Intensive Care - Lectures Flashcards
Outline 8 functions of both the parasympathetic and sympathetic autonomic nervous system.
Which segments of the spinal cord are responsible for which sympathetic functions?
Which 4 Cranial Nerves have sympathetic activity?
Which neuroreceptors act in the PSNS and which in the SNS?
CNs 3, 7, 9, 10
- CN 3 = pupillary constriction when PSNS activated
- CN 7 = Salivation & Lacrimation
- CN 9 = Cough & Gag & Salivary glands in back of throat/mouth
- CN 10 = Vagus nerve
What are the 5 Sympathetic receptors and their actions?
What are the 5 Parasympathetic receptors and their actions?
What are Vasopressors?
List 5 Examples used in ICU.
Vasopressors = Chemical that causes vasoconstriction
2. Noradrenaline
2. Metaraminol
3. Vasopressin
4. Dopamine
5. Adrenaline
What are Inotropes?
List 6 Examples used in ICU.
Inotropes = Chemical that effects heart contractility.
1. Adrenaline
2. Dobutamine
3. Dopamine
4. Milrinone = prevents breakdown of cyclic-AMP
5. Levosimendan = Calcium sensitiser
6. Salbutamol
What are Chronotropes?
List 5 Examples used in ICU.
Chronotropes = Chemical that effects heart rate
1. Adrenaline
2. Dobutamine
3. Salbutamol
4. Atropine
5. Isoprenaline
Adrenaline
- MOA - which 2 receptors?
- 5 Uses?
- 5 Side effects?
- Dose - Shock? Arrest? Anaphylaxis? Infusion? Nebulised?
- Adrenaline = Inotrope, chronotrope & vasopressor
- Causes lactate to rise – but the problem is that you don’t know if it’s the adrenaline or ischemia!
Noradrenaline
- MOA - which 3 receptors?
- 2 Uses?
- 4 Side effects?
- Dose - IV?
- BP rises but HR fairly stable
- Can only give through central line as peripherally it causes tissue necrosis if leak
- Metaraminol can be used peripherally
Metaraminol
- MOA - Direct & Indirect?
- Use?
- 1 Side effect?
- Dose - Bolus? Infusion?
Dobutamine
- MOA - Which receptor?
- 2 Uses?
- 3 Side effects?
- Dose?
Dopamine
- MOA - Which receptors at which doses?
- 3 Uses?
- 3 Side effects?
Vasopressin
- MOA - Which receptors at which doses?
- 3 Uses?
- 3 Side effects?
- Dose - Shock? DI?
- V1 on blood vessels & V2 on kidneys (hold onto water = up BP)
Atropine
- MOA?
- Use?
- 4 Side effects?
- Dose - Max?
Isoprenaline
- MOA?
- 2 Uses?
- 4 Side effects?
- Dose - Time to effect? Dose? Rate?
List 3 Commonalities amongst drugs used in ICU - inotropes/vasopressors?
Commonalities
1. All have very short half-lives (mins) so given by infusion and titrated to effect.
2. Very low bioavailability so parenterally only.
3. Metabolised by MAO and COMT systems to inactive metabolites released in the urine.
What is the equation for blood pressure?
What is the equation for cardiac output?
What is the defintion of shock?
- BP = CO x SVR
- CO = HR x SV
- So low BP can be due to low cardiac output state OR low resistance state.
- Shock = Shock is a state of circulatory failure characterised by inadequate tissue perfusion.
What is Distributive Shock?
- 5 Examples?
- Treatment? (4 points)
Distributive shock = Low BP due to low systemic vascular resistance/vasodilation
1. Septic shock
2. Pancreatitis
3. Spinal cord injury
4. Drug overdose
5. SIRS
Treatment = VASOPRESSOR +/- fluids
- Metaraminol for short term peripheral IV support
- Noradrenaline mainstay of treatment
- Dopamine used less often
- Vasopressin 2nd line if required
What is Cardiogenic Shock?
- 4 Examples?
- Treatment? (3 points)
Cardiogenic Shock = Low BP due to low CO
1. Myocardial infarction
2. Myocarditis
3. Myocardial contusion
4. Drugs/toxins
Treatment = Support with an INOTROPE +/- fluid
1. Dobutamine
2. Adrenaline
3. Milrinone
What is Anaphylactic Shock?
- First line tx?
- 4 Adjuncts?
- Side effects?
- Management algorithm?
Anaphylaxis = Specific form of distributive shock
- First line 0.5mg adrenaline IM
- May require repeat doses +/- infusion
- Adjuncts: 1. Oxygen, 2. IV fluida, 3. Steroids, 4. Salbutamol
- Side effects; tachycardia, flushing, headache
Outline a clinical approach to bradycardia.
Outline the ALS Algorithm for Adults
- 5 things to consider during CPR?
- Drugs - Shockable?
- Drugs - Non-shockable?
- 5 Hs & 5 Ts?
- 5 Post resus care?
Post resuscitation care in the Emergency department
1. Re-evaluate ABCDE
2. 12 lead ECG
3. Treat precipitating causes
4. Evaluate oxygenation and ventilation
5. Begin targeted temperature management (TTM)
List the possible causes of OOHCA (Out of Hospital Cardiac Arrest)
- 4 Cardiac?
- 10 Other causes?
- 6 Investigations to order in ED?
Investigations for OOHCA
1. 12 lead ECG
2. +/- Point of Care Transthoracic ECHO
3. CXR
4. ABG and baseline blood tests
5. CT Head or CTPA – depending on clinical history
6. Cath lab for urgent angiogram = VF/VT & STEMI
Algorithm for OOHCA for patients who have achieved ROSC but remain comatose?
List 8 factors that would make a patient who has had an OOHCA unfavourable for cath lab?
