Shock.students 2.pdf

SHOCK Dr. Deb Jacques RN DNP AGNP-c Student Learning Outcomes Explain the treatment and nursing management of clients with inflammatory heart diseases and valvular problems Identify appropriate pre and post operative nursing care measures used in caring for clients having cardiac surgery Distinguish...

SHOCK Dr. Deb Jacques RN DNP AGNP-c Student Learning Outcomes Explain the treatment and nursing management of clients with inflammatory heart diseases and valvular problems Identify appropriate pre and post operative nursing care measures used in caring for clients having cardiac surgery Distinguish the pathophysiology and clinical manifestations of shock Create a nursing care plan for patient with the tree different types of shock, inflammatory diseases and valvular dysfunctions Defining shock: Inadequate tissue perfusion leading to cellular, organ, and organ system death Causes: 1. Problem with the pump 2. Problem with the tubes 3. Problem with oxygen delivery Reversible if caught in time. Shock-Types Cardiogenic Hypovolemic Absolute hypovolemia Relative hypovolemia Distributive Neurogenic Anaphylactic Septic Obstructive Types of shock Distributive – 66% Septic shock – 94% Anaphylaxis Neurogenic Cardiogenic – 16% Hypovolemic – 16% Obstructive – 2% Swan or PA Catheter Mixed Venous Oxygen Saturation SvO2 = oxygen delivery – oxygen consumption Normal: 65-75% in the pulmonary artery; in the R atrium will be 2-3% lower Abnormalities: High SvO2 Increased O2 delivery – high FiO2, hyperoxia Decreased O2 demand – hypothermia, anesthesia, pharmacologic paralysis, sepsis (inability to uptake oxygen in the periphery) Low SvO2 Decreased O2 delivery Low Hb – anemia, hemorrhage Low SaO2 – hypoxia, suctioning Low CO2 – hypovolemia, shock, arrhythmias Increased O2 demand – hyperthermia, pain, shivering, seizures Lactate and acid/base disturbance Lactate Byproduct of glucose metabolism (glycolysis) Normal: 0.5 mmol/L Mild to moderate: 2-5 mmol/L Above 5 mmol/L - lactic acidosis Elevated levels are associated with: Metabolic acidosis Hypoperfusion Oxygen debt at the tissue and cellular level Elevated lactate = higher risk of mortality Anion Gap – looks at acid/base disturbance Normal anion gap: 3-11 meq/L Base excess: can indicate hypoperfusion and oxygen debt Caution: can be elevated in end stage kidney disease Cardiogenic Shock Occurs when either systolic or diastolic dysfunction of the heart’s pumping action results in reduced cardiac output (CO), stroke volume (SV), and blood pressure. These changes compromise myocardial perfusion, further depress myocardial function, and decrease CO and perfusion. Normal blood flow through the heart Shock-Cardiogenic Problems with our pump Classification and Precipitating factors Mortality rates 50%-usually after a myocardial infarction Systolic dysfunction Inability of the heart to pump blood forward (left ventricle)-MI Diastolic dysfunction Inability of the heart to fill during diastole-cardiomyopathy Dysrhythmias Brady-dysrhythmias and tachydysrhythmias Structural factors Valvular stenosis or regurgitation, ventricular septal rupture or tension pneumothorax Shock-Cardiogenic Clinical Manifestations Cardiovascular Pulmonary Renal Skin Neurologic Gastrointestinal Shock-Cardiogenic Diagnostic Findings Increased cardiac markers Increased B-type natriuretic peptide (BNP) Increased blood glucose Increased BUN ECG (dysrhythmias) Echocardiogram (left ventricular dysfunction) Chest x-ray (pulmonary infiltrates) Hemodynamics in shock Management of Cardiogenic Shock Goal: to restore blood flow to the myocardium Restoring the balance between oxygen supply and demand Thrombolytic therapy Angioplasty with stenting Cardiac catheterization-performed as soon as possible Emergency revascularization Valve replacement Drugs –Table 66-8, pg 1578 Nitrates-decrease the workload of the