WEEK 2 - Shock

Question 1

What is shock?

Answer 1

State of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption.
Body is unable to meet metabolic demands of tissues and cellular metabolism, ATP production is impaired due to hypoxia.
Stages:
1. initial shock
2. compensation
3. decompensation
4. irreversible

Question 2

What is the 1. initial insult state?

Answer 2

Initial insult of injury occurs (blood loss, injury to spine, AMI)
Short period of decreased CO
Decreased oxygen deliver
Difficult to identify, non-specific clinical manifestations
Body is able to quickly adapt and compensate for changes

Question 3

What is the 2. compensation stage?

Answer 3

Body attempts to compensate - maintain CO and tissue perfusion.
Change detected by baroreceptors -> SNS stimulation.
Increased HR, contractility, vasoconstriction.
Chemoreceptors detect increased PaCO2 = increased RR and depth.
RAAS, ADH, water retention to improve blood volume.
Increased glucose metabolism, shift to CHOs.
Clinical manifestations = increased HR and RR, decreased UO.

Question 4

What is the 3. decompensation stage?

Answer 4

Compensatory mechanisms become overwhelmed and fail as insult progresses.
Body is unable to maintain vital organ perfusion.
Increased O2 demand + decreased CO and BP = severe hypoperfusion, hypoxia -> anaerobic metabolism, lactic acid production.
Every organ suffers!

Question 5

What factors influence SVR ? (systemic vascular resistance)

Answer 5

Vessel length
Blood viscosity
Vessel diameter

Question 6

What is the formula for BP?

Answer 6

BP =CO x SVR

Question 7

What is the formula for CO?

Answer 7

CO = HR x SV

Question 8

What factors determine SV ? (stroke volume)

Answer 8

Preload
Contractility
Afterload

Question 9

What are the different types of shock?

Answer 9

Cardiogenic shock (cardiac pump failure)
Hypovolaemic shock (decreased blood volume)
Neurogenic shock (loss of sympathetic tone)
Anaphylactic shock (excessive immune response vasodilators)
Septic shock (vasodilatory toxins)

Question 10

How do you manage a patient with shock?

Answer 10

Early detection = improved pt outcomes.
Primary survey:
A - airway
B - breathing
C - circulation
D - disability 
E - expose

Question 11

What is multiple organ dysfunction syndrome?

Answer 11

The failure of two or more organs due to uncontrolled inflammatory response in a server illness/injury that leads to irreversible organ damage.
Due to endothelial and parenchymal cell injury from hypoxia.
Hyperinflammation & hypercoagulation: oedema formation, cardiovascular instability, endothelial damage and clotting abnormalities
Also affects physiological systems eg. immune, endocrine and haematological.

Mortality 30 – 100% depending on the number of organs affected.

Question 12

How can nurses improve O2 supply and decrease O2 demand?

Answer 12

Decrease anxiety
- Educate visitors
- Deep breathing & coughing 
Keep em warm
Space out activities OR do them all at the same time depending on the pt.
Positioning 
O2 therapy

Question 13

What is cardiogenic shock?

Answer 13

Failure of the cardiac pump resulting in decreased CO and systemic perfusions.
Results in decreased SNS stimulation, compensatory mechanisms, increased myocardial work load, decreased cardiac function, impaired myocardial perfusion and oxygenation.
Insult: LV or RV infarct, severe AMI, cardiac tamponade, PE, valve rupture, post cardiothoracic surgery.

Question 14

What are clinical manifestations of cardiogenic shock?

Answer 14

Low CO, altered GCS, sluggish capillary refill, dusky, pale, cool, clammy peripheries, hypotension, tachycardia/arrhythmias, oliguric/anuric, dyspnoea.

Question 15

How do you manage cardiogenic shock?

Answer 15

Treat the cause - aim to optimise pump action and CO.
HR: to improve myocardial O2 demand.
Preload: reduce pulmonary congestion, IV diuretics, GTN.
Contractility: improve myocardial O2 supply, fix causes, vasoconstrictive agents (dobutamine, intra-aortic balloon pump).
Afterload: GTN, SNP.

