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acute care Flashcards

1
Q

stroke - investigations?

A

BEDSIDE
* Focused history
* Time from stroke onset (for eligibility for acute stroke treatments e.g. tPA)
○ If unclear, ask when they were last known to be unaffected/baseline
○ If person woke up with symptoms, time of onset defined as when patient last awake and symptom-free

  • Level of consciousness - GCS
  • A-E assessment
  • Basic observations especially blood pressure
  • Neurological examination
  • FAST - new facial weakness, arm or leg weakness, speech disturbance
  • Cardiovascular examination
  • ECG - looking for afib

BLOODS
* Blood glucose (rule out hypoglycaemia, glucose <3.3mmol/L)
- lipid profile
- urea and electrolytes (e.g. hyponatraemia causing neurological symptoms, urea for upper GI bleed which is contraindication for thrombolysis)
- cardiac enzymes
- clotting profile
- FBC

IMAGING
* Non contrast-CT head to rule out intracerebral haemorrhage
* Carotid imaging e.g. carotid ultrasound or CT or MRI angiogram

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2
Q

ischaemic stroke management

A

In primary care:
* Immediate emergency admission to stroke unit
* Avoid anti-platelet tx until haemorrhagic stroke has been excluded!

Whilst transferring:
* Supplemental O2 if sats <95% and no contraindications

Short term:

* Exclude hypoglycaemia

ISCHAEMIC STROKE:
* THROMBOLYSIS :Nalteplase or tenecteplase if within 4.5 hours of symptom onset & intracranial haemorrhage excluded by appropriate imaging techniques [should be done within specialist stroke centre)
○ Blood pressure should be lowered to 185/110 mmHg before thrombolysis.

* 24 hours after thrombolysis: antiplatelet (unless contraindicated)

* THROMBECTOMY: considered in patients with a confirmed blockage of the proximal anterior circulation or proximal posterior circulation.  May be considered within 24 hours of symptom onset and alongside IV thrombolysis
* Carotid endarterectomy (if carotid artery stenosis > 70%), angioplasty, and stenting

*patients with disabling acute ischaemic stroke should be started on aspirin ASAP within 24 hours and continued for 2 weeks after stroke onset - when long-term antithrombotic treatment should be started

If atrial fibrillation: 2 weeks of aspirin and then anticoagulate with apixaban

PPI with aspirin for patients with history of dyspepsia associated with aspirin or concurrent use with dual antiplatelet therapy to reduce risk of GI haemorrhage
Aspirin hypersensitivity -> clopidogrel

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3
Q

haemorrhagic stroke management

A
  • Surgical intervention - remove haematoma and relieve intracranial pressure
    • Blood pressure lowering treatment - beta-blockers or ACE inhibitors
    • Do not give rapid blood pressure lowering treatment for:
      ○ Patients with underlying structural cause
      ○ GCS <6
      ○ Early neurosurgery
      ○ Very large haematoma with poor prognosis
    • Do give rapid blood pressure lowering treatment for:
      ○ Patients presenting within 6 hours of symptom onset
      ○ Systolic BP 150-220
      ○ Do not fit any exclusion criteria

Aim for systolic BP 130-139 within 1 hour and sustained for at least 7 days, ensuring that magnitude drop does not exceed 60mmHg within 1 hour of starting treatment

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4
Q

TIA: investigations?

A

BEDSIDE

  • focused history
  • observations
  • cardiovascular examination
  • neurological examination
  • ECG

BLOODS

  • blood glucose
  • FBC
  • clotting profile
  • lipid profile
  • urea and electrolytes

IMAGING

  • diffusion weighted MRI
  • carotid artery duplex
  • CT if on blood-thinners
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5
Q

STEMI management

A
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6
Q

NSTEMI management

A

MONA +

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7
Q

Cardiac arrest management

A
  1. Recognition and Call for HelpConfirm unresponsiveness and absence of normal breathing.
    Call for help and start CPR immediately.
  2. Initiate Basic Life Support (BLS)30:2 Chest compressions: Ventilations (rate: 100-120/min, depth: 5-6 cm).
    Ensure good airway management (head tilt-chin lift or jaw thrust).
  3. Attach Defibrillator/Monitor ASAPAssess rhythm:
    Shockable (VF/pVT): Deliver shock and resume CPR for 2 min.
    Non-shockable (PEA/asystole): Resume CPR for 2 min.
  4. Provide Advanced Life SupportEstablish IV/IO access.
    Deliver drugs during CPR cycles:
    Shockable (VF/pVT):
    1 mg adrenaline (every 3-5 min, after 2nd shock).
    300 mg amiodarone (after 3rd shock; 150 mg after 5th shock if persistent VF/pVT).
    Non-shockable (PEA/asystole):
    1 mg adrenaline ASAP, then every 3-5 min.
  5. Reassess Rhythm Every 2 MinAlternate CPR providers every cycle to maintain quality.
  6. Address Reversible Causes (4 Hs and 4 Ts)4 Hs: Hypoxia, Hypovolemia, Hyper-/Hypokalemia, Hypothermia.
    4 Ts: Tension pneumothorax, Tamponade, Toxicity, Thrombosis (coronary/pulmonary).
  7. Post-Resuscitation CareStabilize airway, breathing, circulation.
    Treat underlying cause.
    Transfer to critical care for further management.
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8
Q

what are the reversible causes of cardiac arrest?

