Summary • NRS 225 Perfusion- Shock, Cardiomyopathy, DIC

• NRS 225 Perfusion- Shock, Cardiomyopathy, DIC Perfusion • Normal Perfusion o 3 Layers: epicardium (outer most); myocardium; endocardium (inner most) o 4 Chambers: 2 atria; 2 ventricles o Pump- Heart; Tubing- Blood Vessels; Fluid- Blood o Systole: ventricular contraction // Diastole: ventricular relaxation: “lub-dub” o Circulation ▪ Pulmonary: right side of heart  lungs ▪ Systemic: left side of heart  body ▪ Coronary: supplies heart o Cardiac Cycle: contraction and relaxation (1 heart beat) o Stroke Volume (SV): amount of blood pumped into aorta from left ventricle with each contraction o Cardiac Output (CO): amount of blood pumped by left ventricle per minute; HR x SV= CO o Mean Arterial Pressure (MAP): average pressure in arterial circulation throughout cardiac cycle ▪ 2x diastolic plus systolic divide by 3 o Sympathetic Tone: smooth muscle surrounding the arteries and arterioles are in a state of partial contraction; increases vasoconstriction o Pulse Pressure: difference of systolic and diastolic BP; early sign of shock ▪ narrowing pulse pressure: common with hypovolemic and cardiogenic shock; reduced CO ▪ widened pulse pressure: common with septic shock o Normal Heart Rate: 60-100 bpm o Normal Blood Pressure: 120/80 // Systolic/Diastolic o Tachycardia: HR 100 o Bradycardia: HR 60 o Factors affecting Pulse: age; gender; exercise; fever; medications; hypovolemia; stress; pathology o Factors affecting Blood Pressure: pumping action of heart; peripheral vascular resistance; blood volume; blood viscosity; age; stress; race; gender; medications; obesity; disease process • Renal System o Functions of Kidneys: filter blood, make urine, protein metabolism, regulates electrolytes, pH/ acid-base balance (hydrogen), regulates BP (RAAS system), production of erythropoietin (RBC production), converts vitamin D into active form o Normal Urinary Output: 0.5-1 mL/kg o RAAS SYSTEM: Renin-angiotensin-aldosterone system ▪ Low BP/hypotension  kidneys release renin  liver makes hormone angiotensinogen  renin converts angiotensinogen into angiotensin I  lungs release enzyme (angiotensin-converting enzyme: ACE) which converts angiotensin I into angiotensin II ▪ Angiotensin II: vasoconstrictive hormone that increases systemic BP, renal perfusion pressure, and GFR • Interrelated Concepts o Acid-Base Balance: respiratory acidosis; metabolic acidosis: retention of CO2; low pH o Cellular Regulation: heart may not provide tissue with enough blood to meet metabolic needs o Cognition: hypoxemia can alter mental state o Comfort: decreased tissue perfusion may manifest as pain; acute and chronic pain o Fluids and Electrolytes: fluid volume excess; hypervolemia; impaired gas exchange and other life- threatening alterations o Intracranial Regulation: altered cerebral blood flow o Oxygenation: altered transport of gasses (oxygen) to tissue SHOCK: decrease in blood flow resulting in adequate oxygenation; state of inadequate blood flow to body organs and tissues; life-threatening; body actively dying; first sign of shock= increased heart rate • Modeling: vasoconstricting in extremities; redness, lines, color change • Catecholamines: Dopamine (neurotransmitter), epinephrine (adrenaline, raise HR), norepinephrine (vasoconstrictor) • Stage 1: Early, Reversible, and Compensatory Shock o Baseline MAP decreases less than 10 mmHg o Increase in HR and respiratory rate; slight increase in diastolic blood pressure o Compensation: vascular constriction and increased HR to assist perfusion o Compensatory Shock: MAP falls 10-15 mmHg; stopping condition causing shock prevents shock from progressing ▪ Compensatory mechanisms are still able to maintain BP and tissue perfusion to vital organs ▪ *Pediatric clients maintain BP until in profound shock* Hypotension in children= late sign ▪ Increased respiratory rate, tissue hypoxia in non-vital organs, decreased bowel sounds ▪ Acidosis and hyperkalemia • Stage 2: Intermediate or Progressive Shock (decompensation: impending doom) o Sustained decrease in MAP more than 20 mmHg from baseline o Compensation mechanisms remain in place; unable to perfuse vital organs- hypoxic o Life-threatening stage; needs immediate intervention o Sodium-Potassium pump fails o HR and vasoconstriction increase, perfusion decreases (heart and brain become hypoxic//other body systems become ischemic and anoxic) o Correction to condition causing shock corrected within 1 hour of onset of progressive shock • Stage 3: Refractory or Irreversible Shock o Anoxia becomes too great for treatment; body no longer responds effectively to interventions o Even if MAP is restored too much cell death to maintain life o Cell death  tissue death  organ death  death of body • Causes of Shock o Problem with heart- cardiogenic o Loss of fluids- hypovolemic o Problem with vascular system- distributive o Condition blocking flow to/from heart- cardiac