- Unwitnessed arrest
- Initial non-VF Rhythm
- Lack of bystander CPR
- > 30 min to ROSC or >30 min of CPR
- Evidence of unresponsive hypoperfusion and microcirculatory failure - eg. pH <7.2 and Lactate >7
- Age >85
- End-Stage Renal Disease (ESRD)
- Non-Cardiac Causes: Cardiac arrest due to drugs, drowning, acute stroke, terminal cancer and trauma, just to name a few non-cardiac causes, are likely to result in poor outcomes post-resuscitation.
What ICU Care is involved for a patient who has had an OOHCA?
- List the 3 Haemodynamic supports?
ICU Care for OOHCA
* Ensure underlying cause identified and treated
* Cardiovascular support = Inotropic support: MAP >65
* Neurological support
What is the Targeted temperature management for a patient who has suffered an OOHCA?
- How?
How?
1. Arctic Sun
2. IV cooling devices
3. Cooling blankets
Outline the natural history of shock post OOHCA?
List 3 features of Global hypoxic brain injury on CT Head?
Which scan can be performed to diagnose brain death? Which sign is visible?
- Loss of grey/white matter differentiation
- Effacement of the sulci & gyri
- Effacement of the ventricles
Brain Death – Nuclear Medicine Perfusion Scan
* Injects die which should cross the BBB, may stop at carotid arteries/foramen magnum as no contrast entering brain = empty box sign.
MET Calls
- What should you do?
- 4 Bedside Investigations?
What is the Adult observation and response chart (AORC)?
- Which 11 parameters are recorded?
- Which vital signs are highly predictive of ICU/HDU admission?
- Outline the escalation protocol?
Adult observation and response chart (AORC)
- Purpose is to identify the deteriorating patient early and escalate to medical review before they become critically unwell.
- Highly sensitive for unwell patients, not very specific.
- Parameters: 1. RR, 2. O2 sats, 3. O2 flow rate, 4. HR, 5. BP, 6. Temp, 7. Conciousness, 8. BSL, 9. UO, 10. Pain score, 11. Intervention
- Certain vital signs are highly predictive of ICU/HDU admission
- Tachypnoea > Low urine output
- Hypotension > Hypertension
- Tachycardia > Fever
What are the normal ranges for the following/when would you escalate care?
- Respiratory rate?
- O2 Sats?
- O2 Flow Rate?
- HR?
- Systolic BP?
- Temp?
Normal Ranges
- Respiratory rate = 10-15bpm
- O2 Sats = >95%
- O2 Flow Rate = 0-6L/min
- HR = 60-100bpm
- Systolic BP = 110-159
- Temp = 36.5-37.5
- Conciousness = Alert (vs. To Voice, To Pain, UnRespons)
List 5 COMMON IMPORTANT MET CALL SCENARIOS?
- What is your approach/management to a MET for “No signs of life”?
COMMON IMPORTANT MET CALL SCENARIOS
1. NO SIGNS OF LIFE
2. HYPOXIA
3. HYPOTENSION
4. LOW GCS
5. TACHYCARDIA
What are the two fundamental causes of a shunt?
- List 9 Causes of of shunt and diffusion abnormality?
- A patient who is hypoxic has a shunt or diffusion abnormality.
- Shunt = An area with perfusion (blood) but no ventilation (oxygen) (and thus a V/Q of zero).
- Diffusion Abnormality = thickening of the alveoli and capillary interface so that gas is unable to diffuse appropriately into the blood.
- Shunt is almost always in the lungs.
- Therefore, you must examine the chest and do a CXR to find the cause!
Outline the management of hypoxia as a MET call?
- Which 3 investigations urgently?
- Which Oxygen delivery system?
Explain an approach to a Hypotension MET Call?
3 Fundamental causes of a hypotensive shock? Exam findings?
Classify the types of shock and their mechanisms.
Outline an approach to a MET call for “Low GCS”? Which examinations? Which 2 investigations?
What are you trying to differentiate between in terms of the cause?
Outline the GCS.
What is the most likely diagnosis? Treatment?
- Most likely diagnosis = Narcotised secondary to opioids
- Treatment = Naloxone 40-400ug IV and stop opioids
What is the most likely diagnosis? Treatment?
- Most likely diagnosis = Intracerebral haemorrhage
- Treatment = Secure airway, urgent CT head, reverse INR
If you get called to a MET for tachycardia, what is the one question you need to ask yourself?
Differentials?
Tachycardia
- Need to answer 1 question and 1 question only……
- Is this a cardiac arrhythmia or sinus tachycardia???
- Study the ECG carefully
Management of a MET call for Tachycardia?
- Which Bedside investigations?
- Which meds? Dose?
In all cases…
1) Give oxygen
2) Vital signs are vital
◦ Pulse and BP especially important
◦ Temperature - Usually tachypnea also
3) Make an early, accurate assessment of GCS
◦ Airway protection compromised if GCS <8
◦ Defibrillate if unconscious (GCS 3)
4) Use “Bedside investigations”
◦ In this case ECG, ABG, BSL, CXR for diagnosis and severity
What is the difference between sepsis and septic shock?
Sepsis represents a spectrum of disease with mortality risk ranging from moderate (eg, 10%) to substantial (eg, > 40%) depending on various pathogen and host factors along with the timeliness of recognition and provision of appropriate treatment.
Septic shock is a subset of sepsis with significantly increased mortality due to severe abnormalities of circulation and/or cellular metabolism. Septic shock involves persistent hypotension (defined as the need for vasopressors to maintain mean arterial pressure ≥ 65 mm Hg, and a serum lactate level > 18 mg/dL [2 mmol/L] despite adequate volume resuscitation.
How do you investigate for causes of respiratory tract infections in any patient? (5 points)
A 40yo indigenous lady from Derby. She is admitted with cough, sore throat and fevers. This has occurred over the last 2-3 days. She is producing a green phlegm.
On examination she is febrile 38.5, tachycardic 120 bpm and saturating 88% on room air. Her blood pressure is low at 90/55 mmHg.
What will your antibiotic management be and why?
