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![◦ For 0 - 10 kg = weight (kg) x 100 mL/kg/day.
◦ For 10-20 kg = 1000 mL + [weight (kg) x 50 ml/kg/day]
◦ For > 20 kg = 1500 mL + [weight (kg) x 20 ml/kg/day]
[Na+] in serum = TBS ÷ TBW ……………………………….equation 1
That means
TBS = [Na+] in serum x TBW ……………………………… equation 2
[Na+]high TBW1 = [Na+]desired (TBW1 + X)
∗ ∗
Where X is the free water deficit. If the desired sodium is 140, rearranging the equation and
solving for X gives you:
X = {([Na+]high – 140) ÷ 140 } TBW1
∗
TBW = Wt (kg) x 0.6 for males
TBW = Wt (kg) x 0.5 for females.
If elderly, use 0.5 for males and 0.45 for females.
To maintain their serum sodium concentrations at 140 mEq/L (140 mmol/L), infants also must
retain approximately 360 mEq (360 mmol) of sodium or 2 mEq/d (2 mmol/d).
Calculating fluid for Maintenance](https://image.slidesharecdn.com/lecture1shockanditsmanagement-250413132201-951daedf/75/Lecture-different-types-of-Shock-and-Its-Management-pptx-32-2048.jpg)
Lecture different types of Shock and Its Management.pptx
- 1. Shock and Its Management prepby shah Fahad Khalid BS Cardiology KMU/IPMS(GM) Lecturer at Abasyn university
- 2. Introduction to shock Possiblecauses of shock Pre-shock symptoms Sign and symptoms Assessment of Shock Patient Generalized Treatment Types of shock Management of each shock type accordingly Monitoring and care to the shock patient Topic Outlines
- 3. Acute circulatoryfailure. Decreased organs perfusion. Inadequate oxygen delivery. End organ dysfunction. Actually it is the imbalance between demand and supply of oxygen. Inability to utilize oxygen A temporary stage of unconsciousness. Shock
- 4. Failure ofoxygen delivery system ◦ Hypoxia ◦ Oxygen deficient environment i.e. high altitude. Injury to the lungs/ Lung disease/ unable to transform oxygen into the blood. ◦ Pneumonia ◦ CHF ◦ Traumatized lungs ◦ Pulmonary embolism ◦ Pulmonary edema ◦ Hemo/hydro/pneumothorax ◦ Respiratory arrest Burns Diarrhea/vomiting (persistent) Spinal injuries (neurogenic) Heart related problems ◦ CHF ◦ MI ◦ Heart attack/cardiac arrest ◦ Arrhythmias ◦ Pericarditis/endocarditis ◦ Pericardial effusion ◦ CAD RBCs related ◦ Anemia ◦ Bleeding disorders ◦ Hemolysis Body fluids (dehydration) Hypotension due to vasodilation or any other causes. Possible Causes of Shock
- 5. Rapid butshallow breathing Feeling to get fainted Dizziness starts Blacking out of eye Nausea Feeling of General weakness Facial flushing Pre-shock Symptoms
- 6. Low Bp Tachycardia (compensatory) Rapid but shallow breathing persists Cold and clammy skin Rapid but weak pulse Dizziness/fainting General weakness Type dependent sign and symptoms ◦ Anxiety or agitation ◦ Seizures ◦ Confusion/ unresponsiveness ◦ Low or no urine output ◦ Peripheral cyanosis ◦ Sweating ◦ Chest pain. Sign and Symptoms
- 7. ABC Protocol ◦Airway ◦ Breathing ◦ Circulation ABCDE Protocols ◦ Airway ◦ Breathing ◦ Circulation ◦ Disability ◦ Exposure BLUE protocol: Bed Side Lung Ultrasonography in Emergency. FALLS Protocol: Fluid Administration Limited by Lungs Sonography. GCS scaling(15) Assessment Protocols
- 8.