heart by dilating coronary arteries Diuretics-reduces preload Vasodilators-reduces afterload B-adrenergic blockers-reduces heart rate and contractility Intraaortic balloon pump (IABP), Ventricular assist device (VAD) Decrease the systemic vascular resistance (SVR) and left ventricular workload IABP LVAD Quick question The nurse understands that a/an _______ is used in the evaluation of cardiogenic shock. A. PA catheter B. LVAD C. RVAD D. IABP Review of important Nursing Assessments VS and hemodynamic readings Neurological status Skin color and temperature labs Shock-Hypovolemic Classification and Precipitating factors Absolute Hypovolemia External loss of whole blood Hemorrhage from trauma, surgery, GI loss (vomiting, diarrhea and bleeding) Loss of other body fluids Excessive diuresis, diabetes insipidus, fistula drainage and diabetes mellitus Relative hypovolemia Pooling of blood or fluids Bowel obstruction Fluid shifts- Burn injuries, ascites Internal bleeding Fractures of long bones, ruptured spleen, hemothorax, severe pancreatitis Massive vasodilation- Sepsis Hemodynamics in shock Shock-Hypovolemic Clinical Manifestations Cardiovascular Pulmonary Renal Skin Neurologic Gastrointestinal Shock-Hypovolemic Diagnostic Findings CBC-D Decreased hematocrit Decreased hemoglobin Increased Lactate Increased Urine specific gravity Electrolytes-changes Hypovolemic/Hemorrhagic shock Management of Hypovolemic Shock Stop the loss of fluid https://www.dhs.gov/stopthebleed Restore the circulating volume- goal is to keep the SBP >90 Fluid resuscitation Types (Table 66-7, pg 1597) 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss) Shock- Distributive Classification and Precipitating factors Neurogenic Shock Hemodynamic consequence of spinal cord injury and/or disease at or above T5 Spinal anesthesia Vasomotor center depression Severe pain, drugs, hypoglycemia, injury Anaphylactic Shock Hypersensitivity (allergic reaction) Contrast media, blood/blood products, drugs, insect bites, anesthetic agents etc Septic Shock Infection-pneumonia, peritonitis, urinary tract, respiratory tract, invasive lines etc At risk patients-Older adults, children < 12 months, patients with chronic diseases, patients receiving immunosuppressive therapy, malnourished, diabetes mellitus and debilitated patients Distributive Shock Neurogenic Shock Decreased cardiac output Decreased CVP and PAOP Decreased SVR Decreased venous oxygen saturation (SvO2 or ScvO2) Hypotension and bradycardia Anaphylactic shock Decreased cardiac output Decreased CVP and PAOP Decreased SVR Decreased venous oxygen saturation (SvO2 or ScvO2) Hypotension and tachycardia Distributive shock Early septic shock Increased cardiac output Decreased CVP and PAOP Decreased SVR Increased venous oxygen saturation (SvO2 or ScvO2) Normal or decreased blood pressure, tachycardia, and hyperthermia Late septic shock Decreased cardiac output Variable CVP and PAOP Variable SVR Decreased venous oxygen saturation (SvO2 or ScvO2) Hypotension, tachycardia, and hypothermia Shock-Distributive Clinical Manifestations Cardiovascular Pulmonary Renal Skin Neurologic Gastrointestinal Shock-Distributive Diagnostic Findings Based on the cause Decreased or increased WBC Decreased Platelets Increased Lactate (2.0-4.0 mmol/L) >2 mmol/L * used as a marker for tissue hypoperfusion. Resuscitation should be targeted to normalize lactic acid Increased Blood glucose Increased Urine specific gravity Decreased Urine NA+ Positive Blood cultures Shock-Septic (Distributive) SIRS- Systemic Inflammatory Response Syndrome Fever >100.9 F, HR > 90, RR > 22, WBC > 12,000, Glucose >140 mg/dL, change in cognition, SPB < 100 mmHg Sepsis- SIRS + infection Severe Sepsis- Sepsis + organ dysfunction, hypoperfusion or decreased BP with lactic acidosis Shock-Obstructive Classification and Precipitating factors Physical obstruction impedes