Consider the eTG for Moderate CAP in adults in tropical regions of Australia
A 40yo indigenous lady from Derby. She is admitted with cough, sore throat and fevers. This has occurred over the last 2-3 days. She is producing a green phlegm.
On examination she is febrile 38.5, tachycardic 120 bpm and saturating 88% on room air. Her blood pressure is low at 90/55 mmHg.
What are the methods available to treat her respiratory failure? (6)
The presented clinical scenario suggests that the patient is experiencing respiratory distress, as evidenced by a low oxygen saturation of 88% on room air. Management of respiratory failure involves addressing the underlying cause, providing supportive measures, and ensuring adequate oxygenation. Here are some methods available to treat respiratory failure in this patient:
A 40yo indigenous lady from Derby. She is admitted with cough, sore throat and fevers. This has occurred over the last 2-3 days. She is producing a green phlegm.
On examination she is febrile 38.5, tachycardic 120 bpm and saturating 88% on room air. Her blood pressure is low at 90/55 mmHg.
How will you manage her cardiovascular system during this illness? (6)
Managing the cardiovascular system in a patient with respiratory distress and signs of sepsis involves a combination of supportive measures, fluid resuscitation, and, if necessary, vasoactive medications. The low blood pressure (hypotension) in this patient suggests the possibility of septic shock, and prompt intervention is crucial.
A 40yo indigenous lady from Derby. She is admitted with cough, sore throat and fevers.
This has occurred over the last 2-3 days. She is producing a green phlegm. On examination she is febrile 38.5, tachycardic 120 bpm and saturating 88% on room air. Her blood pressure is low at 90/55 mmHg. She is a type 2 diabetic and has hypertension. Her baseline creatinine is 120umol/L and today is 200umol/L. How will you reduce the chance of progression to acute renal failure? (10 points)
In the context of a patient with respiratory distress, signs of sepsis, and acute kidney injury (evidenced by an increase in creatinine levels), it’s essential to take a comprehensive approach to reduce the risk of progression to acute renal failure.
What causes of sepsis/septic shock require urgent surgery? (9 Examples)
A 60yo patient with chronic renal failure and haemodialysis 3 times a week is admitted to the emergency department with breathlessness. He has missed his last session of dialysis as his car battery was flat. While you are clerking him, he has a sudden arrest in the resuscitation bay. It is a PEA arrest. His blood gas during CPR show the following:
pH = Acidotic
pCO2 = Hypercapnia
???
Critical Care Masterclass - Torre
What is the broad aim of neurocritical care?
Which 2 parameters are most important to control for this?
What is Cerebral Blood Flow?
- What is the equation for calculating CBF?
- How can we measure it?
- What is cerebral perfusion pressure?
- How is CPP calculated?
- What is the CPP normal range?
Cerebral Blood Flow
- CBF is critical: complete interruption results in loss of conciousness in seconds; permanent neuronal damage in minutes!
- CBF: 750mls/min (15% cardiac output)
- CBF: Via paired internal carotid arteries (70%) and paired vertebral arteries (30%)
- Flow through tubes broadly depends upon pressure difference between two points and the resistance of the tube. This is the same for CBF where the perfusion pressure and cerebral vascular resistance change CBF.
What is the effect of PaO2 on cerebral blood flow?
How is CBF autoregulated? Which ranges?
How can cerebral perfusion pressure be measured/monitored?
(remember the equation)
CCP = MAP - ICP
- Why is intracranial pressure important? (2 things)
- What is the Monroe-Kellie doctrine?
- What are the ICP compensatory mechanisms?
- Describe the intracranial pressure-volume curve?
Intracranial pressure is important for 2 reasons:
1. A factor in cerebral blood flow (CBF)
2. Can deform brain parenchyma and result in herniation syndromes
The Monroe-Kellie Doctrine
- Describes the pressure-volume relationship in the cranial cavity
- The sum of the intracranial contents (brain parenchyma, blood and CSF) is constant within a fixed volume. An increase in one will result in an increase in ICP unless compensated by a reduction in another.
Describe 6 different types of brain herniation syndromes and their complications?
Cerebrospinal Fluid (CSF)
- How much is produced per day?
- Entire volume at any one time?
- Describe the production & pathway of flow of CSF?
CSF: Choroid plexus production, ~500mls/day (21mls/hr), entire CSF volume at any one time is 150mls
What are the 2 types of Hydrocephalus?
How do we classify Traumatic Brain Injuries? (4)
- What is Diffuse Axonal Injury?
- What is the definition of a primary and secondary TBI?
Traumatic Brain Injury
1. Mechanisms: Blunt vs. penetrating
2. Severity: Mild (GCS 13-15), Moderate (GCS 9-12) & Severe (GCS 3-8)
3. Anatomical characteristics of injury: Focal (extradural, subdural & SAH, coup & contra-coup) vs. Diffuse Axonal Injury
4. Pathophysiology: Primary vs. Secondary injury
Extradural Haematoma
- Appearance on CT?
- Location of bleed?
- Usual cause?
- Clinically?
Subdural Haematoma
- Appearance on CT?
- Location of bleed?
- Usual cause?
- Clinically - hx?
Outline the Management of TBI
- General? (14 points)
- Specific? (3)
- What are the indications for an intracranial pressure monitor insertion? (4)
- What ICP & CPP ranges are you aiming for?
- What is resitant/refractory ICP and how is it managed?
Resitant/Refractory ICP
- ICP >20mmHg for 15mins despite general measures (sedation, analgesia, positioning, not seizing, EVD draining etc.)
Management
1. Hyperosmolar therapy: mannitol or hyperosmolar saline
2. Hyperventilate (CO2 30-35mmHG) = Hypercapnia induces cerebral vasodilation and ↑ cerebral blood flow (CBF) and hypocapnia (hyperventilating) = ↓CBF
3. Repeat CT
4. Decompressive craniotomy - needs consideration as may improve ICP and ICU duration but does not necessarily improve outcomes.