- 9. Main types ◦Obstructive Shock ◦ Cardiogenic Shock ◦ Distributive Shock ◦ Hypovolemic Shock Types of Shock
- 10. Actual physicalcause Underlying pathology Optimization of ◦ Cardiac output ◦ Blood pressure ◦ Oxygen delivery Vascular tone restoration Prevent any end organ failure Or at least give supportive therapy (pharmacological/prophylactic). Generalized Treatment
- 11. Obstruction ofblood flow into / out of the heart. Impaired diastolic filling and decreased cardiac output. Causes: ◦ Pulmonary ◦ Circulatory occlusion ◦ Heart itself Acute pericardial tamponade, Pulmonary or systemic hypertension Massive pulmonary emboli occluding >50% of vascular bed. Obstructiv e Shock
- 12. CO isdecreased CVP is elevated, SVR is increased, and Echocardiography is the definitive diagnostic tool for Obstructive shock. Diagnostic Variables
- 13. Parameter Normal value BloodPressure Systolic (SBP) 90-140 mmHg Diastolic (DBP) 60-90mmHg Mean Arterial Pressure (MAP) 70 - 100 mm Hg Cardiac Index (CI) CI=CO/BSA 2.5-4 L/min/m2 Cardiac Output (CO) 4-8 L/min Central Venous Pressure (CVP) (also known as Right Atrial Pressure (RA)) 2-6 mmHg Pulmonary Artery Pressure (PA) Systolic 20-30 mmHg (PAS) Diastolic 8-12 mmHg (PAD) Mean 25 mmHg (PAM) Pulmonary Capillary Wedge Pressure (PWCP) 4-12 mmHg Pulmonary Vascular Resistance (PVR) 37-250 dynes/sec/cm5 Right Ventricular Pressure (RV) Systolic-20-30 mmHg Diastolic 0-5 mmHg Stroke Index (SI) 25 - 45 ml/m2 Stroke Volume (SV) 50 - 100 ml Normal Variables
- 14. The symptomsof obstructive shock are considered emergencies because they can lead to organ failure, tissue death, and death. Symptoms that are associated with neurological function include confusion, loss of consciousness, and inability to concentrate. The symptoms that are related to the heart and its function are chest pain, lightheadedness, and a sudden increase in heart rate along with a faint pulse. Respiratory symptoms consist of shortness of breath and fast but shallow breathing. Other symptoms include sweating, decreased urine output, clammy skin, pallor, and cold hands and feet. Symptoms of Obstructive Shock
- 15. As withall forms of shock, the management of obstructive shock should center around the fundamental components for the treatment of shock. The following should be considered: ◦ Positioning, ◦ Airway and breathing, ◦ Vascular access, ◦ Fluid resuscitation, ◦ Monitoring, ◦ Frequent reassessment, ◦ Lab studies, ◦ Medication therapy, ◦ Expert consultation. Fundamentals of Shock Management:
- 16. Occurs asa direct result of myocardial dysfunction. Heart failure to pump adequately Very rare to occur but often fatal. Diminished Cardiac Output, End organ hypoperfusion Hypoxia Cardiogenic Shock
- 17. Low myocardialcontractility MI Hypotension Systemic vasodilation Coronary artery disease The hallmark is peripheral vasoconstriction and vital end‐organ damage, which stems from ineffective stroke volume and insufficient circulatory compensation. This may, for a while, improve cardia tissue perfusion but it increases the afterload and workload on cardiac muscle increases the damage. Pathophysiol ogy
- 18. In thesetting of CS, classic ACS symptoms and signs are combined with ◦ altered mental status, ◦ hypotension, ◦ arrhythmia, ◦ diminished pulses, ◦ dyspnea, ◦ peripheral edema, ◦ These features reflect an infarction involving >40% of the left ventricle Clinical Presentations
- 19. The fourcommon clinical signs that distinguish cardiogenic shock are ◦ Tachycardia, ◦ Dyspnea, ◦ Jugular vein distention, ◦ Hepatomegaly Increased respiratory effort is often the distinguishing characteristic that sets cardiogenic shock apart from other forms of shock. Primary assessment model (ABCDE) Airway: ◦ typically no airway abnormalities and patent airway Breathing: ◦ tachypena, and pulmonary edema Circulation: ◦ tachycardia, weak or absent peripheral pulses, jugular venous distention, low BP with a narrow pulse pressure, delayed capillary refill, signs of congestive heart failure, and oliguria Disability: ◦ anxiety, confusion, restlessness, drowsiness, and coma Exposure: ◦ pale, cool, and diaphoresis Signs of Cardiogenic Shock:
- 20. ECG ChestX-ray BNP test.(BNP levels below 100 picograms per milliliter (pg/mL)) Investigation
- 21. Unlike other formsof shock which improve with aggressive fluid resuscitation, rapid fluid resuscitation with cardiogenic shock can be counterproductive and may worsen the patient’s condition. Fluid overload and pulmonary edema may occur. Caution should be used when administering fluids in the presence of cardiogenic shock. Manageme nt Of Cardiogeni c Shock
