ACLS : some point not to forget

Pr; < 0.12 Sec

QRS: ,0.12 sec

QT<0.460sec

VF:

FIne vs COarse VF, 

Not VF or pulseless VT

PEA: 

electromechanical Dissociation

narrow complex usually caused by condition iutside the heart but Wide complex usually caused by heart

Not VF or pulseless VT

ASystole:

Pwave might me present but no R wave/ ventricular activity

AFT: 

atial rate 220-350

FLutter wave usually occupieause s 1 big box

AF: 

Atrial rate 300-400

Reenterant SVT: 

220-250 rate usually

P waves are not usallly seen  cause fuses with T wave cause of rapid heart arte

So looks like Sinus tachy but rhythm is fast

Ventricular tachyarrythmia:( check for QT prolonging drugs)( Anti muscaranic)

VT> 30 sec----sustained VT, 

<30 sec duration is Unsustained VT---dont req intervention

3 consecutive PVC: means VT

ventricular rate > 120-250

 p wave present but not seen < AV disscoiation>

Torsa de:

QT prolongation--------increase RRP---so increase risk of arrythmia

* difficult to distinguish type 2b AV block from AF

Pediatric Defib dose is 2-4 J/kg

 bBrady:

if symptomatic----- then gv ATropine 0.5mg I V bolus q 3-4 min---------if no response gv TCP or meds like dopa or epi at a rate of 2-10mcg /min-----------id still no response to TCP the  consider TVP

• During CPR : coronary perfusion pressure > 10mmhg--------------but this cant  be done during cpr so Intra arterial relaxation pressure < 20 mmhg 

end tidal co2--< 10 indicates inadequate CPR..

• Chest recoil ------increase increase coronary perfursion pressure
• 100 heart rate improves ROS and Neurological outcome...( proved)
• for uncoscious pt: tidal volume requirement is around > 500-600ml
• half a bag squeeze is adequate to fill the lungs and chest rise
• Excessive ventilation: cause gastric inflation, decrease venous return and decrease survival

ACLS:

• imp to give complete 2 min of CPR
• Amidarone  for refractory VF/VT
• Epinephrie to all card arrrest pt eveyry 3 -5 min
• Atropine No longer used for PEA and pulseless electrivity or Asystole.

Perfusing rythm:

•  regular monomorphic Wide complex Tachy: If source of Tachy is not known then use Adenosine
• If regular  mono narrow complex tachy---use adenosine
• But for irreg wide complex tachy: dont use adenosine ow cause degn of rythm to VT
• Brady cardia:  Atropine for all brady------if ineffective then use either chronotropic agent like epi or dopa= tc pacer

Suchronised Cardioversion:

•  for unstabel Atrial Fibrillation: dose 120-200 j ( biphasic)
• for unstable AFT or SVT: 50-100 j

for monophasic waveform:

Initial dose 200 j then increase in step wise manner

FOR UNstable VT: initial dose is 100j ---if no response increase the dose

post Cardiac arrest carre:

• Therapeutic Hypothermia is the only intervation shown to improve neurologic recovery: gives esp in coatose pt after ROS and VF as a [resenting rhtythm: cool down body to 32- 34'c for 12-24 hrs
• STMI pt hypothermia and PCI

AIRWAY Management:

• CApnography: most reliable indiactor of ETT and eff of chest compression
• Endtidal co2 normally is 40mmhg...if ineffective chest compression then blood flow to lung decrease and co2 diffusion also decrease ---decreasing endtial c02

 Goals of reperfusion treatment:

•  PCI within 90 min of arrival to ED
• fibrinolytic t/t within 30 min of arrival to ED

 STroke:

pt should recive fibrinolytic t/t within 3 hrs of onset of symp or for slelcted pt windows has been increase to 3-4 and half hrs...( bt not approved by FDA yet)

What happens to brain when we are unconscious?

What happens to your brain as it slips into unconsciousness? A new technique allows researchers to view real-time 3-D images of a patient undergoing anesthesia using the drug propofol, and the findings show that consciousness isn't suddenly switched off, but rather fades as though a dimmer is being dialed down.

The research also suggests that consciousness resides in the connections between multiple parts of the brain, not in any single region. The images show that changes in the anesthetized brain start in the midbrain, where certain receptors for a neurotransmitter called GABA are plentiful.

Drugs like propofol act on these GABA A receptors, mimicking and enhancing the effects of GABA, which inhibits cellular activity. From the midbrain, changes move outward to affect the whole brain; as propofol's message spreads from region to region, consciousness dissolves.

