Catastrophies Flashcards
Xray signs of TAD? What are the pros and cons of Xrays for suspected TAD?
Widened mediastinum
Aortic knuckle double calc sign
Apical Cap
L) pleural effusion
NG/tracheal deviation
Abnormal aortic contour
Pros
- May show suggestive findings
- May show alternate diagnosis
- Can be performed at bedside
Cons
- Poor sens and spec
- Doesnt define extenet/type TAD
- May delay formal investigations
What is the definition of shock?
tissue ischaemia and cellular hypoxia due to one or more of hypoperfusion, increased 02 demand or inadequate 02 utilisation
What are the 5 types of shock?
Cardiogenic
Obstructive
Hypovolaemia
Distributive
Dissociative
What are the clinical signs of failure of fibrinolytic therapy in AMI?
- Persistent or worsening chest pain (particularly if associated dyspnoea and diaphoresis)
- Persistent or worsening STE
<50% resolution of STE at the 60-90min mark on ECG - Persistent or worsening haemodynamic instability
- Development or worsening heart failure
What are the absolute contra-indications to thrombolysis?
Any prior ICH
Known structural intracranial cerebrovascular disease ie AVM
Known brain malignancy
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or coagulopathy
Recent surgery of or encroaching on the brain/spine
Recent significant facial/brain trauma
What are the relative contraindications to thrombolysis?
> 75yrs
Pregnancy
Currently anticoagulated
Intercurrent non-compressible vascular puncture ie subclavian line
Traumatic cardiac arrest
Prolonged CPR >10mins before starting
History of chronic, severe or very poorly controlled HTN
Severe uncontrollable HTN on presentation with diastolic >110 or systolic >180
Known dementia
Recent stroke but >3months ago
Major surgery within 3 weeks
What is the role of thrombolysis in PE?
- Reduces the size of clots and improves pulmonary haemodynamics
- Has not been shown to have a definitive mortality benefit
- Reduces risk of PHTN
- Reduces the rate of further PE’s
- Less safe than catheter directed therapy
What are the risk factors for aortic dissection?
- Hypertension (most common)
- Connective tissue disorders (ie ehlers danlos, Turners and Marfans syndrome)
- Bicuspid aortic valve
- Aortic pathology (anuerysm, haematoma, ulcer)
- Recent aortic cannulation
- Co-arctation of the aorta
- High energy trauma
- Familial history
- Pregnancy and delivery
- inflammatory diseases affecting the aorta (syphilis aortitis, Takayasus, giant cell arteritis)
- Flouroquinolone use
What are the classifications for aortic dissection?
Stanford
- A involves ascending aorta +/- rest of aorta
- B only involves descending
Debakey
- I Involves the ascending +/- rest of the aorta
- II Confined to ascending aorta
- III Only involves the descending
Which rhythms should be synced for shocking?
Any rhythm with a conscious patient should be synced
Cardiac arrest rhythms including unconscious VT don’t shock
What can cause shock in an aortic dissection?
- Pericardial tamponade
- Haemorrhagic shock (ie massive loss into chest or abdomen)
- Tension haemothorax
- Acute aortic regurge
- STEMI from coronary dissection
- Iatrogenic from medications (hydralazine, labetalol etc)
- Pseudohypotension from limb vessel dissection
What is required for a venous air embolism to be fatal?
Air must overwhelm the pulmonary circulations ability to diffuse it
Usually large volume 3-5mls/kg required at a rapid rate (100ml/s)
However the more proximal the entry (ie Right heart cath) the smaller the amount of air required, with fatal doses reported as low as 50mls
What are the most common causes of venous air embolism?
- Surgery, particularly neurosurgery and otolaryngological procedures
- Significant trauma
- Central venous access, both on insertion and removal (ie deep inspiration at moment of removal)
- Barotrauma from ventilation
- Rapid ascent in scuba divers (a form of barotrauma)
- Rapid injection into peripheral lines of large amounts of air (most notably contrast)
What are the potential complications of a STEMI?
- Malignant tachyarrhythmias
- Acute heart failure and APO
- Acute (mitral) valve regurgitation with chordae tendinae rupture
- Free wall rupture and tamponade
- AV blockade and bradyarrhythmias
- Acute RV failure
- Septal rupture
- Dresslers syndrome longer term
How is acute mitral regurgitation often diagnosed and managed?
Usually presents as sudden acute cardiogenic shock with associated pulmonary oedema
Need to reduce SVR so that blood will move down the lower pressure gradient forward instead o backward
- Nitroprusside 0.5 - 10mcg/kg//min for SVR reduction
- IV diuretics such as frusemide
Often have associated acute LV failure, if so needs inotropy
- Dobutamine 1 - 40mcg/kg/min
Often have acute pulmonary oedema
- CPAP or BiPAP starting 5cmH20
