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:
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
A bone marrow biopsy is really a process that takes a tiny sample from the marrow within your bones for examining inside a laboratory. This kind of test can be used to determine if you have an infection, disease, and , or other problems in your bone marrow.
Marrow has the two reliable and liquid elements. If the solid part of the bone is sampled, this is often named a biopsy. Aspiration is the technique utilized to acquire the liquid a part of the marrow.
Bone marrow could be the spongy tissue found out inside your bones. From the much larger bones- like your spine, breastbone, hips, ribs, legs, or skull-bone marrow involves cells in which make white blood cells, Red blood cells, too as platelets. Your very own white blood cells aids in preventing infection, your Red blood cells carry oxygen also nutrition, whilst your platelets stimulate the blood to clot
Troubles with bone marrow can develop lasting, significant well being worries. A bone marrow biopsy is among a lot of tests which can be done to examine the cells of the bone marrow for difficulties or diseases.
Why Is a Bone Marrow Biopsy Done?
If blood screeningexhibitloweramounts of platelets or white or red blood
cells, your physician may
possibly order a bone marrow biopsy.
Problemsas well asillnessesthat couldaffect your
bone marrowinclude:
1- Anemia,all types
2- bone marrow diseases, such as myelofibrosis or myelodysplastic syndrome
3- blood cell illnesses, like as leukopenia or polycythemia
4- cancers of the bone marrow or blood, like as leukemias or lymphomas
5- hemochromatosis, a genetic disorder in which iron builds in the blood
infection, such as sepsis
NB.
A bone marrow biopsy can be a crucial take a look at should you be undergoing cancer treatment, as it might help identify if the most cancers has unfold in your bones
Risks of a Bone Marrow Biopsy
On the other hand in some uncommon situations, the following complications are probable:
A- allergic reaction to anesthesia
B- excessive bleeding
C- infection
D- long-lasting discomfort at the spot exactly where the biopsy was taken
These dangers are rare and most generally take place among individuals who have other situations that weaken their immune systems or decrease their platelet counts
How to Prepare for a Bone Marrow Biopsy?
Your medical doctor will carry out various examinations prior to the biopsy. Through these tests, be sure to tell your physician about any medications you take-including over-the-counter medicines or nutritional supplements-and any known allergies you have got.
Your doctor may possibly ask you to stop taking specific medicines prior to the process. By no means stop taking a medication unless your medical professional instructs you to complete so.
Tell your medical doctor should you be nervous. He or she may well give you a mild sedative that will help you via your process.
Stick to all of your doctor’s instructions before the process. Usually do not overlook to show up on time for your biopsy. You might also choose to arrange to get a ride dwelling.
How a Bone Marrow Biopsy Is Performed?
you will be asked to alter into a hospital gown, Ahead of the test. Then you will stay in your part or rest in your tummy in a area exactly where the process is going to take place.
A doctor or registered nurse will provide you with a nearby sedation to numb the location exactly where the biopsy is going to be used. Usually this may be at the major ridge of your back end hipbone. Occasionally it might be studied from your upper body bone fragments.
You might really feel a brief sting as the anesthesia is injected.
Your medical professional is likely to make a modest cut so a hollow needle can easily get previous the facial skin. The needle then will go in to the bone tissue. It records a cylinder-formed test recognized like a primary sample.
According to the National Institutes of Overall health, some individuals feel a dull discomfort or discomfort because the biopsy is taken, since the inside of the bones cannot be numbed. the Federal Organizations of Wellness, a number of people feel a uninteresting pain or soreness because the biopsy is taken, considering the fact that the inside of the bones can not be numbed, . Even so, not every person will experience this. (NIH, 2010)
Right away following the process, the cut might be bandaged, and you will be used into one more area to relax just before going home.
After a Bone Marrow Biopsy
You could feel some slight discomfort for about per week just after the procedure. That is easily managed with over-the-counter pain relievers. You are going to also need to care for the incision wound, which includes maintaining it dry for 24 hours following the biopsy.
When you happen to be caring for the wound, your bone marrow sample is going to be sent to a laboratory for testing. When the outcomes are back, your doctor may possibly contact you or have you come to their workplace to get a follow-up appointment to talk about the findings.
Abnormal results may be as a result of cancer, anemia, or an additional condition. Your physician may require to order far more tests to confirm a diagnosis or to determine how far the condition has gone. She or he will discuss your treatment options with you and enable you to strategy your subsequent measures during your follow-up appointment.
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:
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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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