My Acute medicine
Card Set Information
My Acute medicine
AKI ARDS ICU Sepsis
AKI, ARDS, ICU, Sepsis
What are the functions of an intensive care unit?
High degree of expertise
High nurse:patient ratio
All used for patients with a critically ill or unstable condition
What does the APACHE II scoring system predict?
The likelihood of mortality or morbidy of ICU patients
What observations are used in the APACHE II scoring?
: Temp, MAP, HR, RR, PaO2
: pH, Sodium, Potasisum Creatinine
: Haematocrit, WBC
What is the signifance of the following in a clinical setting:
- Heart rate
Tachycardia is related to a poor outcome
Tachypnoea occurs in sepsis/PE and other acute disease
Lowers in sepsis and blood loss
Disease affects cellular function
Disease affects metabolism or sepsis/drug
Describe some other important investigations used in ICU, apart from general observations
: Normal suggests adequate perfusion. Hypovolaemia, renal disease.
: Lactate, glucose, [acid/base] = metabolism/perfusion
: Actual/potential tissue damage
What does the SOFA score predict?
Determines the rate and extent of a patient's organ function and failure
What factors are used in the SOFA score?
: <400 = 1, <100 = 4
: <14, <12, <9, <6
: >1.9, >12
: <150, <20
: >145 (2), >382 (5)
Outline the pathogenesis of sepsis
Microorganism invades blood stream
Endo/exotoxins cause mediator release, including NO
Profound vasodilation = renal failure+ albumin enters ECM
Pulmonary oedema + tissue hypoxia
Multiple organ dysfunction syndrome
What are the adverse effects of mechanical ventilation?
Together may cause ARDS
- Define sepsis
- Define severe sepsis
- Define septic shock
SIRS criteria + confirmed or presumed infection
Sepsis with 1 or more organ dysfunctions
Severe sepsis and hypotension unaffected by IV fluids
How are septic patients managed?
1. High flow O2
2. Take 2 blood cultures
3. Investigations; CSF, urine culture, CXR etc
4. Antibiotics, within 1st hour. 1+ active against likely pathogen
5. 250 ml IV crystalloids + consider fluid challenge
6. Vasopressors if severe hypotension
7. Lactate and Hb measured; hypoperfusion/hypovolaemia
- Check urine output constantly
What is the significance of AKI in ICU?
~10% of patients in hospital are at risk of AKI
Directly related to mortality, even at risk stage
Increases likelihood of organ failure
20% of patients in ICU require RRT
What are the classical reasons for renal failure?
: Hypovolaemia, stenosis
: Vasculitis, glomerulonephritis, drugs
: Obstruction, e.g prostate, stone
What are the multi-factorial reasons for AKI?
Theory that many factors cause AKI at once
Many sepsis related
: poor CO + PR = renal ischaemia
Toxin mediated (including rhabdomylysis/drugs)
What are the RIFLE criteria used for?
Assessing measurements (RIF) and outcomes (LE) of AKI (after resuscitation + IV fluids)
: Risk; Creatinine x 1.5, urine <5ml/kg/hr for 6 hrs
: Injury; Creatinine x 2, urine <5ml/kg/hr for 12 hrs
: Failure; Creatinine x 3, urine <3ml/kg/h x 24 hr
: Loss; Persistent ARF= complete function loss >4 weeks
: End stage renal disease
What are the indications for dialysis?
When urine production lowers and urea/creat rises
Renal function related disease; hyperkalaemia, acidosis, uraemia
Survivable injury/decent prognosis (age, ESRD etc.)
Opportunity to stop RRT in future
What is the difference between haemofiltration and dialysis?
: Withdrawal of desirable ions using concentration gradients across a semi-permeable membrane.
: Similar, but positive hydrostatic pressure also used to remove larger solutes. More expensive
If urine output decreases, and urea increaes, how should the patient be managed?
ABCDE to check for hypoxia/hypotension/sepsis
Ensure perfusion (peripheral temp or capillary refill)
Exclude obstruction, e.g. flush catheter/bladder with saline
Next give IV fluids to ensure perfusion/BP
Renal replacement therapy if no difference
: Diuretics should NOT be used
What are the clinical findings of ALI?
: bilateral infiltrates
No evidence of left atrial hypertension
What are the main causes of ALI?
: Pneumonia, aspiration, injalation, fatty emboli
What are the acute pathological mechanisms of ALI?
Type 1 pneumocytes swell and detach from BM after damage
Thrombi in capillaries = V/Q mismatch
Respiratory membrane dysfunction = proteinacious leak
Type 2 pneumocyte damage = reduced surfactant = alveolar collapse
Neutrophil infiltration and cytokine release = damage/thrombi
How does ALI resolve?
Myofibroblast infiltration + exudate = granulation
Type 2 pneumocytes become type 1
Either recovery or 'honeycombing' (end stage fibrotic lung disease)
What co-morbidities are common in ALI?
Chronic liver disease
Chronic respiratory disease
Low serum pH
Acute respiratory distress syndrome
A more severe result of ALI
A Pa/Fi ratio less than 26kPa and persistence, with an associated cause
What does the Murray score measure and estimate?
