Acute Care Flashcards
What is shock?
= a life-threatening failure of oxygen delivery to tissues.
It is a pathophysiological state, which has a number of underlying causes
What is the triad of signs associated with shock?
- Signs of reduced perfusion
• Prolonged capillary refill time
• Reduced urine output
• Altered mental state. - Low blood pressure
- Raised lactate.
Why is lactate raised in a patient with shock?
Anaerobic respiration produces lactate, which accumulates in the blood, causing a hyperlactataemia
End diastolic volume and End Systolic volume
EDV depends on how well the heart is able to fill.
=> Preload
=> Compliance – stretchiness/relaxation of the heart.
ESV depends on how well the heart is able to empty.
=> Contractility – force of contraction
=> Afterload
What are the four broad types of shock?
- Hypovolaemic
- Distributive
- Cardiogenic
- Obstructive
Effect of sympathetic stimulation on heart rate
Increases HR
Effect of parasympathetic stimulation on heart rate
Decreases HR
When does hypovolaemic shock occur?
What are the results of this?
when there is insufficient volume of blood in the intravascular compartment (i.e. a problem with Preload).
Reduces End-Diastolic Volume
Which reduces Stroke Volume
Which reduces Cardiac Output
Which causes low Blood Pressure
Compensation of hypovolaemic shock
Increase in Systemic Vascular Resistance due to peripheral vasoconstriction => Appear peripherally “shut down”
Vasoconstriction limited to least critical organs – skin, gut, kidneys.
Perfusion of vital organs (heart, lungs, brain) maintained.
Increase in Heart Rate => Tachycardia
Signs and Symptoms of hypovolaemic shock
General shock symptoms and signs.
Signs of hypovolaemia/dehydration
Peripheral shut down – cool peripheries, mottled skin
What are the “general” signs of shock?
↓BP,
↓Urine output,
↑CRT
Altered mental state
What are signs of hypovolaemia/dehydration
Sunken eyes, dry mouth, thirst
When does Distributive Shock occur?
when there is failure of vasoregulation (i.e. a problem with the systemic vascular resistance)
This may be due to:
• Loss of sympathetic tone
• Widespread vasodilatation due to toxins
A huge drop in vascular resistance directly causes a drop in blood pressure
Compensation of distributive shock
Tachycardia
May have increased contractility/compliance
Signs and symptoms of distributive shock
General shock symptoms and signs.
Signs of abnormal vasodilatation
=> Flushed complexion, warm peripheries (in contrast with every other category of shock).
When does cardiogenic shock occur?
What can cause this?
Occurs when the heart stops pumping effectively. This may be due to:
- Reduced contractility
- Reduced compliance
- Bradycardia – reduce the cardiac output
- Tachycardia / arrhythmia – prevent the ventricles from filling properly.
Compensation of cardiogenic shock
Will depend on the specific cause – increase in HR/contractility depending on which isn’t affected.
Increase in systemic vascular resistance due to peripheral vasoconstriction
Signs and symptoms of cariogenic shock
General shock symptoms and signs.
Peripheral shut down.
Fluid status may be normal (often overloaded in patients with heart failure)
When does obstructive shock occur?
Occurs when there is blockage of blood flow, either in a great vessel or of the heart itself.
Blockages can affect:
- Preload – vena cava/pulmonary circulation (e.g. compression due to mediastinal shift in tension PTX or massive PE).
- Afterload – aorta (e.g. aortic dissection)
- Compliance – cardiac (e.g. cardiac tamponade)
Compensation of obstructive shock
Increase in systemic vascular resistance due to peripheral vasoconstriction
Tachycardia
Signs and symptoms of obstructive shock
General shock symptoms and signs.
Peripheral shut down
Fluid status may be normal
=> Check neck veins for distension, which may indicate obstruction, rather than fluid overload
Which type of shock will cause a different peripheral temperature?
Distributive shock will cause warm peripheries, whereas other types will cause cool peripheries.
Haemorrhagic shock
= a subtype of hypovolaemic shock
There is a relationship between the volume of blood loss and the signs and symptoms that are observed.
The different classes of haemorrhagic shock allow you to estimate volume of blood loss based on signs and symptoms.
It is important to manage the cause as well as replacing blood/fluid.
Anaphylactic shock
A mixed picture of shock.
- Widespread histamine release has a profound vasodilatory effect which causes a distributive shock.
- Histamine also increases the permeability of the vessels, leading to excessive loss of fluid into the interstitial space (“third-space losses”) – hypovolaemic shock.
How to manage anaphylactic shock
Remove the trigger
Administer adrenaline and antihistamines.
Fluid boluses to correct hypovolaemia
(Steroids?)
How does adrenaline help in managing anaphylactic shock?
acts on adrenergic receptors in the sympathetic nervous system to reverse the systemic vasodilation, acting as a vasopressor.
it also decreases vessel permeability, which helps to prevent further third-space fluid losses.
