Endotracheal Intubation Procedure or ETT is s an emergency procedure that’s often
performed on people who are unconscious
or who can’t breathe on their own. EI maintains an open airway and helps
prevent suffocation.
You may need Endotracheal Intubation Procedure for one of the following reasons:
to open your airways so that you can receive an
anesthetic, medication, or oxygen
to protect your lungs from damage
you’ve stopped breathing or you’re having
difficulty breathing to secure airway
you need a machine (ambu bag or ventilator) to help you breathe
you have a head injury
You need two trial only to intubate the patient in Emergency Department after oxygenation of the patient and suction if needed
if you fail after two trial ,please Dont try adain just oxygenate the patient and use laryngeal mask airway.
Dont waste more time in intubation ,laryngeal mask airway enough and go to search about underling cause to treat.
More serious complications may occur in older adults who have
serious medical problems. These complications are rare but may include:
heart attack
lung infection
stroke
temporary mental confusion
death
Intubation Risks
There are some risks related to intubation, such as:
a buildup of too much water in your tissues
bleeding
a collapsed lung
How
Is Endotracheal Intubation Done?
Watch the video
What
to Expect After Endotracheal Intubation
You may have some difficulty swallowing after the procedure, but
this should go away quickly.
There’s also a slight risk that you’ll experience complications
from the procedure. Make sure you call your doctor right away if you’re showing
any of the following symptoms:
Asbestos: Asbestos can cause a variety of lung
disease from benign pleural plaques tomesothelioma.
Pleural plaques
Pleural plaques are benign and do not undergo malignant change. They are the
most common form of asbestos related lung disease and generally occur after a
latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to
that seen following an empyema or haemothorax. The underlying pathophysiology
is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in
contrast to mesothelioma where even very limited exposure can cause disease.
The latent period is typically 15-30 years. Asbestosis typically causes lower
lobe fibrosis. As with other forms of lung fibrosis the most common symptoms
are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos
is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Patients are usually offered palliative chemotherapy and there is also a
limited role for surgery and radiotherapy. Unfortunately the prognosis is very
poor, with a median survival from diagnosis of 8-14 months.
Lung cancer
Asbestos exposure is a risk factor for lung cancer and also has a synergistic effect
with cigarette smoke.
Aspergilloma
An aspergilloma is a fungus ball which often colonises an existing lung cavity
(e.g. secondary to TB, lung cancer or cystic fibrosis)
Hypertension in pregnancy NICE published guidance in 2010 on the management of hypertension in pregnancy. They also made recommendations on reducing the risk of hypertensive disorders developing in the first place. Women who are at high risk of developing pre-eclampsia should take aspirin 75mg od from 12 weeks until the birth of the baby. High risk groups include:
hypertensive disease during previous pregnancies chronic kidney disease autoimmune disorders such as SLE or antiphospholipid syndrome type 1 or 2 diabetes mellitus The classification of hypertension in pregnancy is complicated and varies. Remember, in normal pregnancy: blood pressure usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks after this time the blood pressure usually increases to pre-pregnancy levels by term Hypertension in pregnancy in usually defined as: systolic > 140 mmHg or diastolic > 90 mmHg or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic After establishing that the patient is hypertensive they should be categorized into one of the following groups: Watch This Video:
A=Pre-existing hypertension :
A history of hypertension before pregnancy or an elevated blood pressure > 140/90 mmHg before 20 weeks gestation No proteinuria, no oedema Occurs in 3-5% of pregnancies and is more common in older women B=Pregnancy-induced HTN (PIH, also known as gestational HTN): Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after 20 weeks) No proteinuria, no oedema Occurs in around 5-7% of pregnancies Resolves following birth (typically after one month). Women with PIH are at increased risk of future pre-eclampsia or hypertension later in life C=Pre-eclampsia: Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours) Oedema may occur but is now less commonly used as a criteria Occurs in around 5% of pregnancies Pre-eclampsia - Pre-eclampsia is a condition seen after 20 weeks gestation characterised by: Watch This Video:
Pregnancy-induced hypertension in association with Proteinuria (> 0.3g / 24 hours). Oedema used to be third element of the classic triad but is now often not included in the definition as it is not specific Pre-eclampsia is important as it predisposes to the following problems: fetal: prematurity, intrauterine growth retardation eclampsia haemorrhage: placental abruption, intra-abdominal, intra-cerebral cardiac failure multi-organ failure Risk factors:
