angel23
Forum Guru
Topics: 42
Posts: 980
|
hello friendz!!
i m starting this new journal for studying IM.....
so tht i should be on track and get motivation from u all....
i l post imp points to remember and everyone is invited to share this for IM
good luck to all
n happy studying
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
ok todays plan is to do emergency medicine
i l report after doing each topic
___________________
God please help me....Haribol!
|
| hir
Forum Guru
Topics: 4
Posts: 525
|
good luck to u dear angel.......................
keep going........................n going................
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
thanks dear hir!!
wen r u starting ur step 3 journal so tht i can see more of u?
i want ur motivation
___________________
God please help me....Haribol!
|
| hir
Forum Guru
Topics: 4
Posts: 525
|
hey...wether i start my journal or not, i m always there for u......just say my name n i ll be there
was working on my applicaiton n today only i m reading all the application material for step-3 n ll start preparing in a day or two..............
but u tell me if u need any help..........
|
| usmlekiller
Forum Guru
Topics: 18
Posts: 1,010
|
gll
___________________
FUTURE 99ER
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
BASIC LIFE SUPPORT
1. make sure pt.is truely unresponsive(gently shaking /calling)
2.call for help
3.position pt on firm,flat surface with faceup
4.open the airway by either jaw thrust maneuver or chin lift
jaw thrust is beeter in a patient with cerical spine injury patient
videos of jaw thrust and head tilt chin lift maneuver
head tilt http://www.emtb.com/8e/video_play.cfm?VideoID=37
jaw thrust http://www.emtb.com/8e/video_play.cfm?VideoID=15
5.check for breathing
if no breathing then perform 2 rescue breathes with abt 2 sec per breathe
6.check for pulse(for atleast 5-10sec)
if no pulse then perform chest compressions 80-100 per min.provide 15 compressions and then 2 ventilations
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
ASYSTOLE
complete absence of electrical activity
Asystole can be primary or secondary. Primary asystole occurs when the heart's electrical system intrinsically fails to generate a ventricular depolarization. This may result from ischemia or from degeneration (ie, sclerosis) of the sinoatrial (SA) node or atrioventricular (AV) conducting system. Primary asystole usually is preceded by a bradydysrhythmia due to sinus node block-arrest, complete heart block, or both.
Secondary asystole occurs when factors outside of the heart's electrical conduction system result in a failure to generate any electrical depolarization. In this case, the final common pathway is usually severe tissue hypoxia with metabolic acidosis
Possible underlying causes include the Hs and Ts.[1][2][3]
Hypovolemia
Hypoxia
Hydrogen ions (Acidosis)
Hypothermia
Hyperkalemia or Hypokalemia
Hypoglycemia
Tablets or Toxins (Drug overdose)
Cardiac Tamponade
Tension pneumothorax
Thrombosis (Myocardial infarction)
Thrombosis (Pulmonary embolism)
Trauma (Hypovolemia from blood loss)
asystole ECG http://www.emsvillage.com/learning_center/ekgs/ek...
Rx continue CPR
have an access to iv line and prepare for intubation
give epinephrine 1mg every3-5min
then give atropine 1mg every 3-5 min
transcutaneous pacing if there is very slow bradycardia
bicarbonate if re existing acidosis(sepsis,renal failure) or TCA overdose
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
VENTRICULAR FIBRILLATION
significant electrical activity on ECG with no signs of organised pattern
History
VF often occurs without forewarning. The following symptoms, while not necessarily specific for SCD or VF, may develop before any major cardiac event:
Chest pain and other angina equivalents
Dyspnea
Easy fatigue
Palpitations
Syncope
Immediately preceding acute cardiac arrest, possible increase in heart rate, presence of premature ventricular contractions (PVCs), or period of VT
Physical
No pulse or respiration
Unconsciousness
Wide and chaotic QRS complexes on cardiac monitor
Causes
Cardiac, structural heart disease
Myocardial ischemia or infarction due to coronary artery disease: Coronary atherosclerosis and its consequences are responsible for approximately 80% of sudden cardiac deaths in the United States.
Cardiomyopathy: Dilated and hypertrophic cardiomyopathies are the second most important cardiac causes of sudden death. The degree of functional and physiologic left ventricular impairment is correlated with the risk of sudden death.
