Shock Huether McCance Ch 26 pp. 624-634 NURS 280/403 – Pathophysiology & Pharmacology I Material is intellectual property, developed solely for use by respective course students. Not to be shared or posted to any platform without faculty consent and permission. Shock • • • • Cardiovascular system fails to perfuse the tissues adequately Inadequate blood flow throughout the body, to the extent that tissues are damaged Even the heart muscle, BV walls and other circulatory parts begin to deteriorate Leads to impaired cellular metabolism • Impaired oxygen use • Cells shift to anaerobic met to extract energy, less efficient lactic acid buildup tissue damage • Na-K+ pumps cannot operate Na/H2O accumulate in cell edema cell injury • Water drawn from intravascular space less circulatory volume • Impaired glucose uptake by cells • • • • Stress hormones & catecholamines released hyperglycemia Fat breakdown to generate fuel Energy stores get depleted after 10 hrs Buildup of toxic end products protein breakdown toxic levels ammonia & urea • Manifestations based on type, often include: • Feeling weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath • Hypotension, tachycardia (but CO & tissue perfusion decrease), increased respiratory rate Impaired Cell metabolism in Shock Patho cont. • 3 stage progression • Compensatory • Tissue perfusion deficient, but not to the degree where cardiovascular system deteriorates • Progressive • Circulatory system begins to deteriorate, compensation fails, leading to a vicious cycle ending in death unless appropriate treatment started. • Irreversible • Has progressed to the point where all treatment inadequate to save person’s life • Organ damage • Respiratory & cardiac failure Types of Shock • Types are classified by cause • • • • • Cardiogenic: heart failure Hypovolemic: insufficient intravascular fluid volume Neurogenic: neural alterations of vascular smooth muscle tone Anaphylactic: immunologic processes Septic: infection Cardiogenic Shock Causes: MI, left vent HF, dysrhythmias, ventricular rupture, myocardial/pericardial infections, massive PE Heart fails as a pump due to decreased contractility Coronary circulation decreases Myocardium further damaged More pump failure Adaptive mechanisms increase heart’s demands for oxygen & nutrients, which further strain the heart Heart can no longer pump adequate volume Result: shock and impaired metabolsim Hypovolemic Shock This type of shock becomes life-threatening when compensatory mechanisms (in orange boxes) are overwhelmed by continued loss of intravascular volume. • Hypovolemic shock • Burns ~ risk • External blood volume losses (hemorrhage, dehydration,) ~ VR, preload, SV, CO • Brief initial rise in BP • release of epi (SNS response) • Liver & spleen add volume by letting out RBCs & plasma • If inadequate compensation decreased perfusion to tissues and organs • Sx: • poor skin turgor, thirst, oliguria, tachycardia when lying sitting & later becomes thready pulse • mental status deterioration, brief initial rise in BP due to increased release of epi, decreased UO hypotension, collapsed neck veins (decreased VR to heart) , poor cap refill, • Anxiety (hyperactive SNS, lack of O2 to brain), decreased pulse pressure, pale moist cool skin • Tx: rapid fluid replacement, blood products, oxygen Neurogenic shock • • • • • • • • Causes: deep gen/spain anesthesia, brain damage, psinl cord injury Widespread massive vasodilation Parasympathetic stimulation Sympathetic inhibition of VSM Causes: trauma to spinal cord, medulla, depressive drugs, anesthesia Blood volume normal but SVR decreases drastically Amount of space containing blood increases Low pressure in vessels nothing to drive nutrients from cap membranes cells Anaphylactic Shock Septic Shock • Bacteria enter blood & are destroyed bu macrophages & other immune cells & complement system • Endotoxins released • Inflammatory mediators released by macrophages • Massive vasodilation & low blood volume • BVs become more leaky