> 40 years old nulliparity (or new partner) multiple pregnancy body mass index > 30 kg/m^2 diabetes mellitus pregnancy interval of more than 10 years family history of pre-eclampsia previous history of pre-eclampsia pre-existing vascular disease such as hypertension or renal disease Features of severe pre-eclampsia: hypertension: typically > 170/110 mmHg and proteinuria as above proteinuria: dipstick ++/+++ headache visual disturbance papilloedema RUQ/epigastric pain hyperreflexia platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome Management: Management: consensus guidelines recommend treating blood pressure > 160/110 mmHg although many clinicians have a lower threshold Oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used Delivery of the baby is the most important and definitive management step. The timing depends on the individual clinical scenario Eclampsia Eclampsia may be defined as the development of seizures in association pre-eclampsia. To recap, pre-eclampsia is defined as: 1) condition seen after 20 weeks gestation 2) pregnancy-induced hypertension 3) proteinuria
Magnesium sulphate is used to both prevent seizures in patients with severe pre-eclampsia and treat seizures once they develop. Guidelines on its use suggest the following: 1) should be given once a decision to deliver has been made 2) in eclampsia an IV bolus of 4g over 5-10 minutes should be given followed by an infusion of 1g / hour 3) urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment 4) treatment should continue for 24 hours after last seizure or delivery (around 40% of seizures occur post-partum) Other important aspects of treating severe pre-eclampsia/eclampsia include fluid restriction to avoid the potentially serious consequences of fluid overload Centrally acting antihypertensives Examples of centrally acting antihypertensives include: methyldopa: used in the management of hypertension during pregnancy moxonidine: used in the management of essential hypertension when conventional antihypertensives have failed to control blood pressure clonidine: the antihypertensive effect is mediated through stimulating alpha-2 adrenoceptors in the vasomotor centre
Hypertention Secondary causes: It is thought that between 5-10% of patients diagnosed with hypertension have primary hyperaldosteronism, including Conn's syndrome. This makes it the single most common cause of secondary hypertension.
Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include: glomerulonephritis pyelonephritis adult polycystic kidney disease renal artery stenosis
Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood pressure: phaeochromocytoma Cushing's syndrome Liddle's syndrome congenital adrenal hyperplasia (11-beta hydroxylase deficiency) acromegaly Other causes include: NSAIDs pregnancy coarctation of the aorta the combined oral contraceptive pill steroids MAOI 3- Isolated systolic hypertension Isolated systolic hypertension (ISH) is common in the elderly, Affecting around 50% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH reduced both strokes and ischaemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is contradicated by the 2011 NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension. Hypertension diagnosis: NICE published updated guidelines for the management of hypertension in 2011. Some of the key changes include: classifying hypertension into stages recommending the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) Why were these guidelines needed? It has long been recognised by doctors that there is a subgroup of patients whose blood pressure climbs 20 mmHg whenever they enter a clinical setting, so called 'white coat hypertension'. If we just rely on clinic readings then such patients may be diagnosed as having hypertension when the vast majority of time there blood pressure is normal. This has led to the use of both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) to confirm the diagnosis of hypertension. These techniques allow a more accurate assessment of a patients' overall blood pressure. Not only does this help prevent overdiagnosis of hypertension - ABPM has been shown to be a more accurate predictor of cardiovascular events than clinic readings. Blood pressure classification: This becomes relevant later in some of the management decisions that NICE advocate. Stage Criteria Stage 1 hypertension Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg Stage 2 hypertension Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg Severe hypertension Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg 4- Diagnosing hypertension:
Firstly, NICE recommend measuring blood pressure in both arms when considering a diagnosis of hypertension. If the difference in readings between arms is more than 20 mmHg then the measurements should be repeated. If the difference remains > 20 mmHg then subsequent blood pressures should be recorded from the arm with the higher reading. It should of course be remember that there are pathological causes of unequal blood pressure readings from the arms, such as supravalvular aortic stenosis. It is therefore prudent to listen to the heart sounds if a difference exists and further investigation if a very large difference is noted. NICE also recommend taking a second reading during the consultation, if the first reading is > 140/90 mmHg. The lower reading of the two should determine further management. NICE suggest offering ABPM or HBPM to any patient with a blood pressure >= 140/90 mmHg. If however the blood pressure is >= 180/110 mmHg: immediate treatment should be considered if there are signs of papilloedema or retinal haemorrhages NICE recommend same day assessment by a specialist NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis) Ambulatory blood pressure monitoring (ABPM): at least 2 measurements per hour during the person's usual waking hours (for example, between 08:00 and 22:00) use the average value of at least 14 measurements If ABPM