Hypovolaemic Shock

Shock can be classified into 3 different types: Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Features of a Hypovolaemic Shock

Hypovolaemic shock is the most commonly occurring type of shock, which is also easily reversible if treated in a timely manner. Features of a hypovolaemic shock include:

  • loss of circulating or intravascular volume
  • impaired tissue perfusion
  • inadequate delivery of oxygen and nutrients
  • may be caused by relative and absolute hypovolaemia, or loss of blood or other fluids

Absolute Hypovolaemia

The phrase Absolute Hypovolaemia refers to external loss of fluids from the body. Fluid loss may be that of whole blood (through trauma or major surgery), loss of plasma (through burns) and loss of other fluids such as massive diuresis (through skin loss), severe vomiting, diarrhoea, and dehydration (through diabetes insipidus – a rare condition unrelated to type 1 or 2 diabetes which causes diuresis and polydipsia, diabetic ketoacidosis, and HONK – hyperglycaemic hyperosmolar non-ketotic coma – coma resulting from very high blood glucose levels in a patient with normal ketone levels; very high blood glucose levels combined with high ketone levels may be due to ketoacidosis).

Internal Haemorrhage

Internal Haemorrhage may be caused by:

  • fractures
  • GI bleeding
  • organ rupture (eg. spleen, liver, and kidneys)
  • pregnancy complications (eg. ectopic pregnancy or post-partum haemorrhage)

Fluid Loss – from intravascular space to extravascular space – may be caused by:

  • burns
  • pleural effusion
  • peritonitis – inflammation of the peritoneum
  • pancreatitis – inflammation of the pancreas
  • ascites – a condition in which fluid collects in spaces within the abdomen

Pathophysiology of Hypovolaemic Shock

  1. relative or absolute hypovolaemia
  2. decreased circulating volume
  3. decreased venous return (decreased preload)
  4. decreased stroke volume
  5. decreased cardiac output
  6. decreased cellular oxygen supply
  7. impaired tissue perfusion
  8. impaired cellular metabolism

Signs & Symptoms

  • impaired consciousness
  • pale, cool, clammy extremities
  • prolonged capillary refill time
  • increased heart rate
  • increased respiratory rate
  • hypotension (SBP <90mmHg & reduced pulse pressure SBP-DBP)
  • reduced urine output
  • metabolic acidosis
  • signs of bleeding (decreased Haematocrit & Haemoglobin)
hypovolaemic shock
Retrieved from https://twitter.com/misirg1/status/1382458804995035144 on 19th January 2023

Management

  1. Identify & Treat the Underlying Cause
  2. Restore Intravascular Volume & Blood Pressure
  3. Redistribute Fluids to Ensure Perfusion
  4. Prevent Shock Progression
  5. Avoid onset of Cardiogenic Shock
  • stop the bleeding by applying pressure to injured site and prepare patient for surgery
  • administer antiemetics for severe vomiting, antidiarrhoeal agents to treat diarrhoea, insulin for dehydration caused by diabetes, and desmopressin for diabetes insipidus
  • establish good venous access through large peripheral lines and central venous catheters
  • insert a urinary catheter to monitor renal perfusion and fluid balance
  • monitor haemodynamic parameters and the patient’s condition, and titrate fluid administration according to patient’s needs
  • crystalloids are electrolyte solutions such as Isotonic (eg. normal saline or RLactate), Hypertonic (eg. 10% Dextrose) or Hypotonic (eg. 0.45% NaCl – Sodium Chloride); these address both fluid and electrolyte loss
  • colloids include blood and its products such as Fresh Frozen Plasma (FFP), as well as synthetic plasma expanders such as Gelafundin (a colloidal plasma volume substitute in an isotonic balanced whole electrolyte solution that can be used for prophylaxis and therapy of hypovolaemia and shock); ADVANTAGES: colloids remain in the intravascular space, restoring fluids faster and with less volume, while blood restores Hgb; DISADVANTAGES: colloids are expensive, may cause reactions, and may also leak out of damaged capillaries, causing additional problems including cardiac failure and peripheral oedema
  • based on the patient’s blood group and cross match, administer infusions of packed red blood cells to increase circulatory volume and oxygen carrying capacity; fresh frozen plasma, platelets, and cryo precipitate (the insoluble portion, or precipitate, that remains when the liquid portion of the plasma drains away) may also be indicated – blood products are commonly administered through a blood warmer so as to prevent or manage hypothermia
  • during surgical procedures such as cardiothoracic surgery, chest and abdominal trauma, and orthopaedic surgery, the patient can receive own blood through the intra-operative blood salvage machine, which collects lost blood through a filtered tube and readministers it within 4 hours; this reduces the risk of reactions and infections, however, it does carry an increased risk of haemolysis and microemboli formation during the collection and administration period
  • pay attention to any arising complications of fluid administration eg. allergic reactions and infection, electrolyte imbalance, dilution of haemoglobin and clotting factors, and pulmonary oedema (higher risk in older adults, and patients with chronic heart failure or renal failure); monitor patient’s urine output and fluid balance, haemodynamic monitoring, fluid responsiveness, and lung sounds
  • haemorrhagic stroke drug therapy may include inotropes and vasopressors (typically adrenaline or noradrenaline and dobutamine) to increase cardiac output and blood pressure for better perfusion; these however increase oxygen demands; ensure secure airway and administer oxygen if needed to treat hypoxia; antifibrinolytics such as tranexamic acid may be required to prevent the breakdown of fibrin, which is the main protein in a blood clot
Retrieved from https://www.getdoc.com/blood-type-basics-blood/ on 19th January 2023