the filling or outflow of blood resulting in reduced cardiac output Cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome, pulmonary embolism Shock-Obstructive Clinical Manifestations Cardiovascular Pulmonary Renal Skin Neurologic Gastrointestinal Diagnostic findings are specific to the cause of the obstruction-need to fix the issue Shock-Obstructive Diagnostic Findings Specific to cause of obstruction Stages of Shock Initial Compensatory Progressive Irreversible (refractory) Initial Occurs at the cellular level No clinical signs at this time Lactic acid is a waste product that is removed by the liver- however, this process requires oxygen which is unavailable because of the decrease in tissue perfusion Compensatory The body activates neural, hormonal, and biochemical compensatory mechanisms-attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis Neurologic System Cardiovascular System Respiratory System Gastrointestinal System Renal System Hepatic System Hematologic System Temperature Skin Progressive Begins as the compensatory mechanisms fail Neurologic System Cardiovascular System Respiratory System Gastrointestinal System Renal System Hepatic System Hematologic System Temperature Skin Irreversible (Refractory)-Multiple organ dysfunction syndrome) Multiple organ failure occurs and death is imminent Neurologic System Cardiovascular System Respiratory System Gastrointestinal System Renal System Hepatic System Hematologic System Temperature Skin Collaborative Care Successful management include: Identification of patients at risk for developing shock Integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis Interventions to control or eliminate the cause of the decreased perfusion Provision of multisystem supportive care Collaborative Care Oxygen and Ventilation Oxygen delivery is dependent on CO2 Increase supply and decreasing demand Continuous monitoring of ScvO2 by a central venous catheter or peripheral arterial line SAO2 CO Hemoglobin Collaborative Care Fluid resuscitation Septic, hypovolemic, and anaphylactic Volume expansion Crystalloids and colloids Two large bore intravenous catheters-antecubital Intraosseous (IO) access *** Use when IV access cannot be obtained Insertion sites include the sternum, proximal and distal tibia and proximal and distal humerus Remove within 24 hours of insertion or as soon as possible Monitor for complications: extravasation or drugs and fluids into the soft tissue, fractures and osteomyelitis https://www.youtube.com/watch?v=KHXSfh2ZRDM Collaborative Care Drugs- see drug therapy table in book Correction of decreased tissue perfusion Through a central venous catheter using an intravenous pump Sympathomimetic-drugs that mimic the action of CNS Vasoconstriction Vasopressor drugs-norepinephrine, dopamine, phenylephrine Vasodilator drugs Decrease afterload-in cardiogenic shock Vasodilator therapy-nitroglycerin (Tridil), nitropresside (Nipride) Collaborative Care Nutritional Therapy Vital to decreasing morbidity Protein-calorie Enteral parenteral nutrition Start within the first 24 hours 10 mL/hr Enhance the perfusion of the GI tract Helps maintain the integrity of the gut mucosa Daily weight Nutritional lab values- serum protein, total albumin, BUN, serum glucose and serum electrolytes Management of Septic Shock QSOFA- Quick Sepsis Organ Failure Assessment Hemodynamic monitoring Central venous catheter 8-12 mm Hg CVP Vasopressors- once CVP is >8 mm Hg (increases BP, decreased stroke volume) Norepinephrine (Levophed), 1st choice Vasopressin –***give along with norepinephrine-infuse at low dose-do not titrate- use cautiously in patients with coronary heart disease Inotropic agents Dobutamine- offset the decrease in stroke volume and increase tissue perfusion Management of Septic Shock Antibiotics Blood cultures, urine cultures, stool and sputum cultures Glucose levels