FUCK PART 2 Flashcards by Claire Jamieson | Brainscape

Q

alcoholism and peripheral neuropathy

-which nutrients

A

-nutrient not absorbed: B12, B6, B1 (thiamine), folic acid

toxic ethanol

impaired blood flow

inflammation

ROS

metabolic- glucose and insulin resistance

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Q

EEG in sleep measure

A

dont measure AP directly; instead measure different in potential and cell body

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Q

waves from high frequency to low frequency (and kind of lower amplitude to higher amplitude)

A

BATD

beta= 13-30Hz
alpha= 8-18Hz
theta= 4-8Hz
delta= 0.5-4Hz

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Q

beta

A

eyes open, awake, concentrate

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Q

alpha

A

eyes closed, relaxed

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Q

theta

A

light sleep

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Q

delta

A

deep sleep

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Q

alpha block/ alerting response

A

alpha –> beta when focus

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Q

which sleep stages have large axial movements and which have no movement

A

move= NREM

no move= REM

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Q

eye movements in sleep stages

A

N1= eye slow roll
rest of NREM= no eye move
REM= rapid

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Q

N1

A

transition from sleep to wake

theta

slow and rolling eye movement

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Q

N2

A

light sleep

K complexes and sleep spindles

no eye movement

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Q

N3

A

deep sleep

delta

thalamus and cortex

minimal eye movement

less if old

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Q

kids sleep

A

50/50 REM and N3

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Q

REM

A

rapid eye movement

no MSK movement (bc GABA)

recall dreams

last sleep stages

theta but NOT synchronized

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Q

sleep architecture

A

1st period is longest, rest are 90-120 mins

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Q

arousal system

A

locus coreulus- NE
raphe nucleus- serotonin
tubermamillary body- histmaine
Ach- many brainstem nuclei
dopamine- periaqueductal gray

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Q

ventrolateral pre optic nucleus (VLPO) release which neurons

A

GABA and galanin

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Q

2 REM states from VLPO

A

REM on= lateral pontine
REM off= pons

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Q

stabilizing nuclei (lateral hypothalamus) in sleep

A

orexin: activate arousal, inhibit VLPO

melanin concentrating hormone (MCH): inhibit arousal

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Q

2 drivers of sleep

A

circadian rhythm
homeostatic signal: adenosine build up
-caffeine is A2a antagonist

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Q

REMon vs REMoff stimuli

A

REMon stimulated by cholinergic input

REMoff stimulated by NE, serotonin, orexin

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Q

melatonin is made where? metabolite of?

A

made in pineal gland

metabolite of serotonin

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Q

dark and light effects an melatonin

A

dark: PVN activates SNS –> release NE and activate pineal gland –> melatonin –> SCN

light: SCN inhibits PVN

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Q

steps to make melatonin

A

tryptophan –> serotonin 5 HTP [[AANAT]] –> N-acetylserotonin [[HIOMT]] –> melatonin

NE (catecholamines) act on beta 1 receptor to make AANAT

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Q

entrain SCN

A

retinohypothalamic fibers relay light

MT2 melatonin receptors

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Q

MT melatonin receptors

A

MT1 decreases sleep latency

MT2 increases sleep time

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Q

narcolepsy

A

excessive daytime sleepiness

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Q

what sleep stage does narcolepsy effect

A

REM intrusion: cataplexy (weak muscle), sleep paralysis, hallucination

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Q

type 1 narcolepsy

A

narcolepsy + cataplexy

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Q

cause of narcolepsy + cataplexy

A

loss of orexinergic neurons (autoimmune, molecular mimicry via strep or infection)

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Q

hypnagogic vs hypnopompic hallucinations in narcolepsy? more common?

A

hypnagogic; while going to sleep

hypnapompic; while awaken (more common)

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Q

what happens in sleep stage or narcolepsy

A

enter REM quickly

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Q

treat narcolepsy

A

antidepressants to increase NE and serotonin and stimulate REMoff

since loss orexinergic neurons and enter REM quickly

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Q

restless leg syndrome and periodic limb movement disorder

A

RLS: when awake? need to move legs, triggered by rest, inactivity, sleep

PLMD: occurs during sleep, kick legs

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Q

RLS and PLMD are? effect which brain area

A

movement disorders- basal ganglia and substantial nigra

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Q

causes of RLS and PLMD

A

iron deficient

increased/ abnormal dopamine

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Q

treat RLS and PLMD

A

with dopamine agonist (even though increase DA in day its decreased at night)