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Cardiogenic Shock

Shock can be classified into 3 different types: Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Cardiogenic Shock

  • impaired ability of the heart to pump blood as it should (left or right ventricle dysfunction), causing systemic hypoperfusion and tissue hypoxia
  • may be caused by cardiac injury (eg. cardiac tamponade), cardiopulmonary arrest, following cardiac surgery, dysrhythmias (severe tachycardia or bradycardia), myocardial tissue necrosis following a Myocardial Infarction, or structural problems (eg. valvular damage or regurgitation, pulmonary embolus, acute myocarditis, papillary muscle rupture, intracardiac tumour, and congenital defects
  • compensatory mechanisms may worsen the situation…eg. reduced cardiac output due to myocardium death causes increased contractility which further increases the heart’s workload and oxygen demand; reduced blood pressure causes the release of catecholamines which leads to vasoconstriction, subsequently leading to a further increase in cardiac workload and oxygen demand

Cardiogenic Shock Signs & Symptoms

  • chest pain or chest trauma
  • altered level of consciousness
  • cool, pale moist skin
  • weak thready pulse
  • tachycardia possibly with dysrhythmias
  • tachypnoea
  • SBP <90mmHg and MAP 30mmHg less than normal
  • urine output <30ml/hr
  • jugular venous distension
  • reduced cardiac output and cardiac index
  • increased PAWP (Pulmonary Artery Wedge Pressure), increased RA (right atrium) pressure & increased SVR (systemic vascular resistance)
  • signs of pulmonary oedema eg. hypoxaemia, crackles, and frothy sputum

