EKG abnormalities, baroreceptors, chemoreceptors Flashcards Preview

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Flashcards in EKG abnormalities, baroreceptors, chemoreceptors Deck (16):

What is torsades de pointes?

this is an polymorphic ventricular tachycardia that can progress to ventricular fibrillation. EKG shows sinusoidal waveforms. long QT predisposes people to torsades de pointes.


What drugs can cause torsades de pointes?

Some Risky Meds Can Prolong QT:
sotolol, risperidone/antipsychotics, chloroquine, macrolides, quinilone and classe Ia and class III antiarrhythmics, thiazides


What electrolyte abnormalities can predispose to torsades de pointes?

low Mg or low K


Treatment for torsades de pointes?

magnesium sulfate


Why is congenital long QT syndrome bad? What is the usual defect in congenital long QT?

it can predispose the patient to torsades de pointes and sudden cardiac death.
usually due to defects in ion channels.


What two common causes of congenital long QT syndrome?

romano-ward: Autosomal dominant type with only cardiac manifestations
Jervell and Lange-Nielsen: autosomal recessive type that also has sensorineural deafness


wolf-parkinson-white: what is the problem? EKG findings? Complication?

there is a fast track between the atria and the ventricles that bypasses the AV node. this causes early depolarization of the ventricles, so you see a delta wave (slow rising up to r wave instead of a normal q wave). may predispose people to reentry circuits and supraventricular tachycardia.


What are the 2 types of second degree heart block?

Mobitz type 1/Wenckebach: progressive lengthening of the PR interval until a beat is dropped. usually asymptomatic
Mobitz type II: dropped beats that aren't preceded by a change in the length of the QR interval, or a 2:1block with 2 or more p waves to each QRS response. often treated with a pacemaker because the block is below the AV node.


What is 3rd degree heart block?

atria and ventricles beat independent of each other. atrial rate faster than ventricular rate. lyme disease can cause 3rd degree heart block.


atrial naturietic peptide

released from ATRIAL MYOCYTES in response to incr. blood volume and pressure.
causes vasodilation and decr. Na resorption in the renal collecting tubule. constricts efferent renal arterioles and dilates afferent arterioles via cGMP- promoting diuresis (and contributing to "aldo escape" mechanism)



brain-type natriuretic peptide
released from VENTRICULAR myocytes in response to incr. tension. similar to ANP with longer half life. used for diagnosing heart failure with good negative predictive value. available in recombinant form for tx of heart failure.


carotid sinus vs. aortic arch receptors: location, what the respond to, innervation

aortic arch transmits via vagus to nucleus solitarious of the medulla. it ONLY responds to incr. BP
carotid sinus is at the dilated region of the carotid bifurcation transmitts via glossopharyngeal nerve to solitary nucleus. it responds to both incr. and decr. BP


carotid massage

incr. pressure on carotid sinus causes incr. stretch and icnr. afferent baroreceptor firing (?). this incr. AV refractory period and decr. HR


What is the Cushing reaction and how is it related to baroreceptors?

response to increased intracranial pressure. it causes hypertension, respiratory depression, and decr. HR.
incr. pressure --> constricted arterioles --> cerebral ischemia and reflex incr. in perfusion pressure --> HTN. HTN causes incr. stretch, an d baroreceptors respond with decr. HR. this causes resp. depression.
often suggests imminent hernaiation


What are the peripheral chemoreceptors? What stimulates them?

carotid and aortic bodies are stimulated by decr. pO2 (less than 60 mmHg), incr. PCO2, and decr. pH


What are the central chemoreceptors? What stimulates them?

stimulated by changes in pH and pCO2 of brain interstitial fluid, which are both obviously influenced by arterial CO2. the don't respond directly to PO2