- 22. Improve cardiac function. Improvecardiac output. Improve tissue perfusion. Decrease myocardial oxygen demand. Any drug that causes an increase in systemic vascular resistance (SVR) (afterload) should be avoided. This includes phenylephrine and norepinephrine which both cause potent vasoconstriction Goals of Manageme nt
- 23. Improve CardiacFunction ◦ Reduce SVR ◦ Dobutamine, milrinone, dopamine, and epinephrine ◦ Nitroprusside, which is a pure vasodilator, it may be necessary to use dopamine or epinephrine to improve perfusion pressure when nitroprusside is administered. ◦ Diuretics may also be used if there is evidence of pulmonary edema or systemic venous congestion. Decreasing Oxygen Demand ◦ intubation and mechanical ventilation, ◦ maintenance of a normal temperature, ◦ and patient sedation. Identification of the etiology is of primary importance because the etiology will direct the course of treatment. Early expert consultation should be obtained. Management Of Cardiogenic Shock
- 24. Inotropic agents.You might be given medications to improve your heart function, such as norepinephrine (Levophed) or dopamine, until other treatments start to work. Aspirin. Emergency medical workers might give you aspirin immediately to reduce blood clotting and keep your blood flowing through a narrowed artery. Take an aspirin yourself while waiting for help to arrive only if your doctor has previously told you to do so for symptoms of a heart attack. Thrombolytics. These drugs, also called clot busters or fibrinolytics, help dissolve a blood clot that's blocking blood flow to your heart. The sooner you receive a thrombolytic drug after a heart attack, the greater your chances of survival. You'll likely receive thrombolytics, such as alteplase (Activase) or reteplase (Retavase), only if emergency cardiac catheterization isn't available. Antiplatelet medication. Emergency room doctors might give you drugs similar to aspirin to help prevent new clots from forming. These include medications, such as oral clopidogrel (Plavix), and platelet glycoprotein IIb/IIIa receptor blockers, such as abciximab (Reopro), tirofiban (Aggrastat) and eptifibatide (Integrilin), which are given through a vein (intravenously). Other blood-thinning medications. You'll likely be given other medications, such as heparin, to make your blood less likely to form clots. IV or injectable heparin usually is given during the first few days after a heart attack. Treatment of Cardiogenic Shock
- 25. Angioplasty andstenting. If a blockage is found during a cardiac catheterization, your doctor can insert a long, thin tube (catheter) equipped with a special balloon through an artery, usually in your leg, to a blocked artery in your heart. Once in position, the balloon is briefly inflated to open the blockage. A metal mesh stent might be inserted into the artery to keep it open over time. In most cases, you doctor will place a stent coated with a slow-releasing medication to help keep your artery open. Balloon pump. Your doctor inserts a balloon pump in the main artery of your heart (aorta). The pump inflates and deflates within the aorta, helping blood flow and taking some of the workload off your heart. Medical Procedures
- 26. Coronary arterybypass surgery. This involves sewing veins or arteries in place at a site beyond a blocked coronary artery. Your doctor might suggest this procedure after your heart has had time to recover from your heart attack. Occasionally, bypass surgery is performed on an emergency basis. Surgery to repair an injury to your heart. Sometimes an injury, such as a tear in one of your heart's chambers or a damaged heart valve, can cause cardiogenic shock. Surgery might correct the problem. Ventricular assist device. A mechanical device can be implanted into the abdomen and attached to the heart to help it pump. This might extend and improve the lives of some people with end-stage heart failure who are waiting for new hearts or aren't able to have heart transplantation. Heart transplant. If your heart is so damaged that no other treatments work, a heart transplant may be a last resort Surgical Procedure
- 27. reduction inintravascular fluid volume. ◦ causes a decrease in stroke volume because of the resulting decrease in preload ◦ Decreases cardiac output. Causes ◦ Dehydration from vomiting and diarrhea, ◦ Hemorrhage, ◦ Decreased intake of fluids, ◦ Pathologic urinary losses (e.g. diabetic ketoacidosis, diabetes insipidus), ◦ Translocation of body fluids (e.g. burns, peritonitis, small bowel obstruction). Hypovolemic Shock
