Shock Introduction PDF

**Shock Introduction** Shock is a complicated yet fascinating condition that unfortunately deserves its reputation as the \'silent killer\'. Shock is an excellent example of the role of feedback loops in ensuring haemostasis, and also what happens when feedback loops start to fail. A sound knowled...

**Shock Introduction** Shock is a complicated yet fascinating condition that unfortunately deserves its reputation as the \'silent killer\'. Shock is an excellent example of the role of feedback loops in ensuring haemostasis, and also what happens when feedback loops start to fail. A sound knowledge of the physiology (especially of the cardiovascular system), pathophysiology and clinical signs and symptoms of shock is important to enable recognition and treatment, especially during the early stages and before shock becomes irreversible. In common, everyday usage, the term shock is often used to describe the psychological effects of trauma i.e. "I was shocked" or "the person looked like they were going into shock" immediately following a traumatic event. When the term is used in an emergency setting to describe anything other than the physiological effects, it can be misleading, and lead to confusion. It may well be the most commonly misused term in emergency medicine. We are going to define shock as an "inadequate cellular perfusion resulting in hypoxia and ultimately cell death" (Greaves et al, 2006). This is due to a global (body wide) reduction in blood flow (or perfusion) to the tissues (Wellington Free Ambulance, 2019). There are many causes of shock, diagnosis of the underlying cause can be difficult in the out-of-hospital environment and treatment can at times be contradictory to other conditions i.e. maintaining an adequate blood pressure in a patient with both a traumatic brain injury and hypovolaemia. This learning package will largely focus on shock secondary to hypovolaemia. The physiology and pathophysiology around hypovolaemic shock is a good starting point to understanding shock and then comparing and contrasting to other forms of shock. In addition, other causes of shock are explored in more detail in **Week 7 -- Sepsis & Septic Shock**, and in the **Anaphylaxis **learning package in Semester 1. +-----------------------------------------------------------------------+ | **Physiology of Perfusion** | | | | Shock is an excellent example of the role of feedback loops in | | ensuring haemostasis, and is also an example of what happens when | | feedback loops start to fail. A sound knowledge of | | the **normal** physiology of the cardiovascular system will help | | understand the mechanism, causes and clinical signs and symptoms of | | shock. | | | | +--------------------------------+--------------------------------+ | | | | **Recommended reading** | | | | | | | | | | Read **Chapter 10 - | | | | | Perfusion** in Paramedic | | | | | principles and practice ANZ: A | | | | | clinical reasoning approach. | | | | | | | | | | This is available through | | | | | the [[ClinicalKey for Nursing | | | | | database]](https:/ | | | | | /weltec.spydus.co.nz/cgi-bin/s | | | | | pydus.exe/MSGTRNGEN/OPAC/EBOOK | | | | | S).** ** | | | +--------------------------------+--------------------------------+ | | | | +--------------------------------+--------------------------------+ | | | | **Watch (& Listen!)** | | | | | | | | | | 1\) The following video from | | | | | the **Khan | | | | | Academy** provides a good | | | | | overview of shock, | | | | | especially in regard to the | | | | | cardiovascular system (7:14 | | | | | minutes).  | | | | | | | | | | 2\) Listen to the following | | | | | podcast from the team at the | | | | | excellent [[The Resus | | | | | Room]](https://www | | | | |.theresusroom.co.uk/) site on | | | | | shock (58:33 minutes): | | | | | | | | | |   | | | +--------------------------------+--------------------------------+ | | | | Body cells and tissue require a constant blood flow to ensure | | adequate supply of oxygen and nutrients, as well as the elimination | | of carbon dioxide and waste products. This constant blood flow (or | | perfusion) is provided by the components of the cardiovascular | | system.   | | | | Moules (2019) states adequate perfusion is dependent on the | | components of the circulatory system: | | | | - an adequate blood volume \[effectively the product\] with | | sufficient oxygen-saturated haemoglobin that is circulating | | through the arteries, arterioles, capillaries, venules and veins | | | | - an adequate pump (i.e. the heart) to provide circulatory force | | | | - sufficient vascular tone (i.e. degree of arteriolar constriction) | | to resist blood flow and maintain adequate arterial pressure, yet | | allow adequate tissue perfusion \[effectively the pipes\] | | | | - sufficient vascular tone in the venules to supply a capacitance | | that is related to the blood volume, and in the venous system to | | ensure blood return to the heart (pp. 163-4). | | | | In addition, the major vessels need to be free of any kind of | | functional obstruction, such as a pulmonary emboli or tension | | pneumothorax (Moules, 2019). | | | | Thus, one way we can begin to examine the physiology of shock is to | | use the **pump/product/pipes** analogy. The pump/fluid/pipes analogy | | is an oversimplification of a very complex system that uses many | | mechanisms to balance blood supply with the body\'s demands. However, | | it is useful in illustrating how shock can occur, (although probably | | less useful in demonstrating how the body reacts to circulatory | | compromise). | | | | **The Three Components of the Circulatory System are:** | | | | - The Heart   (heart rate and contractability, or force i.e. the | | pump) | | | | - The Fluid volume (the blood or product) | | | | - The Container (the blood vessels or pipes) | | | | Any derangement of any of these three components can affect | | perfusion. | | | | ***The Heart*** is the **pump** of the circulatory system, It | | receives blood from the venous system and pumps it to the lungs to | | receive oxygen and  then pumps the blood via arteries etc. to the | | peripheral tissues. ***Stroke volume*** (SV) is the amount of blood | | pumped by the heart in one contraction and is affected | | by **preload**, **contractile force**, and **afterload**. | | | | **Cardiac output** (CO) is volume of blood being pumped by the | | heart per unit time (generally over a minute).  CO is a product of | | the heart rate (HR) and the stroke volume: | | | | **CO = HR x SV** | | | | +--------------------------------+--------------------------------+ | | | | **Watch** | | | | | | | | | | Watch the following online | | | | | lecture from Don Bank\'s on | | | | | the Determinants of Cardiac | | | | | Output (12:06 minutes).  | | | +--------------------------------+--------------------------------+ | | | | ***Blood*** is the **fluid (or product)** of the cardiovascular | | system. It is a viscous fluid, thicker, more adhesive, and slower | | moving than water. Because the cardiovascular system is closed, an | | adequate volume of blood must be present to fill the system. Blood | | transports oxygen, carbon dioxide, nutrients, hormones, metabolic | | waste products, and heat. | | | | ***Blood vessels*** serve as a container (**or pipes**) for the | | cardiovascular system, a continuous, closed, pressurized pipeline | | that moves blood. It includes arteries, arterioles, capillaries, | | venules, and veins and is under the control of the autonomic nervous | | system. They regulate blood flow to different areas of the body by | | adjusting their size and rerouting blood flow through | | microcirculation. | | | | **Maintenance of Blood Pressure** | | | | The cardiovascular system is in a constant state of flux to match | | supply to demand. Many systems work as one to provide the right | | amount of blood supply at the right time.  | | | | Let\'s further define CO in terms | | of **preload** and **afterload** which will affect **cardiac | | output**. | | | | **Preload** is defined as the amount of blood delivered to the heart | | during diastole. It is dependent on venous return (VR). Variable | | venous capacitance (or capacity) can increase or reduce blood return | | to the heart:** increased preload = increased stroke volume**. | | | | The heart will only pump the volume that is delivered to it, so | | alterations in preload will affect ventricular stretch and | | contractility. This is known as the **Frank-Starling | | Mechanism **(note this is a slightly different concept to the | | Starling\'s Law of Capillaries seen in Week  3), which states: | | | | **The greater the preload, the more the ventricles are stretched** | | | | **The greater the stretch, the greater the contractile force of the | | ventricles** | | | | Conversely, any decrease in preload will result in a decrease in | | CO --- an important consideration in the shocked patient! | | | |   | | | | **Afterload** is the resistance against which the heart must pump. In | | order for the aortic valve to open, the ventricular ejection pressure | | must exceed the pressure in the aortic arch. | | | | - When the resistance is overcome, blood can be ejected | | | | - Determined by the degree of arterial peripheral vasoconstriction | | | | - Vasoconstriction = increased resistance = increased afterload = | | decreased stroke volume | | | |   | | | |   | | | | Thus, blood pressure can be seen in the equation: | | | | **BP = CO (HR x SV) x PVR (peripheral vascular resistance)** | | | | **Maintenance of BP** is also a complex mix | | of **short-** and **long-term** controls. | | | | +--------------------------------+--------------------------------+ | | | | **Required Reading** | | | | | | | | | | Read the following section | | | | | in **Chapter 10 - Physiology | | | | | and pathophysiology for | | | | | emergency care **Emergency and | | | | | Trauma Care for Nurses and | | | | | Paramedics (3rd ed.): | | | | | | | | | | - p\. 165 - **Compensatory | | | | | responses** | | | | | | | | | | This is available through | | | | | the [[ClinicalKey for Nursing | | | | | database]](https:/ | | | | | /weltec.spydus.co.nz/cgi-bin/s | | | | | pydus.exe/MSGTRNGEN/OPAC/EBOOK | | | | | S).  | | | +--------------------------------+--------------------------------+ | | | | ***Short term*** consists of neural and chemical controls, which act | | in a feedback loop. In other words, the supply system is demand | | responsive, so when the body\'s demands change, the cardiovascular | | system responds to the changing demand. | | | | Neural control is managed by a specialised cluster of cells in the | | medulla called the **vasomotor center** which, via efferent vasomotor | | fibres, control constriction of the arterioles. The arterioles are | | always in a state of varying constriction called the vasomotor tone, | | this being the principal effector of peripheral resistance. | | | | ***Baroreceptors*** are pressure-sensitive cells located in large | | arteries in the neck and thorax, with the principal sites being in | | the carotid sinuses and the aortic arch. Being responsive to | | hydrostatic pressure, they are capable of sensing a rise or fall in | | BP, and will send impulses to the vasomotor center to effect changes | | in vasomotor tone, and also to the cardiac center for alterations in | | heart rate and contractility. | | | | ***Chemoreceptors*** are located in the aortic arch and in neck | | arteries. They are responsive to changes in oxygen or carbon dioxide | | concentrations in the blood, and also to pH levels. Chemoreceptors | | principal action is to regulate rate and depth of respirations. | | | | *Source: Marieb (2007)* | | | | ***Long term*** mechanisms are for control of blood pressure involve | | the renal system. The kidneys act both directly and indirectly to | | regulate blood pressure. Directly, they act to reduce blood volume. | | When there is an alteration in blood pressure, the rate of filtration | | is increased or decreased, with a corresponding change in urine | | output. | | | | Indirectly, the renin-angiotensin mechanism influences blood | | pressure. When a decrease in arterial pressure occurs, the enzyme | | \'renin\' is released from cells in the kidney. Renin triggers the | | renin-angiotensin pathway that produces angiotensin 11, a potent | | vasoconstrictor which will also increase renal perfusion. It also | | stimulates the adrenal cortex to secrete aldostrerone which enhances | | reabsorption of sodium and the secretion of antdiuretic hormone | | (ADH), which further promotes reabsorption. Water follows sodium, so | | blood volume and blood pressure rise.  | | | | A further mechanism for increasing blood volume is the **transfer of | | interstitial fluid into the intravascular space **(see **Week 3 - | | Fluid therapy**). As blood volume and blood pressure fall, a gradient | | occurs. | | | | ** ** | | | | +--------------------------------+--------------------------------+ | | | | **Watch** | | | | | | | | | | 1\) Watch the following video | | | | | from **Ninja Nerd** on the | | | | | fundamentals of blood | | | | | pressure (40:19 minutes): | | | | | | | | | | 2\) Watch the following video | | | | | from **Ninja Nerd** on the | | | | | regulation of blood | | | | | pressure, especially | | | | | regarding hypotension (42:01 | | | | | minutes): | | | +--------------------------------+--------------------------------+ | | | | **Compensatory mechanisms** | | | | Vasoconstriction effectively reduces (or re-prioritises) the volume | | of the system; this reduces  blood flow is reduced to non-essential | | areas i.e. gut, skin, muscle -- however, the reduced blood volume can | | still perfuse the vital organs (the brain and heart). | | | | The selective vasoconstriction (specifically) is manifested by cold, | | pale skin, cyanosis, and nausea. | | | |  Some regions will experience vasoconstriction and some will | | experience vasodilation. | | | | 65 percent of blood sits in the venous system at any one time (Marieb | | & Hoehn, 2002). When the sympathetic nervous system is activated | | (fight or flight), vasoconstriction causes the blood in these venous | | reservoirs to be squeezed into central circulation. | | | | The spleen acts as another reservoir, holding approx. 300ml of blood. | | When sympathetic stimulation is activated, vasoconstriction squeezes | | as much as 200ml of this blood into the systemic circulation and | | increases the hematocrit by as much as 4 percent (Huether & McCance, | | 2004). If we then add normal saline to replace the lost blood volume, | | it combines with the red blood cells to increase both the volume and | | then oxygen carrying capacity, albeit by a small amount. | | | | In a haemorrhage situation, the red blood cells decrease, the plasma | | increases, or both. Both have the effect of dropping haematocrit, so | | the person ends up with certain symptoms similar to anemia (middle | | slide). So, while you might end up with a relatively normal blood | | volume, the oxygen carrying capacity is greatly reduced.  | | | | **Summary** | | | | The maintenance of adequate perfusion is a complex and constant | | process, occurring beat by beat and with every minor change in | | position and movement. The key regulating variable for perfusion is | | systemic pressure.  A drop in pressure is detected by the | | baroreceptors which cause a reflex increase in heart rate and stroke | | volume and a generalised vasoconstriction (if possible). This assists | | with VR to the heart and should assist with CO (Moules, 2019). | | | | The sympathetic nervous system (SNS) also restricts renal blood flow | | and triggers the release of renin which leads to the production of | | angiotensin II, causing further vasoconstriction and the release of | | aldosterone. Aldosterone increases renal sodium reabsorption, which | | in turn causes more water to be reabsorbed in the kidney tubules. If | | the drop in pressure is not too severe, these homeostatic mechanisms | | will maintain blood pressure and reasonably adequate tissue perfusion | | (Moules, 2019). | +-----------------------------------------------------------------------+ **Stages of Shock** The previous page examined the body's compensation attempts to maintain adequate systemic pressure to ensure appropriate perfusion. If compensation mechanisms stop or are overwhelmed, the lack of oxygen and nutrients and the non-removal of waste products will impair normal metabolism. The cells cannot generate enough adenosine triphosphate (ATP -- the cellular energy-carrying molecule) for their metabolic requirements and are consequently prone to cell death. When cells die, their membranes allow the cell contents to leak into the extracellular space and generate an even more toxic environment for the adjacent cells---resulting in even more cell death. This is an example of a positive (yet vicious-circle) feedback mechanism (Moules, 2019). There are three recognised stages of shocks. It is important to see these stages as a **continuum**; age, gender, underlying fitness and medications will all impact on how an individual patient presents at each stage. Excessive time should not be spent trying to determine what stage your patient is in. However, having an idea of which stage the patient is in can be helpful for determining how aggressive or otherwise your treatment should be. **COMPENSATED SHOCK** The bodies defense mechanisms attempt to preserve major organs (the heart, the brain, lungs and kidneys). Note that both vasoconstriction and vasodilation will occur. - Precapillary sphincters close, blood is shunted towards essential organs. 65 percent of blood sits in the venous system at any one time (Marieb and Hoehn, 2007). When the SNS is activated (fight or flight), vasoconstriction causes the blood in these venous reservoirs to be squeezed into central circulation. Selective vasoconstriction effectively reduces the vascular container, meaning reduced blood volume can still perfuse the essential organs (heart, brain and kidneys). Blood flow to non-essential organs (gut, skin and skeletal muscle) is diminished.  The following image shows the **relationship** between** blood flow velocity** and **total cross sectional area** in various blood vessels of the systemic circulation: *Image: https://www.studyblue.com/notes/note/n/exam-1/deck/2095530 * The key message here is that most of the circulating blood volume is located in non-essential areas. When these are closed down secondary to vasconstriction, large volumes of blood are then forced into the core, preferentially perfusing the heart, lungs, and brain. So the body has some pretty good compensatory mechanisms which will cope with mild to moderate blood loss and maintain blood pressure at a decent level. However, if blood loss continues, the compensatory reserves are exhausted and a rapid deterioration follows. - The spleen acts as another reservoir, holding approximately 300 ml of blood. When sympathetic stimulation is activated, vasoconstriction squeezes as much as 200 ml of this blood into the systemic circulation and increases the hematocrit by as much as 4 percent (Huether and McCance, 2004). If we then add normal saline to replace the lost blood volume, it combines with the red blood cells to increase both the volume and then oxygen carrying capacity, albeit by a small amount. These two images further show the impact of reducing arterial diameter (vasoconstriction) and vasodilation on blood flow: ***Image: http://hyperphysics.phy-astr.gsu.edu/hbase/ppois2.html*** ***Image: http://hyperphysics.phy-astr.gsu.edu/hbase/ppois4.html*** ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- This diagram shows the effect of reducing the arterial diameter, but the opposite is also true. If blood volume and therefore blood pressure drops, reducing the arterial diameter will have a dramatic effect on increasing the blood pressure again. Note the pressure to restore normal flow rate; the numbers increase exponentially, showing the dramatic reduction in blood flow that occurs secondary to occlusion. It also suggests how powerful vasoconstriction is at increasing blood pressure.  Vasodilation and vasoconstriction have dramatic effects on blood flow. Again, when blood volume is decreased, widespread vasoconstriction is very effective at restoring blood pressure.  - Increased heart rate and strength of contractions. However, as seen in the following image, increasing tachycardia will only increase cardiac output to a certain point, beyond which the CO is likely to fall again. Maximum heart rate can be estimated by the equation: 220 -- age. For an 80 year old therefore, their max heart rate may be 140/min. At this point they are physiologically maxed out and have no reserve. Athletes are used to these high heart rates, so it is important to recognise when the rate reflects a critical physiological state and when it doesn't.  ***Image: www.slideshare.net*** - Increased respiratory function, bronchodilation. These increases may not be dramatic or even readily noticeable, so accurate recording is important to notice any change. The body defense mechanisms will continue until the problem is solved or shock progresses to next stage. - Increased heart rate, possible tachycardia - Decreased skin perfusion; cold, pale skin, cyanosis and nausea - Alterations in mental status Some medications such as metoprolol (or other B- blockers etc) can hide signs and symptoms. Some or any of these signs may be present. Compensated shock can be difficult to detect as the markers can be quite subtle. There is no substitute for careful patient assessment, accurate recording of vital signs, and good history taking including mechanism of injury (MOI). Of the vital signs, an increase in the respiratory rate may be your first indication of change. For this reason practice and maintain your ability to accurately count respirations. **Don\'t guesstimate**! This should result in a raised index of suspicion that a state of shock exists. **DECOMPENSATED SHOCK** This is the stage on the shock continuum sees the compensation mechanisms start to be overwhelmed or fail. The speed of this failure will again depend on the patient\'s age, gender, fitness and history. The physiological response of decompensated shock : - Precapillary sphincters open, blood pressure falls - Cardiac output falls - Blood surges into tissue beds, blood flow stagnates - Red cells stack up in rouleaux (i.e. start to \'clump\' together) The decompensated stage is easier to detect than compensated shock: - Prolonged capillary refill time - Marked increase in heart rate - Rapid thready pulse - Agitation, restlessness, confusion - Decreased BP **IRREVERSIBLE SHOCK** In this stage, Compensatory mechanisms