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
signs of bleeding (decreased Haematocrit & Haemoglobin)
Retrieved from https://twitter.com/misirg1/status/1382458804995035144 on 19th January 2023
Management
Identify & Treat the Underlying Cause
Restore Intravascular Volume & Blood Pressure
Redistribute Fluids to Ensure Perfusion
Prevent Shock Progression
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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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
signs of pulmonary oedema eg. hypoxaemia, crackles, and frothy sputum
Management
Treat Underlying Cause to Prevent Further Damage & Preserve Healthy Myocardium
Enhance Pumping Effectiveness by Increasing Cardiac Output
Improve oxygen perfusion in the heart as well as other organs and tissues
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 diureticseg. 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)
providethrombolytic 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 vasodilatorseg. 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
Retrieved from https://www.facebook.com/jamajournal/photos/a.10158814898548341/10158814906348341/?type=3&locale=zh_HK on 19th January 2023
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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.
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.
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:
inadequate blood flow reaching the tissues
inadequate delivery of oxygen and nutrients to the cells
cell starvation due to oxygen and nutrient deprivation
cell death
multiple organ failure
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
Retrieved from https://www.pinterest.com/pin/34762228362737082/ on 11th January 2023
The 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.
Decrease in Cardiac Output
Decrease in tissue perfusion
Cells switch from aerobic to anaerobic respiration
Accumulation of Lactic Acid
Lactic Acidaemia (Low pH)
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)
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:
In the final stage of shock, the patient becomes unresponsive to treatment, experiences multiple organ failure, eventually leading to death.
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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.
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);
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:
Neurogenic Shock – happens following a spinal injury, head injury, or opiate overdose;
Septic Shock – happens following a severe infection which causes the casualty’s blood pressure to drop to a dangerously low level;
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
identify cause of shock
control cause of shock
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
maintain casualty’s body temperature – this helps in avoiding hypothermia, which would disrupt an open wound’s clotting process, leading to longer bleeding time
administer high-concentrated oxygen if available
increase ventilation by opening windows if inside
call 112 for assistance
monitor casualty for deterioration – if casualty is in recovery position, attempt to maintain shock position i.e. elevated legs, if possible
provide reassurance at all times
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
wear gloves to protect self
control bleeding through direct pressure or using a pressure dressing
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 tourniquetis 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:
History
Signs & Symptoms
Pain & Tenderness
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 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.
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
Obtain information directly from patient; ask questions regarding family history (parents or siblings), degree of pain, how it all started, etc.
Assess symptoms to make sure they are coronary-related
Monitor for ECG changes: check for signs of Ischaemia and MI
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)
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)
Acute Coronary Syndrome Treatment
Morphine: decrease anxiety and pain associated with ACS
Oxygen: monitor SP02 and administer Oxygen on demand
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.
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