Steroids in managing anaphylaxis
usually hydrocortisone
likely to reduce the likelihood of a biphasic anaphylaxis (i.e. a second event), rather than having any role in correcting the current abnormalities.
Septic Shock
A mixed picture – Bacterial endotoxins have an effect of:
- Widespread vasodilatation (causing distributive shock)
- Increasing vessel permeability (causing hypovolaemia through third-space losses).
Management of septic shock
Remove trigger - urgent antibiotics
Fluid boluses to correct hypovolaemia
In cases refractory to fluid boluses, referral to HDU or ITU for infusion of vasopressors
Neurogenic shock
occurs when there is an injury to the central nervous system above the T6 level
=> total loss of sympathetic tone whilst leaving vagal stimulation unopposed.
profound vasodilatation causing a distributive shock, but potentially with no tachycardia as compensation due to the loss of sympathetic stimulation
What should be considered in a case of distributive shock with paradoxical bradycardia
neurogenic shock - ?injury to the brain or spinal cord
Management of neurogenic shock
Any/all of:
- Fluid resuscitation
- Vasopressors to reverse systemic vasodilatation
- Inotropes to increase myocardial contractility
- Chronotropes to correct the Bradycardia
Prolonged supportive measures during recovery (~1-3 weeks)
Examples of vasopressors
vasopressin (ADH), adrenaline, noradrenaline, etc
Examples of inotropes
dopamine, isoprenaline, adrenaline, noradrenaline, etc
Examples of chronotropes
atropine, adrenaline, dopamine, etc.
Effects of shock on the heart
Increased HR may lead to myocardial ischaemia, though coronary perfusion is preferentially maintained
Effects of shock on the kidney
pre-renal AKI due to reduced perfusion
Effects of shock on the brain
Cerebral perfusion is maintained for as long as possible
Depending on degree and duration of shock - can get hypoxic brain injury
Effects of shock on the lungs
reduced perfusion can cause Type 1 respiratory failure acutely, even after resuscitation
Effects of shock on the gut
Reduced perfusion can cause mucosal ischaemia - may lead to stress ulceration over time
Initial monitoring in shock
A-E assessment (and regular reassessment)
Obs repeated regularly
Hourly Urine Output monitoring – Insert urinary catheter
Blood gas - for lactate, and for acid-base/respiratory status
Bloods
ECG
Monitoring in severe/refractory cases of shock
Admission to HDU (Level 2)/ITU (Level 3)
Advanced monitoring:
- Central Venous Pressure monitoring via Central Venous Catheter (CVC/Central Line)
- Invasive Blood Pressure monitoring via Arterial Line (A-Line)
- Continuous cardiac monitoring
Management of Shock
High-flow (15L) oxygen via a non-rebreathe mask
Establish IV access early
IV fluid resuscitation (unless obvious Cardiogenic shock)
Treat the Cause
- Vasopressors (if SVR impaired)
- Inotropes (if Contractility impaired)
- Chronotropes (if HR impaired)
- Cardioversion (if arrhythmias present) – chemical or DC
Don’t forget to reassess and escalate if needed.
When is DKA considered severe?
What should be done?
Ketones >6 pH <7.1 HCO3 <5 / anion gap >16 K+ <3.5 GCS <12 SpO2 <92% SBP <90 Pulse >100 or <60
HDU/ITU must be contacted
Why is potassium monitoring important in DKA?
Potassium levels can fluctuate severely during DKA
=> osmotic diuresis (due to glucosuria) leads to a total body K+ (and phosphate) depletion.
=> Life threatening hypokalaemia can occur with insulin infusion.
BUT Serum potassium levels may not mirror this and may be low/normal/high.
So continuous monitoring of potassium is essential and replacement may be required.
when is cardiac monitoring required with a K+ infusion?
if rate >20 mmol/hour
Management of HHS
- IV Fluid replacement – to replace loss caused by the hyperglycaemia
- IV insulin – to bring the blood glucose level down.
=> but often very sensitive to insulin and require much lower doses than in DKA.
= > Aim is to reduce glucose levels slowly. - Treat any underlying cause, if known
- Refer to diabetes specialist nurse – education for prevention of further emergencies.
What is considered hypoglycaemia?
glucose <4.0 mmol/L
What are some causes of hypoglycaemia?
Delayed/missed meals
Low carbohydrate content in meals
Unplanned or strenuous exercise
Taking too much insulin
What are some symptoms of hypoglycaemia?
Fatigue, Sweating, Pallor, Headache Tachycardia
Management of hypoglycaemia - conscious patient who is able to swallow
If conscious and able to swallow:
- 15–20 g of fast-acting carbohydrate
- Repeat treatment after 10–15 minutes, up to a maximum of 3 treatments in total.