Management

  1. Treat Underlying Cause to Prevent Further Damage & Preserve Healthy Myocardium
  2. Enhance Pumping Effectiveness by Increasing Cardiac Output
  3. Improve oxygen perfusion in the heart as well as other organs and tissues
  4. Increase oxygen supply and reduce oxygen demand of the heart
  • provide oxygen therapy through supplementary oxygen or mechanical ventilation due to cardiac ischaemia and chest pain
  • administer morphine for analgesia and sedation, and promote rest
  • if patient has pulmonary oedema, administer diuretics eg. furosemide or bumetanide, and oxygen whilst monitoring haemodynamic status and ABGs of the patient; diuretics reduce fluid accumulation which causes a decrease in preload – monitor for fluid and electrolyte imbalance
  • provide mechanical reperfusion through PCI (percutaneous coronary intervention) eg. angioplasty and coronary stents, or a coronary artery bypass graft (CABG)
  • provide thrombolytic therapy through pharmacologic agents eg. streptokinase, urokinase, tissue plasminogen activator TPA, which dissolve clots in coronary artery BEFORE cardiogenic shock sets in; ATTENTION: watch out for bleeding!
  • provide drug therapy that helps improve cardiac output by increasing cardiac contractility, decreasing preload and afterload, and stabilising the heart rate
  • provide fluids with great caution since this increases risk of pulmonary oedema
  • administer inotropes (eg. dobutamine or milrinone) to improve contractility and reduce afterload, and vasopressors (eg. adrenaline or noradrenaline) to increase contractility, vasoconstriction, blood pressure, and heart rate NOTE: inotropes and vasopressors can be given in combination
  • administer vasodilators eg. nitrates to reduce oxygen demands by reducing preload through venous dilation, reducing afterload by arterial dilation due to less resistance, increasing oxygen supply to the myocardium due to coronary vasodilation, but ATTENTION – vasodilators cause hypotension!
  • treat arrhythmias with anti-arrhythmic drugs eg. amiodarone to help increase time for ventricular filling
  • make use of the intra-aortic balloon pump – a long balloon attached to a large bore catheter inserted through the femoral artery to the descending aorta, with the balloon tip placed just below the aortic arch, and the bottom tip above the renal artery; the attached machine helps by inflating the balloon with helium at the start of diastole when the aortic valve closes, and rapidly deflating it at the start of ventricular systole, just before the aortic valve opens; ATTENTION to possible complications eg. dislodgement of clots, limb ischaemia / neuropathy (check pedal pulses), bleeding (check clotting time before insertion and removal), infection, balloon rupture, and improper position
  • if indicated, the Left Ventricular Assist Device may be used – flow pump which is placed across the aortic valve into the left ventricle; it draws blood continuously from the left ventricle to the proximal aorta; may be used prior to transplantation or long term for transplantation-ineligible patients
  • the VA-ECMO is a device through which deoxygenated blood is drained through the central vein; blood is then oxygenated outside of the patient’s body, before being returned through the large artery; it helps improve aortic flow and organ perfusion, however, it may increase afterload and worsen pulmonary oedema; note increased risk of acute kidney injury, severe bleeding, lower limb ischaemia, and stroke
  • if indicated, a patient with cardiogenic shock may undergo surgical interventions such as human heart transplantation, repair of septal, ventricular, or papillary muscle rupture, or valve repair or change
Retrieved from https://www.magonlinelibrary.com/doi/abs/10.12968/bjca.2021.0055?journalCode=bjca on 20th January 2023
cardiogenic shock
Retrieved from https://www.facebook.com/jamajournal/photos/a.10158814898548341/10158814906348341/?type=3&locale=zh_HK on 19th January 2023

Cardiogenic Shock and Intra-aortic Balloon Pump => https://www.youtube.com/watch?v=mADxD7C8jBw


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The Definition, Classification and Pathophysiology of Shock

In order to understand how to care for a patient in shock, we must first understand the pathophysiology of shock, as well as how to assess, diagnose, and manage it through appropriate nursing interventions. The most common types of shock are the Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Throughout this blogpost we will be looking in detail at the definition, classification, and pathophysiology of shock.

What is Cardiac Output?

Cardiac Output (CO) is the volume of blood ejected from the heart over 1 minute. In adults, normal Cardiac Output is between 4-6L/min.

Cardiac Index (CI) is a haemodynamic parameter related to the cardiac output from the left ventricle in 1 minute to body surface area (BSA). In adults, normal Cardiac Index should be between 2.5-4L/min/m2.

Stroke volume (SV) is the volume of blood pumped out of the left ventricle during each systolic cardiac contraction.

Mean Arterial Pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole.

Systemic Vascular Resistance (SVR) is the resistance in the circulatory system which affects the blood pressure and the flow of blood. SVR is also a component of cardiac function, eg. vasoconstriction leads to an increased SVR.

Formulas:

Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)

Cardiac Index (CI) = Cardiac Output (CO) / Body Surface Area

Mean Arterial Pressure (MAP) = Cardiac Output X Systemic Vascular Resistance (SVR)

Cardiac Output Determinants

  • HEART RATE – influenced by both the sympathetic and parasympathetic system, as well as by intrinsic regulation
  • STROKE VOLUME – determined by cardiac preload (PL), afterload (AL), and cardiac contractility (CC).

Preload determinants

Preload (PL) is the stretching force exerted on the ventricle by the blood contained within at the end of diastole.

The Starling’s Law of the Heart indicates that increased volume returned to the heart causes an increase in Cardiac Output, however, following a certain increase in volume returned causes a decrease in Cardiac Output.

