnal dip
• Systolic blood pressure variation shows an increase in incidence of cardiovascular mortality.
• Good control of HTN: Acute coronary syndrome incidence reduced by 25%, stroke by 30%, heart failure by 50%

• In patient with good control of HTN, incidence of:

• Acute coronary syndrome to be reduced by 25%
• Stroke to be reduced by 30%
• Heart failure to be reduced by by 50%

Blood Pressure   

• Optimal BP < 11575mm of Hg 
• Race dependent value: If Systolic blood pressure (SBP) more than 20 mm, diastolic blood pressure (DBP) by 10 mmhg then the cardiovascular mortality risk increases
• Morning hours will have higher chances of increased blood pressure.

Classification

Home based BP monitoring (HBPM)

• >135/85mm Hg
• 7 days: Morning / Evening
• Discard 1^st day value
• 6 days: average
• Cuff size: 80% of arm circumference
• Width: >40%
• Rest: 5 min
• After smoking / coffee consumed: wait 30 min
• BP measure both arms 
• BP measure legs 

White coat HTN

• BP normal at home but increase in clinic
• Can develop HTN in future

Masked HTN

• BP normal in clinic but elevated at home (stage1)
• Need anti-hypertensive medicine

Causes Of Hypertension (HTN)

• Most common cause of HTN: Essential HTN/ idiopathic
• Most common cause of secondary HTN: Renal Parenchymal disease
• Secondary HTN (America): Obstructive sleep apnea

• Most common congenital cause of HTN is Coarctation of Aorta
• In Coarctation of Aorta (Post ductal), BP in upper limb is higher and BP in lower limbs is lower

Unequal Blood Pressure in left/right arm is seen in

• Takayasu’s arteritis (Important cause of renal artery stenosis in India)
• Supravalvular AS (Aortic Stenosis): William syndrome (Conda Effect)
• Coarctation of Aorta (Pre ductal)
• Aortic Dissection: (acute) antegrade

Secondary Causes of HTN

• Renal parenchymal disorder  
  • Chronic Kidney disease
  • Chronic glomerulonephritis
• Renovascular HTN 
  • Fibromuscular dysplasia in young age
  • Atherosclerosis in old age
• Metabolic syndrome/ syndrome X
  5 components of metabolic syndrome:
  • Centripetal obesity
  • Insulin resistance
  • Hypertriglyceridemia
  • Low HDL 
  • HTN
    3 out of 5 should be present for diagnosis
• Obstructive Sleep Apnea (OSA) 
  • Fluctuation of heart rate during sleep increases the stress on the heart and that manifests into HTN and left ventricular hypertrophy
  • During apnea episode there is bradycardia (oxygen cut off from body) and due to hypoxia, the person tries to breathe in and then there is cortical arousal – oxygen goes inside and there is sudden increase in the HR
• Endocrinological 
  • Hypothyroidism (Isolated diastolic HTN)
  • Thyrotoxicosis
  • Pheochromocytoma episodic HTN
  • CONN syndrome
  • OCP: due to secondary aldosteronism
  • Acromegaly: increased Growth hormone
  • Neurogenic: Spinal cord transection (At T6 or above: unopposed sympathomimetic outflow to heart)
  • Cushing reflex: decreased HR and increased BP 

Mendelian causes

• Liddle syndrome (Autosomal Dominant)
  • Overactivity of ENac – causes more salt/H₂O to retain in the body
  • HTN with loss of K+/H+ causing hypokalemia alkalosis
  • Low aldosterone, low renin, and high blood pressure
  • Treatment: Amiloride (ENac blocker)
• Gordan syndrome
  • Autosomal Dominant
  • Mutations are WNK-1/ WNK-4: gain of function - Thiazide dependent
  • Na/Cl cotransport in Distal Convoluted Tubule 
  • HTN due to more Na/Cl retaining in the body
• Polycystic kidneys 
  • Autosomal Dominant in adults, Autosomal Recessive in pediatrics
    USG criteria:
  • Should have 2 or more cyst in kidney
  • Adults: hepatic cyst
  • Pediatric: hepatic fibrosis
  • Destruction of parenchyma in kidney causes reduction in GFR and Renin levels increases resulting in HTN
    • Abdominal pain
    • GI manifestations
• Pheochromocytoma 
  • Autosomal Dominant
  • Associated with MEN-2A (Sipple Syndrome), MEN-2B, Von hippel lindau, Neurofibromatosis-1
• Congenital adrenal hyperplasia (CAH)
  • 17-α hydroxylase deficiency (Autosomal Recessive), causes increase in Aldosterone and thus HTN
  • 11 – hydroxylase deficiency (Autosomal Recessive) causes increase in Deoxycortisol which stimulates ENaC and cause HTN

Work up for newly diagnosed HTN patients

• Echocardiography: Left ventricular hypertrophy
• Fasting blood sugar, 
• lipids
• Serum electrolytes
• TSH
• Urine microscopy, Albumin Excretion Rate (AER) Urine albumin/Urine creatinine = (30-300 mg/gm)
• BUN, Serum creatinine Na+/K+, uric acid values

Target Organ Damage

• Eyes 
• Brain 
• Kidneys 
• Aorta 
• Heart

Heart damage

• 1st to damage 
  • Left ventricular hypertrophy
  • Increased oxygen demand 
  • Subendocardial ischemia 
  • ST depression 