A

5Hs, 4Ts, 1N

* Hypoxia - O2
* Hypovolaemia - ?haemorrhage. Fluid, blood, urgent surgery to stop the haemorrhage
* Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia, and other metabolic disorders - IV calcium chloride in presence of hyperkalaemia, hypocalcaemia, and calcium channel blocker overdose
* Hypothermia - old people do not shiver! Reduced ability to thermoregulate. Drowning!
* Hypoglycaemia

* Tension pneumothorax - may follow attempts at central venous catheter insertion.
	○ Decompress rapidly by thoracostomy or needle thoracocentesis and then insert a chest drain
* Tamponade - typical signs of distended neck veins and hypotension cannot be assessed during cardiac arrest.
	○ Cardiac arrest after penetrating chest trauma or after cardiac surgery
	○ Needle pericardiocentesis or resuscitative thoracotomy
* Toxic substances - supportive, antidotes if available
* Thromboembolic - massive PE Thrombolytic drug immediately & 60-90 minutes CPR

Naloxone

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9
Q

order of ECG changes of acute STEMI

A
  • hyperacute T waves
  • ST elevation
  • Q waves
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10
Q

investigations after ECG shows STEMI

A
  • troponin
  • investigations for complications: BNP, echo
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11
Q

complications of MI

A

FAM

  • failure (left ventricular, right ventricular, CCF)
  • arrhythmias (VT, VF)
  • murmurs (papillary muscle rupture MV, intraventricular septum rupture VSD)
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12
Q

causes of a dominant R wave in lead VI

A
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13
Q

young person having MI with no risk factors - what is likely cause?

A

cocaine induced

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14
Q

chest pain + normal(ish) ECG causes?

A

pulmonary embolus

dissection

abdominal causes:
- perforation
- pancreatitis
- cholecystitis

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15
Q

diagnosing MI in atypical patient

A
  • bilateral radiation (worse in right than left)
  • pain on exercise
  • diaphoresis
  • vomiting
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16
Q

a super important question to ask with any symptom

A

is this presentation the same as the last time they presented with that same thing

17
Q

why do women have worse prognosis with acute care

A
  • painless MIs more common

atypical sx:
- SOB
- sleep disturbance
- fatigue

18
Q

VT

A

3 broad complex QRSes

19
Q

___ is to asthma what BM is to diabetes

A

peak flow

  • do before and after nebulisers!
20
Q

asthma not responding to treatment - one differential to think about?

A

pneumothorax

21
Q

back in IVDU

A

discitis until proven otherwise

22
Q

to rule out with acute abdo

A

black bowel

retrocaecal appendicitis

ectopic

torsion

23
Q

tachycardia + narrow pulse pressure + tenderness to ribs

A

bleed!

splenic or liver

24
Q

grades of haemorrhagic shock

A

grade 1: low BP

grade 2: diastolic rises

grade 3: systolic drops

25
Q

treating different grades of shock

A
26
Q

types of shock

A

Septic
Haemorrhagic
Neurogenic
Cardiogenic
Anaphylactic

27
Q

septic shock

A

Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.

Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3.

Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ failure have severe sepsis and those with refractory hypotension -septic shock.

During the septic process there is marked activation of the immune system with extensive cytokine release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those of excessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for attention:

Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous search for the source of infection.
Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.
Modulation of the septic response. This includes manoeuvres to counteract the changes and includes measures such as tight glycaemic control. The routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with anastomotic leaks, abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery the aim should be to undertake the minimum necessary to restore physiology. These patients do not fare well with prolonged surgery. Definitive surgery can be more safely undertaken when physiology is restored and clotting, in particular, has been normalised.

28
Q

neurogenic shock

A

This occurs most often following a spinal cord transection, usually at a high level. There is a resultant interruption of the autonomic nervous system. The result is either decreased sympathetic tone or increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance mediated by marked vasodilation.

This results in decreased preload and thus decreased cardiac output (Starling’s law). There is decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types of shock peripheral vasoconstrictors are used to return vascular tone to normal.

29
Q

cardiogenic shock

A

In medical patients the main cause is ischaemic heart disease. In the traumatic setting, direct myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but they are less useful in delineating the extent of myocardial trauma than following MI.

When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the most likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may require intra-aortic balloon pump as a bridge to surgery.

30
Q

anaphylactic shock

A

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.

Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated. Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible.
Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the middle third of the thigh.

Common identified causes of anaphylaxis

food (e.g. Nuts) - the most common cause in children
drugs
venom (e.g. Wasp sting)
31
Q

most likely cause of chemical nausea - ie feeling nauseous all the time but vomiting small amounts

A

renal impairment
infection
medication
hypercalcaemia

32
Q
A

y6 (13 decks)

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