Question 16

What is hypovolaemic shock?

Answer 16

A significant reduction in intravascular volume due to large blood/fluid loss resulting in decreased CO.
Loss of fluid:
vomiting, diarrhoea, polyuria, burns, ascites, ‘third spacing.’
Loss of blood: trauma, surgical, fractures, retroperitoneal, abdominal.

Question 17

What are the clinical manifestations of hypovolaemic shock?

Answer 17

Hypotension, tachycardia, sluggish capillary refill, altered GCS, thready pulse, thirst, oliguria, arrhythmias.

Question 18

What is the management for hypovolaemic shock?

Answer 18

Aim to minimise fluid loss and restore volume - must treat cause!
Surgery, compression,
HR: optimise to improve myocardial O2 demand.
Preload: fill to restore volume, warm crystalloids, even blood product administration.
Contractility: improve myocardial O2 supply
Afterload: permissive hypotension.

Question 19

What is neurogenic shock?

Answer 19

Shock due to the interruption of autonomic pathways resulting in decreased vascular resistance and vagal tone.
Insult above level of T6
Eg. trauma, post anaesthesia, cerebral ischaemia, drugs.

Question 20

What are the clinical manifestations of neurogenic shock?

Answer 20

SBP < 90-100 mmHg
HR < 80 bpm
Hypothermia

Question 21

What is the management of neurogenic shock?

Answer 21

Extent of injury determines management.
Spinal stabilisation and supine position, surgical fixation.
SVR: inotropes to squeeze vessels
HR: atropine or pacing to fix bradycardia
Preload: filling
Hypothermia: active external warming
Monitor respiratory function, bowel chart, pressure ulcer care, DVT prophylaxis

Question 22

What is anaphylactic shock?

Answer 22

Systemic vasodilation due to type 1 hypersensitivity immune response.
Production of IgE post exposure to an antigen.
Mast cell degranulation = release of histamine.
H1 receptors: contracts bronchial smooth muscle, increases vascular permeability, extreme vasodilation.
Insult: food, drugs, insects.

Question 23

What are clinical manifestations of anaphylactic shock?

Answer 23

Stridor, wheeze, cough, difficulty breathing, anxiety, dizziness, angioedema, utricaria, erythema, hives, hypotension, altered GCS

Question 24

What is the management for anaphylactic shock?

Answer 24

Treat cause - remove aggregator.
IM/IV adrenaline ASAP: fix SVR
α receptor agonists: causes vasoconstriction and reduces oedema.
β receptor activity dilates bronchial airways, increase force of myocardial contraction, suppresser histamine and leukotriene release.
Closely monitor CVS and Resp, pt with airway oedema may require intubation.
Fluids, steroids

Question 25

What is septic shock?

Answer 25

Sepsis + persistent hypotension (MAP ≤65mmHg) + lactate ≥2mmol/L (despite adequate volume resuscitation).
Activation of immune response and massive inflammatory response: microvascular thrombus, vasodilatation, increased vascular permeability, immunosuppression.

Insult: gram –ve bacteria, gram +ve bacteria (staphylococcus aureus), fungi, viruses. Severe cases often remain unknown.

Question 26

What are the clinical manifestations of septic shock?

Answer 26

Tachycardia, hypotension, febrile, tachypnea, altered GCS, oliguria/anuria, deranged renal function, jaundice, clotting abnormalities, ARDS, WCC > 12,000

Question 27

What is the management of septic shock?

Answer 27

Treat cause - early recognition!
IV Abs in the first hour
CO = HR x SV (preload, contractility, afterload) Preload: fill, fluid resuscitation
Afterload/SVR: squeeze! Vasoconstriction -> inotropes Monitor: lactate, urine output
Minimise oxygen demands in all ways possible.
Severity of the patient: adequate nutrition renal filtration, ventilation, sedation, surgical intervention