Dilated
Hypertrophic
Arrhythmogenic right ventricular cardiomyopathy or dysplasia
Aortic stenosis
Aortic dissection
Pericardial tamponade
Congenital heart disease
Myocarditis
Cardiac, no structural heart disease
Catecholaminergic polymorphic ventricular tachycardia and right ventricular outflow tract tachycardia
Mechanical (commotio cordis) or electrical accidents
Preexcitation (including Wolff-Parkinson-White syndrome)
Heart block
Drug-induced QT prolongation with torsades de pointes
Channelopathies
Long QT syndrome
Short QT syndrome
Brugada syndrome
Noncardiac respiratory
Bronchospasm
Aspiration
Sleep apnea
Primary pulmonary hypertension
Pulmonary embolism
Tension pneumothorax
Metabolic or toxic
Electrolyte disturbances and acidosis
Medications or drug ingestion
Environmental poisoning
Sepsis
Neurologic
Seizure
Cerebrovascular accident - Intracranial hemorrhage or ischemic stroke
Drowning
Algorithm
Activate emergency response system.
Initiate CPR and give oxygen when available.
Verify patient is in VF as soon as possible (ie, AED and quick look with paddles).
Defibrillate once.
Adult - Device specific or 200 J for biphasic waveform and 360 J for monophasic waveform
Children - 2 J/kg
Resume CPR immediately without pulse check and continue for 5 cycles.
One cycle of CPR equals 30 compressions and 2 breaths.
Five cycles of CPR should take roughly 2 minutes (compression rate 100 per minute).
Do not check for rhythm/pulse until 5 cycles of CPR are completed.
During CPR, minimize interruptions while the following are performed:
Secure intravenous access.
Perform endotracheal intubation.
Once intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 8-10 breaths per minute.
Check rhythm after 2 minutes of CPR.
Repeat a single defibrillation if still VF or pulseless VT with rhythm check. Use the same dose as the initial defibrillation for adults, and use 4 J/kg for this and all subsequent defibrillations for children.
Resume CPR for 2 minutes immediately after defibrillation.
Continuously repeat the cycle of the following:
Rhythm check
Defibrillation
2 minutes of CPR
Vasopressors
Give vasopressor during CPR before or after shock when intravenous or intraosseous access is available.
Administer epinephrine 1 mg every 3–5 minutes.
Consider administering vasopressin 40 units once instead of the first or second epinephrine dose.
Antidysrhythmics
Give antidysrhythmic during CPR before or after shock.
Administer amiodarone 300 mg IV/IO once, then consider administering an additional 150 mg once.
Instead of or in addition to amiodarone, administer lidocaine 1-1.5 mg/kg first dose, then additional 0.5 mg/kg doses up to a maximum total of 3 mg/kg.
If undulating polymorphic ventricular tachycardia suggestive of torsades de pointes (TdP), administer 1-2 g magnesium IV/IO.
Administer sodium bicarbonate 1 mEq/kg IV/IO in cases of known or suspected preexistent hyperkalemia or tricyclic antidepressant overdose.
Lidocaine and epinephrine can be administered through the endotracheal (ET) tube if IV/IO attempts fail. Use 2.5 times the IV dose.
Correct the following if necessary and/or possible:
Hypovolemia
Hypoxia
Hydrogen ion (acidosis) - Consider bicarbonate therapy.
Hyperkalemia/hypokalemia and metabolic disorders
Hypoglycemia (Check fingerstick or administer glucose.)
Hypothermia (Check core rectal temperature.)
Toxins
Tamponade, cardiac (Check with ultrasonography.)
Tension pneumothorax (Consider needle thoracostomy.)
Thrombosis, coronary or pulmonary - Consider thrombolytic therapy if suspected.
Trauma
Refractory or recurrent VF
Lack of response to standard defibrillation algorithms is challenging.
After initial amiodarone bolus, consider continued amiodarone therapy with 1 mg/min IV for 6 hours, then 0.5 mg/min for 18 hours.
If ongoing ischemia is the suspected cause of recurrent VF, consider emergent cardiac catheterization and angioplasty, and intra-aortic balloon pump placement.
Postresuscitative care
Antidysrhythmics used successfully should be continued. Maintain amiodarone at 0.5-1 mg/min and lidocaine at 1-4 mg/min.
Control any hemodynamic instability by administering vasopressors as indicated.
Check for complications (eg, aspiration pneumonia, CPR-related injuries).
Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).
