Pathology of Hypertension Flashcards Preview

Cardiovascular Block > Pathology of Hypertension > Flashcards

Flashcards in Pathology of Hypertension Deck (21)
Loading flashcards...

Risk Factors for Primary HTN

Family History
Reduced nephron number
High sodium diet
Excessive alcohol consumption
Physical inactivity
Diabetes and dyslipidemia
Personality traits and depression


Consequences of HTN

Asymptomatic: pre=HTN and established HTN

Oligosymptomatic: proteinuria, L ventricular hypertrophy, retinopathy

Symptomatic: CKD, A fib, systolic/diastolic dysfunction, coronary artery disease, dementia, TIA

Polysymptomatic/End Stage: end stage renal disease, ventricular tachycardia/fib, CHF, MI, and stoke


Primary vs. Secondary HTN

Primary (Essential) Hypertension
No identifiable cause
The most common form of HTN 90%
Tends to develop gradually over many years

Secondary Hypertension
Caused by an underlying medical condition
CKD, OSA, RAS, Hyperaldosteronism etc.
Tends to appear suddenly
BP’s are generally higher


Resistant Hypertension

A BP that remains above the goal in spite of:
compliance with maximum doses of 3 antihypertensive medications from different classes, ideally including a diuretic
BP Controlled but requires 4 or more medication
Reversible causes identified and addressed


Accelerated and Malignant HTN

Accelerated Hypertension
Severe HTN with recent progression in the presence of retinal hemorrhages and exudates
Without papilledema

Malignant HTN - 1928
Severe HTN with CNS involvement (papilledema)
Long-term prognosis much improved


HTN Urgency vs. Emergency

Hypertensive Urgency
Acute rise in BP with severe HTN
SBP > 180 mmHg
DBP > 110 mmHg
Without acute end-organ damage

Hypertensive Emergency
Acute rise in BP with severe HTN
SBP > 200 mmHg
DBP > 130 mmHg
With acute ongoing end-organ damage
Aortic dissection, heart failure
Stroke, renal failure, papilledema

Depends on the clinical state of the patient NOT the absolute level of blood pressure
Rapid rise in BP more important


White Coat Effect

White-coat resistance may be present in patients with consistently significantly elevated BP but no evidence of target organ damage

How to Screen:
Consider repeated at-home BP measurements to rule out white-coat resistance
Where available, 24-hour ambulatory BP monitoring (ABPM) may be used for further diagnostic evaluation


Automated BP

Automated office BP measurement has several advantages:
Minimizes potential for user error
Enables efficient collection of multiple BP readings
Reduces patient anxiety and aids in detection of white-coat effect
Average of 5 BP readings taken 1 minute apart, while patient is alone in room, has been shown to approach average waking BP

Home BP measurement is a useful tool:
Average of as few as 6 readings may achieve similar accuracy for measurement of true ambulatory BP as ABPM
May improve adherence to the treatment regimen
Affordable and accessible

Patients should be trained in proper BP measurement technique
Patients should utilize validated monitors to ensure accuracy (wrist or finger cuffs should be avoided)
Patients should bring new devices to clinic to confirm accuracy


Pathogenesis of BP

Maintenance of arterial BP is necessary for organ perfusion

Arterial BP = CO x SVR
(HR x Stroke Volume) x Vasoconstriction

Think of the components as:
HR = Heart and nervous system
SV = Kidneys (size of vascular compartment)
SVR = Arteries/arterioles


Kidneys and BP

The kidney is a central regulator of the electrical, chemical, and mechanical, forces that control BP

Electrical: SNS and Brain
Chemical: RAAS, Cytokines, and Neurohormones
Mechanical: HR, vasodilation/constriction, volume control

Kidney impairment or dysfunction = increase in afferent activity, which amplifies central, or systemic sympathetic outflow
Causes HTH, LVH, ventricular arrhythmias, and sudden cardiac death


Primary Electrical Component of BP

Primary electrical component of BP control is the sympathetic nervous system (SNS)

The SNS is part of the body’s autonomic nervous system
Operates without conscious control

The SNS connects the brain, heart, blood vessels, and kidneys, each of which plays an important role in the regulation of BP


Secondary HTN Clues

Young age of onset
Sudden onset
HTN Emergency/End organ damage

Features of a recognized underlying cause:
Flash pulmonary edema – normal EF ?
Moon facies, truncal obesity, hirsutism and striae = Cushing's
Elevated Cr (>30%) after ACE/ARB?
Episodic headache, sweating and tachycardia = drug use or pheochromocytoma
Asymmetric renal size?

Hyperaldosteronism, renal artery stenosis, and Cushing’s are the big three


Obstructive Sleep Apnea and HTN

Coexistence of HTN and OSA is observed in 30% patients
OSA is common in patients with resistant HTN
Cross sectional studies indicate that the more severe the sleep apnea, the less likely BP is controlled despite increasing number of medications

Mechanism of HTN:
Hypoxemia = ↑ SNS activity = ↑CO and SVR

CPAP effect on BP is modest but significant:
~ 2 mmHG, much larger in some patients


Target Organ Damage – Triage

Brain: Stroke or Encephalopathy

Heart: decompensated heart failure, aortic dissection, acute coronary syndrome

Kidneys: acute renal failure


Arteriole Diameter: Pressure and Resistance

Flow = Pressure/Resistance

As pressure goes up the resistance must go up to maintain it
From MAP of 45-145 can maintain, but once pressure goes up too much it cannot maintain as well past a point


Cerebral Autoregulation

Normotensive to Hyperperfusion: girl that is used to having normal BP and then pregnancy causes BP to rise and get symptoms because sudden change

HTN: blood vessels get good at resisting high pressure and will be asymptomatic because used to it


Posterior Leukoencephalopathy

Edema predominately of the white matter of
the parieto-occipal regions and post. fossa

Brain is trapped and cannot adapt as well
Usually reversible and better prognosis than stroke or bleed


Retinopathy Findings

The optic disc is swollen with indistinct borders
Venous tortuosity with multiple cotton wool spots
Flame-shaped hemorrhages
Punctate hemorrhages


Secondary HTN and Emergencies

Suspect secondary HTN in ALL cases of hypertensive emergency

Atherosclerotic Renal Artery Stenosis
Suspect with HTN Emergency and Flash pulmonary edema


Drug Interactions

Certain medications or other drugs may cause elevated BP or inhibit the effects of antihypertensive medications:
NSAIDs and cyclooxygenase-2 (COX-2) inhibitors
Sympathomimetic drugs (ephedra, phenylephrine, cocaine, amphetamines)
Herbal supplements
Anabolic steroids
Appetite suppressants
Oral contraceptives


Mechanisms of Action of Major Medication Classes

ACEIs: decrease production of angiotensin II

ARBs: bind and block the angiotensin AT1 receptor

DRIs: directly inhibit renin

β-blockers: reduce renin release

Diuretics: inhibit water and sodium retention

CCBs: dilate arteries and reduce peripheral resistance

α-blockers: block vasoconstrictor effects of NE

Centrally acting agents: act on the hypothalamus to reduce sympathetic outflow