Module 9 - Circulatory Disorders (1).pdf

Circulatory Disorders ACP 222 – MODULE 9 Objectives Understand the pathophysiology, s/s and treatment of the following conditions: Shock Syndromes ◦ • Cardiogenic Shock ◦ • Low-Volume Shock (Absolute Hypovolemia) ◦ • Hypovolemia ◦ • High-Space Shock (Relative Hypovolemia) ◦ • Neurogenic (Spinal) ◦...

Circulatory Disorders ACP 222 – MODULE 9 Objectives Understand the pathophysiology, s/s and treatment of the following conditions: Shock Syndromes ◦ • Cardiogenic Shock ◦ • Low-Volume Shock (Absolute Hypovolemia) ◦ • Hypovolemia ◦ • High-Space Shock (Relative Hypovolemia) ◦ • Neurogenic (Spinal) ◦ • Sepsis ◦ • Mechanical (Obstructive) Shock Endocrine Disorders ◦ • Catecholamine Excess ◦ • Thyroid Storm EENT ◦ • Retinal Hemorrhage ◦ • Papilledema Obstetrics ◦ • Pre-eclampsia and ◦ • Eclampsia Neurological ◦ • Vasovagal Syncope ◦ • Hypertensive Encephalopathy The components of perfusion Oxygenation Pump (heart) Container (blood vessels) Fluid (blood Volume) Administer oxygen, an provide ventilation if needed. If it is a rate problem, fix the rate, if it is obstructive problem can you fix the obstruction? If it’s a failing heart can you fix it? Does the vessels need to be constricted? Are they broken, open or leaking? Fill the tank with isotonic solution or blood if needed Stroke Volume x Pulse Rate = Cardiac Output (L/min) Factors that affect stroke volume or pulse rate will affect the cardiac output. Afterload (pressure of blood against the aorta) Preload (pressure of the blood entering the heart from the right side) Myocardial contraction (Heart failure, infarcts) Myocardial contractility (dysrhythmias) heart-rate-ekg-ecg-heart-beat - Scope (stanford.edu), Hand Squeezing Red Heart Shape Vector Stock Vector (Royalty Free) 1278117661 | Shutterstock Half Full Heart Stock Illustrations – 170 Half Full Heart Stock Illustrations, Vectors & Clipart – Dreamstime, Cardiac rehabilitation research (eventscloud.com) The ability of the heart to fill and expand Absolute Hypovolemia Loss of blood volume 2 types: Exogenous - Hemorrhage ◦ (blunt, penetrating wounds, traumatic vascular injuries Endogenous - Fluid loss is contained inside the body ◦ Dehydration ◦ Plasma losses (burns) ◦ Anaphylaxis (mix with relative hypovolemia) ◦ Third space losses (peritonitis, ascites) ◦ Osmotic losses (DKA) When the blood volume loss causes too low blood pressure to maintain tissue perfusion, hypovolemic shock occurs. Blood Volume Females ◦ 65ml/kg blood Males ◦ 70 ml/kg blood Childs blood volume ◦ 80-80 ml/kg •Blood loss for an adult of 1 L of blood or more produces significant changes in vital signs •Bodies can not tolerate acute blood loss of 20% or more of the total blood volume. •Infants and children have less blood volume then adults •Compensation for blood loss is related to how fast blood loss occurs Relative Hypovolemia If the vascular system became fully dilated it can hold up to 25 L of blood When vascular system becomes dilated causing too low blood pressure to maintain tissue perfusion, high space shock or distributive shock occurs. ◦ Neurological Shock ◦ Anaphylactic shock ◦ Sepsis shock (mix with hypovolemic) Shock Shock occurs when inadequate tissue perfusion occurs Inadequate tissue perfusion occurs with poor cellular exchange of: ◦ Oxygenation ◦ Waste exchange ◦ Nutrient delivery Compensation for Decreased Perfusion