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Q

Obstructive sleep apnea

A

> 5 OA or hypopnea episode in 1 hour

> 15= severe

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Q

apnea vs hypoapnea

A

apnea= no air for >10 secs

hypoapnea= >30% reduction in airflow for 10 secs

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Q

what sleep stage is OSA worse in

A

REM

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Q

causes of OSA

A

pharyngeal collapse from negative pressure

obesity, male

co2 sensitivity

septal deviation or nasal polyps

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Q

diagnose OSA

A

polysomnogram

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Q

parasomnia

A

abnormal behaviour that Arise from or during sleep

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Q

types of parasomnias

A

sleep walking
sleep terrors
REM sleep behaviour disorder

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Q

who and what sleep stage does sleep walking and sleep terrors happen in

A

N3, kids

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Q

sleep walking and sleep terrors

A

SW: N3, early evening

ST: scream, N3, tachycardia, hyperventilate

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Q

REM sleep behaviour disorder (parasomnia)

A

act out dreams; kick, punch

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Q

who does REM sleep behaviour disorder happen in

A

older

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Q

REM sleep behaviour disorder from

A

neurodegeneration of interneurons that cause paralysis in REM

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Q

HIV and peripheral neuropathy

A

-distal symmetric
-inflammatory demyelinating polyradiculoneuropathy
-AIDS drugs can cause toxic neuropathies
-CD8+

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Q

chemotherapy induced peripheral neuropathy

A

glove and stoking

platinum [ ] in tissue

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Q

shingles cause

A

herpes varicella zoster

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Q

shingles and peripheral neuropathy

A

latent; post herpetic neuralgia

dermatomes

infect perineurial satellite cells

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Q

triad of Lyme disease and peripheral neuropathy

A

cranial nerve palsy

radiculitis

aseptic meningitis

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Q

A

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Q

what are causes of acute pericarditis

A

viral-coxackie A and B, echovirus and idiopathic most common

strep, staph, TB, RA, SLE

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Q

what makes pain in acute pericarditis better

A

sitting up and leaning forward

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Q

acute pericariditis

A

common, fibrinous inflammation

pericardial friction rub

increased ECF= pericardial effusion

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Q

diagnose acute pericariditis

A

echocardiography

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Q

prognosis of acute pericaridits

A

self resolve or NSAID, aspirin

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Q

complication of acute pericarditis

A

cardiac tamponade, progress to constrictive pericarditis

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Q

constrictive pericarditis

A

pericardium scars after acute pericarditis

restrict cardiac filling

decrease end diastolic volume, venous congestion, fatigue, neck vein distended, hepatosplenomegaly

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Q

pericardial tamponade (complication of acute pericarditis)

A

accumulate fluid, obstruct flow to ventricles

can cause obstructive shock

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Q

myocarditis can lead to

A

dilated cardiomyopathy, conduction blocks

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Q

causes of myocarditis

A

echovirus, coxsackie, Lyme, tryponosmitatis cruzi, SARS CoV2, rickets

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Q

pathophysiology in myocarditis

A

adaptive immune response: form granuloma, release cytokines, alter ECM, fibrosis and dialtion

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Q

mehcanism in bacterial endocarditis

A

vegetation + thrombus

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Q

what part of the heart does bacterial endocarditis involve

A

valve

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Q

pathophysiology in bacterial endocarditis

A

form thrombus –> bacteria colonize it –> break off and cause stroke or obstruction

vegetation: mass of platelets, fibrin etc. –>break off and spread

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Q

causes of bacterial endocarditis

A

from bacteria: dental/ gingival

bad, acute: strep, staph, enterococcus

less bad, slow: HACEK

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Q

symptoms of bacterial endocarditis

A

fever, anorexia, heart murmur, splenomegaly, myalgia…

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Q

infective endocarditis key findings

A

osler nodes, janeway lesions, roth spots

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Q

Lyme disease is caused by

A

barrelia burgdoferi

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Q

Lyme disease need

A

a réservoir animals

baby ticks (nymphs) better at transmitting disease

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Q

Lyme disease binds what proteins in the body

A

complement regulatory proteins

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Q

2 stages of Lyme disease

A

stage 1: erythema migrans rash

stage 2: effect many organs via blood vessels –> myocarditis, CNS, joints, arthritis