ECG finding http://www.ecglibrary.com/vf.html
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
nice site for all ECG s
http://www.ecglibrary.com/
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
VENTRICULAR TACCHYCARDIAS
Ventricular tachycardia (VT) is a tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute and wide QRS complexes. VT may be monomorphic (originating from a single focus with identical QRS complexes) or polymorphic (may appear as an irregular rhythm, with varying QRS complexes). Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.
No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following:
Rate greater than 100 beats per minute (usually 150-200)
Wide QRS complexes (>120 ms) (becoz of slowed conduction thru purkinge fibres)
Presence of atrioventricular (AV) dissociation
Fusion beats
Ventricular tachycardia may develop without hemodynamic deterioration. Nevertheless, it often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation (VF).
History: Most patients present to the ED with symptoms of either ischemic heart disease or hemodynamic compromise. Symptoms may include the following:
Chest pain
Palpitations
Dyspnea
Anxiety
Diaphoresis
Nausea
Physical: Findings generally reflect the degree of hemodynamic instability.
Symptoms of congestive heart failure (CHF)
Dyspnea and hypoxemia
Rales from pulmonary edema
Jugular venous distention
Hypotension
Mental status changes
Anxiety
Agitation
Lethargy
Coma
Causes: VT generally is a symptom of CAD or structural heart disease.
VT can be triggered by electrolyte deficiencies (eg, hypokalemia, hypocalcemia, hypomagnesia).
Use of sympathomimetic agents (from relatively benign caffeine to more potent agents such as methamphetamine or cocaine) may stimulate VT in vulnerable hearts.
Drugs that prolong the QT complex (eg, type 1A antiarrhythmics, droperidol and related antiemetics) may predispose to VT, particularly torsade de pointes.
quinidine ,TCA's and phenothiazines predispose to VT
torsades may be associated with hypomagnesemia
Rx.During the initial assessment, once real-time cardiac monitoring or 12-lead ECG has established VT as the diagnosis determine if the VT is stable or unstable, even as the ABCs are reassessed in the secondary survey.
Unstable VT
Unstable VT is characterized by symptoms of insufficient oxygen delivery such as chest pain, dyspnea, hypotension, or altered level of consciousness, indicating that rate and stroke volume are not providing adequate cardiac output.
synchronised cardioversion is done(100J-360J)
stable VT
first give iv lidocaine....
if persistent give iv procainamide
still persistent give iv amiodarone
Mg is given for torsades
In chronic VT
if LV dysfunction:implantable cardioverter defibrillator device
if no LV dysfunction: beta blocker + amiodarone
non sustained :Beta blockers
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
TORSDES DE POINTES
TDP, often referred to as torsade, is an uncommon variant of ventricular tachycardia (VT). The underlying etiology and management of torsade are, in general, quite different from those of garden-variety VT. The management of torsade with group IA antidysrhythmic drugs can have disastrous consequences.
Torsade is defined as a polymorphous VT in which the morphology of the QRS complexes varies from beat to beat. The ventricular rate can range from 150 beats per minute (bpm) to 250 bpm. The original report described regular variation of the morphology of the QRS vector from positive to net negative and back again. This was symbolically termed torsade de pointes, or "twisting of the point" about the isoelectric axis
Causes
Prolongation of the QT interval may be congenital, as seen in the Jervell and Lange-Nielsen syndrome (ie, congenitally long QT associated with congenital deafness) and the Romano Ward syndrome (ie, isolated prolongation of QT interval). Both of these syndromes are associated with sudden death due to either primary ventricular fibrillation or torsade that degenerates into ventricular fibrillation.
Prolonged QT is found in only 0.25-0.3% of deaf-mute children.
Brugada syndrome is characterized by a coved ST segment in the right precordial leads. The syndrome may cause sudden death due to polymorphic VT resembling TdP.
The acquired conditions that predispose one to torsade either decrease the outward potassium current or interfere with the inward sodium and calcium currents, or fluxes.
The electrolyte disturbances that have been reported to precipitate torsade include hypokalemia and hypomagnesemia. Close observation is required in predisposed patients, such as those with cirrhosis or hypothyroidism.
Hypokalemia and hypomagnesemia, in turn, cause a delay in phase III (ie, reprolongation) and form the substrate for emergence of the dysrhythmia.
Antiarrhythmic drugs reported to be etiologic include class IA agents (eg, quinidine, procainamide, disopyramide), class IC agents (eg, encainide, flecainide), and class III agents (eg, sotalol, amiodarone).