- 28. Increased HR, Increased afterload, and/or Increased contractility. Those are altered in compensation to hypovolemia, a viable effort to maintain CO. But alteration is the key to diagnose hypovolemic shock. Compensatory Mechanisms In Hypovolemia
- 29. The PrimaryAssessment acronym stands for Airway, Breathing, Circulation, Disability, and Exposure. A: Typically the airway of the child with hypovolemic shock will not be significantly affected. B: The patient may experience some Breathing changes and this may be recognized by a nonlabored tachypnea. (With no effort) C: The most notable changes will likely be seen with circulation. These circulation changes include tachycardia, narrowing pulse pressure, possible systolic hypotension, capillary refill time > 2 seconds, cool/pale skin, weak to absent peripheral pulses, reduced urine output. D: Disability or neurological changes include decreased level of consciousness. E: Exposing the patient to observe the skin and extremities will often reveal cool, pale, and mottled extremities Sign and Symptoms (ABCDE Acronyms)
- 31. • compensatory mechanismscan maintain systolic blood pressure. This window of time is classified as compensated shock. If compensatory mechanisms fail and hypotensive shock (low systolic BP) develops, the chances of survival and recovery are significantly decreased
- 32. ◦ For 0- 10 kg = weight (kg) x 100 mL/kg/day. ◦ For 10-20 kg = 1000 mL + [weight (kg) x 50 ml/kg/day] ◦ For > 20 kg = 1500 mL + [weight (kg) x 20 ml/kg/day] [Na+] in serum = TBS ÷ TBW ……………………………….equation 1 That means TBS = [Na+] in serum x TBW ……………………………… equation 2 [Na+]high TBW1 = [Na+]desired (TBW1 + X) ∗ ∗ Where X is the free water deficit. If the desired sodium is 140, rearranging the equation and solving for X gives you: X = {([Na+]high – 140) ÷ 140 } TBW1 ∗ TBW = Wt (kg) x 0.6 for males TBW = Wt (kg) x 0.5 for females. If elderly, use 0.5 for males and 0.45 for females. To maintain their serum sodium concentrations at 140 mEq/L (140 mmol/L), infants also must retain approximately 360 mEq (360 mmol) of sodium or 2 mEq/d (2 mmol/d). Calculating fluid for Maintenance
- 33. Excessive vasodilationand impaired distribution of blood flow. Anaphylactic and septic shock Neurogenic shock Distributive Shock
- 34. Hyperdynamic statedevelopment. Inadequate tissue perfusion Intraorgan shunting Hypotensive state with increase mixed venous oxygen saturation. Early Septic Shock (warm or hyperdynamic) ◦ Reduced diastolic Blood Pressure ◦ Flushed warm extremities ◦ Brisk capillary refill from peripheral vasodilation and increased cardiac output. Late Septic Shock (cold or Hypodynamic) ◦ Decreased myocardial Contractility ◦ Paralyzed microvascular tone ◦ Pressure dependent reduction in organ perfusion (Hypoperfusion) Pathophysiology
- 35. Anaphylactic ◦ DecreasedSVR; histamine release from mast cells after activation of antigen bound immunoglobulin (IgE) ◦ Increased prostaglandins Neurogenic Shock ◦ Loss of sympathetic tone due to severe injury to the nervous system. Pathophysiology (anaphylactic/ neurogenic)
- 36. Anaphylaxis ◦ Respiratorydistress ◦ Wheezing ◦ Urticarial rashes ◦ Angioedema ◦ High grade fever in septic shock Clinical Signs
- 37. CBC Urinalysis Electrolytes Blood urea Nitrogen (BUN) Creatinine Glucose Urine cultures Blood cultures Possible ABGs or VBGs Serum lactate Total Circulating blood Volume (TCBV) Microcirculatory Imaging Thoracic bioelectrical Impedance (TBI) In case of pneumonia ◦ Sputum gram stain and cultures Intra-abdominal pathology or hepatic insufficiency ◦ Serum bilirubin ◦ ALP, ALT, AST ◦ PT/aPTT, INR ◦ Amylase, lipase DIC suspicion ◦ PT/aPTT, fibrin split products, fibrinogen levels, platelets level. ECG,CT scan, X-ray etc. TEE/TTE Arterial Catheters, Venous Catheters Work up
- 38. DDx PCWP (pulmonarycapillary wedge pressure) Cardiac Output Cardiogenic Shock increased Decreased (due to mechanical defect) Extra Cardiac obstructive Shock 1. Pericardial tamponade 2. Pulmonary embolism Increased Normal or decreased Decreased Decreased Hypovolemic Shock Decreased Decreased Distributive Shock 1. Septic Shock 2. Anaphylactic Shock Normal or decreased Normal or decreased Increased or normal Increased or normal
Editor's Notes
- #3 Septic shock - This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative bacteria i.e. Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body. Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins produce a similar syndrome. Anaphylactic shock - Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. Neurogenic shock - Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension.