Circulatory Shock

Review key cardiovascular physiology terms: Cardiac output & vascular function curves Cardiac output (HR & SV) Intrinsic blood flow regulaiton Baroreceptor reflex Shock is the state in which reduced cardiac output, vasodilation, or low blood volume leads to tissue hypoperfusion and cell death. Four types of shock: – Distributive, which is the most common form – Hypovolemic – Cardiogenic – Obstructive (which is the least common). Be aware that these types of shock can co-exist in a patient. Three stages of shock: – Nonprogressive (aka, compensated) – Progressive – Irreversible Treatment can generally be summarized with the acronym VIP: – Ventilate (administer oxygen) – Infuse (administer fluids) – Pump (administer vasoactive agents that facilitate circulatory pumping). Be aware that the treatments can vary by type of shock and the underlying causes; for example, in some cases, fluid infusion can cause more harm than good. Reperfusion injury: Reperfusion of the tissues can cause additional injury due to increased production of superoxide and hydroxyl radicals. Multiple organ dysfunction syndrome: Aka, multiple organ failure describes the progressive dysfunction of two or more organs. Nonprogressive stage is characterized by physiological adaptations that compensate for the effects of shock and allow for recovery. – Compensation relies on negative feedback mechanisms that respond to low tissue perfusion by increasing cardiac output and/or increasing arterial pressure to ensure adequate blood supply. Progressive stage is characterized by positive feedback mechanisms in which shock facilitates the progression of shock. – Reduced blood supply to the myocardium weakens the heart's ability to contract. – Sustained lack of blood to the brain leads to depression of the vasomotor center, which leads to loss of sympathetic activation. – As a result of slow flow and buildup of metabolic wastes, blood in the small vessels begins to agglutinate and obstruct flow. – Hypoxic capillaries become leaky, and release fluid into the tissues; this exacerbates low blood volume and cardiac output. – Ischemic tissues and/or bacteria release toxins that cause further cell damage. – As a result of hypoxemia, the tissues begin to break down, especially in the liver, lungs, and myocardium. – Because the tissues are malfunctioning, acidosis develops. Lactic acid is especially elevated as tissues shift to anaerobic metabolism, which is why we measure lactic acid levels in suspected cases of shock. Irreversible stage is fatal – a patient cannot be saved, even with medical intervention, because the high-energy compounds necessary for cellular functioning are depleted. – Thus, early recognition and treatment of shock is crucial for saving a patient's life. Consider how the following signs and symptoms are predictable given the causes and effects of shock. Shock leads to low arterial pressure. – However, be aware that hypotension may be minimal, initially, due the body's physiological responses to reduced blood pressure, such as increased sympathetic activity. Altered mental states, such as confusion, can develop when brain doesn't receive sufficient oxygen. Tachycardia can occur due to increased sympathetic activity. Lactic acid levels rise because the cells shift to anaerobic metabolism. Skin changes are common, and depend on the cause of shock, but can produce clamminess, flushing, cold, or other changes. Oliguria is common due to reduced renal perfusion. Important things to keep in mind are:

• Different types of shock can overlap.
• Discovery of the underlying cause is key to treatment.
• Shock can be volume-related or output-related.

Volume-Related Causes Distributive Shock: shift in distribution of blood volume. Septic shock is the most common form of all shock types; it is the result of bacterial infection. Anaphylactic shock is the result of a severe allergic reaction; bee stings, foods such as peanuts, latex, and some medications are among the most common causes of anaphylactic shock. Neurogenic shock can occur; this is most often the result of trauma to the CNS. Hemodynamic changes: Each of these types of distributive shock induce significant vasodilation. To remember this, recall that vasodilation is triggered by various toxins (i.e., bacteria), inflammation (i.e., allergy), and suppression of the sympathetic nervous system (i.e., CNS). Distributive shock is often associated with normal, or even high, cardiac output due to high venous return (which is, itself, due to the vasodilation). As we'll see, high cardiac output is unique to distributive shock. Preload is reduced due to capillary leakage and transfer of fluid from the intravascular to the extravascular tissues. Skin changes: Distributive forms of shock often produce flushing of the skin. More specifically, the skin of patients in anaphylactic shock are often warm and itchy (think of an allergic reaction). patients with septic shock experience fever and chills; and, patients in neurogenic shock typically have dry skin. Treatment: Administration of fluids and vasopressors to increase cardiac output and arterial pressures; epinephrine is given for anaphylactic shock. Hypovolemic shock: loss of blood volume Associated with internal or external hemorrhaging, severe burns, very low fluid intake, and vomiting or diarrhea (recall that dehydration, and, therefore, hypovolemic shock are particularly common in sick children in low-income countries). Hemodynamic changes: Preload and cardiac output are reduced; to compensate for low blood volume, systemic vascular resistance increases (via vasoconstriction and fluid retention). Skin Changes: Cold, clammy skin Treatment: administration of fluids and controlling the bleeding or fluid loss. Output-Related Causes Cardiogenic shock: structural/mechanical problems in the heart. Results form cardiac defects that produce abnormal contractility, rhythm, or structures; thus, common causes are myocardial infarction, arrhythmias, valve dysfunctions, and drugs. Hemodynamic changes: Dysfunctional pumping reduces cardiac output, and, as in hypovolemic shock, systemic vascular resistance increases*** in response to low arterial pressure. Preload, however, may increase. Skin: Cold and clammy. Treatment: Underlying causes must be treated, and vasopressors or inotropes may be provided to improve blood pressure and flow. Obstructive shock: extracardiac causes, including cardiac tamponade, pulmonary embolism, and tension pneumonothorax. Cardiac output is reduced as a result of extracardiac obstructions that inhibit ventricular filling or emptying. Systemic vascular resistance increases, but preload is variable. Skin: Cold and clammy. Treatment: Remove the obstruction, administer medications to improve blood pressure and flow.