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Q

Lyme disease can cause inflammation in what

A

myocarditis

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Q

diagnose lyme

A

2 tiered serological testing and EISA immunoblot test

antibodies so dont know if past or current infection

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Q

endocarditis microbes virulence factors - strep

A

strep have dextrans to adhere to thrombotic vegetation or valve damage
-bind platelet fibrin complexes
-fimA

fibronectin is usually hidden by endothelium, but exposed by strep

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Q

virulence factors in strep (bacterial endocarditis)

A

dextrans and fimA and mucopolysaccharide biofilms

also exposes fibronectin

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Q

endocarditis microbes virulence factors - s aureus

A

produce tissue factor to build clots, invade vegetations

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Q

endocarditis microbes virulence factors - HACEK

A

in oral cavity to blood stream via floss or dental work

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Q

what entrains clock genes

A

zeitgebers: light/dark, food, exercise

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Q

clock genes synchronized to 24 hours via

A

-synchronized to 24 hours via melatonin

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Q

clock genes for the intrinsic rhythm of

A

the rest of the body NOT the SCN

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Q

melatonin is carried by

A

albumin

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Q

melatonin paracine signal to the

A

retina

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Q

melatonin increases antioxidant enzyme

A

superoxide dismutase and glutathione peroxidase

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Q

what does melatonin block

A

block Bax proapoptotic and caps 3

inhibit COX and prostaglanding= anti-inflammatory

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Q

melatonin as analgesic

A

decrease pain via MT1 and MT2

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Q

melatonin is localized in the

A

mitochondria

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Q

sleep deprivation and mens and Womens health

A

decrease testosterone

follicular fluid- ROS and infertile (melatonin is protective)

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Q

what hormones increase and decrease in sleep

A

increase: TSH, GH, prolactin

decrease: cortisol, NE, E

melatonin suppressed GnRH (puberty?)

Q

melatonin and immune response

A

Th1 response

NK

Q

diet and sleep

A

high fat diet changes clock genes

Q

hypothyroid and peripheral neuropathy

distal or proximal?
axonal degeneration or myelin desegmentation?

A

proximal myopathy and carpal tunnel

primary axonal degeneration

Q

how does hypothyroid cause peripheral neuropathy

A

weight gain and water retention, mucopolysaccharides, hyaluronic acid

energy deficit from nutrient oxidation: decease ATP, accumulate glycogen, decrease Na+/K+ pump

Q

Hepatitis B or C more common in peripheral neuropathy

A

Hepatitis C

Q

what does hepatitis C have for peripheral neuropathy

A

cyroglubulimenia (a protein leading to vasculitis)

Q

mechanisms of hepatitis B and C (autoimmune) and peripheral neuropathy

A

-directly invade liver and nerves

-liver metabolizes drugs and toxins

-B12 and folate deficiency from chronic liver disease

Q

leprosy is caused by

A

mycobacterium leprae

Q

leprosy affects peripheral neuropathy via

A

direct nerve damage

Q

3 types of leprosy

A

-tuberculoid leprosy
-lepromatous leprosy
-borderline leprosy

Q

tuberculoid leprosy and peripheral neuropathy

A

asymmetric, around skin lesion

Q

lepromatous leprosy and peripheral neuropathy

A

extensive bilateral symmetric distal

Q

borderline leprosy and peripheral neuropathy

A

severe

Q

most common leprosy that causes peripheral neuropathy

A

borderline leprosy

Q

seizures are

A

an electrical disturbance

Q

types of serizures

A

focal seizure

generalized seizures (tonic clonic, absence etc)

Q

focal seizures

A

1 region of brain effected

EEG shows epileptiform spikes (medial temporal or inferior frontal lobe)

Q

types of focal seizures (1 region of brain)

A

-intact or impaired awareness (impaired= cant respond to environment, automatic behaviour)

-motor or non motor

Q

generalized seizures impact

A

both hemispheres of the brain

Q

typical absence seizures vs atypical absence seizure

A

typical = brief loss of consciousness but not posture, common in kids, looks like “blanking out”

atypical= longer loss of consciousness

Q

tonic-clonic seizures cause

A

metabolic

Q

common type of seizure

A

tonic-clonic seizure

Q

tonic-clonic seizure

A

contract for 10 seconds then relax for 1 minute

post-ictal phase: unresponsive, flaccid, incontinence

Q

atonic seizures vs mycolonic seizure

A

atonic; lose muscles for 1 second

mycologic; brief muscle contraction

Q

epileptic spasm (seizure)

A

in infants, flex or extend trunk and proximal

Q

epileptogenesis

epileptogenic factors

precipitating factors

A

epileptogenesis: make brain tissue hyperexcitable

epileptogenic factors: lower seizure threshold

precipitating factors: trigger seizure

Q

spread activations in seizures (hyper excitable)