Eyes

• Hypertensive retinopathy
  • Earliest Fundus findings
    • Stage I: focal attenuation of arterioles (earliest)
    • Stage II: I+A-V nipping (Salu sign)
    • Stage III: I+II+flame shaped hemorrhage, cotton wool spots
    • Stage IV: I+II+III+Papilledema

Brain 

• Hemorrhagic stroke 
• Most common site: putamen 

Kidneys

• GFR reduces progressively
• CKD

Aorta

• Aortic dissection 
  • Tearing chest pain in interscapular area
  • Antegrade travel of dissection can manifest neurological features like horner syndrome
  • Diagnosis:
    • Trans Esophageal Echocardiography: in unstable patients
    • CT angiography: Tennis ball appearance
  • Treatment:
    • Type A (Tear in front, anteriorly) → surgery
    • Type B (Tear present behind)
    • Unrecordable BP→ Surgery
    • BP normal to low→ Esmolol (to retard the progression of tear)
    • HTN crisis: labetalol

When to treat HTN as per ACC/AHA

• ASCVD risk increased: <130/80
• ASCVD risk not increased: > 140/90
• Age > 65 year: > 130/80

Treatment

• Lifestyle modification
  • D.A.S.H (dietary approaches to stop hypertension): reduced intake of sodium and increased of potassium
  • Physical activity
• If the patient is HTNsive despite the lifestyle modifications, then switch to drugs
• < 55 years 
  • “ACE inhibitor”, in case of dry cough, angioedema then switch to “ARB” 
  • ACEI/CCB
  • ACEI+ CCB+Thiazides
• >55 years 
  • CCB
  • CCB + ACEI + Thiazides

Resistant HTN

• At least 3 classes of anti HTN concurrently used in patient
• Must include Thiazide (at least 2 weeks)
• Improper BP measurement should be ruled out
• Cox-1(-), cocaine, steroids
• Excess salt intake, obesity
• Alcohol intake
• Noncompliance of patient

Uses Of Anti-Hypertensive

ACE inhibitors

• Acute coronary syndrome -post MI
• Diabetic nephropathy
• Ischemic nephropathy (Unilateral RAS)
• Heart failure with reduced ejection fraction
• Chronic hyperkalemia K⁺
  • Patiromer
  • K⁺ biding Resin (SPS)
  • Na zirconate

β- Blockers (Cardio selective)       

• Carvedilol
• Metoprolol
• HTN + Chronic stable angina, congestive heart failure

Aldosterone antagonist

• Used in patients of heart failure with preserved ejection fraction

α- Blockers

• HTN in patients having BPH use Prazosin
• HTN in Pheochromocytoma use Phenoxybenzamine
• End stage renal disease (diabetic nephropathy) use α- blocker

Hypertensive Urgency

• If BP > 220/130 mm Hg but life-threatening end-organ damage is absent

Hypertensive Emergency/ Crisis

• If BP > 220/130 mm of Hg + target organ damage is present

Goal/ Objective:

• Reduce MAP by 25% within 2 hours (Mean Arterial Pressure) or maintain BP 160 / 100 mmHg
• Presence or absence of target organ damage defines the urgency or emergency than recorded numerical values.

Malignant HTN

• Fibrinoid necrosis occurs in the vessels supplying various parts in the body and the mortality rate increases ↑↑ by 50% in 6-12 months
• Retina: hemorrhage 
• Brain: putamen bleed intra parenchymal bleed
• Kidney: nephrosclerosis 
• Blood vessel: Microangiopathic hemolytic anemia
• Hypertensive encephalopathy, sodium nitroprusside is used 

Stroke + HTN

• Thrombolysis (Reteplase < 4.5 hours)

Ischemic stroke

• Thrombolytic candidate
  • To initiate thrombolysis, BP <185/110
  • To lower BP, Give: Nicardipine
• Not a thrombolytic candidate
  • If BP is 220/130 mmHg (first lower BP)

Intracerebral Hemorrhage

• Target BP 130-140mmHg

In patients with postoperative HTN / MI/ Unstable Angina/ Acute decompensated CHF 

Give: IV Nitroglycerin

In patients of “Adrenergic Crisis” in pheochromocytoma surgery 

• Nitroprusside is used along with Phentolamine

Pheochromocytoma

• Pre op: Oral phenoxybenzamine

• Intra op: Phentolamine 
• Intra op + HTN crisis: Nitroprusside
• Heart failure: IV Nitroglycerin

Target Blood Pressure

• Target BP/ Goal to be maintained in patients with HTN: < 135-140/ 85-90 mm of Hg
• Target HTN along with Diabetic nephropathy = < 130/80 mm of Hg
• BP Malignant HTN: 160/110 mm of Hg to be maintained by using antihypertensives or Mean Arterial Pressure should be reduced by 25% over 2 hours
• CKD grade I-III: ACEI/ARB + Thiazide + CCB
• eGFR< 30ml/min: Diuretic, Metazolone
• ESRD
  • CCB/amlodipine
  • alpha blocker.

That is everything you need to know about Hypertension for your Medicine preparation. For more interesting and informative blog posts like this download the PrepLadder App and keep reading our blog!