Flashcards in Cardio L14 Hypertension Deck (45):
Diastolic (and systolic) blood pressures vary widely in the population and show a normal distribution.
20% of adults
Isolated Systolic Hypertension
Isolated elevation in systolic pressure alone with normal diastolic pressures. Common in the elderly and is predominantly due to increased stiffness/reduced compliance of the large blood vessels including the aorta.
White Coat Hypertension
Rise in Blood pressure while being examined by a physician e.g. fight or flight response.
Primary (essential) Hypertension
95% of cases, no cause identified.
2-5% of cases with a defined underlying cause.
Uncommon but important because it may be curable.
1. The majority of hypertensive patients are asymptomatic and it is discovered during a routine physical examination.
2. The “classic” symptoms of headache and nosebleeds do not appear to occur more frequently than in the general population, except in very severe hypertension.
Signs of hypertension
1. High BP
2. Signs due to organ damage
3. There may be signs due to the underlying cause in secondary hypertension.
Organ damage: from hypertension Brain Symptoms:
1. Longstanding hypertension leads to microaneurysms that may rupture to cause haemorrhagic strokes (CVE, CVA)
2. Atherosclerotic plaques may embolise or cause thrombosis resulting in a cerebral infarct.
3. Occlusion of small penetrating branches may result in multiple tiny infarcts resulting in cavities known as lacunae.
Heart effects froms hypertension
1. Left ventricular hypertrophy in responding to chronic elevation of afterload that may lead to congestive cardiac failure.
2. Accelerated coronary atherosclerosis predisposing to ischemia and infarction.
Aorta and peripheral vasculature damage from hypertension
1. Peripheral vascular disease
2. Abdominal aortic aneurysm “tripe A” >6cm
3. Aortic dissection
Kidney symptoms from hypertension
Produces nephrosclerosis, which in severe hypertension may lead to a leak of protein into urine (proteinuria) and chronic renal failure.
Retina damage form hypertension
1. Only location where arteries can be directly visualised using an opthalmoscope.
2. The changes depend upon the severity and duration of the elevated blood pressure (grades I-IV)
Suspicion of Secondary Hypertension:
1. Young age onset (180/110)
4. Signs of underlying pathology
5. Sporadic (i.e. no history in history degree relatives)
6. Refractory to drug treatment.
Causes of secondary hypertension
• Renal (Chronic Failure, Renal Artery stenosis)
• Mechanical (coarctation of the aorta)
• Endocrine (Conn’s Sundrome, Cushing’s syndrome, Phaeochromocytoma, Acromegaly, thyroxtoxicosis)
• Drugs (e.g. oral contraceptive)
• Pre-eclamptic toxaemia
Renal artery stenosis
• Atherosclerosis in elderly man
• Fibromuscular dysplasia in young woman
• Abdominal bruit
• Activation of RAA system results in hypokalaemia
• Goldblatts experiment
Coarctation of the Aorta
• 1. Congenital narrowing often distal to origin of left subclavian
• BP in arms > legs
• Weak or absent femoral pulses
• Midsystolic murmur between scapulae
• Notched appearance of ribs on CXR due to shunting of blood through enlarged arteries
• Adrenal tumour (adenoma
• Often asymptomatic
• Produces Hypokalaemia
• Excess Glucocorticoids
• Cushinggoid appearance including moon face, hisutism, acne, central obesity and proximal muscle wasting
• Catecholamine secretin gtumour (often of the adrenal medulla)
• Oaroxysms of aniexty, sweating, palpitation snad hypertension
• Placental ischaemia leads to release of agents causing endothelila dysfunction, vasoconstriction and reduced pressure matriuresis resulting in hypertension
• Occurs in 7-10% of pregnancies
• Can lead to fits (eclampsia) and maternal death
• Important to monitor BP throughout pregnancy
• Excessive production of growth hormones e.g. pituitary tumour
• Occurs after fusion of epiphyseal plates
• Example → Grave’s disease (autoimmune)
• Excessive secretion of thyroid hormones
Produces hypertension through an increase in blood volume and cardiac output
What is the pathophysiology of essential hypertension:
Determinants of mean arterial pressure:
Total peripheral resistance
Cardiac output determined by
Stroke volume → Preload (CVP), afterload, contractility
Heart rate → Para/Symp
Total peripheral resistance determined by
Pathophysiology of Hypertension:
1. An imbalance between CO and TPR
2. In early stages CO seems to ne increased and TPR is normal
3. Disease progression leads to LVH that compromises diastolic filing and reduced CO
4. Change sin blood vessels leads to increased TPR
What causes elevated TPR:
1. Narrowing of the small arteries due to hypertrophy of the tunica media
2. Rarefaction, a reduction in the number of vessels per unit volume of tissue
3. Barareceptor reflex becomes reset at a higher set point. This is believed to be a consequence and not causes of hypertension.