is not tolerated or declined HBPM should be offered. Home blood pressure monitoring (HBPM): for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated BP should be recorded twice daily, ideally in the morning and evening BP should be recorded for at least 4 days, ideally for 7 days discard the measurements taken on the first day and use the average value of all the remaining measurements Interpreting the results 1) ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension) treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greater 2) ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension) offer drug treatment regardless of age 5- Hypertension management: NICE published updated guidelines for the management of hypertension in 2011. Some of the key changes include: classifying hypertension into stages recommending the use of ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM) calcium channel blockers are now considered superior to thiazides bendroflumethiazide is no longer the thiazide of choice Managing hypertension 1) Lifestyle advice should not be forgotten and is frequently tested in exams: A low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg caffeine intake should be reduced the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight 2) ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension) treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greater 3) ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension) offer drug treatment regardless of age For patients < 40 years consider specialist referral to exclude secondary causes. Step 1 treatment: patients < 55-years-old: ACE inhibitor (A) patients > 55-years-old or of Afro-Caribbean origin: calcium channel blocker Step 2 treatment: ACE inhibitor + calcium channel blocker (A + C) Step 3 treatment: add a thiazide diuretic (D, i.e. A + C + D) NICE now advocate using either: chlorthalidone (12.5-25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide 6- NICE define a clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated doses as resistant hypertension. They suggest step 4 treatment or seeking expert advice Step 4 treatment: 1) consider further diuretic treatment if potassium < 4.5 mmol/l add spironolactone 25mg od if potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic treatment 2) if further diuretic therapy is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker Patients who fail to respond to step 4 measures should be referred to a specialist. NICE recommend: If blood pressure remains uncontrolled with the optimal or maximum tolerated doses of four drugs, seek expert advice if it has not yet been obtained. Blood pressure targets Age < 80 years, Clinic BP 140/90 mmHg, ABPM / HBPM 135/85 mmHg Age > 80 years, Clinic BP 150/90 mmHg , ABPM / HBPM 145/85 mmHg New drugs: Direct renin inhibitors: e.g. Aliskiren (branded as Rasilez) by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I No trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists adverse effects were uncommon in trials although diarrhoea was occasionally seen only current role would seem to be in patients who are intolerant of more established antihypertensive drugs 7- Malignant hypertension Basics: severe hypertension (e.g. >200/130 mmHg) occurs in both essential and secondary types fibrinoid necrosis of blood vessels, leading to: retinal haemorrhages, exudates, and proteinuria, haematuria due to renal damage (benign nephrosclerosis). can lead to cerebral oedema → encephalopathy Features: classically: severe headaches, nausea/vomiting, visual disturbance however chest pain and dyspnoea common presenting symptoms papilloedema severe: encephalopathy (e.g. seizures) Management: reduce diastolic no lower than 100mmHg within 12-24 hrs bed rest most patients: oral therapy e.g. atenolol if severe/encephalopathic: IV sodium nitroprusside/labetolol
The ST segmentis a flat, isoelectric part of ECG in between the ending from the S wave (J point) and the start of the T wave.
It signifies the actual interval in between ventricular depolarization and repolarization.
The most significant reason for ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.
Causes of ST Segment Elevation:
Watch this Video:
Acute myocardial infarction
Coronary vasospasm (Printzmetal’s angina)
Pericarditis
Benign early repolarization
Left bundle branch block
Left ventricular hypertrophy
Ventricular aneurysm
Brugada syndrome
Ventricular paced rhythm
Raised intracranial pressure
Morphology of the Elevated ST segment
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Myocardial Infarction
Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology as follows
ST Segment Morphology in Other Conditions:
Pericarditis
BER
LBBB
LV aneurysm
Brugada
Patterns of ST Elevation
Acute ST elevation myocardial infarction (STEMI)
Causes ST segment elevation and Q-wave formation in contiguous leads, either:
Septal (V1-2)
Anterior (V3-4)
Lateral (I + aVL, V5-6)
Inferior (II, III, aVF)
Right ventricular (V1, V4R)
Posterior (V7-9)
There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + aVL typically produces reciprocal ST depression in lead III (see example below)..
Anterolateral STEMI
Coronary Vasospasm (Prinzmetal’s angina)
This will cause a design of ST elevation that's very like acute STEMI - i.e. localized ST elevation with reciprocal ST depression happening throughout attacks of chest pain. Even so, unlike acute STEMI the ECG changes are usually transient, reversible with vasodilators and never commonly ASSOCIATED with myocardial necrosis. It might be difficult to distinguish both of these situations based on the ECG alone.