Measures alveolar consolidation, Pa02/Fi02 ratio and lung volume
Used to estimate the severity of ARDS
Outline the clinical presentation of ARDS
Within 1-2 days of insult
Progressive, severe dyspnoea and dry cough
What are the clinical findings of ARDS?
Diminished air entry into lung base
May be unexpectedly normal
What are the systemic effects associated with ARDS?
Pulmonary manifestation of systemic response
Pulmonary hypertension/Right heart failure (thrombi)
What investigations are appropriate in ARDS?
: Patient's well being
Transbronchial/open lung biopsy
Outline the treatment of ARDS
High 02 to maintain tissue xygenation
Fluids used to prevent shock, but may cause late damage via oedema
Support other failing organs
What are the clinical features of respiratory failure?
RR <8 or >30 (slow = exhaustion)
Exhaustion/accessory muscle use
Confusion/convulsion 2nd to hypoxia
Prolonged expiratory phase, maybe with wheeze
Low GCS 2nd to hypercapnia
Tachycardia or late bradycardia
How does O2 therapy administration differ in COPD
: High flow 02 used and steadily decreased
: Low flow 02 used and steadily increased, with GCS, RR and ABGs monitored
The percentage of O2 inspired that participates in gas exchange in the alveoli
Differs from Pa02 as it is unaffected by V/Q
When are fixed performance masks used?
When Fi02 must be a known, acceptable amount
E.g. in COPD where 02 delivery is essential but must be monitored
What are the indications for respiratory support?
Time needed to investigate/treat underlying condition
How can CPAP
In unilateral or lobar diseases, CPAP forces blood out from the ventilated to the 'dead space'
In fully compliant lungs, CPAP can increase pulmonary vascular resistance
Flattening diaphragm may increase expiratory muscle use
In pneumothorax, GI bleeds etc. positive pressure a bad thing
Define and outline some 'rescue therapies'
A procedure which aids the treatment of respiratory failure but doesn't rely on gas exchange
: Vasodilation improves oxygenation (no effect on outcome)
: Blood removed from body and CO2 removed.
What are the causes of unilateral effusions found on a CXR?
What are the causes of bilateral effusions found on a CXR?
Heart or renal failure
What are the findings of ARDS on a CXR?
Diffuse alveolar shaddowing/patchy opacity
Effusions are not a major feature
What are the findings of heart failure or fluid overload in a CXR?
Interstitial thickening occurs across the lung, highlighting the lobules
Underlying lung is normal, with effusions
What are the problems with diagnostic imaging in ICU?
Suboptimal positioning and exposure, which varies between images
Magnification of mediastinal contours
Reduced kilovoltage of portable units = underexposure and motion blur
Describe some commonly used IV fluids
: Different ionic concentrations in solute. Associated with oedema
: Larger molecules e.g. albumin; preserve osmotic pressure (helpful in oedema)
Outline the process and purpose of a fluid challenge
An end point is selected (e.g. normal HR, GCS, perfusion)
250ml given rapidly; response monitored
Patient reassessed, especially SV
No response = further challenge and continued treatment
What is the mechanism of action of catecholamines?
: Inotropy via calcium release, chronotropy via calcium channel opening = Increase CO and ischaemia
: Vasodilation via calcium uptake into sarco. ret. = smooth muscle relaxation and greater muscle 02
: Vasoconstriction via G proteins = increase PR
What are the effects of Dobutamine?
B1 and B2 receptor effect (3:1 ratio of strength)
Strong inotrope, weak chronotrope
What are the effects of noradrenaline?
Alpha agonist, slight B activity
Vasoconstriction, weak inotropy/chronotropy
Reliable increase in BP and cardiac blood flow
What are the effects of adrenaline?
Mainly Beta agonist in lower doses
Increase pulmonary pressure and peripheral ischaemia
What are the effects of PDE inhibitors?
Used if catecholamines ineffective/resistant
Increase cAMP = calcium entry = inotropy (not via beta receptors)
What are the effects of vasopressin?
Used in refractory septic shock
V1a receptor = inotropy and noradrenaline sensitivity
V2 receptor = increased ion/water uptake in kidneys
Describe the CV monitoring of a septic patient
Goal to monitor BP and CO
Tissue oxygenation measured (not ABG)
If low value despite normal ABG, CO insufficient
What does MEWS predict?
"Modified Early Warning Score"
Guide used to quickly determine the degree of illness
: SBP, HR, RR, temp and GCS
The more the patient's diverse from the norm, the greater the score
Apart from OBs, what other investigations are important in acute medicine? What do they indicate?
: Hypovolaemia, renal disease, overhydration, drugs. Normal = adequate perfusion
: lactate, glucose, acid/base. Metabolic function and perfusion
: Associated with actual or potential tissue damage
What are the problems with the measurements used in the RIFLE criteria?
Several conditions can cause a drop in urine production unrelated to renal failure
Creatinine can also be affected by other conditions (e.g. diabetes, muscle mass)