A

increase K+, RMP higher

accumulate Ca2+

activated NMDA receptor, increase Ca2+

Q

epilepsy effects sleep

A

decrease REM, change NREM

Q

taenia is a

A

tapeworm

Q

tania tapeworm from

A

raw meat; pass in stool

Q

taenia tapeworm invades

A

invades the intestinal wall and muscles and brain

Q

2 types of invasions by Tania tapeworm

A

cysticerosis
neurocysticerosis

Q

cysticerosis
neurocysticerosis

from taenia tapeword

A

cysticerosis- muscle infected

neurocysticerosis- brain infected, common in low income countries

Q

neurocysticerosis from taenia tapeworm impacts the brain

what is the polymorphism

causes

A

MMP polymorphism increase BBB permeability

major cause of seizures

Q

what causes sleeping sickness

A

trypanosoma bruceli (tse tse fly)

Q

trypanosoma bruceli (tse tse fly) and sleeping sickness

common in

lasts how long

symptoms

diagnose

impact on sleep

A

S.S Africa

last 3 years, fatal

fever, headaches

invade CNS, disturb sleep and cause neuropsyhiatric disorders

diagnose: CSF

no change in sleep time: increase daytime sleep, and nighttime insomnia (like narcolepsy)

Q

what is around a single nerve fiber

A

endoneurium

Q

vitamin B12 deficiency neuropathy

antibodies target what?

GI symptoms

A

pernicious anemia- cobalamin defieicny

antibodies target parietal cells and decrease intrinsic factor

atrophic gastris and achlorhydria

Q

B12 defiant and what thing

A

decrease intrinsic factor

Q

B12 is need for what 2 cycles

A

1 carbon cycle: b12 as coenzyme for homocysteine –> methionine for RNA and DNA

myelin synthesis: methylmalonyl coA –> succinyl coA

Q

what can cause b12 deficiency

A

nitrous oxide

Q

which fibers are effected in b12 deficient neuropathy

A

large fibers

small fibers are OK

Q

signs in B12 deficient neuropathy

A

bad gait, hyperreflexia, absent achilles reflex

hand goes numb 1st

Q

2 types of degeneration that cause peripheral neuropathy

A

axonal degernation and segmental demyelination

Q

% of peripheral neuropathy caused by axonal degeneration vs segmental demyelination

A

90% axonal
10% demyelination

Q

2 types of axonal degenration

A

distal axonal degeneration

neuronopathy

Q

what is the mechanism in distal axonal degeneration

A

wallerian degeneration; degeneration after area of compression/ injury

Q

distal axonal degeneration

A

distal part, neruon cell body and proximal axon are spared

wallerian degeneration

Q

neuronopathy (a type of axonal degeneration)

A

degeration of neuron cell body and axon (i.e. autoimmune)

Q

segmental demyelination

A

myelin sheath detonates, underlying axon is ok

hereditary or immune

macrophages remove the debris

recovery and remyeliantion via Schwann cells but decreased internodal length

Q

types of segmental demyeliantion

A

primary demyelination: injure Schwann cells or myelin sheath

secondary demyelination: underlying axon abnormality

Q

hypertrophic neuropathy (from segmental demyelination)

A

repeated demyelination and remyelination = accumulate supernumerary Schwann cells= onion bulb

Q

large vs small sensory fibers

A

large= proprioception and vibration

small= pain and temperature

Q

peripheral neuropathy causes

A

metabolic: DIABETES, thyroid

B12 defieint

systemic: HIV, Lyme, hepatitis, leprosy

toxic, alcohol, chemotherapy

Q

types of peripheral neuropathy

A

polyneuropathy= symmetrical

radiculopathy/polyradiculopathy= asymmetrical

mononeuropathy= 1 nerve

multiple mononeuropathies (mononeuropathy multiplex)

plexopathy= brachial or lumbosacral plexus; 1 limb

neuronopathy= nerve cell body, ganglion cells, proximal and distal

Q

diabetic neuropathy what type of neuropathy

A

usually distal symmetric stocking and glove but could be many

Q

pathway in diabetic neuropathy

A

polyol pathway

Q

poll pathway and diabetic neuropathy

A

high blood sugar >7mmol activates the poly pathway

glucose into sorbitol via aldose reductase and NADPH

Q

immune and vascular problems in diabetic neuropathy

A

immune: antiphospholipid antibodies

vascular: decrease NO, decrease Na+/K+ ATPase, decrease free carnitine and myoinostiol, increase homocystinemia

