Hypertensive- Shock Flashcards Preview

Term 5 - PathoPhysio > Hypertensive- Shock > Flashcards

Flashcards in Hypertensive- Shock Deck (16):

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Coarctation of the Aorta:

  • Congenital narrowing of the aorta distal to the origin of the left subclavian artery
  • Blood pressure is elevated in the arms, head, and chest but lowered in the legs
  • Because of low renal blood flow, plasma renin level is increased
  • Stimulation of Renin-angiotensin-aldosterone system in a positive feedback manner
  • Elimination of the constriction by resecting the narrowed segment of the aorta usually cures the condition

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Renal causes for hypertension:

  1. Constriction of one or both renal arteries 
  2. Tumors of the renin-secreting juxtaglomerular cells 
  3. Ureteral obstruction: Increase in renal interstitial pressure and stimulation of renin secretion  
  4. Acute and chronic glomerulonephritis:
    • a) Activation of RAAS and/or
    • b) ECF volume expansion due to abnormal salt and water handling by the kidneys.
  5. Liddle's syndrome: a condition in which there is abnormal Na+ retention due to over-activation of the epithelial sodium channels (ENaC)


Liddle’s syndrome

  • Young patient presenting with high BP
  • H/O family members with early onset severe hypertension
  • Autosomal dominant transmission
  • Suppressed renin
  • Suppressed aldosterone
  • Abnormality of epithelial sodium channels (ENaC) in distal nephron


Adrenal Gland Disorders:

  1. Conn’s syndrome (primary hyperaldosteronism) -
  2. Excess secretion of cortisol (Cushing’s syndrome) -
  3. Hypersecretion of deoxycorticosterone (DOC) in congenital adrenal hyperplasia
  4. Glucocorticoid remediable aldosteronism (GRA): An autosomal dominant disorder in which ACTH produces prolonged hypersecretion of aldosterone as well as glucocorticoids. The genes encoding aldosterone synthase and 11-hydroxylase are 95% identical and located close together on chromosome 8 
  5. Pheochromocytoma - disorder of adrenal medulla.


HTN related to Insulin Resistance:

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Clinical Presentation of HTN:

  • The hypertensives present with:
    • Myocardial infarction
    • Congestive heart failure 
    • Strokes of thrombotic and hemorrhagic origin 
    • Hypertensive encephalopathy 
    • confusion, disordered consciousness, and seizures 
    • Renal failure


Physical findings in HTN:

  • Observable changes are generally found only in advanced cases. These include:
  • Left ventricular hypertrophy and cardiac enlargement and a loud S2
  • Bruits in the renal artery on auscultation
  • Hypertensive retinopathy - narrowed arterioles seen on funduscopic examination; retinal hemorrhages and exudates along with papilledema


Venous return (VR)

  • Venous return is the amount of blood received by the right atrium per minute
  • In normal person, it is same as cardiac output (5 L/min)
  • The pressure gradient between the right atrium and the peripheral veins is the driving force for VR
  • Higher the gradient, greater will be the venous return;
  • Lower the gradient, less will be the venous return
  • Factors that increase this gradient improve VR
  • Factors that increase venous return are:
    • Negative intrathoracic pressure
    • Increase in total blood volume (preload)
    • Contraction of skeletal muscles
    • •Increase in vascular tone of systemic veins


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The factors that change the cardiac and vascular function curves

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  • Immediate effect of reduced contractility: (Point B)
    • There is a reduction in CO; This soon changes due to the compensatory changes in the heart
  • Compensated failure: (Point C)
    • Blood volume expansion has partially restored the CO by Starling’s mechanism; This gradually progresses to massive volume expansion
  • Decompensated failure: (Point D)
    • As failure progresses, there is severe reduction in contractility despite extreme increase in preload due to overstretching of ventricle.
  • At this point, increase in preload is harmful to heart!

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