Shock Lecture Notes PDF

Shock Lecture 19 Unit 3 Table of contents 1. Introduction 2. Cardiogenic shock 3. Hypovolemic shock 4. Distributive shock 5. Obstructive shock 1. Introduction Categories of shock - there are four types of shock : cardiogenic, hypovolemic, distributive, and obstructive. - diagnosin...

Shock Lecture 19 Unit 3 Table of contents 1. Introduction 2. Cardiogenic shock 3. Hypovolemic shock 4. Distributive shock 5. Obstructive shock 1. Introduction Categories of shock - there are four types of shock : cardiogenic, hypovolemic, distributive, and obstructive. - diagnosing shock depends on a few key measures: - shock index (HR/systolic BP) > 1 - blood lactate levels > 2 mmol/L - additional information is required to diagnose the type of shock 3 2. Cardiogenic shock SVR = systemic vascular resistance Characteristics - occurs when the heart pumps inefficiently. - despite normal vascular volume (and normal BP early on), the following occurs: SV= preload - afterload *cardiac output* CO= HR x SV if afterload increases= stroke volum decreases CO decreases leading to hypotension. - etiology: 1) mechanical (myocardial infarction, heart failure, blood backs up heart contusion, valvular regurgitation, cardiac tamponade) or 2) arrhythmogenic (arrhythmias, bradycardia or extreme tachycardia) = tachycardia inficcient because not enough time to fill up blood between 4 2. Cardiogenic shock Characteristics - mechanical and arrhythmogenic causes affect the efficiency of the heart’s activity. - a decrease in CO results from a dec. in heart contractility or an inc. in afterload. - to compensate, adrenal stimulation releases E and NE to inc. HR , but this also causes vasoconstriction (inc. the afterload). decrease SV overtime cardiac hypertrophy -> death - low BP causes renin release and angiotensin II triggers more vasoconstriction, further affecting afterload. 5 2. Cardiogenic shock diastolic = how much blood overall in blood Characteristics - when coronary artery perfusion is impaired, cardiac function worsens. - signs and symptoms include cyanotic nail beds and lips, dec. in systolic BP (but normal diastolic BP). output is dec. due to dec. renal perfusion and - urine RAAS activation. - insufficient perfusion of neural tissue can cause encephalopathy (confusion, lethargy). part of multi organ failure 6 2. Cardiogenic shock Treatment - cardiac output is commonly improved by increasing stroke volume; not by increasing contractility but by dec. afterload and/or maintaining adequate cardiac tissue perfusion. - manipulating contractility increases in oxygen demand by the heart, which should be avoided in certain patients. - two intervention types include 1) surgery and 2) pharmacological. 7 2. Cardiogenic shock Treatment: surgical interventions - intra-aortic balloon pump (i.e. counterpulsation) can improve cardiac perfusion and afterload. - a balloon is inserted into descending aorta via catheter and inflated during ventricular diastole and deflated during ventricular systole. balloon is battery powered - inflation during diastole ensures more blood reaches the cardiac tissues ; deflation during systole ensures adequate ventricular ejection.. - valve replacement is required in patients with aortic or Mitral regurgitation. 8 2. Cardiogenic shock inotropes = impact contractility Treatment: pharmacological interventions - vasodilators (nitroprusside or nitroglycerin) can dilate systemic arteries to dec. afterload and improve stroke volume. - in patients where cardiac perfusion is not a problem, positive inotropes can improve SV by inc. cardiac contractility; dobutamine and milrinone do this AND cause arterial vasodilation. 9 2. Cardiogenic shock Treatment: pharmacological interventions chronotropes = impact heart rate - arrhythmias causing tachycardia may require cardioversion (electrical synchronization) or negative chronotropes. - arrhythmias causing bradycardias may require a pacemaker or positive chronotropes. - arrhythmias caused by medication overdose (beta-blockers or calcium channel blockers) require antidotes (glucagon or calcium gluconate). 