Q

anti-arrhythmic medications

A

prevent Na+ influx
beta blockers
block K+; prolong refractory
block Ca2+

Q

cardiac ischemia findings on ECG

A

inverted T wave
ST elevation

Q

3 types of conduction block

A

1 2 and 3 degree

Q

1st degree AV conduction block

A

prolonged PR, asymptomatic, increased vagal tone of fibrous

Q

two types of 2nd degree AV conduction block

A

type 1 (wenckebach): progressive prolong of PR until QRS is dropped

type II: consistent PR, QRS suddenly drops, more serious –> progress to 2rd degree and cardiac arrest

Q

3rd degree AV conduction block

A

no impulse from atria reach ventricles

bradycardia, heart failure, syncope, decrease CO

regular P and QRS, but not coordinated, slow HR

Q

ECG findings in all conduction blocks

A

1st degree= prolong PR

2nd degree type I= progressively prolong PR until QRS dropped

2nd degree type II= consistent PR, QRS suddenly drops

3rd degree= regular P and QRS but not coordinated

Q

% of primary vs secondary hypertension

A

90% primary
10% secondary

Q

mechanism in primary hypertension

A

increased tone and resistance in arterioles, release less NO, arteroscleosis (deposit ECM, hypertrophy)

vascular changes in kidney (regulate BP)

increase SNS: alpha 1 vasoconstriction, increase ADH, increase renin and AT 2

increase WBCs to kidneys

increase Na+ –> Th17 and ILC3

insulin resistance and obesity

Q

what are the systems most frequently impacted in secondary hypertension

A

kidneys and SNS

also OSA, medication, endocrine…
hyperthryoid= increase SBP
hypothyroid= increase DBP

Q

diagnosis of hypertesnion

A

> 180/110 = immediate diagnosis

automated: >135/ 85 or >130/80 if diabetic

in office: >140/90

Q

hypertensive urgency

A

systolic >180 or diastolic >120

Q

hypertensive emergency

A

end organ damage

Q

malignant hypertension

A

> 180/120, end organ damage, fibrinoid necrosis

Q

antihypertensive medications

A

-Ca2+ channel blockers

ACE inhibitors: decrease angiotensin and vasoconstriction and stop ACE from desrtroying bradykinin (so bradykinin can increase and increase NO to vasodilate)

AT2 receptor (ARB) blockers

alpha receptor blockers: decrease NE and E

Q

type of reaction in vasculitis? immune?

A

inflammation and necrosis

Th1/ Th17

type III hypersensitivity reaction: immune complex

Q

secondary vasculitis

A

hepatitis, autoimmune, medications

Q

types of vasculitis

A

temporal arteritis
polyarteritis nodosa
thromboangitis obliterans
granulomatous with polyangitis

Q

most common type of vasculitis, especially in elders

A

temporal arteritis

Q

temporal arteritis affects

A

large arteries

Q

pathology in temporal arteritis? arteries effects? symptoms?

A

patchy granulomatous, caroitd artery branches: temporal and ophthalmic

temporal headache, vision loss, poly myalgia rheumatica

Q

diagnosis and treatment of temporal arteritis

A

diagnose: ESR/CRP, ultrasound of temporal artery

treat: glucocorticoids

Q

polyarteritis nodosa cause

A

hepatitis B

Q

polyarteritis nodosa effects

A

medium and small arteries

Q

ogans in polyarteritis nodosa

A

many organs, but rarely lungs

kidney (increase BP)
MSK (arthritis, myalgia)
peripheral neuropathies (mono multiplex)