Pericarditis
Pericarditis will cause popular concave ST segment elevation together with PR segment depression in several leads, usually including I, II, III, aVF, aVL, and V2-6. There's reciprocal ST depression as well as PR elevation in leads aVR and V1. Spodick’s sign - a downward sloping TP segment - can also be seen.
Pericarditis
Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments.
There is reciprocal ST depression and PR elevation in aVR.
Spodick’s sign is present.
Benign Early Repolarization
BER will cause slight ST elevation along with tall T-waves mostly within the precordial leads. Is really a normal variation commonly observed in youthful, healthy and balanced patients. There's frequently notching from the J-point - the “fish-hook” pattern. The actual ST changes might be much more prominent at more slowly heart rates and also disappear in the existence of tachycardia.
Benign Early Repolarization
There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)
Left Bundle Branch Block
In left bundle branch block, the ST segments and also T waves reveal “appropriate discordance” i.e. they're directed reverse towards the essential vector of the QRS complex. That creates ST elevation and upright T waves in leads with a negative QRS complex (predominant S wave), whilst developing ST depression as well as T wave inversion in leads along with a positive QRS complex (dominant R wave).
Left Bundle Branch Block
Note the ST elevation in leads with deep S waves — most apparent in V1-3.
Also note the ST depression in leads with tall R waves — most apparent in I and aVL.
Left Ventricular Hypertrophy
LVH leads to a very similar pattern of repolarization abnormalities as LBBB, with ST elevation within the leads with deep S-waves (usually V1-3) as well as ST depression/T-wave inversion in the leads along with tall R waves (I, aVL, V5-6).
Left Ventricular Hypertrophy
Deep S waves with ST elevation in V1-3
ST depression and T-wave inversion in the lateral leads V5-6
Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to ASSOCIATED left posterior fascicular block.
Ventricular Aneurysm
This is an ECG pattern for residual ST elevation and deep Q waves observed in affected individuals with past myocardial infarction. It's ASSOCIATED with extensive myocardial injury and paradoxical movement of the left ventricular wall during systole.
Ventricular Aneurysm
There is ST elevation with deep Q waves and inverted T waves in V1-3.
This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.
Brugada Syndrome
This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.
Brugada syndrome
There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.
Ventricular Paced Rhythm
Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.
AV Sequential Pacing
Raised Intracranial Pressure
Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is ASSOCIATED with widespread, deep T-wave inversions (“cerebral T waves”).
ST elevation due to traumatic brain injury
Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.
Less Common Causes of ST segment Elevation
Pulmonary embolism and acute cor pulmonale (usually in lead III)
Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
Hyperkalaemia
Sodium-channel blocking drugs (secondary to QRS widening)
J-waves (hypothermia, hypercalcaemia)
Following electrical cardioversion
Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease
Transient ST elevation after DC cardioversion from VF
J waves in hypothermia simulating ST elevation
Causes of ST Depression
Myocardial ischaemia / NSTEMI
Reciprocal change in STEMI
Posterior MI
Digoxin effect
Hypokalaemia
Supraventricular tachycardia
Right bundle branch block
Right ventricular hypertrophy
Left bundle branch block
Left ventricular hypertrophy
Ventricular paced rhythm
Morphology of ST Depression
ST depression can be either upsloping, downsloping, or horizontal.
Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD.
Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
Posterior MI manifests as horizontal ST depression in V1-3 and is ASSOCIATED with upright T waves and tall R waves.
ST depression: upsloping (A), downsloping (B), horizontal (C)
ST segment morphology in myocardial ischaemia
Reciprocal change
ST elevation in III
Reciprocal change in aVL
ST segment morphology in posterior MI
Patterns of ST depression
Myocardial Ischaemia
ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.
NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought.
LMCA Occlusion
Reciprocal Change
ST elevation during acute STEMI is ASSOCIATED with simultaneous ST depression in the electrically opposite leads:
Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).
Reciprocal ST depression in aVL with inferior STEMI
Reciprocal ST depression in III and aVF with high lateral STEMI
Posterior Myocardial Infarction
Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.
Posterior MI
De Winters T Waves
This pattern of upsloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.
De Winter’s T Waves
Digoxin Effect
Treatment with digoxin causes downsloping ST depression with a “sagging” morphology, reminiscent of Salvador Dali’s moustache.
Hypokalaemia
Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.
Hypokalaemia
Right ventricular hypertrophy
RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.
Right ventricular hypertrophy
Right Bundle Branch Block
RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.
Right bundle branch block
Supraventricular tachycardia
Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment.
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