Drop in BP causes: Baroreceptors (carotid sinuses and aortic arch) – vasoconstrictor center in the medulla ◦ vasoconstriction Renin- angiotensin aldosterone system – releases antidiuretic hormone from the pituitary gland ◦ Vasoconstriction ◦ Sodium and water retention Hypoperfusion to the cells causes: Spleen may release RBC Adrenal glands release epinephrine and norepinephrine ◦ Increases cardiac output ◦ Vasoconstricts (shunts blood to vital organs) If hypoperfusion continues the body will not be able to compensate and will lead to impaired cellular metabolism Impairment of Cellular Metabolism Inadequate tissue perfusion results in impaired cellular metabolism Inability to use oxygen and glucose for cellular metabolism results in anaerobic metabolism which causes: ◦ Lactic acid production leads to Metabolic acidosis ◦ Decreased oxygen affinity for hemoglobin ◦ Changes in electrolytes ◦ Decreased ATP production – leads to ion pump dysfunction (inflex of sodium, efflux of potassium) ◦ catecholamine and cortisol release – glycogenolysis – elevated glucose and ketone formation. Compensated Shock (early shock – warm shock – normal tensive shock ) Decompensated Shock (late shock – cold shock – hypotensive shock) •Volume drop of 15-30% •Volume drop of 30% or more •Weakness, lightheaded •Hypotensive •Pale, diaphoresis •Altered Mental Status •Tachycardia •Cardiac Arrest •Decreased urinary output •Weakened peripheral pulses The BP is the last measurable factor of distinguishing shock – if you detect a drop in BP shock is well developed. Late Shock As shock progresses multi organ dysfunction syndrome occurs ◦ ◦ ◦ ◦ ◦ Renal failure Respiratory failure Myocardial depression Liver failure Leads to DIC (disseminated intravascular coagulation) Relative Bradycardia The patient will remain in bradycardia despite the catecholamine release. Medications: ◦ Betablockers ◦ Calcium Channel blockers 20% of patients who have an internal bleed in their abd will not show tachycardia Hypotensive BP for Pediatrics • A BP lower than the PALS BP chart is considered hypotensive • Any decrease in systolic BP of 10 mmHg from the baseline should prompt you to assess for other conditions and signs of shock • Hypotension defined by systolic BP and age use the 5thcentile of BP calculation • Bradycardia with hypotension is an ominous sign Case Questions You have a hypotensive patient in the rhythm on the screen. A&O x 0 70/42, P 160, R 24, pale cool, diaphoretic skin What type of shock is this patient experiencing? Cardiogenic Shock Cardiogenic shock is caused by a pump fail: ↓ cardiac output ↓ vital organ perfusion ↓ systemic vascular resistance more ↓ coronary artery perfusion Clinical Presentation: ◦ Reduced cerebral perfusion -> decreased LOC ◦ Peripheral vasoconstriction ◦ Pale, Cool skin ◦ SPO2 may not be accurate ◦ Respirations ◦ rapid and shallow ◦ Heart rate ◦ usually, tachycardia unless bradycardia is involved ◦ Poor Renal Perfusion ◦ Minimal or absent renal output ◦ left side heart failure ◦ Pulmonary edema chest sounds crackles ◦ right side heart failure ◦ Pedal edema ◦ JVD present ◦ Decreased cardiac output ◦ Hypotensive Cardiogenic Shock Treatment: ◦ Oxygenation, Ventilation, Possible CPAP/BIPAP ◦ Supine position (unless Pulmonary edema is present) ◦ IV TKVO (no fluid bolus) ◦ pulmonary edema ◦ rate related (Symptomatic Bradycardia/Symptomatic tachycardia) ◦ IV fluid therapy includes: ◦ systolic less than 90 or Map less then 65 attempt 250 ml bolus ◦ Cardiac Contusion – only enough fluid to maintain 80-90 systolic until perfusion returns ◦ Address the problem ◦ Dysrhythmia, STEM… ◦ Vasopressors: (choose depending on situation) ◦ Dobutamine – increases contractility may cause vasodilation ◦ Dopamine with Dobutamine ◦ Norepinephrine (vasoconstriction) with Dobutamine (contractility) ◦ Norepinephrine (vasoconstriction) ◦ Transport consideration ◦ PCI ◦ Trauma center Case Question You have a patient that was involved in an MVC. They were a driver and the steering wheel hit their chest. He is exhibiting SOB, has cyanosis to his lips On exam you find: ◦ Distending neck veins. ◦ Muffled heart tones ◦ Pulsus paradoxus ◦ Clear chest sounds ◦ Pale cool diaphoretic skin A&O x 3 BP 78/50, Pulse of 118 bpm, Resps 30 (New Message) Chest Injuries After an Accident - Sherrod & Bernard, P.C. (sherrodandbernard.com) Case Questions You have a 28-year-old patient that has been involved in an assault The patient is extremely SOB has cyanosis to the lips, is pale, cool, diaphoretic, no radial pulse. On assessment you find ◦ absent chest sounds to the right side ◦ JVD is present BP 80/60 P – 120 R – 30 SPO2 – 60% Rib Injuries In BJJ: Causes, Diagnosis And Prevention - Grappling Insider Obstructive Shock Caused from mechanical impediment of blood flow. A condition causes obstruction of venous return and/or arterial outflow from the heart. Clinical Presentation ◦ Hypotension ◦ Tachycardia ◦ Respiratory distress ◦ Cyanosis ◦ JVD ◦ Tracheal Deviation (tension pneumothorax) Treatment: ◦ High flow Oxygen, Ventilation, Intubation if needed ◦ Treat the underlying cause if you can. ◦ Tension pneumothorax – treat when found ◦ Pericardial Tamponade ◦ Administer only enough fluid to maintain perfusion 80-90 systolic ◦ Manage arrhythmias if they occur Case Question You have a patient that was climbing a tree and fell from the tree at a 20 ft height, landing on their back (on a tree root). They have pink, warm skin to their arms, legs and chest. On assessment you note the patient is not able to feel their legs BP is 80/60 Pulse - 78 SPo2 94% Resps 10. Weighing the Pros & Cons of Current Spine Immobilization Techniques - JEMS: EMS, Emergency Medical Services - Training, Paramedic, EMT News Distributive Shock Neurogenic Shock Neurogenic shock • Loss of spinal cord function below site of injury • Loss of sympathetic tone • Relative bradycardia (unopposed vagal tone) • Cutaneous vasodilation • Typically, with cord injuries above T6 Disruption of sympathetic nervous system • Loss of sympathetic tone • Venous & arterial vasodilation • Decreased venous return • Decreased stroke volume • Decreased cardiac output • Decreased cellular oxygen supply • Impaired tissue perfusion • Impaired cellular metabolism Distributive Shock Neurogenic Shock Sign/Symptoms • Hypotension • Bradycardia or normal range rate • Hypothermia • Warm, dry, skin • Flaccid paralysis below lesion • Potential for inadequate ventilations Treatment • Monitor respiratory / ventilatory status • Oxygenation – be prepared to intubate • Fluid resuscitation - 20 ml/kg prior to fluid therapy • BP at 90 systolic or peripheral pulses are maintained • head injury at MAP of 70 • Vasopressors • Norepinephrine (vasoconstriction) • Bradycardia - Epinephrine Infusion (Alpha and Beta) • Prevent