"Our jaws ricocheted off the ground, and I won't say the words we used when we first saw the video," says lead author Dr. Brian Pollard, professor of anesthesia at the University of Manchester, who presented the results at the European Anesthesiology Conference in Amsterdam on Saturday. "We just sat there and stared, dumbfounded and kept repeating it. We're the first people in the world ever to see the brain becoming unconscious, that's quite a sobering thought."

Although anesthesia has been widely used since 1846, when a dentist first demonstrated the effects of ether at Massachusetts General Hospital, until recently very little has been understood about how it works. Even though scientists know that anesthetic drugs like propofol affect GABA in the brain, how that actually eliminates consciousness still remains a mystery.

Pollard explains, however, that propofol alters "the balance between inhibition and excitation in the brain," shifting the balance of activity toward the inhibitory circuits. At first, this produces a paradoxical result.

"When inhibition is inhibited, you first move into a stage of excitation or mania," he says, noting that this usually occurs too quickly to be observed with modern anesthesia. But the brief sense of euphoria that some people experience before losing consciousness from propofol may reflect this loss of inhibition (and may also account for Michael Jackson's taste for the drug).

"You then begin to inhibit the excitation and the patient becomes more sedated and loses consciousness," he says. That's why in the video the brain appears to become more active while unconscious: it's showing the increased action in inhibitory circuits.

Read more: http://healthland.time.com/2011/06/15/real-time-video-first-look-at-a-brain-becoming-unconscious-under-anesthesia/#ixzz1PxfDpaRN

hypercoagulation

case: young female patient with k/c/o prothrombin gene mutation( probably heterogenous) presented with rt arm swelling and tenderness around PICC line( peripherally inserted central cath for total parentral nutrition as she had small bowel ischemia few yrs back 2ndry to prothrobin gene mutation).

denied chest pain, cough, fever, ...
we did doppler for rt brachial vessels which came negative so she dint have any DVT in arm...

Dx: probably superficial vein thrombophlebitis..
Rx: intially we gave her heparin but when doppler came negative we stopped and discharged her on ice pack locally, acetaminophen and coumadin for her hypercoagulable state....

Increased pulm vascular markings : Chest Xray

Pulm edema vs consolidation vs fibrosis

when Consolodation: u will see airbronchogram: markings for bronchi..and complete white out of that part of lung instead of fluffy markings or lines...
Fibrosis: white lines
edema: interstitial edema: small lines...while alveolar edema:  white small nidules

pulm fibrosis:



pulm edema: see fluffy white lesions






consolidation: see complete white out of lung









extensive scarring, fibrosis

Reading chest xray

reading Chest Xray








Following are the points to see  in Chest Xray:

1. check for rt  and LT side
2. Looks whether is well centralized or not,...check for medial end of Clavicle ...both should be at equi level from spine..i f not then it difficult to comment about cardiomegaly, medistinal deviation..     whichever end is more close to spine-----mediastinum is deviated on that side...           6th ant rib level or 9th post rib level        
3. look for exposure....if u see four spinal process then its well exposed...if over exposed then it looks translucent( like emphysema)
4. Looks for cardio and costophrenic angle...all should be  acute...if nt then its abnormal....also look for Diaphragmatic contour...if flattened ---then probably some lung disease....Both diaohragm are at
5. divide the lungs field into 3 section....Upper: above the anterior end of 2nd rib.....middle: between 2nd anf 4th rib...lower: below 4th rib...compare both lung field...
6. check Apical area ...esp behind the Clavicle for TB lesion then check lower lung filed for all 4 angle,,
7. check trachea...and trace it upto carina...should be patent
8. Cardiac: Let side border is made  by Aortic knob, pulm conus, lt atrium and Lt ventricle while rt side border is made by  SVC and rt atrium
9. Vascular markings: Lower lobe vessels are more prominent compare to Upper lobe coz of Gravity...If not then Cardiac problem.. rt side vessels look more prominent than lt side...

few other points...

• how to say number of thoracic vertebra using chest xray??:--- check anterior end of 1st rib which is connected to 1st thoracic vertebera...
• if engorged upper lobe vessels: probably it's puml veins...due to CCF
• Kerly A line: prominent vascular markings in upper lobe
• Kerly B lines: in Lower lobe of lungs on peripheral side ----which suggest fluid between septa...
• Carinal Ange is around 90...any angle above 90 is abnormal probably coz of Lt atrial enlargement----( lt atrium lies just below carina)
• batt wing's appearance:  Enlargement of hilar vessels....in Acute pulm edema..

SAH treatment

Medical stabilization is aimed at preventing early complications, including brain edema, hydrocephalus, and rebleeding, as well as the late complication of vasospasm. Treatment options include bed rest with elevation of the head of the bed to 30 degrees, nimodipine (a calcium channel blocker to prevent vasospasm), seizure prophylaxis, antiemetics, analgesia, and labetalol or other agents as needed for blood pressure control.