Retrieved from https://ecgwaves.com/topic/pressure-volume-curves-preload-afterload-stroke-volume-wall-stress-frank-starlings-law/ on 10th January 2023

Preload determinants include:

  • VOLUME OF BLOOD RETURNED TO LEFT VENTRICLE – influenced by venous return, total blood volume, and atrial kick
  • LEFT VENTRICLE COMPLIANCE (stretching ability) – influenced by the stiffness and thickness of the muscle wall

Examples: in Hypervolaemia, preload is too low, whilst in Congestive Heart Failure, preload is too much.

Afterload Determinants

Afterload (AL) is the resistance (a.k.a. Systemic Vascular Resistance SVR) that the heart must overcome to push blood into the systemic circulation.

An increase in Afterload causes an increase in the required effort and oxygen demand by the heart, eg. vasoconstriction increases Systemic Vascular Resistance, total blood volume and viscosity.

To reduce the heart’s workload we can provide therapeutic nursing management, including the administration of vasodilators.

pathophysiology of shock
Retrieved from https://www.studypk.com/articles/nursing-mnemonics-preload-vs-afterload/ on 10th January 2023

Cardiac Contractility Determinants

Cardiac Contractility (CC) is the force by which the heart contracts. CC is determined by:

  • VENOUS RETURN – Starling’s Mechanism
    • STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM
    • INCREASE IN INTRACELLULAR CALCIUM (Ca++) – such as after use of Digoxin
    • PHARMACOLOGICAL INTERVENTIONS – eg. administration of Inotropes
Retrieved from https://step1.medbullets.com/cardiovascular/108003/cardiac-output-and-variables on 11th January 2023

Shock Definition

Shock can be defined as an acute widespread process of impaired tissue perfusion resulting in cellular, metabolic and haemodynamic changes, causing an imbalance between cellular oxygen supply and demand. Shock leads to death if not controlled in time.

Normal tissue perfusion requires:

  • adequate blood volume
  • adequate cardiac pump
  • effective circulatory system

Impairment of any of the above, thus, impairment in normal tissue perfusion, may lead to SHOCK…

Impaired oxygen perfusion causes:

  1. inadequate blood flow reaching the tissues
  2. inadequate delivery of oxygen and nutrients to the cells
  3. cell starvation due to oxygen and nutrient deprivation
  4. cell death
  5. multiple organ failure
  6. death

Classification of Shock

Shock can be classified into 3 different types. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Hypovolaemic Shock

Hypovolaemic shock is the most commonly occurring type of shock, which is also easily reversible if treated in a timely manner. Features of a hypovolaemic shock include:

  • loss of circulating or intravascular volume
  • impaired tissue perfusion
  • inadequate delivery of oxygen and nutrients
  • may be caused by relative and absolute hypovolaemia, or loss of blood or other fluids
Retrieved from https://twitter.com/misirg1/status/1382458804995035144 on 19th January 2023

Cardiogenic Shock

  • impaired ability of the heart to pump blood as it should (left or right ventricle dysfunction), causing systemic hypoperfusion and tissue hypoxia
  • may be caused by cardiac injury (eg. cardiac tamponade), cardiopulmonary arrest, following cardiac surgery, dysrhythmias (severe tachycardia or bradycardia), myocardial tissue necrosis following a Myocardial Infarction, or structural problems (eg. valvular damage or regurgitation, pulmonary embolus, acute myocarditis, papillary muscle rupture, intracardiac tumour, and congenital defects
  • compensatory mechanisms may worsen the situation…eg. reduced cardiac output due to myocardium death causes increased contractility which further increases the heart’s workload and oxygen demand; reduced blood pressure causes the release of catecholamines which leads to vasoconstriction, subsequently leading to a further increase in cardiac workload and oxygen demand
Retrieved from https://www.facebook.com/jamajournal/photos/a.10158814898548341/10158814906348341/?type=3&locale=zh_HK on 19th January 2023

Distributive Shock

  • impaired distribution of circulating blood volume
  • vasodilation
  • capillary leaks

Distributive Shock is further sub-classified into 3 other types of shock:

SEPTIC SHOCK:

While sepsis is defined as a life-threatening organ dysfunction caused by dysregulated host response to infection, a septic shock is defined as a subset of sepsis in which underlying circulatory, cellular and metabolic abnormalities and profound enough to substantially increase the risk of mortality.

