Shock Emergency Medicine seminar work.pptx

This seminar focuses on the essentials of managing shock in emergency situations.
Topics include:
- Types of shock: Overview of hypovolemic, cardiogenic, distributive, and obstructive shock.
- Recognizing Shock: Identifying signs and symptoms quickly and accurately.

1. :

2. Limited Energy Lactic Acid  MAP ( Mean arterial BP ) : the average arterial pressure throughout one cardiac cycle at which a sufficient level of perfusion is maintained. 

3. inadequate blood perfusion - a critical lif e - t h reatening condition of and delivery of nutrients for normal tissue and cellular function due to fall in blood pressure which could lead to hypoxia, ischemia, tissue necrosis and ultimately organ failure. “ Death due unde r - perfusion of tissues “ Initially - may be rever s ible but life threatening if not treated promptly  ”Multi Organ failure “ - Mortality rate: 20% (1 of 5 reaches irreversible stage). Could be defined by any number of parameters : Systolic Blood pressure <90 mmHg or MAP <60/65 mmHg Urine output <0.5 mL/ Kg / Hr. Clinical signs of shock

4. Hemodynamic V a r i a bl e s C o m pe n s a ti o n “ S y m p a th e tic “ P r o b lem w i t h t h e p u m p “ H e a r t “ Too Fast Too Slow  Vessels Diameter

5. There are basically two main causes of shock : 1. Low Cardiac Output 2 . Low Sy s temic Vascu l ar resistance Loss Of Contractility Low Intravascular Volume Diffuse Peripheral Vasodilation According to the cause of shock , they divided shock into Major types : Four CO 1. Cardio genic : cardiac disorder  due to contractility prelo a d 2. Hypovolemic : due to Extracellular fluid volume depletion . SVR 3. Distributive : leading to abnormal distri b ut i on of blood flow to tissues 4. Obstructive : physical obstruction of the great vessels or the CO heart.  despite Normal Contractili t y .

6. four There are stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next. H y p o p e rfus i on H y p o x ia Anerobic Metabolism ( Glycolysis ) Lactic acidosis By-product : Lactic Acid Lactate Metabolism in poorly perfused liver Activation of physiological compensatory mechanisms Acidosis h y p e rventil a tion hypotension sympathetic system (Due to stimulation of baroreceptor in Carotid Sinus and Aortic Arch) catecholamines vasoconstriction HR the first sign of shock is t a chycardia hypovolemia ADH and RAA System water retention Increase in RAS (Angiotensin, ADH ,Aldosterone ) will decrease the urine output

7. If the cause of the crisis not successfully t r eated , the shock will proceed to the progressive stage and the compensatory mechanisms begin to f a i l. continuous decreased perfusion of the cells sodium ions build up within cell will be injured potassium ions leak out ( Hyperkaliemia due to cell lysis ) anaerobic m e t a b oli s m continues incre a sing the body's metabolic acidosis the arteriolar smooth muscle relax the BP start to decrease, and hydrostatic pressure will increase and leads to edema The heart's functioning continues to spiral downward , and the kidneys usually shut d o w n completely. Cells in organs and tissues throughout the body are injured and dying . The endpoint of this Stage is patient death Positive Feedback ( Shock produces Shock )

8. Diagnosis of Shock and differentiation between types  mainly Clinically General : hypotension (systolic BP LESS than 90 mmHg) Tachycardia (<100/min) “early sign” rapid, shallow respiration (lactic acidosis) weakness and fatigability multi-organ damage : CNS : drowsiness, confusion , coma , death renal : oliguria (urine output <.5 ml/kg/hour) , anuria specific signs and symptoms due to shock etiology:

9. Shock is clinically diagnosed based on pt.'s signs and symptoms and vital signs (BP ,T , HR,RR) other … .: brief focused History and physical examination (to know etiology) ECG monitoring ( pulse , Pressure ) ischemic changes, electrical alternans which is alternating amplitudes of the QRS complex , S1Q3T3 pulse oximetry (O2 sat .)/ ABG 4- labs : CBC electrolyte, LFT , KFT Lactate levels High levels  high mortality (esp. in septic shock) Helpful in identifying shock (esp. when bp is normal ) PT,PTT ( Thrombocytopenia , as well as coagulation studies such as a prolonged prothrombin time may clue towards coagulopathy as a cause of hemorrhagic shock .) Septic shock  blood culture ,urinalysis , chest x-ray Anaphylactic shock  serum tryptase levels (marker released from mast cells) 5- if still not diagnosed do : - echocardiogram - pulmonary artery catheter

10. CBC HIGH NORMAL LOW Hematocrit in non- hemorrhagic hypov olemic shock , due to hemo c o n c e nt r ation Hemorrhagic shock because a person loses red blood cells and a proportional amount of plasma with it. Eosinophil anaphylaxis leukocytes Leukocytosis may indicate septic shock Or Response to stress to any type of shock leukopenia or presence of immature neutrophils ca lled band cells are more specific for sepsis .

