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.

Bronchiectasis

check out the following video for Bronchiectasis CXray...

http://www.youtube.com/watch?v=Kk4x7DPJtRI&feature=player_embedded

Hypertensive emergency

Case: we had one patient presented with epistaxis from left nose and blood pressure of 210/130--------pt had nasal septum surgery 1 week back.....pt dint have any altered consciousness nor pappiloedema...U/a was normal...
Dx: As there is vascular injury but no end organ damage..so he has hypertensive urgency...
Rx: he was give hydralazin...bp came down to 160/100..... was given anterior nasal packing and Abx for nasal packing: ampi+sulbactam....
after 2 days he improved and was discharged...


A sudden rise in blood pressure to >180/120 mm Hg that is associated with end-organ damage is termed a hypertensive emergency

• Accelerated HTN is a sudden, marked elevation in blood pressure associated with end-organ damage but no papilledema (although retinal hemorrhage and exudates are often present).
• Malignant hypertension is a sudden, marked elevation in blood pressure accompanied by end-organ damage including papilledema.
• Hypertensive encephalopathy is a malignant HTN accompanied by cerebral edema, which presents with headache, nausea, vomiting, restlessness, and confusion.
  
  Hypertensive encephalopathy versus stroke: Onset is usually sudden in ischemic or hemorrhagic stroke but insidious in hypertensive encephalopathy..
  
  
  What is the difference between urgency and emergency?
  Urgency denotes severe hypertension (HTN), typically with diastolic blood pressure (DBP) > 130 mmHg, without symptoms or evidence of end-organ damage. The term accelerated hypertension falls in this category, where retinal exudates and hemorrhages are often present.
  Emergency is an acute, life-threatening elevation in BP with evidence of vascular injury + end-organ damage. The term malignant hypertension falls in this category, typified by papilledema.
  
  
  What causes the end-organ damage?Failure of autoregulation to regulate pressure in the arterioles and capillaries with increasing HTN results in disruption of the vascular endothelium. Fibrinoid necrosis results from deposition of plasma elements in the vascular wall, causing narrowing of the vascular lumen. Tissue ischemia as well as leakage of blood and plasma from affected vessels then results, causing end-organ damage.
  
  
  
  What is the treatment for specific hypertensive emergencies?
  

  Goal is the rapid lowering of mean arterial pressure by approximately 20-25% or to a DBP of 100-110 mmHg over 2-6 hours. However, in aortic dissection, the goal is to lower SBP to 100-120 mmHg and MAP below 80 mmHg ASAP, while patients with acute ischemic stroke or hypertensive encephalopathy may require slightly higher BP initially due to cerebral autoregulation.

  
  

  Malignant hypertension with retinal changes and/or hypertensive encephalopathy - Treatment of choice is a rapid, short-acting IV agent, such as nitroprusside (dose: 0.25-0.5 m g/kg/min to a max of 8-10 m g/kg/min; acts within seconds and lasts only a few minutes). Acts as both a veno- and vasodilator. Limited by cyanide or thiocyanate toxicity, especially with prolonged use or in renal insufficiency; do not use for more than 48 hours if possible (antidote is sodium thiosulfate). Other rapid-acting IV agents include labetolol (20mg IV bolus, 0.5-2 mg/min IV gtt), which is both an alpha- and beta-adrenergic blocker; and nicardipine (5-15 mg/hr IV gtt), which is a peripherally-acting calcium-channel antagonist. A newer medication, fenoldopam (0.1-1.6 m g/kg/min IV gtt), which is a pure dopamine agonist, has the advantage increasing renal blood flow and sodium excretion.

  What about hypertensive urgency?
  
  

  The goal is a reduction in blood pressure to 160/110 over several hours with conventional oral therapy. The oral medication used may vary with the clinical scenario - for example, beta-blockers and nitrates would be preferred in patients with coronary disease, while ACE-inhibitors might be useful in patients with a history of diabetes, scleroderma, or congestive heart failure. Loop diuretics are often very helpful initially in asymptomatic patients who are not volume-depleted. Nifedipine is generally not recommended due to rapid hypotension and possible precipitation of ischemic events, while clonidine often causes sedation and dry mouth as well as orthostatic hypotension and may require careful monitoring. There is no proven benefit in the rapid reduction of blood pressure in asymptomatic patients with severe HTN.

  
  

  
  

  check out this link for info: http://intmedweb.wfubmc.edu/blurbs/cards/hypertensive.html

Cold air causing cough

One of my friend always complain that her son starts coughing if he is exposed to cold air/windy weather....I saw him coughing even if he passes frozen section in grocery stores....

The cold weather cough can be caused from a couple of sources.

When you breath in cold air, your lungs contract (tighten) just like any tissue does when exposed to cold. Once you come inside and start breathing warm air, the lung tissue rapidly expands. That sudden expansion can cause the cough reflex. It is a similar reaction to what new runners experience when their lungs start to grow and expand. You'll often see new runners chuging along and hacking out a few coughs.


Your body will work as best it can to deal with the sudden change as best as it can. Taking a moment to cool down before heading inside is excellent advice. If you have a garage or somewhere that would serve as a step between the two extreme temps it would be a good place to cool down in. (Assuming there aren't too many fumes from cleaners etc. in there.)

Only other thing that comes to mind is to try and inhale through your nose while you are cooling down. Conchae inside your nose that serve to adjust the temp/humidity of your inhaled breath to a more acceptable level. They also work as a bit of a 'screen' or filter to help keep some of the junk we breathe out of your lungs.

I'm guessing the tea/coffee you drink would assist your upper airway (mouth/nose) in warming the air you inhale by increasing the temperature in those areas. 

Renal

Some Lab Values to remember

1. Acute Renal Failure:  When Cr starts increasing at a rate > 0.3mg/dl/ 48 hrs...or increase in s.Cr by 25% from baseline..
2. BUN/ Cr ratio:   10-15-----------------Intrarenal etiology,     <10 ------------------Pre renal
3. Normal Cr-  0.7 to 1.2 mg/dl ( but in pregnance it never goes more then 1mg/dl)
4. Normal BUN  = 20 to 24
5. Normal GFR = 120 ml/ min

• Whne pt is having ARF dont forget to check serum k+ level..give keyxalate and insulin+ d50.
• In diabetic patient keep checking Urine protein, microalbumiuria--------if present suggest low protein, Low salt diet and Give ACE inhibitors...maintain blood glucose level...also check for retinopathy which is uaually associated with diabetic nephropathy
• In hypertensive patient also check for proteinuria...
• in chronic renal failure pt, donr forget to prescribe Vit D and Iron.
• The fractional excretion of sodium (FENa) is useful in diagnosing pre-renal ARF. FENa is less than 1 % in many patients with prerenal ARF. Intravenous hydration is the mainstay of treatment.

NASH

obese pt with elevated LFTs but normal viral hepatitis profile and not taking hepatitis induced medication ...

with elevated lipid profile-----------consider Non alcoholic steatotic hepatitis....

Hepatitis c and Alcohol abuse

we all know that treatment of Hep c is INF and Ribavarin but if pt is alcoholic dont start the treatment ....send him for drug abuse counselling...once pt stops EToh ---u can start treatment