10 3. Hypovolemic shock Characteristics - occurs due to diminished blood volume , i.e. inadequate filling of vascular compartment. - hypovolemic shock occurs when at least 20% of total vascular volume is lost. - acute vascular volume loss occurs due to 1) loss of fluids from GI tract (vomiting, diarrhea, NG suctioning), 2) excessive skin loss (diaphoresis, burns), 3) renal losses (abuse of diuretics), and 4) blood loss (GI bleed, uterine bleed, trauma, triple A rupture). Triple A= abdominal aortic aneurysm 11 3. Hypovolemic shock mean arterial pressure, important because signifies how much blood can perfuse tissues Characteristics - as blood volume falls, SV falls while arterial pressure is initially maintained. - pressure is maintained due to sympathetic-triggered inc. in HR and vasoconstriction. - dec. SV with inc. vasoconstriction initially causes diastolic pressure to inc. while systolic pressure remains the same. - CO falls and hypoperfusion occurs before hypotension is apparent; after 35-45% blood loss, CO and arterial pressure fall to zero. 12 3. Hypovolemic shock SV= preload - afterload Compensatory mechanisms preload is decrease =SV decreased - most immediate (within minutes) is sympathetic activation to inc. CO and maintain BP. - specifically, tachycardia, inc. cardiac contractility, vasoconstriction ; E/NE release can further stimulate cardiac output. - as long as arterial pressure remains above 70 mmHg, the brain and heart can remain adequately perfused. 13 3. Hypovolemic shock Compensatory mechanisms - early maintenance mechanisms work to move interstitial fluid into plasma , while later compensatory mechanisms further inc. vascular volume: - endocrine response to conserve water and sodium by the kidneys. ALD + ADH / RAAS activation - trigger the thirst reflex. 14 3. Hypovolemic shock Compensation: how and why? - as vascular volume decreases … capillary hydrostatic pressure dec. , decreasing filtration; this results in greater reabsorption. - glomerular filtration dec. , triggering renin release (and ALD and ADH release) to inc. water (RAAS) and sodium retention. - osmoreceptor activation inc. ADH release and the thirst reflex. 15 3. Hypovolemic shock As blood loss progresses… - vasoconstriction continues in the skin, muscles, and abdominal organs. - this leads to anaerobic respiration and cellular injury. 16 3. Hypovolemic shock Signs and symptoms - somewhat proportional to amount of blood lost. - thirst, inc. HR, cool and clammy skin, dec. arterial pressure, dec. urine output, and changes in mentation. - lab tests will monitor hemoglobin levels and hematocrit to assess severity of blood loss. - acute fatal hemorrhagic shock occurs due to metabolic acidosis, coagulopathy, and hypothermia. 17 3. Hypovolemic shock Signs and symptoms - inc. HR is an early sign of hypovolemic shock. - BP is acutely preserved as CO is maintained and vasoconstriction occurs. - as shock progresses , resp. rate inc. and breaths become deeper due to hypoperfusion and acidosis. - restlessness occurs due to intensifying sympathetic activation; this progresses to dec. mentation. 18 3. Hypovolemic shock Treatment - controlling underlying cause and restoring perfusion are key. - surgical correction (of blood loss) and oxygen administration may be necessary. - frequent monitoring of HR, BP, and urine output are necessary. - immediate intravenous infusion of fluids and later, when stabilized, blood transfusion may be - necessary. plasma volume expanders can be used to inc. colloid pressure. 19 4. Distributive shock Characteristics - this type of shock occurs due to a drop in vascular resistance resulting from massive vasodilation from: 1) inadequate secretion of epinephrine and norepinephrine; and 2) inflammatory cytokine production. - there are three types: neurogenic shock , anaphylactic shock , and septic shock. 20 4. Distributive shock Neurogenic shock - as during spinal shock , brain injury , use of depressant drugs, anesthesia, hypoglycemia (as with an insulin reaction). - inability to stimulate the release of E/NE from the adrenal medulla. - unlike other types of shock, HR is lower than normal , and it is usually temporary. - treatment requires maintaining blood pressure by administering: phenylephrine, norepinephrine, epinephrine, or vasopressin. 