What are the 4 Types of Strokes - give definitions?
What is not considered a stroke? (3)
Ischaemic Stroke
- Define an Acute Ischamic Stroke?
- Define a TIA?
- What is the difference between the two?
- Aetiology of Ischaemic Stroke? (5)
- BE FAST detection of stroke?
Aetiology of Ischaemic Stroke
1. Atherosclerosis (large vessel) - eg. carotid artery stenosis
2. Cardioembolic - eg. atrial fibrillation
3. Small vessel occlusion - eg. lacunar strokes
4. Strokes of other determined aetiology - eg. vasculitis, carotid dissection
5. Strokes of undetermined aetiology = “cryptogenic strokes”
Ischaemic Stroke
- Which imaging investigations are indicated? What will they show?
Ischaemic Stroke
- What is the management? (2 specific)
Intracerebral Haemorrhage
- 2 Aetiologies?
- What kind of bleed are they often associated with? Complication?
- Why does damage actually occur?
- What are the principles of management?
- BP Target range?
Intraventricular haemorrhage
- Often associated with intraparenchymal haemorrhage (extension of it into the ventricles) or subarachnoid haemorrhage
- Prone to result in obstructive hydrocephalus
Damage
- Occurs because the intracranial environment is disrupted: direct pressure effects (local compression/more general high ICP) & biochemical toxicity because of blood products themselves (Hb, iron, thrombin)
What is the issue with any posterior fossa mass?
- What is in the posterior fossa?
Subarachnoid Haemorrhage
- Aetiology?
- Clinically?
- Appearance on CT?
- Definitive mx options? (2)
SAH Aetiology
- Vast majority associated with aneurysm (80%)
- Often in younger patients
Clinically
- Presents with “thunderclap” headache, worst headache of my life, maximal intensity in seconds
- Brief LOC, vomitting, focal neurological signs, photophobia, meningism may all be present
Complications of SAH
- List 3 neurological comps?
- 3 general comps?
- What comp is of particular importance? Timeframe? Monitoring? Prevention? Treatment?
- What is vasospasm?
Complications of SAH
While there may be many neurological (eg. re-bleed, seizures, hydrocephalus etc), and general complications (pneumonia, arrythmias, DTV etc.) of particular importance for SAH is Delayed Cerebral Ischaemia
Delayed Cerebral Ischaemia
- A clinical syndrome of focal neurological deficits that develop in some patients between days 4 & 14 after SAH.
- “Vasospasm” is the angiographical narrowing of the blood vessels
- The two are often used synonymously, although they are not altogether the same. Other factors contribute to DCI.
What is the definition of Sepsis?
- Why was a new definition proposed?
Definition = Sepsis is life-threatening organ dysfunction due to a dysregulated host response to infection.
Definitions
* In 2016 revised definition of sepsis was released – “SEPSIS-3”
* Previous definition from Surviving Sepsis Guidelines (2001) – be aware of the existence of a previous definition “SEPSIS 2”
* Original definitions developed in 1991 “SEPSIS 1”
Describe the difference between an infection, sepsis, septic, shock and MODS?
- Definition of Septic Shock theoretically vs. Clinically?
What is a SOFA Score?
What are 4 problems with SOFA?
Issues with SOFA
1. Hard to memorise the table
2. What if you don’t know the patient’s baseline score?
3. You can get a point for closing your eyes!
4. What if you’re in a hospital that doesn’t use dobutamine or dopamine?
Sepsis
- Why is SOFA important?
- What can make SOFA easier?
- What is Septic Shock? Clinical Criteria?
Outline the Pathophysiology of Shock.
- Activators?
- Receptors?
- Amplifier?
- The result?
Pathophysiology of Sepsis - Arises from interaction between 2 components:
1. Pathogen – bacteria, virus, fungus or parasite
2. Host – immune response to pathogen, inflammatory cascade, activation of coagulation system
- Presence of cytokines, vasoactive mediators, activated coagulation products results in end- organ effects which leads to clinical syndrome of sepsis
Inflammation in sepsis results from pathogen triggered host cell response – leading to activation of the innate and adaptive immune systems.
What are the Steps in generation of septic shock?
Steps in generation of septic shock
1 - Inflammatory response with WBC activation, complement system activation, coagulation system activation, decreased anticoagulant activation.
2 - Results in:
1. Increased vascular permeability leading to hypovolaemic shock.
2. Vasodilation leading to distributive shock.
3. Myocardial depression leading to cardiogenic shock.
4. Intravascular thrombosis leading to microcirculatory disturbances and cell ischaemia.
3 - Tissue hypoperfusion from above mechanisms leads to organ ischaemia and multiorgan failure.
Can also cause activation of the coagulation pathway = thrombi = DIC
What are 7 mechanisms by which organs are actually damaged in septic shock?
Pathogenesis of Sepsis: Organs damaged by:
1. Interstitial oedema
2. Microvascular thrombosis
3. Reduced red cell deformability.
4. Vasodilation and hypotension
5. Cardiomyopathy (sepsis induced)
6. Direct (organisms)
7. Indirect (inflammation)
What are the Common causes of sepsis in ICU?
Sepsis - Clinical Presentation
- Manifestations of Infection? (6)
- Manifestations of Organ Damage? (5)
Sepsis - Clinical Presentation
- Variable depending on host, organism, site of infection, and clinical course - eg. may not illicit a host response as immunocompromised.
- Categorised as manifestation due to infection & organ damage
What are the Principles of Management of Sepsis? (Surviving Sepsis Campaign)
- What is the aim of investigations?
- Which investigations would you consider?
Principles of Management – Surviving Sepsis Campaign
1 - Investigations - The aim of investigations is to
1) identify the source of infection
2) Guide specific therapy (guide source control & Abx choice/duration)
3) Diagnose DDxs (abdominal sepsis may prove to be pancreatitis)
2 - Specific Therapy
3 - Supportive Therapy
Describe the Specific Therapy Management of Sepsis
- 2 Components of Specific Therapy?