obstructive • Diagnostic Testing: o Hemoglobin and Hematocrit: concentration- low: hemorrhage; high: dehydration o ABGs: decrease in pH (acidosis), decrease in O2, and increase in CO2 o Serum Electrolytes: shock progression: glucose decreases, sodium decreases, potassium increases o BUN/ Creatinine, Urine Specific Gravity, Osmolality: renal function; decreased renal function= decreased renal perfusion; all values will increase o Blood Cultures & WBC Count: sepsis; CBC with differential o Serum Cardiac Enzymes: elevated with cardiogenic shock: lactate dehydrogenase, creatine phosphokinase, & serum glutamic-oxaloacetic transaminase o Central Venous Cath: information regarding preload of heart, cardiac dynamics, fluid balance, medication effects • Treatment: o Pharmacologic Therapies o Oxygen Therapy o Fluid Replacement: increase blood volume & tissue perfusion; Normal Saline, Lactated Ringers o Narrowing pulse pressure (except septic-wide pulse pressure; vasodilation) o “Fill the tank then press it”: restore perfusion, then give pressor Compensated Shock: stage during which interventions and rapid transport are most effective Decompensated Shock • Tachycardia (HR 100) • Delayed capillary refill • Pallor • Anxiety, agitation, restlessness • Shallow, rapid breathing (tachypnea) • Shortness of breath • Nausea or vomiting • Weak pulse • Clammy skin • Marked thirst • Feeling of impending doom • Altered mental status • Falling blood pressure • Labored, irregular breathing • Ashen, mottled, cyanotic skin • Thready or absent pulse • Dull eyes, dilated pupils *obvious signs and symptoms; patients move rapidly to death; no vascular resistance can maintain adequate circulation * critical organs are hypoperfused Hemodynamic Pressure Monitoring: assesses cardiovascular functioning • Measures pressure within vessels; HR, arterial blood pressure, central venous or right atrial pressure, pulmonary pressure, cardiac output • Intra-Arterial Pressure Monitoring: inserted directly into artery o allows for direct and continual systolic, diastolic, blood volume, and MAP monitoring o allows for easy ABG and blood gas sampling; allows for monitoring of vasoactive drugs ▪ Arterial BP: • CO- blood volume and ability of ventricles to fill and pump blood • SVR: systemic vascular resistance- vessel diameter; affected by RAAS, SNS input, hormones (epi, norepi, ANP, vasopressin) ▪ MAP: average pressure in arteries throughout circulation during cardiac cycle; MAP= COxSVR • Calculated by: 1/3 of pulse pressure to diastolic BP • Decreased organ perfusion- MAP 50 or less • Hypertension or Vasoconstriction- MAP of 105+ • Venous Pressure Monitoring: (CVP and right atrial pressure): measures of blood volume, venous return, and right-heart filling pressures o Primarily: monitor fluid volume status o Measuring venous and atrial pressure: catheter inserted into Internal Jugular Vein or Subclavian Vein o Right- Sided HF: pressures are elevated o Normal Values: 2-6 mmHg ▪ Decreased: hypovolemia and shock ▪ Increased: fluid overload, vasoconstriction, and cardiac tamponade • Pulmonary Artery Pressure Monitoring: PA catheter swan-ganz catheter o Evaluates left ventricle and cardiac functioning ▪ Inserted in Internal Jugular Vein or Subclavian Vein into Right Atrium right ventricle  pulmonary artery  small branch of vasculature • Measures pressure of: right atrium, pulmonary artery, left ventricle ▪ PAWP- pulmonary artery wedge pressure: used to assess left ventricular function • Normal Values: 8-12 mmHg o Decreased: hypovolemia o Increased: left ventricle failure, pericardial tamponade ▪ Cardiac Index: CO per square meter of body surface area Signs and Symptoms of Shock: (most common for all shock) • Pallor; cold, clammy skin • Feeling of sickness and weakness • Restlessness, anxiety, confusion, depression, apathy • Low BP, rapid HR, weak pulse • Rapid, shallow breathing • Unconscious • Thirst Irreversible Shock: terminal stage of shock • Damage to cells and organs death will ultimately occur • Aggressive resuscitation & transfusions will NOT be enough to save a life Multiple Organ Dysfunction Syndrome • Sequence of cell damage: massive release of toxic metabolites and enzymes o Metabolites release from dead cells o Microthrombi form o MODS: first in liver, heart, brain, and kidney EXEMPLAR: Hypovolemic Shock What is it? - Low fluid volume: blood or fluids What causes it? - Dehydration: burns, loss of fluid - Hemorrhage (substantial blood loss= 1,000 mL) How will it present? - affects all body systems - tachycardia, Pulse: slight increase  rapid, thready pulse - low BP - vasoconstriction; cool, pale, clammy skin - altered LOC - cyanosis, oliguria to anuria Risk factors: - older adults, babies, pregnancy - high risk lifestyle Nursing Care: - monitor PT/INR, platelet counts, aPTT - PT: 10-15 s./ INR: 1-1.2 s. - Platelets: 150-400K - aPTT: 35 s. - restore fluids with NS or Lactated Ringers (no liver failure patients)