Pathology of Hypertension Flashcards
Risk Factors for Primary HTN
Age Obesity Family History Race 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
Considerations:
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
Uncontrolled/refractory
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?
Hypokalemia?
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