hypothermia • Assess for other potential causes of shock (multisystem) •Sepsis is SIRS plus a systolic BP of less than 90mmHG or 40mmHG from baseline BP Distributive Shock Sepsis Most common causes: • gram-negative or gram-positive bacteria • Fungi • (rarely)viruses It can be a complication following burns, trauma, surgery, or illness. Causes widespread of • Inflammation • Coagulation • Suppression of fibrinolysis If SIRS involves more than one organ system, it is considered MODS. •Sepsis progression: • Inflammatory response occurs • Blood vessels Dilate (loss of resistance) • Systemic Inflammatory Response (SIRS) • Leak (loss of volume) Distributive Shock Sepsis Inflammatory Response: • Cell wall of organism contains Endotoxins • Endotoxins from bacteria signal release of cytokines and other mediators that circulate throughout the body and cause a number of responses • Endotoxins release inflammatory mediators (systemic inflammatory response) • Vasodilation & increase capillary permeability • Shock due to alteration in peripheral circulation & massive vascular dilation Hypotension and hypoperfusion with lactic acidosis occurs. ◦ Low blood pressure, high lactate levels and signs of organ dysfunction are seen. Distributive Shock Sepsis Is the patient history suggestive of new infection? • Pneumonia • UTI • Acute abdomen infection • Meningitis • Skin/soft tissue infection • Bone joint infection • Wound infection • Catheter related Blood stream infection • Endocarditis • Implantable device infection Distributive Shock Sepsis Phase 1: Early Shock ◦ Fatigued, anorexic ◦ Fever (or hypothermic) ◦ Edema ◦ Tachycardic ◦ Tachypnea and or dyspnea ◦ Altered mental status (especially >65) ◦ Hypotensive ◦ Skin may be flushed, warm and dry or cool and mottled Phase 2: Late shock: ◦ Changes in mentation ◦ Tachypneic ◦ Significant tachycardia ◦ Decreased blood pressure ◦ Vasoconstriction ◦ Skin pale and cool ◦ Decreased Urine output Distributive Shock Sepsis Treatment ◦ Oxygenation, ventilation ◦ Antipyretic if indicated ◦ Fluid Boluses 20 ml/kg x 2-3 ◦ Use a vasopressor Norepinephrine 1st choice ◦ Antibiotics Severe/ life threatening allergic reaction Antigen exposure ◦ Drugs, bites, contrast, blood, foods, vaccines Distributive Shock Anaphylaxis Body stimulated to produce IgE antibodies specific to antigen ◦ IgE binds to mast cells & basophils ◦ Histamine is released Blood vessels ◦ Dilate (loss of resistance) ◦ Leak (loss of volume) Bronchoconstriction Increased mucus production Most often occurs 60 minutes after exposure Re-exposure to antigen 8-11 hours -> S/S may reoccur 3-4 hours after initial symptoms are cleared Distributive Shock Anaphylaxis Signs and symptoms ◦ Urticaria, erythema, pruritis ◦ Angioedema ◦ Respiratory collapse: ◦ Stridor ◦ Wheezing ◦ Bronchorrhea ◦ Circulatory collapse ◦ Tachycardia ◦ Vasodilation ◦ Hypotension Distributive Shock Anaphylaxis Treatment ◦ Epinephrine IM x 3 ◦ (bronchospasm) Ventolin and Atrovent NEBs x 3 ◦ Antihistamines (Benadryl) ◦ Corticosteroids(Dex/Prednisone)-reduce the inflammation ◦ Fluids 20mg/kg bolus x 3, titrate to MAP 65mmhg Continued anaphylaxis Do you need to use an epi push-dose epi Epi infusion. Glucagon therapy for people of beta blocker therapy with continued hypotension Hypovolemic and Hemorrhagic Shock Caused by fluid loss -Absolute hypovolemia. ◦ Decreased intravascular volume ◦ ↓ venous