- Timing, Delivery & Choice of Abx?
- Source control by organ? Examples?
Sepsis - Specific Therapy
1 - Antimicrobials
- Therapies targeting the aetiological agent (ie. the infection - the specific agent that has resulted in the sequelae of organ dysfunction.
2 - Source Control
- This means identifying and removing the microbioligical source of infection, controlling ongoing contamination, & restoring premorbid anatomy & function
- Early (as soon as medically & logistically possible)
- Examples: abscess drainage, abdominal washout/repair GIT perforation, drainage cholangitis (cholescytectomy or via ERCP), pyelonephritis (eg. nephrostomy or JJ stent), debridement of necrotising soft tissue infection, removal of implanted devices.
Sepsis - Supportive Therapy
- Definition?
- 5 Components? 7 Additional therapies?
- Why do we give fluids & vasopressors/inotropes?
- Which fluids & how much?
- Which vasopressors? Which inotropes?
- Monitoring?
Sepsis - Supportive Therapy
= Provision of therapy to optimise organ function, prevent further deterioration and allow for recovery whilst infection and resulting sepsis is specifically treated.
1. Fluid resuscitation
2. Vasopressor/inotrope
3. Additional therapies: Oxygen/ventilation, Renal replacement therapy, glucose control, stress ulcer prophylaxis, DVT prophylaxis, blood products, nutrition
4. Disposition decision
5. Communication/Goals of Care
Sepsis - Supportive Management: Additional Therapies
- Role of Hydrocortisone?
- When to transfuse with Packed Red Cells?
- When to initiate actrapid infusion?
- Role of Vitamin C?
- Remember adrenaline also causes an increase in lactate which is an issue as you don’t know if you’re making the ischemia worse hence why noradrenaline is preferred.
- Don’t tend to transfuse patients with sepsis with PRBC unless bleeding/low Hb
Sepsis - Organ Supports: Cardiovascular
- What are the clinical problems with the CVS system in septic shock? (4)
- Resuscitative Care?
- Target MAP?
- Distributive shock most common – warm peripheries but 10% cardiogenic so peripherally shut down
- Avoid normal saline as its acidic, CSL = more balanced
- Cardiac ischemia – MI if underlying IHD
- Target MAP to >65mmHg – usually done with volumne & vasopressors – 1st = noradrenaline (but this has to be given via a central line so start with metaraminol/aramine peripherally
- Need an arterial line if in septic shock to monitor MAP
Sepsis - Organ Supports: Respiratory
- What are the clinical problems with the Respiratory system in septic shock? (4)
- Resuscitative Care?
Sepsis - Organ Supports: Neuro/Metabolic
- What are the neurological & metabolic problems clinically in septic shock? (3)
- Resuscitative Care?
- BSL Target range?
- Aim for a BSL of 6-10 in ICU – insulin infusions to keep down
Sepsis - Organ Supports
- Temperature?
- Skin changes?
- AKI - Dialysis indications?
- AKI very common in septic shock – prerenal (hypovolemia & vasodilation with hypotension, also microthrombi 2o to DIC) & intrarenal (nephrotoxins – NSAIDs/ACE inhibitor) = Drop urine output & rise creatinine
- Treat: good MAP >65/blood volume & cease any nephrotoxins & careful with contrast & remove any possible post-renal causes (blocked catheters etc)
- Indications for acute renal dialysis = AEIOU
Supportive Care for ICU Patients - FAST HUGS IN BED?
- What is the definition of Renal Failure?
- What is the definition of AKI? 3 Components of AKI?
- Which Criteria are used to determine the extent of AKI?
Definition of Renal Failure = Functional or structural abnormalities or markers of kidney damage including abnormalities in blood, urine, tissue or imaging tests present for less than 3 months.
- Complete loss of kidney function.
Components of Acute Kidney Injury (AKI) – NOT THE SAME AS FAILURE = AKI is an abrupt (1 to 7 days) and sustained (more than 24 hours) decrease in kidney function.
1. Abrupt onset
2. Creatinine rise
3. Oliguria
RIFLE Criteria
- RIFLE stands for Risk, Injury, Failure, Loss & End Stage Renal Disease.
- The ADQI formulated the RIFLE criteria in 2004 to allow for AKI to be objectively and uniformly defined.
RIFLE CRITERIA FOR AKI
- Why do we use the RIFLE Criteria? (7 Reasons)
- What are the implications of RIFLE?
- What are some of its limitations/ issues?
Why use RIFLE Criteria?
1. Early detection of AKI
2. Consensus definition of AKI
3. Understand epidemiology of AKI
4. Defined groups for controlled trials
5. Develop animal models
6. Validate diagnostic tests
7. Classify severity = determine mortality and outcome
Issues with RIFLE = you may not know a patients baseline creatinine – what is their ‘normal’? Also, people may be in renal failure but they’re on a diuretic so making urine + creatinine levels not that high in a tiny old lady with small muscle mass (might go from 50 to 130) but still not classified as renal failure.
AKI
- List 5 Major contributing factors?
- Clinical features?
Major Contributing Factors to AKI
1. Septic shock
2. Major Surgery
3. Cardiogenic shock
4. Hypovolemia
5. Drugs
Clinical manifestations
- Fluid overload & pulmonary oedema = Congestive cardiac failure
- Electrolyte imbalance (K+, Po4-)
- Hyperkalaemia (cardiac arrythmias) – often asymptomatic until arrest
- Hormonal imbalance
- Uremic Symptoms: Encephalopathy (confused), bleeding (platelet dysfunction), pericarditis (pericardial effusion), neuropathy
- Tachypnoea compensating for metabolic acidosis
Causes of AKI?
8 Drugs causing AKI in ICU?
**Drugs causing AKI in ICU **
1. Radiocontrast agents
2. Aminoglycosides
3. Amphotericin
4. NSAID’s/ ACE inhibitors/ ARB’s
5. Acyclovir
6. Cyclosporin
7. Tacrolimus
8. Beta-lactams
- 10 Steps in Investigate plan for AKI?