21 4. Distributive shock Anaphylactic shock - occurs due to a severe systemic allergic reaction mediated by the release of vasodilators, like histamine. - arterial and venous dilation and inc. capillary permeability occur. - often accompanied by laryngeal edema , angioedema , hives , bronchospasm, uterine and GI smooth muscle contraction, and circulatory collapse. 22 4. Distributive shock Anaphylactic shock - causes include allergic reactions to medications (like penicillin), food, and venoms. - severity depends on intensity of allergy and level of exposure to the allergen. - epinephrine (i.e. Epipen) is administered first; causes vasoconstriction and dilates bronchi/bronchioles. - antihistamines can be administered next. - prevention is key. 23 4. Distributive shock Septic shock - it is associated with severe infection. - severe sepsis causes hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia, and obtundation. - septic shock occurs with severe sepsis and begins with hypoperfusion despite fluid replacement and can lead to… - a systemic inflammatory response, causing tachycardia, tachypnea, inc. body temp., inc. white blood cell count, and hyperglycemia. 24 4. Distributive shock Septic shock - infections will cause: 1) activation of neutrophils, monocytes, and endothelial cells, 2) the release of proinflammatory mediators , 3) neuroendocrine reflexes (HPA axis and sympathetic activation) and 4) activation of complement and coagulation and inhibition of fibrinolytic systems. 25 4. Distributive shock Septic shock: manifestations - hypotension occurs due to dec. in vascular resistance. - edema occurs due to endothelial damage, which inc. capillary permeability. - metabolic acidosis occurs due to hypoxia, causing inc. levels of anaerobic respiration. - altered cognition occurs with reduced cerebral blood flow. 26 4. Distributive shock Septic shock: treatment - inflammation and infection must be managed, and oxygen administration can prevent cellular injury. - fluid administration is necessary to counter vascular fluid loss. - vasoconstrictive agents counter inflammatory vasodilatory compounds. - positive inotropes can inc. CO to inc. tissue perfusion. 27 5. Obstructive shock Characteristics - occurs from a mechanical obstruction of blood flow through the great veins, heart, and lungs. - drop in preload or increase in afterload causes a drop in SV and CO; thus, dec. in blood pressure. blocks blood from going to left side of heat - common causes include : pulmonary embolism, cardiac tamponade and tension pneumothorax. fluid in pericardial space lungs compress heart 28 5. Obstructive shock Characteristics - primary manifestation is elevated right heart pressure, due to impaired right ventricular function. - other signs include inc. central venous pressure and jugular vein distension. - treatment includes surgical intervention: embolectomy, pericardiocentesis, or chest tube insertion. 29 6. Multiorgan system failure Due to ischemia of major organs - metabolic acidosis due to lactic acid production causes tachypnea. - encephalopathy causing cognitive impairment. - NSTEMI due decreased perfusion of cardiac tissues. - acute kidney injury causing oliguria, inc. creatinine, and uremia. - abdominal pain due to acute mesenteric ischemia. - ischemic hepatitis causing elevated liver function test results. 30 Overview Types of shock Manifestations caused by: Body’s reflexive response to ↓ BP Comments: Decreased stroke Massive Vasoconstriction Increase HR volume vasodilation Cardiogenic ✔ ✔ ✔ Exceptions: AV block, beta-blocker overdose Hypovolemic ✔ ✔ ✔ Obstructive ✔ ✔ ✔ Neurogenic ✔ Commonly see bradycardia Anaphylactic ✔ ✔ Septic ✔ ✔ 5. Review Questions - What are the stages of shock and their associated symptoms? - How is blood pressure maintained during compensated shock? - What are the series of events that cause a patient to go decompensated? - What is irreversible shock? - What are the differences between hypovolemic, cardiogenic, obstructive and disruptive shock? - What is the etiology, compensatory mechanisms, manifestations and treatments for all types of shock? 32