  • microorganism entry into the patient’s body
  • dysregulated host response characterised by excessive peripheral vasodilation, causing maldistribution of blood volume, over-perfused peripheral areas and under-perfused central areas
  • is the major cause of admission in the critical care setting

Septic Shock may originate from the community (>80% of cases) or during a stay in a healthcare facility.

ANAPHYLACTIC SHOCK:

  • severe antigen-antibody reaction causing histamine release
  • signs & symptoms include vasodilation, hypotension, bradycardia, increased capillary permeability, bronchospasm, laryngeal oedema, and stridor

NEUROGENIC SHOCK:

  • disruption of sympathetic nerve activity below the level of a spinal cord injury or disease
  • signs & symptoms include vasodilation, hypotension, bradycardia, warm dry skin, and loss of thermoregulation

Obstructive Shock

  • obstructive shock is often classified with cardiogenic shock
  • obstructive shock is mechanical obstruction which impedes the heart from generating adequate cardiac output
  • examples of obstructive shock include Tension Pneumothorax, Pericardial Tamponade and Pulmonary Embolus
pathophysiology of shock
Retrieved from https://www.pinterest.com/pin/34762228362737082/ on 11th January 2023

The Pathophysiology of Shock

pathophysiology of shock
Retrieved from https://slideplayer.com/slide/17204705/ on 11th January 2023

Initial Stage

Within the initial phase of shock, effects are very subtle and at cellular level. An increase in serum lactate indicates metabolic acidosis due to cells switching from aerobic to anaerobic respiration.

  1. Decrease in Cardiac Output
  2. Decrease in tissue perfusion
  3. Cells switch from aerobic to anaerobic respiration
  4. Accumulation of Lactic Acid
  5. Lactic Acidaemia (Low pH)
  6. Cellular Damage

Compensatory Stage

During the compensatory stage of shock, the patient’s body attempts to improve tissue perfusion through neural, chemical, and hormonal compensation, mediated by the sympathetic nervous system.

NEURAL COMPENSATORY MECHANISMS

  • increased Heart Rate and Cardiac Contractility
  • arterial and venous vasoconstriction
  • circulation lessens within the peripheries and becomes more focused on vital organs perfusion

CHEMICAL COMPENSATORY MECHANISM

  • chemoreceptors detect acidosis and stimulate hyperventilation so more Carbon Dioxide is exhaled

HORMONAL COMPENSATORY MECHANISMS

Hormonal compensatory mechanisms aim to increase the blood pressure to cause an increase in tissue perfusion.

  • the anterior pituitary gland is stimulated, causing secretion of ACTH (Adrenocorticotropic Hormone), which then stimulates the adrenal cortex to produce glucocorticoids (glucagon), which causes an increase in blood glucose level
  • the adrenal medulla is also stimulated, causing the release of adrenaline and noradrenaline, which result in vasoconstriction, leading to an increased Blood Pressure and increased Heart Rate
  • renin response is activated, which facilitates the conversion of Angiotensinogen into Angiotensin II; this conversion causes vasoconstriction, release of aldosterone (which leads to sodium retension), and release of antidiuretic hormone (ADH) by the posterior pituitary gland (which leads to water retention)
pathophysiology of shock
Retrieved from https://en.wikipedia.org/wiki/Renin%E2%80%93angiotensin_system on 11th January 2023

SYMPTOMS EXPERIENCED DURING THE COMPENSATORY PHASE:

  • cold, clammy skin
  • drop in urine output
  • tachycardia
  • tachypnoea
  • hyperglycaemia

Progressive Stage

  • compensatory mechanisms start failing
  • shock cycle continues indefinitely
  • anaerobic respiration causes energy exertion within the cells
  • cells are unable to function, and irreversible damage occurs (Mitochondria become unable to use oxygen for the production of energy, and Lysosomes release digestive enzymes which then cause further cellular damage)
  • utilisation of the limited oxygen delivered into the cells becomes problematic