What happens to the large elastic arteries?
1. Accelerated ageing results in elastic fragmentation and increased wall stiffness.
2. The reduced compliance results in a larger pulse pressure for a given stroke volume.
What happens to the pulse wave:
1. Steeper upslope due to reduced compliance
2. Augmentation die to bigger reflected pressure wave
3. Increased pressure wave velocity
What causes the medial hypertrophy?
2. Familial and racial tendencies indicating a genetic component.
3. Epi association with salt intake and alcohol intake indicating an environmental component
Causative theories of essential hypertension?
1. Neurogenic or stress
2. Salt imbalance/renal hypothesis
3. Depression of sodium pump in cell membranes
4. Endothelial dysfunction
5. Metabolic Syndrome (Reaven’s syndrome)
6. Cushing reflex
Neurogenic or stress
1. Excessive sympathetic response to emotional stress produces bouts of reversible hypertension
2. Repeated episodes induce hypertrophy of the tunica media
3. Some experimental evidence e.g. in laboratory animals psychogenic stress has been shown to cause hypertension.
Salt imbalance/renal hypothesis
1. An increase in arterial pressure tends to cause the kidneys to increase excretion of salt and water (pressure diuresis) until arterial pressure returns to normal
2. An imbalance between salt intake and excretion could increase ECF volume, CVP, Co and hence MAP resulting in medial hypertrophy
Depression of sodium pump in cell membranes
• There is reduced activity of the sodium pump of the red blood cell membrane in hypertensive patients
• Theory suggests there may be an increase in an endogenous digoxin-like factor that results in abnormal sodium handling and increased smooth muscle tone via knock-on effects upon calcium handling.
• 1. Vascular endothelial cells produce a number of potent local vasoactive agents
• In hypertension there is impaired production of nitric oxides and increased production of the vasoconstrictor endothelin
Metabolic Syndrome (Reaven’s Syndrome)
• Epi several cardiovascular risk factors appear to cluster together (obesity, hypertension, glucose intolerance and hyperlipedeamia)
• Proposed (and contested) that these represent a single syndrome
• Suggested final common pathway of vascular damage and hypertension
• Hyperinsulineamia can alter calcium handling in cells, produce Smooth muscle hypertrophy and increase sympathetic nervous activity
• Raised ICP reduces cerebral blood flow resulting in ischaemia of brainstem
• Icreased sympathetic tone raises TPR and in attempt to increase MAP and cerebral blood flow
• Barareceptor response to increased MAP results in increased parasympathetic tone and bradycardia
• Preterminal phase of traumatic head injury
• Could brainstem atherosclerosis result in hypertension by this mechanism
1. Weight reduction
2. Reduction in alcohol intake
3. Reduction in salt intake
4. Regular physical exercise
5. Meditation, yoga
Pharmacological treatments first time drugs
1. thiazide diuretics
3. Ca channel blockers
4. ACE inhibitors
5. All receptor blockers
Second time drugs
• Alpha blockers
• Direct vasodilators – hydralazine
• Centrally acting alpha agonists – alphamethyldopa
Malignant Hypertension: a medical emergency: epi
1. Sudden and marked rise in BP often to levels aboce 200/120
2. If untreated majority of patients will die within 6-12 months
Pathologically of malignant hypertension
there is fibrinoid necrosis of the arterioles
Malignant hypertension Characterised by
Focal neurological deficits (hypertensive encephalopathy)
Acute pulmonary oedema
Acute renal failure