- 6 Principles of Management of AKI?
- Indications for dialysis?
- Contrast Nephropathy - Definition? 3 Risk factors? Mechanism? Management?
Principles of Management of AKI
1. Treat & Reverse underlying cause
2. Optimize intravascular volume status - DO NOT allow hypovolaemia!
3. Optimize cardiac output / BP - MAP >70mmHg (usually >65 but they need good renal perfusion + usually these patients are slightly hypertensive anyway so they can cope)
4. Avoid nephrotoxins.
5. Dialysis if required = supportive only
- Acidemia <7.2 but only if they won’t get better quickly.
- HyperK = no.1 elecytrloyte imbalance dialysis is used for given the rapid changes & lethal complications
Rhabdomyolysis
- Definition?
- 9 Causes?
- 4 Complications?
- 5 Clinical Features/Results on ixs?
- 5 Management?
Rhabdomyolysis
Rhabdomyolysis is the breakdown of skeletal muscle fibres with leakage of potentially toxic intracellular contents into the systemic circulation, characterised by elevated plasma creatine kinase, myoglobinuria and risk of renal impairment.
How do you breathe?
Define: Inspiration & Expiration
Where is the CO2 control centre?
Where is the O2 control centre?
How do you breathe?
* Create a negative pressure in our chest compared to the atmosphere (zero)
* Inspiration = Active contraction of the diaphragm and intercostal muscles generates a negative intrathoracic pressure relative to the atmosphere so gas flows into the lungs from the mouth
* Expiration = Passive relaxation of the muscle groups creates a positive intrathoracic pressure relative to atmosphere so gas flows out of the lungs via the mouth.
Why can it be dangerous to give O2 to CO2 Retainers/COPD patients?
Define and explain the 2 types of respiratory failure?
RF Occurs when the pulmonary system can no longer meet the demands of the body.
- Type 2 = brain or CNS telling you not to breath (hypoventilation) or brain telling you to breath but musculoskeletal cannot (eg. Diaphragm paralysis – phrenic nerve)
Type I RF
- What is a Shunt? 6 Most Common Causes?
- 6 Most Common Causes of Diffusion Abnormality?
Type II RF
- 7 Neurological Causes?
- 4 Musculoskeletal Causes?
Commonest causes of shunt: area of lung which is perfusion with blood but no air/O2 (V/Q= small, zero)
1. Atelectasis
2. Pneumonia
3. Aspiration
4. Pleural effusion
5. Pneumothorax
6. Pulmonary Haemorrhage
Commonest causes of diffusion abnormality:
1. Acute Pulmonary Oedema (APO)
2. ARDS
3. Interstitial lung diseases
4. Atypical pneumonia
5. Pneumonitis of any cause
6. Vasculitis
How do we treat T1RF?
- How do you improve oxygenation? (2)
- How do we increase the FiO2? (6)
- What is Mean Airway Pressure?
- How do you increase the mean airway pressure? (3)
MEAN AIRWAY PRESSURE = The average pressure in the airways over a whole respiratory cycle (inspiration and expiration).
What is Non-Invasive Ventilation (NIV)?
- What are the 2 common modes of NIV used?
- Patients must? (3)
- Patient must not? (5)
- NIV Common Indications - 2 CPAP? 2 BIPAP?
- Settings - 2 CPAP? 5 BIPAP?
NIV Common Indications
CPAP
1. Type I respiratory failure (e.g. acute pulmonary oedema
2. OSA (upper airway splinting)
BIPAP
1. Type II respiratory failure (including Type I and II respiratory failure, e.g. COPD)
2. Post extubation for patients with increased risk of needing reintubation
High Flow Nasal Oxygen
- How does it work?
- What does it require?
List 5 Indications for invasive ventilation and give examples for each.
- Compare the processes of Inspiration and Expiration in Spontaneous vs. Mechanical Ventilation.
Indications for Invasive Ventilation
1 - Airway issue - eg. Reduced tone causing airway collapse OR Anatomical issue
2 - Type I RF - eg. APO, PE, Pneumonia, ARDS
3 - Type II RF - eg. COPD, Asthma OR Respiratory muscle function OR Intra-abdominal hypertension
4 - Work of breathing - eg. Shock states
5 - Facilitate a procedure/ intervention - eg. Surgery, MRI, Interventional radiology
What are the 2 modes of Mechanical Ventilation?
- What is the difference between Pressure Control and Volume Control? Give examples of each?
- Which mode is better for treating critically ill patients?
Modes of Mechanical Ventilation
1 - Controlled ventilation
- Ventilator does all the work
- You set how often, how long and how much the ventilator inflates the patients lungs
2 - Supported ventilation
- The patient does some of the work
- The patient triggers and the ventilator pressure supports patients inspiratory efforts.
There is no definitive evidence that any one mode of ventilation is superior to another for treating critically ill patients.
What is ARDS?
- 4 Diagnostic features?
- 4 Common Causes?
ARDS - Acute Respiratory Distress Syndrome
ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue, characterised by hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.
- Basically acute pulmonary oedema that isn’t caused by cardiac failure
Ventilation Basics - Case 1
* A 90kg man is intubated for a prolonged seizure.
* Initial settings: SIMV Tv 500mls, RR 12, PEEP 5, IE ratio 1:2
* His initial PaCO2 is 53mmHg.
* What will you do?
= Increase his minute ventilation by:
1. Increase his respiratory rate & 2. Increase his tidal volume
What is your management approach for this patient?
How will you resuscitate this patient?
Management
1. Initially»_space; Resuscitation
2. Treatment of bleeding
3. Treatment and prevention of complications
How will you resuscitate this patient?