Drug interactions with the antihistamines astemizole (recalled from US market) and terfenadine (recalled from US market) can precipitate torsade; these drugs should never be used with class IA, IC, or III agents.
Astemizole and terfenadine, in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics, have been reported to precipitate torsade and sudden death.
Grapefruit juice has been shown to slow the hepatic metabolism of these antihistamines as well as other drugs and to prolong the QT interval in patients taking astemizole or terfenadine (recently taken off the market by the US Food and Drug Administration [FDA]).
Clinical implications of this interaction are unclear.
Other drugs that prolong the QT interval and have been implicated in cases of torsade include phenothiazines, tricyclic antidepressants, lithium carbonate, cisapride, highly active antiretrovirals (HAARTs), high-methadone, anthracycline chemotherapeutic agents (eg, doxorubicin, daunomycin), some fluoroquinolones, and any other medication using the CYP3A metabolic pathway. Ranolazine, an antiangina agent, also prolongs the QTc, but torsade is a rare complication of this therapy.
Risk factors
Female gender
History of syncope or resuscitated arrest
Congenital deafness
Family history of sudden death
Treat hypokalemia if it is the precipitating factor and administer magnesium sulfate in a dose of 2-4 g intravenously (IV) initially.
Magnesium is usually very effective, even in the patient with a normal magnesium level.
If this fails, repeat the initial dose, but because of the danger of hypermagnesemia (depression of neuromuscular function) the patient requires close monitoring.
Other therapies include overdrive pacing and isoproterenol infusion. Most (75-82%) torsade de pointes (TDP) rhythms are started by a pause. Pacing at rates up to 140 bpm may prevent the ventricular pauses that allow TDP to originate.
The patient with torsade who is in extremis should be treated with electrical cardioversion or defibrillation
___________________
God please help me....Haribol!
|
| docdoc9
Forum Guru
Topics: 63
Posts: 521
|
http://in.youtube.com/watch?v=77q52lO99KE&fea...
good link for BLS and ACLS
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
thanks docdoc9
tht was really helpful....very nice link
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
PULSELESS ELECTRICAL ACTIVITY
Pulseless electrical activity (PEA) is a clinical condition characterized by loss of palpable pulse in the presence of recordable cardiac electrical activity. PEA also is referred to as electromechanical dissociation (EMD).
PEA may result from various etiologies and has a spectrum of manifestations. Patients may present with recordable aortic pressures and absent peripheral pulses from weak cardiac contractions or severe peripheral vascular disease. These patients are classified as having pseudo-PEA. True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity.
Causes
PEA is classified on the basis of etiology. It also may be classified by the presence or absence of aortic pressure. This differentiation is more practical because the etiology often is unclear. Occasionally, an aortic pressure may be recorded by invasive monitoring (ie, in pseudo-PEA), or cardiac contractions may be found by echocardiography (ie, normotensive PEA). Peripheral pulses may be absent because of very low aortic pressures or peripheral vascular disease. Approximately half of all patients may have an aortic pressure detectable by invasive monitoring. Also, patients with pseudo-PEA usually are younger, have a normal QRS interval, and are more likely to respond to epinephrine than patients with no aortic pressure. In one study, 77% (14/18) of patients with pseudo-PEA responded to epinephrine.
Pulmonary - Respiratory arrest
Mechanical - Cardiac tamponade, massive myocardial infarction, cardiac rupture, tension pneumothorax, auto-PEEP, severe congestive heart failure (CHF)
Preload and afterload changes - Severe hypovolemia, massive pulmonary embolus, sepsis
Metabolic changes - Hyperkalemia, hypothermia, drug ingestion (tricyclic antidepressant overdose, digitalis overdose, calcium channel and beta-blockers)
Postdefibrillation PEA after prolonged ventricular fibrillation and electrical cardioversion
Postdefibrillation PEA is characterized by the presence of organized electrical activity, occurring immediately after electrical cardioversion and in the absence of palpable pulse. This may be the cause in as many as 60% of patients who experience PEA after defibrillation.
Postdefibrillation PEA may be associated with better prognosis than continued ventricular fibrillation. A spontaneous return of pulse is likely, and cardiopulmonary resuscitation (CPR) should be continued for as long as 1 minute to allow for spontaneous recovery.
A further recommendation is to discontinue administration of epinephrine at this time to avoid precipitating ventricular fibrillation.