During the progressive stage, organ systems start to fail…

  • Myocardial Hypoperfusion causes decreased Cardiac Output leading to ventricular failure, enabling shock to progress further
  • Decreased Cerebral Blood Flow causes CNS dysfunction, causing failure of the sympathetic nervous system, failure of the thermoregulation mechanism, cardiac and respiratory depression, and altered mental status
  • Impaired Coagulation leading to microclot formation, which may cause Disseminated Intravascular Coagulation (DIC)
  • Renal Vasoconstriction & Hypoperfusion causes decreased urine output and increased creatinine, which may also lead to Acute Tubular Necrosis (ATN)
  • GastroIntestinal Tract Hypoperfusion causes decreased peristalsis (decreased bowel sounds), release of Gram-negative bacteria (which worsens shock), and liver hypoperfusion due to deranged LFTs
  • Pulmonary Vasoconstriction along with microemboli, parenchymal inflammation, and alveolar oedema all lead to respiratory failure (Acute respiratory distress syndrome ARDS)

SYMPTOMS EXPERIENCED DURING THE PROGRESSIVE PHASE:

  • electrolyte imbalance
  • metabolic acidosis
  • respiratory acidosis
  • peripheral oedema
  • tachycardia
  • arrhythmias
  • hypotension
  • pallor
  • cool clammy skin
  • altered level of consciousness
  • reduced bowel sounds

Refractory Stage

In the final stage of shock, the patient becomes unresponsive to treatment, experiences multiple organ failure, eventually leading to death.


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Bleeding and Shock First Aid

In the acronym DR ABC, C stands for circulation. Signs of circulation compromise to watch out for include bleeding or shock symptoms.

The Human Circulatory System

The human circulatory system comprises of the heart, the blood vessels, and the blood. All these components need to be working efficiently so that every tissue within the body is supplied with oxygenated blood.

Shock Causes

A decrease in blood pressure and SPO2 indicate circulatory failure – the brain is slowly dying due to lack of oxygen, and so, it triggers a defense mechanism: SHOCK.

Any issue affecting the heart, the blood vessels, or the blood volume, may lead to a decrease in the body’s blood circulation, leading to a reduction in blood pressure and volume, which in return cause a decrease in tissue perfusion.

Decreased Cardiac Output = Decreased Circulating Volume & Pressure = Reduced Venous Return

Types of shock include:

  1. cardiogenic shock
  2. obstructive shock
  3. neurogenic shock
  4. septic shock
  5. anaphylactic shock
  6. hypovolaemic shock

Causes of shock can be divided into 3 categories:

1. Decrease in the Pumping Action of the Heart

A drop in cardiac output can result in a:

  1. Cardiogenic Shock – this may happen due to a heart defect or disorder (cardiogenic = issue originating from the heart itself) eg. Congestive Heart Failure (CHF) or Ischaemic Heart Disease (IHD);
  2. Obstructive Shock – this may happen due to cardiac compression in cases such as in cardiac tamponade (bleeding within the pericardial space) and tension pneumothorax (air accumulation in the pleural space which compresses the lungs and decreases venous return to the heart).

2. Blood Vessel Dilation

Following vasodilation, which refers to the dilation of the blood vessels, a casualty can suffer a distributive shock:

  1. Neurogenic Shock – happens following a spinal injury, head injury, or opiate overdose;
  2. Septic Shock – happens following a severe infection which causes the casualty’s blood pressure to drop to a dangerously low level;
  3. Anaphylactic Shock – happens following a severe allergic reaction

NOTE: due to a biochemical process in the body, chemicals released cause vasodilation, which then causes either a septic shock or an anaphylactic shock.

3. Blood or Fluid Loss

Severe bleeding or severe dehydration can lead to a hypovolaemic shock. This happens due to the drop in blood volume.

Progressive Shock Clinical Indicators

  • initial weak rapid pulse that eventually becomes thready or absent (body increases heart rate to compensate due to lack of blood; eventually, drop in cardiac output = drop in stroke volume = weak heartbeat)
  • initial rapid irregular breathing that eventually becomes laboured and dyspnoeic
  • initial pale skin that eventually becomes cold, clammy and mottled (happens since the body compensates lack of oxygen circulation by sending it in the most important areas rather than in the extremities)
  • cyanosis – signifies established hypoxia
  • weakness and fatigue – signifies cerebral hypoxia (lack of oxygen in the brain)
  • confusion and disorientation
  • altered level of response leading to unresponsiveness…casualty is now at risk of cardiac arrest!