11. Swan Ganz Catheter Data : Direct : RA Pressure PA Pressure RV Pressure PCWP Mixed venous oxygen saturation Indirect : Cardiac output ( Fick Equation ) SVR ( Flow Equation )

12. Primary survey: Control ABC A: airways : cervical spine protection , keep airway patent Maintain airways opining by basic maneuvers ,  . head tilt – chin left, and jaw thrust in case of spinal injury Incubation If Not breathing Unconscious with GCS<8 Anaphylactic shock B: Breathing : mechanical ventilation Include assessing Ventilation and oxygenation

13. C: Circulation with hemorrhage control :IV fluid (firstly establish 2 large bore IV line) ± blood transfusion (if it’s difficult to find iv access e.g. hypovolemic shock, Then interosseous line should be inserted) *Give 250 ml of IVF under observation (except Cardiogenic shock) Central venous access (IJV, Subclavian or femoral line should be obtained if blood products or prolonged infusion of vasopressors are be given) A small bolus of IV crystalloid fluid may be given initially as a “fluid challenge”, which assesses the person’s response to fluids. Parameters like the mean arterial blood pressure or the urine output may be used to assess responsiveness. For example, hypovolemic and septic shock usually respond well to fluids, whereas cardiogenic and obstructive shock do not.

14. Measure the plus (the carotid or femoral artery for 10 second) Capillary refill time (adult normal refill time<2 sec.,peds <3sec.) Check the JVP Control the external hemorrhage by direct firm pressure with a sterile dressing placed over the site Assess body temperature and skin specific treatment for each shock type *main indicator for successful treatment is urine output

15. most common type Vasoconstriction Blood Loss Fluid Loss Hallmarks : Low CO Low Cardiac pressures High SVR Tachycardia Cool and Clammy hands Signs of dryness P a l e “ B lo o d L o s s “ Flat Veins

16. V om i t ing diarrhea s w e a t i ng burns External :, penetrating injury, surgical Internal : rapture AAA , solid organ injury Causes Of Hypovolemic Shock : 1- Hematemesis 2- Hematochezia , melena 3- Hemoptysis 4-Hematuria 5- Chest or abdominal pain 6- Abdominal swelling 7- Bruises or skin discoloration

17. **The shock index (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone.

18. Control ABC hemorrhage resuscitation external bleeding : compression initially internal bleeding : need surgical intervention Replace fluids : IV fluid crystalloid (isotonic ): ringer lactate or normal saline(for every 100ml blood loss give 300ml crystalloid fluid) colloid (hypertonic): plasma substitutes (1 platlets:1 fresh frozen plasma: 1packed RBCs) Support BP : vasopressors

19. P r o b lem w i t h t h e p u m p “ H e a r t “ caused by any disease, or event, which prevents the heart muscle from pumping strongly and consistently enough to circulate the blood normally Direct injury : infarction(MI), contusion, trauma Indirect mechanism arrhythmia, constrictive pericarditis, valvular disease, severe anemia Vasoconstriction Hallmarks : Low CO High Cardiac pressures High SVR Tachycardia * Cool and Clammy hands Fluid Overload symptoms  Jugular venous distention ( high RV Pressure )or Pulmonary congestion / edema ( high LV Pressure ) { Pulmonary rales / c r a c k l e s a n d t a c h yp n e a } Low pulse pressure {HF}

20. Diagnosis of primary cause : ECG Echocardiogram LAB Investigations : m y o c a r d i a l i n f a r c ti o n  t r o p o n in congestive heart failure  brain- natriuretic peptide Management : 1- ABC ( IV fluid are likely to be harmful , instead we give t h e m d i u r etics “ T h is i s r e l ati v e a cc o r d ing t o p a t i e n t c a s e ” ) vasopressor : dopamine (dose dependent adrenergic agonist effects ) to improve cardiac contractility inotrope : dobutamine ( Pure Beta agonist ) / Milrinone (increase the heart's contractility and decrease pulmonary vascular resistance) Treat underlying cause The intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction

21. a balloon device inserted percutaneously and advanced up to the aorta. T h e device synch ronizes with t h e cardiac cycl e. It infla t e s during early diastole, which increases diastolic coronary blood flow, and then it deflates during systole, reducing the afterload and dramatically improving cardiac output. But because IABPs sit within the vasculature, they increase the risk of thrombosis, and therefore individuals need to be anticoagulated with medications like heparin)

22. S u rr ounding the heart In the great vessels  NORMAL Cardiac tamponade Constrictive pericarditis Tension pneumothorax In the Heart itself ( Valve) Aortic stenosis -Pulmonary embolus -IVC obstruction Hallmarks : Low CO despite normal contractility High SVR Tachycardia Cool and Clammy hands Fluid Overload symptoms  Jugular venous distention or Pulmonary congestion / edema { Pulmonary rales / crackles and tachypnea } / Anasarca .