Rx
For a patient in whom PEA is suspected, the American Heart Association - Advanced Cardiac Life Support (AHA-ACLS) guidelines protocol recommends the following:
Initiate CPR.
Place an intravenous line.
Intubate the patient.
Assess blood flow using Doppler ultrasound.
Correct hypoxia by administering 100% oxygen.
Once these basic measures are in place, reversible causes should be sought and corrected, which include the following:
Hypovolemia
Hypothermia
Hypoxia
Acidosis
Hypokalemia/hyperkalemia
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolus
Acute myocardial infarction
Drug overdose (eg, tricyclic antidepressants, digoxin, calcium channel blockers, beta-blockers)
The clinical scenario usually provides useful information. Some examples include the following:
In a previously intubated patient, tension pneumothorax and auto-PEEP are more likely to occur.
In a patient on dialysis, consider hyperkalemia.
In a patient with prior myocardial infarction or CHF, myocardial dysfunction is likely.
A core temperature should always be obtained if the patient is thought to have hypothermia.
In patients diagnosed with hypothermia, resuscitative efforts should be continued at least until the patient is rewarmed because patient survival is possible even after prolonged resuscitation.
Other components of the evaluation include the following:
Measure QRS duration since it has prognostic significance. Patients with QRS duration of less than 0.2 second are more likely to recover, and high-dose epinephrine may be administered.
Invasive monitoring (eg, arterial line) may be placed if it does not cause a delay in delivering standard ACLS care.
Absence of pulses should be confirmed by Doppler examination.
Echocardiography, if available, may assist with identifying the presence of cardiac contractions (pseudo-PEA). Patients with pseudo-PEA may have a rapidly reversible cause (eg, auto-PEEP, hypovolemia). Echocardiography also is invaluable in identifying cardiac tamponade, right ventricular enlargement, myocardial dysfunction, cardiorrhexis, or ventricular septal rupture.
In refractory cases, if the patient has suffered chest trauma, a thoracotomy may be performed, provided adequate expertise is available.
Once reversible causes are identified, they should be corrected immediately. This process involves needle decompression of pneumothorax, pericardiocentesis for tamponade, volume infusion, correction of body temperature, and administration of thrombolytics or surgical embolectomy for pulmonary embolus.
Resuscitative pharmacology includes epinephrine (1 mg IV q3-5min). If this therapy fails, a class IIb (acceptable, possibly helpful) regimen is to administer higher doses of epinephrine. Little data strongly recommends one regimen over the other. Higher doses include the following:
Intermediate - Epinephrine (2-5 mg q3-5min)
Escalating - Epinephrine (1 mg, 3 mg, or 5 mg q3min)
High dose - Epinephrine (0.1 mg/kg IV push q3-5min)
If the underlying rhythm is bradycardiac (ie, heart rate <60 beats per min) associated with hypotension, then atropine (1 mg IV q3-5min, not to exceed 0.4 mg/kg) should be administered. This is considered the total vagolytic dose, beyond which no further benefit will occur. Note that atropine may cause papillary dilation, and this sign then cannot be used to assess neurological function.
Sodium bicarbonate may be administered only in patients with severe systemic acidosis, hyperkalemia, or a tricyclic antidepressant overdose. The dose is 1 mEq/kg. Routine administration is discouraged because it worsens intracellular and intracerebral acidosis and does not appear to alter mortality rate.
Prompt initiation of a cardiopulmonary bypass may have a role in carefully selected patients. This maneuver requires availability of expertise and support services. Patient selection is paramount because it should be used only in patients who have an easily reversible etiology of cardiac dysfunction. In an animal model, initiation of prompt cardiopulmonary bypass resulted in a higher rate of success in returning circulation than administration of high- or standard-dose epinephrine. Cardiac pacing can result in electrical capture but does not necessarily increase incidence of mechanical contractions; hence, this procedure is not recommended.
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
pulseless electrical activity alogrithm
Attached Files:
image_Pulseless_Electrical_Activity_Algorithm[1].jpg (376 KB, 2 downloads)
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
time for cooking n break
will come back in 45mins
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
ok back after a long break!!
had some household work
now back to studies
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
ATRIAL DYSARRYTHMIAS
___________________
God please help me....Haribol!
|
| angel23
Forum Guru
Topics: 42
Posts: 980
|
BRADICARDIA
___________________
God please help me....Haribol!
|
|
| |
| | | | | | | | | | | | | | | | | | | | |