have failed, cell death has begun and vital organs have begun to falter and fail. It cannot be differentiated in the field. - The patient may be resuscitated but may die later of SIRS, ARDS, renal and liver failure or sepsis (or a combination). - Organs have been deprived of oxygen for too long and cells have died causing multiple organ failure (brain, lungs, heart, kidneys). - Development of DIC (Disseminated Intravascular Coagulopathy) **DIC (DISSEMINATED INTRAVASCULAR COAGULOPATHY)** Disseminated intravascular coagulation (DIC) is a paradoxical condition characterised by both bleeding and thrombosis. DIC is always secondary to another condition, such as severe trauma, sepsis or burns or certain haemalogical disorders (Oatley & Dunleavey, 2019). DIC results from the release of pro-inflammatory cytokines, and is characterised by simultaneous activation of blood coagulation, consumption of clotting proteins, generation of thrombin, activation of platelets and secondary activation of the fibrinolytic system. Microclots form within the capillaries and deplete clotting factors in the circulating blood faster than the liver and bone marrow can replace them, resulting in haemorrhage. Intravascular clots obstruct the capillaries causing ischaemia in the tissues. The fibrinolytic system is activated to dissolve the clots and potent fibrin degradation products trigger further bleeding (Oatley & Dunleavey, 2019). The mortality rate for DIC has been given as 40--80% in patients with severe trauma, sepsis and burns (Oatley & Dunleavey, 2019). It is difficult to provide accurate statistics around mortality rates because this is so connected with other factors, such as the underlying disease process. Note that DIC is often insidious in its presentation and small signs may alert suspicions. Be aware of bleeding from previous venepuncture sites, mucous membranes or the sclera and conjunctiva, particularly in the context of a clinically deteriorating patient (Oatley & Dunleavey, 2019). +-----------------------------------+-----------------------------------+ | | **Required Reading** | | | | | | Read the following sections | | | in **Chapter 10 - Physiology and | | | pathophysiology for emergency | | | care **Emergency and Trauma Care | | | for Nurses and Paramedics (3rd | | | ed.): | | | | | | - pp. 793-794 -** Disseminated | | | intravascular coagulation** | | | | | | - p\. 167 - **Trauma induced | | | coagulopathy and the triad of | | | death** | | | | | | ** **These are available through | | | the [[ClinicalKey Student | | | database]](https://we | | | ltec.spydus.co.nz/cgi-bin/spydus. | | | exe/MSGTRNGEN/OPAC/EBOOKS).  | +-----------------------------------+-----------------------------------+ **Summary** There are certain patients that despite our best efforts, due to the nature of their injuries or illness, the pathway described will occur and death will be the result. Mattox (2003) states that only 6-8% of patients suffering blunt or penetrating trauma will exhibit post traumatic hypotension. Of this cohort, 1/3rd will die regardless of intervention, 1/3rd will survive regardless of treatment or not, and the outcome of the final third will be dependent on treatment. Interestingly (and positively), the definition of irreversible shock may change as advanced multi-trauma care begins to save those who would otherwise have been considered unsalvageable. This can be seen in the Major Trauma Pathways and in cardiac arrest secondary to trauma. If the patient has good prognostic features keep resuscitating aggressively, including calling for whole blood (potential game-changer) and tranexemic acid. **Types of Shock** +-----------------------------------+-----------------------------------+ | | **Required Reading** | | | | | | 1\) Read the following sections | | | in **Chapter 10 - Physiology | | | and pathophysiology for | | | emergency care **Emergency and | | | Trauma Care for Nurses and | | | Paramedics (3rd ed.): | | | | | | - pp. 165-167 | | | -** Hypovolaemic Shock** | | | | | | - pp. 167-169 -** Distributive | | | shock (includes septic shock | | | and anaphylactic shock)** | | | | | | - p\. 169 -** Neurogenic shock* | | | * | | | | | | - pp. 169-170 -** Cardiogenic | | | shock** | | | | | | - p\. 170 -** Obstructive shock | | | ** | | | | | | This is available through | | | the [[ClinicalKey Student | | | database]](https://we | | | ltec.spydus.co.nz/cgi-bin/spydus. | | | exe/MSGTRNGEN/OPAC/EBOOKS).  | | | | | | 2) [**[Guideline 4.1 - | | | Shock]**](https://cpg | | |.stjohn.org.nz/tabs/guidelines/sh | | | ock-and-trauma-eas/page/shock-eas | | | ) in | | | the [[Emergency Ambulance Service | | | (EAS) Clinical Procedures and | | | Guidelines]](https:// | | | cpg.stjohn.org.nz/tabs/guidelines | | | ), | | | especially the **Causes of | | | Shock**commentary. This includes | | | commentary on **Hypoadrenal | | | shock,** a rare but | | | life-threatening cause of shock | | | caused by inadequate levels of | | | circulating cortisol. | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | | **Watch** | | | | | | The following podcast featuring | | | Dr. Craig Ellis and Dan Ohs from | | | St John provides an excellent | | | overview on the types and causes | | | of shock (15:27 minutes): | | | | | | [[https://player.vimeo.com/video/ | | | 268677244]](https://p | | | layer.vimeo.com/video/268677244)  | +-----------------------------------+-----------------------------------+ **HYPOVOLEMIC SHOCK** This is shock due to loss of intravascular fluid volume. Hypovolaemia can occur secondary to either blood loss from haemorrhage (\'[[controlled]](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/hypovolaemia-from-controlled-bleeding-eas)\' or \'[[uncontrolled]](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/hypovolaemia-from-uncontrolled-bleeding-eas)\', or [[fluid loss]](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/hypovolaemia-from-fluid-loss-eas) (examples include severe burns, excessive diarrhoea or vomiting, perspiration, etc.). Possible causes: - Internal or external hemorrhage - Traumatic hemorrhage - Long bone or open fractures - Severe dehydration from GI losses - Plasma losses from burns - Diabetic ketoacidosis - Excessive sweating Also can result from internal third-space loss Possible causes: - Bowel obstruction - Peritonitis - Pancreatitis - Liver failure resulting in ascites [**[CARDIOGENIC SHOCK]**](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/spinal-cord-injury-eas) Causes: - Chronic progressive heart disease - Rupture of papillary heart muscles or intraventricular septum - End-stage valvular disease Patients may be normovolemic or hypovolemic \ May have pulmonary oedema - Pump failure (cardiogenic shock) Inadequate function of the heart - the heart muscle can no longer generate enough pressure to circulate blood to all organs. Causes a backup of blood into the lungs which results in pulmonary oedema +-----------------------------------+-----------------------------------+ | | **Thinking point** | | | | | | Cardiogenic shock is generally | | | secondary to some 'insult', with | | | acute myocardial infarction the | | | most common cause of cardiogenic | | | shock. Other causes include | | | pulmonary embolism, dysthymia, | | | cardiac tamponade or aortic valve | | | rupture. Cardiogenic shock has a | | | high mortality | | | rate [unless] the | | | underlying problem is corrected | | | in a timely manner; as noted in | | | the CPGs, there are only two | | | interventions in the | | | out-of-hospital setting that | | | significantly alter outcomes:  | | | | | | - Initiating fibrinolytic | | | therapy for STEMI when | | | indicated | | | | | | - Transporting the patient to a | | | hospital with a cardiac | | | catheter room/lab for PCI | | | | | | A clear history (both of | | | presenting complaint and medical | | | history etc.) as well as 12 lead | | | ECG and vital signs is thus key. | | | | | | The use of fluid therapy in | | | cardiogenic shock is tricky | | | and [**[Guideline 3.13 -- | | | Cardiogenic | | | shock]**](https://cpg | | |.stjohn.org.nz/tabs/guidelines/ca | | | rdiac-eas/page/cardiogenic-shock- | | | eas) outlines | | | a cautious approach. The patient | | | will often be pale, cold, | | | tachycardiac, and with shortness | | | of breath, pulmonary oedema | | | (crackles) and/or a dysrhythmia. | | | These signs and symptoms will | | | limit the indication for fluid | | | therapy.  | | | | | | - Cardiogenic shock secondary | | | to poor left ventricular | | | function, for example from an | | | acute anterior, anteroseptal | | | or anterolateral STEMI, is | | | unlikely to respond to fluid | | | therapy and may make | | | pulmonary worse by increasing | | | end diastolic volume.  | | | | | | - Cardiogenic shock secondary | | | to poor right ventricular | | | function, for example, an | | | acute inferior myocardial | | | infraction, is more likely to | | | respond to fluid therapy as | | | the patient will have a | | | decreased preload.  | | | | | | I believe that these cautions | | | from the CPGs reflect the danger | | | of fluid overloading these | | | patients and inducing (or | | | enhancing) pulmonary oedema. | | | Nevertheless, there will be times | | | when the patient's main problem | | | is life-threatening hypotension | | | in the presence of one or more of | | | SOB, pulmonary oedema (crackles) | | | and/or dysrhythmia but where | | | these are a minor issue. In this | | | setting the benefits of | | | administering | | | fluid [might] outweig | | | h | | | the risks -- seek clinical | | | guidance.  | | | | | | Again, this requires caution and | | | a balance between maintaining | | | perfusion to heart and other | | | vital organs and the high risk of | | | developing pulmonary oedema. The | | | guideline asks for small bolus, | | | between 250-500ml, repeated as | | | required up to 1 litre. You must | | | stop if the patient shows signs | | | or symptoms of pulmonary oedema. | | | When administering these small | | | fluid boluses, ask the patient if | | | their breathing is improving etc | | | plus monitor for improvement for | | | other signs of shock - LOC, | | | CRT/skin etc (HR and BP may be | | | affected by medications). | | | | | | Remember, these patients are also | | | extremely fragile. They are using | | | all of physiological reverse so | | | any increased sympathetic nervous | | | stimulation etc. (i.e. moving | | | patient) may cause rapid | | | deterioration. You must request | | | ICP back up. | | | | | | You will cover cardiogenic shock | | | in more detail in Year 3 | | | cardiology paper. | +-----------------------------------+-----------------------------------+ [**[NEUROGENIC SHOCK]**](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/spinal-cord-injury-eas) Shock resulting from inadequate peripheral resistance due to widespread vasodilation. Common causes: - Spinal cord injury - Central nervous system injuries No sympathetic response Neurogenic shock is a pipe problem. +-----------------------------------+-----------------------------------+ | | **Thinking point** | | | | | | What signs and symptoms would you | | | expect to see in a patient with | | | neurogenic shock? | | | | | | How would you treat these | | | patients? | | | | | | **Tip**: make sure you | | | distinguish between a spinal cord | | | injury (and shock) caused by | | | multi-trauma (i.e. from a | | | high-speed road traffic crash, | | | where the shock may be caused by | | | hypovolaemia etc.) and shock | | | caused from an **isolated spinal | | | cord injury** (i.e. from a | | | collapsed rugby scrum, with nil | | | other injury).  | | | | | | Refer to the **Thoracic injuries | | | & multi trauma learning | | | package **in Week 10 for more | | | information. | +-----------------------------------+-----------------------------------+ [**[SEPTIC SHOCK]**](https://cpg.stjohn.org.nz/tabs/guidelines/infection-eas/page/sepsis-eas) Shock resulting from systemic vasodilation. Systemic increased vascular permeability Usually a result of gram (-) bacteria infection Development of bacteremia septic shock Vessel and content failure Caused by: - Severe bacterial infections, toxins, or infected tissues - Toxins damage vessel walls, causing them to leak and become unable to contract well. Leads to *[dilation]* of vessels and loss of plasma, causing shock. We will cover septic shock in more detail in **Week 7 - Sepsis & septic shock**. [**[ANAPHYLACTIC SHOCK]**](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/anaphylaxis-eas) Widespread hypersensitivity reaction to a specific antigen resulting in vasodilation, peripheral pooling, relative hypovolemia leading to decreased perfusion and impaired cellular metabolism Provokes an extensive immune & inflammatory response: - Vasodilation - Increased permeability - Peripheral pooling - Tissue edema Sudden onset and death can occur in minutes: - Anxiety - Difficulty breathing - GI cramps - Edema - Urticaria - Pruritis Allergic Reactions: Vasodilation = produces drop in **[BP]**. +-----------------------------------+-----------------------------------+ | | **Clinical tip** | | | | | | Be careful to differentiate | | | between a severe allergic | | | reaction and anaphylaxis. True | | | anaphylaxis is a life-threatening | | | emergency, while a severe | | | allergic reaction, while serious, | | | is unlikely to be. Encountering | | | life-threatening anaphylaxis is | | | quite rare, and an increasing | | | number of patients with known | | | anaphylaxis carry an Epipen, | | | allowing them to self-administer | | | adrenaline. It is however | | | encountered from time to time, | | | and is a situation that requires | | | urgent action. | | | | | | In addition, fluid therapy will | | | be far more effective | | | post-adrenaline administration. | | | In anaphylaxis, the capillaries | | | dilate and become more permeable | | | (leakier). This causes the blood | | | pressure and the central venous | | | pressure to drop and the plasma | | | part of the blood passes out of | | | the leaky capillaries and into | | | the interstitial space. | | | Adrenaline will vasoconstrict the | | | dilated blood vessels and reverse | | | the permeability. Once the | | | vessels are back to their normal | | | diameter and are no longer | | | leaking, the intravenous fluid | | | will remain in the vascular | | | space.   | +-----------------------------------+-----------------------------------+ **OBSTRUCTIVE SHOCK** Obstructive shock is caused by a clinical condition causing obstruction of blood flow into, or out of the heart. The patient may retain a relatively healthy cardiovascular system and operating baroreceptors, but tissue perfusion is compromised by an obstruction in a major vessel (Moules, 2019). Examples include: - An embolism in a major artery, lung or major vein, for example, a pulmonary embolism (which is caused by inadequate right ventricular function as a result of increased afterload) - Tension pneumothorax (causing inadequate right ventricular filling as a result of raised intrathoracic pressure) - Cardiac tamponade (causing inadequate cardiac filling) Clinical manifestations vary according to the site of the obstruction.  **Recognition of shock** +-----------------------------------+-----------------------------------+ | | **Watch** | | | | | | The following podcast featuring | | | Dr. Craig Ellis and Dan Ohs from | | | St John provides an excellent | | | overview on assessing the | | | severity of shock (14:17 | | | minutes).  | | | | | | In this podcast Dan and Craig | | | provide a very clear description | | | of the classic signs and symptoms | | | of shock (especially hypovolaemic | | | shock) and link these signs and | | | symptoms to projected volume | | | loss. In addition, Dan and Craig | | | provide interesting commentary on | | | the potential 'over-treatment' of | | | adult patients and the | | | 'under-treatment' of paediatric | | | patients. Thanks to St John for | | | the use of the video. | | | | | | [[https://player.vimeo.com/video/ | | | 268677014]](https://p | | | layer.vimeo.com/video/268677014) | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | | **Required Reading** | | | | | | The following guidelines in | | | the [[Emergency Ambulance Service | | | (EAS) Clinical Procedures and | | | Guidelines]](https:// | | | cpg.stjohn.org.nz/tabs/guidelines | | | ) each | | | provide information on | | | defining shock, either in terms | | | of hypovolaemia/poor perfusion or | | | severe shock: | | | | | | - [**[Guideline 4.1 - | | | Shock]**](https:/ | | | /cpg.stjohn.org.nz/tabs/guideline | | | s/shock-and-trauma-eas/page/shock | | | -eas) | | | | | | - [**[Guideline 4.6 - | | | Hypovolaemia from | | | uncontrolled | | | bleeding]**](http | | | s://cpg.stjohn.org.nz/tabs/guidel | | | ines/shock-and-trauma-eas/page/sh | | | ock-eas) | | | | | | - [[**Guideline 4.7 - | | | Hypovolaemia from controlled | | | bleeding** ]](htt | | | ps://cpg.stjohn.org.nz/tabs/guide | | | lines/shock-and-trauma-eas/page/h | | | ypovolaemia-from-controlled-bleed | | | ing-eas) | | | | | | - **G[[uideline 4.8 - | | | Hypovolaemia from fluid | | | loss]](https://cp | | | g.stjohn.org.nz/tabs/guidelines/s | | | hock-and-trauma-eas/page/hypovola | | | emia-from-fluid-loss-eas).** | | | | | | Pay particular attention to the | | | difference in signs of shock or | | | hypovolaemia/poor perfusion in | | | Guidelines 4.1, 4.7 and 4.8 and | | | the signs of severe shock in | | | Guideline 4.6. Defining severe | | | shock may require the recognition | | | of trends over a time period i.e. | | | increasing tachycardia, a falling | | | blood pressure and/or level of | | | consciousness as well as your | | | initial assessment i.e weak | | | radial pulses, prolonged | | | capillary refill time, inability | | | to obey commands. Note also the | | | consistent commentary around | | | blood pressure. **Blood pressure | | | is a poor guide of severity of | | | shock - after all, the bodies | | | compensation mechanisms are all | | | focused on maintaining systemic | | | pressure!** Blood pressure may | | | only begin to fall when shock is | | | severe and blood pressures varies | | | with age, sex, degree of fitness | | | and medications. | +-----------------------------------+-----------------------------------+ A knowledge of the clinical signs and symptoms of shock is important to enable recognition, and allow treatment to begin. Shock is referred to as the \'**Silent Killer**\' because so often it is unrecognised in the early (but treatable) stages. The clinical implications of this are very significant.  We must not become focused solely on the blood pressure! In young, healthy individuals, 1500 mL - 2000 mL  (15 - 30%) blood loss is required before a decrease in BP is observed! We must become good at assessing **perfusion status**, and not become focused on one small component.  "**Cue recognition**" is vital.  It is important that as a paramedic you recognise developing shock early, not late when it is irreversible.  This means a high index of suspicion (Greaves et al, 2006). The following table is an example of a systematic and standardised **Perfusion Status Assessment **(PSA). You should be familiar with the format of this assessment following your use of the related Respiratory Status Assessment (RSA) in Trauma/Medical II. Like the RSA, the PSA model can be utilised rapidly for time critical (\'Big Sick\') patients, as well as for patient\'s who are less acute. This model is adapted from the Ambulance Victoria PSA (a version of which can be seen in **Table 4.3 - Perfusion Status Assessment** on page 38 of *Paramedic Principles, 2015*). In addition, the model incorporates key aspects of the New Zealand Early Warning Score Vital Sign Chart, which was developed as part of the Health Quality and Safety Commission\'s, patient deterioration programme (Health Quality & Safety Commission, 2017). Please however that that this version of the Perfusion Status Assessment has not been validated in practice or is it specifically endorsed by either St John Ambulance or Wellington Free Ambulance. [[Click here for a downloadable copy of the PSA.]](moodleappfs://localhost/_app_file_/var/mobile/Containers/Data/Application/5646C75F-EF25-42C8-8C97-45A0D2E00948/Documents/sites/2ad3b6cda7ecae7627fda94748a3f414/filepool/PSA%202019%20v3_f45e6a8d27cdc340ca18c2b0a26ce61e.pdf) Note that by the time the patient has an altered level of consciousness they have extremely poor perfusion. This is important to recognise; we deal with many unconscious patients who are stable haemodynamically (for example, CVA, EtOH or drug overdose, post-ictal, hypoglycaemia), but when the unconsciousness has a cardiac or hypovolaemic cause, it is often pre-terminal. **Extremes of age.** Recognising shock can be difficult in any patient, but some patient sub-groups offer particular challenges. Both immature and aged body systems have limited ability to compensate for shock. At one end the systems are immature, and at the other systems are debilitated through age and injury. ***Paediatric*** The heart has not developed stretch receptors, so it is not capable of increasing stroke volume. Tachycardia is the only response the pediatric heart can make to circulatory insufficiency. This physiological feature, plus a child\'s significant capacity for vasoconstriction, means that a fall in blood pressure is a very late sign of shock. In addition, children have a greater proportion of circulating blood per body weight; 8 - 9 percent (or 80 -- 90 mL/kg).  However, absolute volume is less.  Therefore, a 500 mL loss, for example, may be very serious. In comparison, circulating blood volume of an adult is 7 percent of the lean body mass (70 mL/kg). A 70 kg adult thus has 5000 mL of circulating blood. +-----------------------------------+-----------------------------------+ | | **Required reading** | | | | | | Read the following sections | | | in **Chapter 35 - Paediatric | | | emergencies **in** **Emergency | | | and Trauma Care for Nurses and | | | Paramedics (3rd ed.): | | | | | | - pp. 969-972 - **Shock** | | | | | | - pp. 972-975 -** Dehydration** | | | | | | This is available through | | | the [[ClinicalKey Student | | | database]](https://we | | | ltec.spydus.co.nz/cgi-bin/spydus. | | | exe/MSGTRNGEN/OPAC/EBOOKS).  | +-----------------------------------+-----------------------------------+ ***Geriatric*** The heart has limited ability to respond with a tachycardia due to injury or disease. Also the patient may be taking a beta blocker. Ischaemic heart disease (IHD) may limit the ability to stretch to increase stroke volume. The patient may be taking an anticoagulant (warfarin, clopidigrel, dipyridimole, aspirin) which will limits the body's ability to clot at the site of any hemorrhage. Co-morbidities such as IHD, stroke, diabetes can impact on the body's ability to compensate. Many elderly people do not hydrate well, with their only fluid intake being the cup of tea they take at mealtimes, which may be little more than 1 litre a day. While the body may have adapted to this level of hydration and cope relatively well, when deprived of fluid intake, dehydration leading to hypovolemic shock can occur. +-----------------------------------+-----------------------------------+ | | **Thinking point** | | | | | | A scenario not uncommon to | | | paramedics is the elderly patient | | | who has had a fall, and is not | | | found for 24 hours or greater. | | | | | | Consider how you would treat such | | | a patient, if they appear | | | normotensive, with reasonable | | | heart rate, but poor skin turgor. | | | | | | Would you give this patient | | | fluids, if so, how much? | | | | | | This example is to illustrate | | | that shock need not be a high | | | drama, big ticket item, but can | | | occur in more subtle ways. | +-----------------------------------+-----------------------------------+ ***Pain*** The impact of pain, either independent or in conjunction with shock can help mask or distract from the signs and symptoms of shock. The physiological response to pain i.e increased HR, increased RR, altered LOC (distracted, agitated) , pale/clammy skin mimic the signs and symptoms of shock. We can begin to treat the patient\'s pain but instead of being suspicious when the signs and symptoms do not improve following opiates etc, we continue to provide more pain relief and/or don\'t prioritise prompt transport to an appropriate facility. By the time shock becomes overt, it is usually on the borderline of irreversible. ***Question: How can we distinguish between hypovolaemia and the pain response? *** **Answer**: Treat for the worst! In the presence of signs and symptoms (plus a suggestive mechanism of injury or index of suspicion) we assume that shock is present until proven otherwise. In my opinion it better to \'overcall\' (or more accurately, assume the worst) 19 times than be caught out on the 20th and be the cause of someone's death due to under-calling it and not wanting to look like you're overreacting. This is cognitive bias which we must be aware of and actively challenge.  Lastly, note the impact that **underlying fitness** can have on a patient\'s clinical response. A fit person may compensate very well and have few signs and symptoms; for example, a heart rate of 95 bpm may be normal for an elderly man with heart problems, but may reflect serious compromise in an athlete whose resting HR is 40 bpm. **Treatment** +-----------------------------------+-----------------------------------+ | | **Required Reading** | | | | | | The following guidelines in | | | the [[Emergency Ambulance Service | | | (EAS) Clinical Procedures and | | | Guidelines]](https:// | | | cpg.stjohn.org.nz/tabs/guidelines | | | ) set | | | out the key treatment priorities, | | | principles and key information | | | for the treatment of | | | hypovolaemia: | | | | | | - [**[Guideline 4.6 - | | | Hypovolaemia from | | | uncontrolled | | | bleeding]**](http | | | s://cpg.stjohn.org.nz/tabs/guidel | | | ines/shock-and-trauma-eas/page/hy | | | povolaemia-from-uncontrolled-blee | | | ding-eas) | | | | | | - [**[Guideline 4.7 - | | | Hypovolaemia from controlled | | | bleeding]**](http | | | s://cpg.stjohn.org.nz/tabs/guidel | | | ines/shock-and-trauma-eas/page/hy | | | povolaemia-from-controlled-bleedi | | | ng-eas) | | | | | | - [[**Guideline 4.8 - | | | Hypovolaemia from fluid | | | loss** ]](https:/ | | | /cpg.stjohn.org.nz/tabs/guideline | | | s/shock-and-trauma-eas/page/hypov | | | olaemia-from-fluid-loss-eas) | | | | | | Take special note in the | | | different thresholds for starting | | | fluid therapy for each guideline. | | | Guidelines 4.7 and 4.8 has a | | | lower threshold for commencing | | | fluid therapy (i.e. if the | | | patient has signs of poor | | | perfusion or hypovolaemia) | | | compared to Guideline 4.6, where | | | fluid is started only if the | | | patient is severely shocked. This | | | allows relative hypovolaemia | | | prior to surgical control of the | | | bleeding (although we don\'t want | | | to let the patient bleed to | | | death!). | +-----------------------------------+-----------------------------------+ In emergency medicine, few things are more controversial than the treatment of shock. Evidence based medicine (EBM) has certainly had a profound effect on the way we approach the treatment of the shocked patient. In practice, we do not treat a shocked patient, per se. Any trauma or medical patient should be treated as presented and treatment modalities should be flexible enough to take into account changes in patient condition. Patient management is a dynamic situation, and the ability to make changes based on the presentation by anticipating what may happen next is how a paramedic should be dealing with the prospect of shock. We don't have procedures for dealing with shock, we have guidelines. It is not "if the patient has X, we do Y" but rather common sense and the practical application of sound theoretical knowledge. **Trends** The most important tool in a paramedic's armoury is observation. By carefully observing a patient, and accurately recording those observations, trends can be identified, which allow us to determine changes in patient condition, to predict further deterioration, and adjust our treatment plan. **Treatment** 1. **Airway and Breathing** -- needs to be manage appropriately. Good ventilation is important as is good oxygenation. High-flow O2 via non-rebreather. Anything impeding ventilation will need to be fixed. Consider: - Upper airway compromise, through injury or disease. Bronchospasm, FBO, maxillo-facial injuries, structural damage to trachea, blood, secretions, vomitus. - Chest/lungs; rib \#'s, haemothorax, pnuemothorax, diaphragm rupture, pulmonary oedema 2. **External bleeding controlled** -- direct pressure, elevation, wound packing (if appropriate). A tourniquet may be needed in a "life versus limb" situation. **Guideline 4.6  - Hypovolaemia from uncontrolled bleeding **provides updated advice on tourniquet application (p.184).  3. **Internal bleeding **is less simple to identify, but some bleeds not obvious. Careful assessment may elicit grounds for suspicion. - Chest - usually obvious on auscultation, examination etc. The lungs will be affected fairly quickly, whereas the abdomen or pelvis can absorb a very large amount of blood before it clinically manifests itself - Abdomen (and retro-peritoneal) -- not obvious - Pelvis -- not obvious - Long bone - obvious - External - obvious +-----------------------------------+-----------------------------------+ | | **Thinking point** | | | | | | Shock following blunt trauma is | | | usually caused by blood loss, but | | | it is important to exclude | | | tension pneumothorax: | +-----------------------------------+-----------------------------------+ 4. **Warmth** - the ability to generate warmth requires energy, as does clotting cascade. If a patient has decreased energy, oxygen etc., their body will prioritise warmth over clotting (i.e. hypothermia will contribute to coagulopathy). You need to keep the patient warm, especially if have exposed patient to find and stop any bleeding or for an examination. Remove wet clothing and dry the patient as soon as possible, keep the patient covered with blankets whenever possible and keep the interior of the ambulance as hot as possible. **Treatment