Q

skin findings in polyarteritis nodosa

A

raynauds
pupura and nodules

Q

raynauds in which vasculitis

A

polyarteritis nodosa

Q

Thromboangitis obliterans effects the

A

medium and small arteries

Q

who is thromboangitis obliterans most common in

A

men, smokers

Q

thromboangitis obliterans presentation

A

distal arm and leg –> occlusion and ischemia –> ulcers and claudication

Q

vessels impacted by granulomatous with polyangitis

A

small and medium arteries and veins

Q

granulomatous with polyangitis symptoms

A

URTI, LRT, kidney: sinus, dyspnea, renal failure

flaring disease

Q

diagnose granulomatous with polyangitis

A

cANCA

Q

what are ANCAs

A

anti-neutrophil cytoplasmic antibodies

increase cell surface expression in inflammation

Q

p-ANCA and c-ANCA

A

p-ANCA: nucleus, bind myeloperoxidase

c-ANCA: cytoplasm, bind proteinase 3

Q

Raynauds presentation

A

bilateral, asymmetric ischemia of fingers and toes

rarely ulcers or gangrene

Q

raynauds cause

A

transient vasopasm

Q

raynauds worse with

A

cold and stress

Q

raynauds and autoimmune

A

lupus

Q

3 phases of raynauds

A

vasoconstrict (white)
cyanosis (blue)
hyperemia (red) - blood flow restored

Q

SA node location

A

right atrium, near vena cava

Q

heart rate is found on ECG by

A

R-R interval

300/ # of boxes

Q

rhythms on ECG

A

regular
regularly irregular
irregularly irregular (atrial fibrilation)

Q

normal sinus rhythm criteria

A

SA as pacemaker
regular or regularly irregular

each P wave followed by QRS
each QRS has a P wave before
constant PR interval
QRS <100ms (2.5 boxes)

Q

long PR interval=

A

AV node dysfunction

Q

QT varies with

A

heart rate

Q

QT corrected

A

QTc = QT/ (square root of R-R)

Q

abnormal Q wave

A

MI

Q

ST segment pathology

A

elevated: STEMI, hyperkalemia, RBBB

depressed: NSTEMI, hypokalemia, LBBB

Q

T wave problems

A

tall: hyperkalemia
small: hypokalamie
inverted: MI, ventricular hypertrophy

Q

P wave problems

A

-different pacemaker if it changes beat to beat

-absent= atrial fibrillation

-more P waves than QRS= heart block

Q

3 causes of dysrhythmias

A

re-entry
ectopic foci or abnormal automaticity
triggered activity

Q

re-entry

A

normal depolarization enters ischemia area and cant contract –> slower conduction

if complete refractory then depolarize= tacchycardia

area of fast and slow conductance

Q

ectopic foci or abnormal automaticity

A

increase Ca2+ decrease K+

scar tissue changes electrolytes (inhibit Na+/K+ - accumulate Na+/Ca2+)

make non-pacemaker cells automatic= ectopic foci

IR K+ = decrease refractory period

Q

triggered activity

A

normal AP then abnormal ventricular depolarization before AP complete

i.e. premature ventricular contractions

Q

most common type of dysrhythmia

A

atrial fibrillation

Q

atrial fibrillation has ___ p wave

A

no

Q

what dysrhythmia is the leading cause of stroke

A

atrial fibrillation

Q

atrial fibrillation findings

A

ectopic foci, re-entry

irregular irregular HR

Q

atrial flutter

A

re-entry bc of fibrosis

atrial rate 300bpm

Q

sinus tachycardia

A

increase HR and CO

from exercise, stress, excess catecholamine OK, bad if at rest

Q

paroxysmal supraventricular tachycardia

A

at atria or AV node

re-entry

Q

premature ventricular contraction- what is it initiated by

A

heartbeat from the purkinje fibers

Q

premature ventricular contraction on an ECG

A

wide QRS; single, double, triple

Q

premature ventricular contraction - what dysrhythmia

A

ectopic nodal automaticity, triggered activity, re-entry

Q

idioventricular rhythm - what on an ECG

A

no p wave, prolonged QRS

Q

idioventricular rhythm- what happens

A

SA node isn’t working, ventricles take over

Q

HR in idioventricular rhythm

A

slow regular, <50bpm

Q

ventricular tachycardia cause

A

ischemic heart disease

life threatening

Q

ventricular tachycardia HR

A

100-250bpm, > 3 ventricular beats

Q

ECG for ventricular tachycardia

A

wide QRS

Q

dysrhythmias in ventricular tachycardia

A

re-entry, triggered activity, enhanced automaticity

Q

CO and SV in ventricular tachycardia

A

decreased

Q

ventricular tachycardia can lead to

A

ventricular fibriliation

Q

HR and CO in ventricular fibrillation

A

irregular, >300bpm, decreased CO

Q

what can ventricular fibrillation lead to

A

sudden cardiac death in minutes

Q

dysrhythmias in ventricular fibrillation

A

purkinje automaticity, re-entry , triggered activity

Q

ECG in ventricular fibrillation

A

no P wave, QRS or T wave

Q

trosades de points is a type of

A

ventricular tachycardia

Q

ECG on torsades de pointes

A

twisting ECG, varied QRS

prolonged QTc (prolonged repolarization)

Q

torsades de pointes can progress to

A

ventricular fibrillation; cardiac death