- GCS of 13 = probably maintaining own airway but risk of aspiration, would not intubate at this point as there are risks of anaesthesia + hypovolaemic shock
- PR = 125bpm and a BP of 90/60
- O2 – probably via nasal prongs (high flow if hypoxic) as don’t want to be vomiting into a mask
- Large bore (16/18 gauge) IV access + Aggressive fluid resus (CSL +/- Packed red cells) + Coags + G&H
Causes of Haematemesis
- 2 Common?
- 2 Less frequent?
- 3 Rare?
What signs on clinical examination would you look for to indicate chronic heavy alcohol intake?
- 3 specific signs?
- 3 organ specific effects & their signs?
What is the Empirical Medical Therapy for GI bleeds?
- Everyone gets a PPI, not just ulcers as variceal bleeds can predispose.
- Terlipressin = IV Vasopressin analogue with a longer half-life than vasopressin (4-6hrly) but vasopressin needs an infusion as its half life is only approx. 1hr
Options whilst waiting for endoscopy
1. Continue to correct coagulopathy and fluid resuscitate, transfer to ICU for further management.
2. Place a Minnesota tube/ Sengstaken-Blackmore tube to compress bleeding varices.
- Only for those who are intubated.
- Need to do an xray once tube in before you inflate the gastric balloon to make sure in the stomach!
- Can leave this balloon in for hours if the bleeding has stopped.
- If ongoing bleeding then bleed is coming from higher up so can inflate the esophageal balloon.
Which scoring system attempts to identidy patients at risk of adverse outcomes following acute upper GI bleeding?
- 5 Scoring Parameters?
Rockall risk scoring system attempts to identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding.
The patient returns to ICU no longer bleeding with surgically controlled varices. What medical therapies are available to treat bleeding varices? (6)
- What are 4 possible complications of an acute upper GI bleed and their treatments?
- Control of BP
- Correction of coagulopathy
- Terlipressin - analog of vasopressin which causes a local vasoconstriction of splanchnic blood vessels.
- Propranolol is a non-selective betablocker which has been shown to reduce the risk of bleeding in patients with confirmed varices. However, it is not recommended to treat actively bleeding varices and should not be immediately started. It is usually commenced around 2 weeks after control of the bleeding as a prophylactic.
- IV antibiotics are recommended (ceftriaxone)
- IV Proton pump inhibitor to reduce any acidity in oesophagus.
A patient who presents with an acute upper GI bleed from varices is confirmed to have alcoholic cirrhosis and portal hypertension.
- What are 2 scoring systems for cirrhosis?
- Give 2 advantages and 2 disadvantages of the Child-Pugh?
Only use if someone has liver cirrhosis otherwise a healthy normal person will still get a score of 5.
What is the MELD Score?
- What is it used for?
- 1 Pro & 1 Con?
MELD Score
- Model for End Stage Liver Disease
-
On day 5 post variceal banding for an acute upper GI bleed, the patient begins to vomit blood again. What are the 3 options for management now?
- Repeat endoscopy is possible. It is probable that further rebleeding represents severe portal hypertension that will only cause futher rebleeds in the future. The options are
- TIPSS = Endovascular procedure attempting to directly bypass portal vessels into the hepatic veins via tunnels made by the liver parenchyma.
- Liver transplant (if a candidate)
- Conservative mx (palliative care)
TIPSS = Trans jugular intrahepatic portosystematic shunt
* Effective but associated with a high mortality (50%)
* Often precipitates encephalopathy as blood from the GIT which hasn’t been through the liver for detoxification is now being shunted straight back into circulation.
Outline the Upper GI Bleed Protocol at SCGH.
What blood products are available?
Packed Red Blood Cells
- How many mls/bag?
- Hb transfusion trigger?
- How much does each unit raise the Hb by?
- How fast is it available?
Packed Red Blood Cells
* Approx 300mls per bag
* Transfusion trigger is 70g/L
* Each unit raises the Hb by 10g/L
* How fast?
- O neg or O pos (immediate)
- Group specific (10 mins)
- Full cross match (45 mins)
Platelets
- How is it made?
- What does it contained?
- Under which 2 processes has it undergone?
Fresh Frozen Plasma
- How many mls?
- Contents?
- Which diseases is it useful in?
Platelets
- Adult platelet unit is made from 4 identical ABO donors donation of a single unit = “pooled platelets”
- Contains a small amount of plasma also
- Leucodepleted and irradiated
Fresh Frozen Plasma
* 200mls
* Contains all coagulation factors and protein
* Can be used in diseases where multiple factors are deficient e.g. liver disease or disseminated intravascular coagulation (DIC) or for warfarin reversal
Do you need to use blood type specific platelets when transfusing to a patient?
Which blood groups are safe when giving FFP?
No, but this is still attempted when possible as there are still a few mls of plasma which could icite a mild reaction.
- What is cryoprecipitate?
- What is cryodepleted plasma and what is it used for?
What are the risks of blood transfusions?
What is TRALI?
TRALI = Tranfusion Related Acute Lung Injury
- Present with dyspnoea, hypoxia and fever
- CXR looks like APO
- Treatment is supportive: Oxygen, Positive pressure ventilation, Diuresis, Stop transfusion
- Usually resolves within 3 days
- 5% mortality
- Multiparous females highest risk donors as their plasma has more antibodies in it
- Tracing of reactions to donors is done and donors can be excluded.
What problems are associated with massive transfusion?
Risks of a Massive Blood Transfusion
1. Acidosis
2. Hypothermia
3. Coagulopathy
4. Electrolyte imbalances
5. Citrate toxicity
6. Transfusion-related lung injury
7. Transfusion-associated circulatory overload
What are the Definitions of a Massive Transfusion?
Why do we replaces in a 1:1:1 ratio?
Definitions of Massive Transfusion
- 10-unit transfusion in 24 h
- Transfusion of an entire blood volume in 24 h (70ml/kg)
- Replacement of 50% blood volume over 3 h
- Trauma is the most common reason for massive transfusion
What is Acute traumatic coagulopathy?