23. insult cause: (Excessive Peripheral Vasodilation ) + Leaky Blood Vessels ( Endothelial dysfunction ) Abnormal distribution of blood to the organs :  A W A Y f r o m v i t al o r g a ns -- - O r g a n f a il u re  T O W A RD S k in -- - H o t S h o ck Hallmarks : LOW SVR Normal or high CO Warm skin Cardiac pressures variable according to degree of leakage .

24. Inflammation In the blood stream Systemic i n f l a mm a t o r y response syndrome Keep Clinical Picture in mind Confirmed infection Reversible elevated lactate, or decreased urine output  30ml/kg Multiorgan dysfunction syndrome Septic shock + Irreversible Organ failure and mostly liver failure SOFA score: The sequential organ failure assessment score (SOFA score),  known as the sepsis- related organ failure assessment score, is used to track a person's status during the stay in an intensive care unit (ICU) to determine the extent of a person's organ function or rate of failure.

25. Septic shock is the most common cause of distributive shock. Caused by an overwhelming systemic infection resulting in vasodilation and increased permeability of the blood vessels leading to hypotension. The primary infection is most caused by bacteria , but also may be by fungi , viruses or parasites . Early (warm) = compensated Due to hyperdynamic state vasodilation Warm ,flushed skin Inc HR Inc RR Dec BP Fever Normal or Inc. CO Late “cold” = decompensated Dec CO Clod , clammy extremities Hypothermia sever hypotension Oliguria Coma

26. -- confirmed by : - CBC and blood culture - identifying primary source : pneumonia , pyelonephritis , meningitis , peritonitis ,abscess … etc.) Initially, IV antibiotics (broad spectrum) at maximum dosages. Antibiotics for more rare organisms or antifungal medications may be required if there is no clinical response or if suspicion for an atypical organism (i.e., immunocompromised). If cultures are positive, antibiotics can be narrowed based on sensitivity testing . Fluid administration to increase mean BP (may require many liters of fluid). Vasopressors (Norepinephrine, dopamine, phenylephrine) may be used if hypotension persists despite aggressive IV fluid resuscitation CRP / ESR

27. A type of di s tr ibutive shock t hat re sults from widespread sy s t e mic allergic reaction to an antigen Most common causes : Drugs ( ex: Antibiotics ) Insects :bee stings Food (ex:nuts) Could be : Immunologic ( IgE mediated ) Non – Immunologic ( Anaphylactoid reaction ) Anaphylactic Response: Vasodilatation Increased vascular permeability Bronchoconstriction Increased mucus production Increased inflammatory mediators' recruitment to sites of antigen Note : Anaphylactic Shock (Hypotension ) Vs Anaphylactic reaction ( No hypotension )

28. Cutaneous manifestations (s ome of the most severe cases of anaphylaxis present in the absence of skin findings). Urticaria, erythema, pruritis, angioedema Respiratory compromise stridor, wheezing, bronchorrhea, resp. distress Circulatory collapse tachycardia, vasodilation, hypotension * Symptoms usually begin within 60 minutes of exposure *Faster the onset of symptoms = more severe reaction *Biphasic phenomenon (Biphasic anaphylaxis is a second episode of anaphylaxis. It happens with no additional exposure to the allergen.) occurs in up to 20% of patient's 2 nd episode *most common sign  skin reaction *Most dangerous sign ( laryngeal edema )

29. Clinical diagnosis( airway compromise, hypotension, cutaneous involvement) Look for exposure to drug, food, or insect Non pharmacotherapy epinephrine and H1 antihistamines. -Adrenergic agonists (eg, epinephrine ) Allergen (remove it) Airway management (eg, ventilator support with bag/valve/mask, endotracheal intubation) High-flow oxygen Cardiac monitoring and/or pulse oximetry Fluid resuscitation with isotonic crystalloid solution Supine position (or position of comfort if dyspneic or vomiting) with legs elevated Pharmacotherapy The primary drug treatments for acute anaphylactic reactions are - H1 Antihistamines (eg, diphenhydramine, hydroxyzine) -H2 receptor antagonists (eg, cimetidine, ranitidine, famotidine ) - Bronchodilators (eg, albuterol) - Corticosteroids (eg, methylprednisolone, prednisone) to prevent reccunt atta -Vasopressors (eg, dopamine)

30. a slow heart rate The classic symptoms include due to loss of cardiac sympathetic tone (unopposed vagal tone ). Low blood pressure occurs due to to dilation of the peripheral blood vessels and decreased systemic vascular resistance as a result of lacking sympathetic tone which in turn causes pools of blood staying within the extremities and not being redirected to the core body. B R A D Y C A R DIA

31. 1. Supine or Trendelenburg position ( Immobilize the patient ) IV fluids 2. Judicious use of as the mainstay of treatment 3.Vasoconstrictors to restore venous tone ( V a s o p r esso rs ) 4. Correct the underlying problem .