priorities** Develop an ***ACTION PLAN*** An action plan should take into consideration: - Patient condition, and predict possible changes in status - The resources available to you; fire, police, ICP back up, helivac/trauma pathways - The difficulties in the incident; extrication of patient, environment, family or bystanders helping or impeding, risk of violence **Time to Hospital** In many situations the presence of any shock is a marker for an unfavorable outcome. In some situations, such as blunt or penetrating trauma, it\'s not so much that the patient needs to be in the ED, but rather the operating theatre, for surgical repair. In such cases, time taken to initiate treatment outside hospital must be used well, and only prudent interventions attempted. Greaves et al (2006) provides the following treatment priorities: 1. Identify patients at risk of bleeding/shock 2. Identify shock 3. Control of compressible haemorrhage 4. Urgent transport for surgery You will note where IV insertion and fluid therapy come in the list of treatment priorities; it may mean that in some situations that the IV and fluid therapy is not attempted in order to expedite transport to hospital (and definitive care i.e. surgery). The key here (once airway and ventilation is managed) is to recognise shock, control compressible bleeding (direct pressure, tourniquet etc) and urgent transport (including accessing trauma pathways) with any other interventions en-route. +-----------------------------------+-----------------------------------+ | | **Watch & Listen** | | | | | | 1\) The following video from | | | George Clicquot outlines the | | | pharmacology of shock and | | | trauma, with a focus | | | on **tranexamic | | | acid** (TXA), **adrenaline **and  | | | **metaraminol**. | | | Pay special attention to TXA, | | | as this is within the paramedic | | | ATP, while an increased | | | knowledge | | | about adrenaline and metaraminol  | | | will | | | help when making decisions | | | about calling for | | | assistance** **(19:42 minutes): | | | | | |   | | | | | |   | | | | | | 2\) Listen to the following | | | from **The Resus Room** team on | | | shock in trauma (76:35 | | | minutes): | | | | | |   | | | | | |   | | | | | | This podcast follows on from | | | their previous podcast on shock; | | | there will be some crossover but | | | will focus specifically on | | | current concepts around | | | hypovolaemic shock, traumatic | | | coagulopathy, controlling | | | external haemorrhage, blood | | | pressure targets & permissive | | | hypotension, fluid choices and | | | TXA. | +-----------------------------------+-----------------------------------+ **Fluid Therapy** **FLUID THERAPY** Fluid replacement remains a controversial subject in the management of shock. Many modalities have been embraced and discarded over the years, as new ideas have emerged, often without much science behind them. Techniques such as the trendelenberg position, use of MAST, colloid fluids, and aggressive crystalloid fluid infusion and others have come and gone. With the rise of evidence-based medicine, and its application to pre-hospital care, a relatively new discipline, new thinking has been embraced. With Hypovolemic shock from blunt or penetrating trauma, aggressive fluid resuscitation has been shown to worsen outcomes. Fluid therapy may: - Displace a developing clot - Dilute clotting factors - Promote hypothermia and secondary metabolic derangements - Delay surgical access while repeated attempts are made to gain IV access However, it is not acceptable to allow someone to bleed to death either! A compromise must be reached. ***Permissive (or relative) Hypotension*** is a term which reflects current thinking on fluid resuscitation. This reflects the aim of keeping the blood pressure at a low level to prevent any fresh clot from being displaced. In large animal models, the clot is displaced at approximately 80mm/Hg. This level is reproducible in both blunt and penetrating trauma models (Mattox 2003). "Popping the clot" can lead to a greater loss of whole blood, with the dilution of clotting factors. So are we actually helping the patient by infusing large volumes of crystalloid fluid? Conversely, we don't want the patient to exsanguinate (bleed to death!). As some pressure is required for the perfusion of vital organs, Greaves et al (2006) advocates administering enough fluid to maintain a radial pulse, as opposed to blood pressure targets. Their recommendation is to give boluses of 250ml, until a radial pulse is palpated; only giving more if the pulse is lost. The management technique is somewhat different in non-hemorrhagic shock. When the vascular container (the pipes) is intact, but leaky, the use of fluid to expand volume is a little different. With non-traumatic hypovolemia, septic and anaphylactic shock, fluid administration can be more aggressive. The most common cause of cardiogenic shock is MI, (pump failure), but the cause can be obstructive, as in cardiac tamponade or pulmonary embolus. The prognosis is usually poor. Treatment should consist of boluses of 250ml saline until a radial pulse is palpated or the patient becomes short of breath. Neurogenic shock from isolated spinal cord injury may also require a more cautious approach to fluid therapy, especially if there has been a concurrently loss of cardiac function due to the spinal cord injury. ***Immediate Post Traumatic Hypotension ***is a presentation paramedics encounter rarely and is a significant predictor of poor outcome. More often we may encounter trauma or medical patients with significant potential to deteriorate if not managed correctly. Maintaining an appropriate index of suspicion is important, as is accurate patient assessment and recording. Application of critical thinking and clinical practice of a high standard should be the hallmark of the professional paramedic. ***Hypovolaemia from other causes*** Hypovolaemia can occur secondary to either blood loss from haemorrhage, or fluid loss (examples include severe burns, excessive diarrhoea or vomiting, perspiration, etc.). There are now three CPGs relating to these different conditions with slightly different approaches to fluid therapy for each condition. By now, we should be familiar with the 'main' hypovolaemia guidelines (Guideline 4.6 and Guideline 4.7) but remember the third hypovolaemia guideline ([**[4.8 - Hypovolaemia from Fluid Loss]**](https://cpg.stjohn.org.nz/tabs/guidelines/shock-and-trauma-eas/page/hypovolaemia-from-fluid-loss-eas)). This is a new guideline in the 2019 CPGs and deals with hypovolaemia that does not clearly fit into another section. Examples include diarrhoea and vomiting or dehydration (fluid has moved from vessels into interstitial space) - look for a history of fluid loss or decreased fluid and food intake and decreased energy. Other indicators of dehydration that should be taken into account include: ambient temperate (has there been increased sweating in hot temperatures), tenting, dry mucus membranes (check tongue and below eyes), and history suggestive of reduced oral fluid (decreased urine output, especially in children and the elderly) or solids intake. Dehydration often accompanies other conditions, e.g., influenza +/- dehydration (and thus fluid loss via respiration etc). If there are signs of UTI, consider increased urination plus decreased fluid intake due to pain on urination. If you undertake a PSA, you should be on the lookout for dehydration. This guideline could also be used for correcting treatment-induced hypotension (e.g. midazolam, GTN, Ceftriaxone administration).