What values should you be aiming to maintain in resus?
Acute Traumatic Coagulopathy
- Coagulopathy disorder precipitated by tissue injury and shock.
- Results in hyperfibrinolysis and hypocoagulability (probably mediated by dysregulation of the Protein C system).
- Present in nearly 25% of patients with major trauma.
- 3-4x the mortality compared to those without.
What is Tranexamic acid?
What is Factor VIIa?
Outline the Blood Product Guidelines for Major Haemorrhage in Adults?
Outline the SCGH Massive Transfusion Protocol?
Tranexamic Acid
* = An anti-fibrinolytic = Blocks fibrin breakdown
* Always always always………… 1gm bolus, 1gm 8 hourly
* If some is good, more is better!
* Highly side effect in VERY high doses = seizures, otherwise very safe.
Factor VIIa
- Uncontrolled haemorrhage that is not amenable to surgical or interventional radiological therapies.
- In a salvageable patient with:
1. Optimal blood component therapy (INR, APTT, platelets and fibrinogen all in the normal range),
2. pH 7.2, and
3. normothermia (T>34C)
- Can be given to Jehovah’s witnesses
Define:
- An Acid?
- pH?
- Base?
Acid
- Proton Donor
- More acid = higher H+ concentration
- E.g.: CO2 + H2O –> H2CO3, carbonic acid + H+ + HCO3-
pH
- negative logarithm of H+ concentration
- H+ concentration is measured
- Smaller pH = higher H+ concentration = more acid
Base
- Proton Acceptor
- More base = lower H+ concentration
- What is the definition of base excess?
- What is the normal pH of plasma? Why?
- List 3 Physiological Buffers?
What is the Henderson - Hasselbalch equation?
What are the 2 ways the body compensates for acid-base changes?
- How quick?
- pH (7.4) – acidaemia, alkalemia
- CO2 (40) [mmHg] - respiratory acidosis, respiratory alkalosis
- H2CO3 (25) [mmHg] - metabolic acidosis, metabolic alkalosis
What is the difference between an ABG and a VBG?
ABG vs VBG
Venous blood gas is becoming popular in ED setting (less invasive) than arterial blood gas.
Metabolic Acidosis
- What is the Anion Gap? What does it help differentiate?
- Equation?
- 4 Differentials for a High Anion Gap Metabolic Acidosis?
- 3 Causes of Normal AG Metabolic Acidosis?
Metabolic Acidosis / AG
- Anion Gap helps differentiate the cause of metabolic acidosis
- High AG vs normal AG metabolic acidosis
- Normal AG = 12 mmol/L = Na+ - (HCO3- + Cl-)
Metabolic Alkalosis
- Causes?
- How does Hypoventilation result in Respiratory Acidosis?
- How does Hyperventilation result in Respiratory Alkalosis?
Blood Gas Analysis - Differentials
- 4 Respiratory acidosis?
- 8 Respiratory alkalosis?
- 5 Metabolic alkalosis?
- 4 AG positive Metabolic acidosis?
- 3 AG negative Metabolic acidosis?
ABG Interpretation - Case 1
A postoperative patient on patient controlled analgesia (hydromorphone). The nurse finds patient somnolent. His SpO2 is only 88%. pH 7.25, PaCO2 55 mmHg, Bic 25 mmol/L
ABG Interpretation - Case 2
A patient presents with a one-day history of productive cough, fevers and SOB. CXR shows RML opacity. SpO2 is 90% on RA. pH 7.55, PaCO2 30 mmHg, Bic 22 mmol/L
ABG Interpretation - Case 3
18 y patient with diabetes type I, vomiting for 2 days, confused. P125, BP 90/45, afebrile, RR 35/min. SpO2 96%. pH 7.05, PaCO2 25 mmHg, HCO3- 12 mmol/L, BE -18, AG 18, BSL 32, urine ketones +
ABG Interpretation - Case 4
Patient with COPD exacerbation. SpO2 90% on RA. pH 7.29, PaCO2 75 mmHg, Bic 32 mmol/L.
ABG Interpretation - Case 5
Patient on long-term diuretic.
pH 7.48, PaCO2 48 mmHg, Bic 34 mmol/L
ABG Interpretation - Case 6
44 year old patient following extensive prolonged plastic surgical operation. pH 7.25, PaCO2 44mmHg, Bic 16 mmol/L Na+ 140 mmol/L, Cl- 112 mmol/L, K+ 4.8
ABG Interpretation - Case 7
77 year old male with smoking history, chronic exercise intolerance, frequent chest infections. Currently feeling well without signs of respiratory distress.
U&E: Na+ 139 mmol/L, K+ creatinine= 3.9 mmol/L, Bic 35 mmol/L, urea 2.6mmol/L, creatinine 77 micromol/L
What will the pH and CO2 likely be?
ABG Interpretation - Case 8
81 year old patient with COPD has now increased sputum production
exercise intolerance with widespread wheeze on auscultation. Previous
ABG = pH 7.4, PaCO2 65, Bic 30 mmol/L.
pH 7.25, PaCO2 85 mmHg, Bic 30 mmol/L
ABG Interpretation - Case 9
81 year old patient with COPD has now increased sputum production
exercise intolerance with widespread wheeze on auscultation. Previous
ABG = pH 7.4, PaCO2 65, Bic 30 mmol/L.
pH 7.25, PaCO2 85 mmHg, Bic 30 mmol/L
ABG Interpretation - Case 10
45 year old male post laparotomy. Now vomiting and in pain.
pH 7.46, PaCO2 32 mmHg, Bic 23 mmol/L
ABG Interpretation - Case 11
24 year old female with septic shock and acute renal failure
requiring mechanical ventilation.
pH 7.25, PaCO2 40 mmHg, Bic 18 mmol/L
ABG Interpretation - Case 12
22 year male with vomiting and abdominal pain presents with shock.
Na+ 144, Cl- 95, K+ 4.2, Bic 14
