NRS 225 Perfusion- Shock, Cardiomyopathy, DIC

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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)