return (pre-load) ◦ ↓ ventricular filling pressure ◦ ↓ stroke volume ◦ ↓ Cardiac Output ◦ Inadequate tissue perfusion Causes ◦ Trauma ◦ Non-traumatic blood loss ◦ Vaginal / OB ◦ GI ◦ GU ◦ Vascular ◦ Burns ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ Dehydration Vomiting Diarrhea Diuresis Sweating Third space losses Pancreatitis Peritonitis Bowel obstruction Hypovolemic and Hemorrhagic Shock Signs and Symptoms: ◦ Agitation/anxiousness ◦ Nausea/vomiting ◦ Decrease urine output ◦ Tachycardia ◦ Tachypneic ◦ Weak pulses ◦ Skin cool & diaphoretic 30% volume loss ◦ Altered mental status ◦ hypotension Hypovolemia Non-Bleeding Maintain oxygenation, ventilation IV fluid administration to maintain MAP of 65 ◦ 20 ml/kg fluid bolus 2-3 x (prior to vasopressors) Hypovolemic and Hemorrhagic Shock Vasopressors ◦ Norepinephrine is 1st choice Treat Cause / Condition of fluid loss Example: ◦ Antiemetic ◦ Treatment of Osmotic Loss (ie) DKA/HNKS Pediatric - 4-2-1 Method for Maintenance Fluid from Dehydration Examples: 8 kg Infant 4 ml/kg/hr -> 1st 10 kg 2 ml/kg/hr -> 2nd 10 kg Total: 4ml x 8 kg = 32 ml /hr 15 kg child 4 ml x 10 kg = 40 ml/hr 1 ml/kg/hr -> for each kg over 20 kg +2 ml x 5 kg = 10 ml/hr Total -> add the volumes to find ml/hr Total: = 50 ml/hr 5% dextrose in 0.9% saline (except neonate) 30 kg child 4 ml x 10 kg = 40 ml/hr Can be initiated with 0.9% Saline + 2 ml x 10 kg = 20 ml /hr Maintenance Fluid solution and rate must be discussed with a physician prior to administration + 1 ml x 10 kg = 10 ml / hr Total: 70 ml/hr Hypovolemic Shock with bleeding Identify the source of bleeding Internal / external Control bleeding Administer TXA when indicated **Keep patient warm** Administer fluid therapy: ◦ LR or 0.9% normal saline - Do NOT delay transport / Start IVs enroute Administer Blood when available Monitor calcium levels when blood is administered due to citrate (causes hypocalcaemia) ◦ Most massive transfusion protocols include the administration of Calcium New reviewed on the effects of... - US Tactical Medicine | Facebook Hypovolemic Shock with bleeding Consider blood after reassessment of treatments remaining in shock: ◦ after 2 – 3 L of isotonic fluid ◦ 40 ml/kg with pediatrics ◦ Or a hemoglobin less than 80 Transfusion Therapy ◦ Type O RH – universal donor ◦ Do not contain major blood groups of A or B Type ◦ Can be used for females of childbearing age ◦ If O RH- blood is not available, O+ can be used in: ◦ Males or Females not of childbearing age Administering 1 unit of PRBC’s will raise hemoglobin approximately 1 gram/dL or 10 gram/L Massive transfusion protocols ◦ PRBC: Platelets: Fresh Frozen Plasma 1:1:1 ratio Administration of blood and Reactions Must be given with NS line ◦ Check ID, ABO group, Rh type and expiration date ◦ Ideally ran through 18 gauge or larger IV ◦ Document transfusion reaction Transfusion Reactions ◦ Usually occur in first 15 minutes after administration began ◦ Signs/ Symptoms ◦ Fever ◦ Back pain ◦ Bloody urine ◦ Chills ◦ Flank Pain ◦ Flushing of the skin ◦ Fainting or dizziness Transfusion Reaction Treatment ◦ Stop the transfusion ◦ Flush line with NS ◦ Check blood products to make sure they match patient ◦ Transport all products with patient to receiving for testing ◦ Contact Medical direction – for treatment care plan ◦ Assess and provide supportive care ◦ Manage BP ◦ Fever – consider acetaminophen ◦ Urticaria (1-3%), can consider antihistamines ◦ If reaction is anaphylactic ◦ administer IM epi, Benadryl, Bronchodilators ◦ Inform transfusion service of reaction ◦ Pulmonary Edema – Supportive care Catecholamine Excess (sympathetic Crisis) Think You Have ‘Normal’ Blood Pressure? Think Again - The New York Times (nytimes.com) Excess catecholamines can result in a hypertensive crisis: Causes: Abrupt D/C of oral or transdermal clonidine medication ◦ Clonidine is an central alpha 2 agonist agent ◦ Used to treat - ADHD, Tourette syndrome, Antihypertensive agent, pheochromocytoma tumors Pheochromocytoma ◦ Rare adrenal tumor ◦ History of - headache, alternating periods of normal and elevated BP, tachycardia and flushed skin with asymptomatic periods. ◦ Sympathomimetic Toxicity of Drugs ◦ Cocaine, amphetamines, PCP, LSD ◦ Cause - tachycardia, diaphoresis, chest pain and mental status changes. ◦ MAOI (monoamine oxidase inhibitor) and Tyramine ◦ MOIO used to treat – depression, Parkinson's Catecholamine Excess (sympathetic Crisis) Treatment: Symptomatic crisis (sympathomimetic drugs toxicity), clonidine abrupt withdrawl and MOAI toxicity ◦ ◦ ◦ ◦ Manage airway, oxygenation and ventilation if needed. Initiate and IV Treat with benzodiazepines if treatment does not resolve hypertensive crisis – discuss with medical direction the use of nitroglycerin Do not use Beta Blockers – can result in increased vasoconstriction and increased BP. Pheochromocytoma Manage airway, oxygenation and ventilation if needed Patient will need special care at the hospital (discuss with medical direction) Thyroid Storm Thyroid affects all organ systems, and it is responsible for: ◦ Increasing metabolic rate ◦ Heart rate ◦ Ventricle contractility ◦ Muscle and CNS excitability 2 thyroid hormones – ratio 20:1 ◦ Thyroxine T3 (main) (20) ◦ Triiodothyronine T4 (1) Hyperthyroidism ◦ Excess circulating hormone from the thyroid gland dysfunction ◦ Graves disease most common cause Thyroid storm ◦ The extreme manifestation of thyrotoxicosis T4 940+ Hyperthyroidism Illustrations, Royalty-Free Vector Graphics & Clip Art - iStock | Hyperthyroidism eyes, Hyperthyroidism eye (istockphoto.com) Causes that can create a thyroid storm: ◦ Infection ◦ Stress ◦ Myocardial Infarction ◦ Trauma ◦ Pregnancy Thyroid Storm Hypothyroidism research: A long-term effort | NIH MedlinePlus Magazine Signs and symptoms of hyperthyroidism: ◦ Heat intolerance – diaphoresis ◦ Lethargic/weak ◦ Weight loss / muscle wasting ◦ Dry eyes ◦ Hypertension ◦ Diarrhea ◦ Pale skin (anemia) ◦ Hair loss Signs and symptoms of thyroid storm in addition to hyperthyroid S/S: ◦ High Fever ◦ Palpitations ◦ severe tachycardia (10% of patients will be in atrial fib) ◦ Dyspnea ◦ Heart failure ◦ Decreased Level of consciousness Thyroid Storm Treatment ◦ Supportive therapy ◦ Support airway, breathing and ventilation ◦ Cardiac monitoring ◦ Passive cooling (for fever) ◦ Acetaminophen administration (for fever) ◦ Check glucose levels and treat as needed ◦ Treat dehydration – fluid bolus to maintain MAP 65 ◦ Discuss maintenance fluid management with medical direction Education - TRAUMA YELLOW Hypertension associated with loss of the blood -brain barrier and cerebral edema causing increased ICP. MAP exceeds 150 mmHg Hypertensive Encephalopathy Symptoms ◦ 1st - headache, nausea, vomiting ◦ Leads to - seizures, altered LOC to unconsciousness ◦ Mimic a CVA -> sudden blindness, aphasia, hemiparesis Treatment: ◦ Support Oxygenation (if needed) ◦ Monitor ECG ◦ Initiate an IV NS TKVO ◦ Treat as stroke if they meet the criteria ◦ *** Lower the BP by no more than 1/3 in a controlled manner over 30-60 mins. (should be done in the hospital unless end-organ damage is occurring) ◦ Treat with Labetalol to reduce BP ◦ Do not use Nitroglycerin ◦ It dilates cerebral arteries too fast causing problems with the autoregulation system Pregnancy Hypertension Pre-existing Chronic hypertension • Prior to pregnancy and occurs prior the 20 week of pregnancy but not later than 12 weeks after delivery. • Greater /= 140/90 -> greater systolic of 110 increases the risk of CVA, cardiovascular problems Gestational Hypertension Develops after 20th week of pregnancy and continues to post-partum. • Increased risk for placental abruption, preeclampsia, low birth weight. Hypertensive Emergency ◦ A BP of systolic of 160 or higher or a diastolic of 105 or greater requires emergency management of antihypertensive medications. (labetalol) Pre-Eclampsia / Eclampsia Pre-Eclampsia ◦ Hypertension greater than 140/90 on two occasions 4 hours apart at 20 weeks of gestation until 4-6 weeks after deliver with either new onset of proteinuria or sudden increase in proteinuria or onset of HELLP syndrome Risk factors ◦ renal disease and diabetes Increased risks of: ◦ Pre-mature labor ◦ low birth weight ◦ abruptio placentae ◦ placental development impairment o the fetus ◦ impaired liver and renal functions ◦ pulmonary edema ◦ Eclampsia – Tonic-colonic seizures Symptoms: headache, nausea, vomiting, visual disturbances and abdominal pain, edema. Eclampsia, occurs when the patient experiences a seizure in the presence of s/s consistent with pre-eclampsia. -> treated with Magnesium Sulfate. HELLP syndrome ◦ Hemolysis, elevated liver enzymes, low platelet counts. ◦ Variant of pre-eclampsia ◦ 20 weeks gestation up to 7 days post partum ◦ Needs immediate delivery of the fetus Clinical Presentation: ◦ Hypertension 140/90 or higher ◦ Edema in legs ◦ Abdomen pain (RUQ) ◦ Headache ◦ Visual changes ◦ Nausea and vomiting ◦ Severe vaginal bleeding Papilledema Is bilateral Edema of the head of the optic nerve due to increased intracranial pressure. (diagnosed by an optometrist) Retinal Hemorrhages From the abrupt increase in venous pressure from elevated intracranial pressure. Caused by: ◦ Shaken baby syndrome - Rapid deceleration and acceleration of the child’s brain against their head. ◦ Rapid deceleration injuries Causes blindness Case Questions You have responded to a 70-year-old male patient that had a syncope episode in church at a funeral. The patient is wearing a shirt and tie. BP 100/70, R – 20, SPo2 94%, glucose 5.8 mmol/l, temp 36.8C Sinus rhythm at 62 bpm What relevance does the shirt and tie have to this case? Old Man The Bench In Park - Free photo on Pixabay - Pixabay Summary – Discussed the following topics Shock Syndromes ◦ • Cardiogenic Shock ◦ • Low-Volume Shock (Absolute Hypovolemia) ◦ • Hypovolemia ◦ • High-Space Shock (Relative Hypovolemia) ◦ • Neurogenic (Spinal) ◦ • Sepsis ◦ • Mechanical (Obstructive) Shock Endocrine Disorders ◦ • Catecholamine Excess ◦ • Thyroid Storm EENT ◦ • Retinal Hemorrhage ◦ • Papilledema Obstetrics ◦ • Pre-eclampsia and ◦ • Eclampsia Neurological ◦ • Vasovagal Syncope ◦ • Hypertensive Encephalopathy