Shock First Aid

  1. identify cause of shock
  2. control cause of shock
  3. assist casualty in shock position – elevate legs by about 30cm to increase venous return; if casualty is conscious but dyspnoeic, a semi-sitting position helps provide better breathing
  4. maintain casualty’s body temperature – this helps in avoiding hypothermia, which would disrupt an open wound’s clotting process, leading to longer bleeding time
  5. administer high-concentrated oxygen if available
  6. increase ventilation by opening windows if inside
  7. call 112 for assistance
  8. monitor casualty for deterioration – if casualty is in recovery position, attempt to maintain shock position i.e. elevated legs, if possible
  9. provide reassurance at all times
bleeding and shock
Retrieved from https://persysmedical.com/blog/hypothermia-prevention/trauma-triad-of-death/ on 18th September 2022

NOTE: The term vasoconstriction refers to constriction of the blood vessels. It can be clinically indicated in blood pressure results that show a difference of about 20 only between the systolic and diastolic readings. In such case, the pulse is weak or not palpable.

Bleeding

Bleeding amount depends on what it is originating from:

  • ARTERIES – spurting blood, pulsating flow, bright red colour
  • VEINS – steady, slow blood flow, dark red colour
  • CAPILLARIES – slow and even flow

Bleeding severity depends on the injury body site, blood loss volume, time frame of blood loss volume, casualty’s age (worse in children and the elderly), and casualty’s health status prior to the injury.

Catastrophic bleeding refers to bleeding in which 30% of blood volume is lost. Such bleeding takes priority over Airway and Circulation in the DR ABC acronym.

The major consequence of blood loss is a hypovolaemic shock (explained further up). During this type of shock, the heart becomes unable to pump enough blood throughout the body due to severe blood or fluid loss. This leads to organs shutting down.

External Bleeding First Aid

  1. wear gloves to protect self
  2. control bleeding through direct pressure or using a pressure dressing
  3. monitor and provide first aid for shock

Notes:

  • In bleeding circumstances without signs of shock, elevation is not recommended anymore.
  • Indirect pressure (pressing on arteries eg. on femoral or brachial artery) is not a recommended bleeding control technique anymore.
  • If direct pressure method fails, you may use an emergency bandage, tourniquet, or haemostatic agents, all of which require prior specific training.
  • In catastrophic bleeding first aid, one may pack the wound with a towel. Worrying about an infection is not a primary concern at this point, since catastrophic bleeding may lead to loss of life.
  • Haemostatic Agents can be poured on wounds to stop catastrophic bleeding. Only materials specifically prepared for bleeding purposes may be used
  • A tourniquet is a device that helps apply pressure to a limb or extremity to limit the flow of blood. It may be used in emergency situations, during surgery, or in the post-operative rehabilitation period.
  • Normal use tourniquets are orange in colour, while the Combat Application Tourniquet (CAT) is usually black.

Internal Bleeding

Internal bleeding may be caused as a disease process eg. due to a stomach ulcer, or trauma.

Common sites of serious internal bleeding include the head, the chest, the abdomen and pelvis.

Internal bleeding is more difficult to diagnose, since it usually doesn’t show. The worst type of internal bleeding happens in the pelvic area, right in the retroperitoneum.

Recognition of internal bleeding may be done through:

  1. History
  2. Signs & Symptoms
  3. Pain & Tenderness
  4. Revealed Internal Bleeding (eg. internal bleeding in the head may produce trickling blood out of orifices such as from the ear)

Types of Internal Bleeding:

  • Otorrhoea – blood coming out of the ear
  • Rhinorrhoea – blood coming out of the nose
  • Haemoptysis – coughed out blood
  • Haematemesis – vomited blood
  • Haematuria – bleeding in the urine
  • Rectal Bleeding – bleeding coming out of the intestines
  • Bruising
Retrieved from https://psnet.ahrq.gov/web-mm/coming-undone-failure-closure-device on 18th September 2022

NOTE: If there is suspicion of internal bleeding, it NEEDS TO BE ASSUMED! Monitor for ABC compromise and signs of shock, and provide first aid as needed!


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Acute Coronary Syndrome – STEMI, NSTEMI, Necrosis and Angina

Acute coronary syndrome refers to a range of conditions associated with sudden reduced blood flow to the heart. Such conditions include:

STEMI – a very serious MI during which one of the heart’s major arteries is more than 70% blocked. An ST segment elevation is an abnormality detected on the 12-lead ECG in STEMI. Treat immediately!

NSTEMI – non-ST elevation MI: may progress to STEMI so treat with importance.

MINIMAL MYOCARDIAL NECROSIS – cardiomyocytes cell death related to irreversible myocardial injury.

UNSTABLE ANGINA – experiencing pain even when resting (may progress to STEMI if undiagnosed or not treated in time).

STABLE ANGINA – experiencing pain during exacerbating physical activity.

Plaque Rupture Triggers

  • Vulnerable Plaque – eg. Statin therapy causes plaque to become vulnerable
  • Inflammatory Cytokines
  • Emotional Stress – can change the physiological status of the body through high BP, increased heart rate etc.
  • Physical Stress – strenuous exercise in unfit individuals
  • Plaque Rupture – thin fibrous cap with lipid beneath makes plaque susceptible to rupture

Myocardial injury extent depends on facturs such as the oxygen demand of the affected tissue, tissue response (younger individuals usually respond better and deal in a better way with an MI than older individuals), rate of flow etc.

Myocardial Infarction Symptoms

  • pain, pressure and heat sensation usually in the chest area but possibly radiating to the jaw, back, left arm or both arms;
  • sweating, clammy cold skin, tachycardia
  • weakness, nausea and vomiting
  • mild fever
  • dyspnoea

NOTE: an individual may experience a MI but still be asymptomatic!

Diagnosis of an Acute MI

  1. Obtain information directly from patient; ask questions regarding family history (parents or siblings), degree of pain, how it all started, etc.
  2. Assess symptoms to make sure they are coronary-related
  3. Monitor for ECG changes: check for signs of Ischaemia and MI
  4. Monitor serum cardiac biomarkers: necrosis causes sarcolema disruption, releasing macro-molecules in circulation
  5. Monitor Troponin I & T (absent in healthy individuals, rise 3-4hrs after a MI and peak at 18-36hrs before declining slowly within 10-14 days)
  6. Monitor Creatinine Kinase (CK): injury to the heart is marked as an elevation in CK; CK-MB rises 4-8hrs post MI and peak by 24hrs before returning to normal in 48-72hrs; a 2nd CK-MB indicates a re-infarction (can be noticed easier as CK-MB returns to normal quicker)
STEMI Q Wave MI

Acute Coronary Syndrome Treatment

  • Morphine: decrease anxiety and pain associated with ACS
  • Oxygen: monitor SP02 and administer Oxygen on demand
  • Anti-Ischaemic Therapy: Beta-Blockers, Nitrates and Calcium Channel Blockers (CCB are not to be administered in case of heart block or heart failure)
  • Anti-Thrombotics – Aspirin (300gm) & Clopidogrel (300-600mg loading dose, then 75mg): balance platelet aggregation
  • Anti-Coagulants – Enoxaparin OR IV Heparin OR Fondaparinux OR Bivalirudin (the latter only for patients undergoing Percutaneous Coronary Intervention)
  • Statin: anti-cholesterol drug that reduces infarction and mortality
  • ACEi: helps control blood pressure – excellent drug for patients with low ejection fraction

Percutaneous Coronary Intervention VS Thrombolytics

PCI vs Thrombolytics
Accessed from https://www.researchgate.net/figure/Advantages-and-disadvantages-of-thrombolysis-vs-PPCI_tbl1_230724181 on 29th January 2021

Myocardial Infarction Complications

Myocardial Infarction Complications
Assessed from https://www.pinterest.com/pin/191403052899246797/ on 29th January 2021

Cardiogenic Shock

Cardiogenic shock is caused by either a massive Myocardial Infarction or a valve issue. If a patient presents with a prominent jugular vein, low blood pressure and high heart rate consider as emergency…monitor closely!

Below you can find a collection of videos that can help provide a more visual approach to Acute Coronary Syndrome.

Acute Coronary Syndrome Detailed Overview

Special thanks to the creator of the featured videos on this post, specifically Youtube Channel Armando Hasudungan and Thrombosis Adviser.

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