- Once glucose >4mmol/L, long-acting carbohydrate should be given to prevent blood glucose from falling again.
Management of hypoglycaemia - if unconscious/unable to swallow/seizures
- Glucagon or glucose 10% (or 20%) infusion.
- Long-acting carbohydrate should be given as soon as possible.
(Patients who have received glucagon require a larger portion of long-acting carbohydrate to replenish glycogen stores)
What is self harm?
self-poisoning or self-injury, irrespective of the apparent purpose of the act.
=> it’s not an illness itself but is more or less dangerous behaviour that should alert us to an underlying problem, difficulty or disorder.
What is suicide?
= an intentional self-inflicted act that results in death
Suicide - epidemiology
~10 deaths per 100,000 in the UK
1/3rd of all suicides in the UK are men in their 40s and 50s
~90% are suffering from a psychiatric disorder at the time of death
Risk factors for self harm
F:M = 1.5 : 1
Increased incidence in some ethnic groups
Previous self-harm (40% of people who present have a history of self-harm)
Diagnosis of personality disorder
Alcohol / drug misuse
Lower socioeconomic status, social isolation
Hopelessness, impulsivity, poor problem-solving ability
Sexual abuse, traumatic life events
Recent significant life events
Risk factors for suicide
Statement of intent and access to means
Psychiatric illness – depressive illness, early schizophrenia, comorbidity, recent discharge from hospital
History of previous self-harm,
History of violence
Family history of self-harm and suicide
Social isolation, unemployed, lower social class, single, Significant life events e.g. bereavement
Painful physical illness
Impulsive personality traits
Male
Older age
Factors associated with HIGH Risk:
- Recurrent and persistent suicidal ideation,
- Hopelessness, Agitation, Intoxication,
- Delusions of control, poverty, guilt,
- Impulsive personality traits, poor engagement with services
Suicide in post-partum period
women presenting in the post-partum period.
Deaths in post-partum period are more likely to be by violent means
Postpartum psychosis is associated with 70x risk
Assessment of self harm/suicide
History
Assessment of Mental State
Management of self harm/suicide
involves a Bio-psychosocial approach to minimise risk to self and others
is discharge safe or is admission needed?
What is sepsis?
a life-threatening organ dysfunction due to a dysregulated host response to infection
what is septic shock?
= a subset of sepsis where particularly profound circulatory, cellular and metabolic abnormalities substantially increase mortality
Recognising sepsis
Previously, the SIRS criteria were used (with sepsis being SIRS + evidence of infection)
Now, NEWS2 scores are used
NEWS2 score of 5+ should trigger a sepsis screen if one of the risk factors is present, or if a HCP is concerned.
Risk factors for recognising sepsis
- Extremes of age (<1 or >75)
- Impaired immune system (chemotherapy, comorbidities, long-term steroids).
- Recent invasive procedure (e.g. surgery, trauma, etc.)
- Broken skin (indwelling lines, IVDU, cuts/burns/blisters)
Also some more specific risk factors in pregnancy and neonates.
What infections are the most common causes of sepsis?
- Pneumonia
- UTI
- Abdominal infection
- Skin, soft tissue, bone/joint infections
- Other infections – endocarditis, device-related, meningitis, etc.
What things count for “suspicion of infection” ?
Suggestive diagnostic results
Clinical suspicion
Signs of infection – e.g. fever, high/low temperature, sweating, flushing; but with no suggestion of source.
How is sepsis diagnosed?
SOFA Score - the “Official” diagnostic criterion for diagnosis of organ dysfunction (and therefore Sepsis)
Can only really be used in critical care situations
Therefore, “red flag” sepsis criteria used more frequently
RED FLAG SEPSIS
- Objective evidence of new or altered mental state
- Systolic BP ≤90 mmHg, or a drop of >40 mmHg from the patient’s normal
- Heart rate ≥130 beats per minute
- Respiratory rate ≥25 breaths per minute
- Requirement for Oxygen supplementation to maintain saturations of 92% or above (or 88% in COPD)
- Skin signs – such as a non-blanching rash, mottled or ashen appearance, or cyanosis
- A Lactate level of 2 or higher
- Recent chemotherapy
- Anuria for 18 hours, or <0.5ml/kg/hr if catheterised
If any one of these is present, START SEPSIS SIX.
AMBER SEPSIS
mostly match up with the red flag criteria, with a lower threshold for each
- Concern from relatives about the patient’s mental status
- An acute deterioration in the patient’s functional ability (“off legs”)
- Immunosuppressed
- Trauma/Surgery/Procedure in the last 8 weeks
- Respiratory rate between 21 and 24
- Systolic BP between 91-100
- Heart rate between 91-130, or any new abnormal heart rhythm
- Temperature <36°C
- Clinical signs of wound infection
If any one of these are present, FURTHER REVIEW REQUIRED.
