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Blood is shunted away from the skin, muscle, and GI tract and goes to the heart, brain, and kidneys Etiology Heart – heart fails to pump blood efficiently enough to keep vascular container filled Blood – serous loss of blood Blood vessels – dilation of blood vessels Compensated vs. Decompensated Compensated Compensated shock is when the body’s responses keep the circulatory system functioning at normal or near normal levels. Clinical Manifestations Tachycardia Tachypnea Decreased urinary output Skin pale and mottled, extremities cool Increased capillary refill time AMS – 1st sign of decreased O2 to the brain Decompensated Decompensated shock is when circulatory system begins to fail despite efforts to compensate Clinical Manifestations Skin pale Weak rapid pulse N/V and thirst – GI system slows down because blood is being shunted away Decreased level of consciousness Hypotension Decreased capillary refill Dilated pupils Severe acidosis – respiratory and then metabolic Oliguria/anuria Tachypnea – shallow, rapid breathing Hypovolemic Shock Hypovolemic shock is decreased intravascular volume leading to multiple organ failure due to inadequate perfusion. Decreased blood is the etiology, leading to decreased preload and cardiac output. Can be due to loss of blood, plasma, or fluid and electrolytes. Hemorrhagic is due to trauma. Non-hemorrhagic is due to diarrhea, vomiting, burns, and dehydration. Clinical Manifestations CNS – AMS Skin – pale, dusky, clammy skin with cyanosis and diaphoresis Renal – decreased urine output CVS – tachycardia, weak pulses Respiratory – tachypnea, shallow breathing GI – mesenteric ischemia Metabolic – respiratory acidosis, followed by metabolic acidosis Retinal hemorrhages, cotton wool spots, and conjunctival petechiae Diagnosis CBC, platelets Electrolytes BUN/Cr UA Lactic acid level D-dimer, fibrinogen, fibrin split products – DIC Radiological diagnostic tests Pregnancy test in females – r/o ruptured ectopic pregnancy Management ABCs Intubation/oxygen Control hemorrhage IV hydration/resuscitation including fluid bolus – 20-40cc/kg over 10-20min. Cross matched blood Treat acidosis with ventilation and fluids Vasopressors only after fluid challenge – Dobutamine for BP >100; vasodilator, which reduces preload and afterload. Good for CHF patients. No renal effect. Dopamine for BP 70-100; inotropic and vasopressor effects. Lower doses produce renal and mesenteric vasodilation. Higher leads to cardiac stimulation and renal vasodilation, which increases HR and myocardial O2 demand. Dopamine does not cross the BBB. 10mg/kg/min produces vasoconstriction. NE is only used for severely decreased BP (<70) Cardiogenic Shock Cardiogenic shock is due to decreased pumping ability of the heart. Decreased contractility reduces ejection fraction and cardiac output. Etiology Systolic dysfunction – MCC is MI Diastolic dysfunction – cardiomyopathy Valvular dysfunction – mitral regurgitation Cardiac arrhythmias – VT/VF CAD – anterior wall MI PE – due to RVH Clinical Manifestations Signs of MI Pulmonary edema if RVH or JVD if RVH S3 from CHF AMS Pale cool skin Hypotension Tachycardia Decreased urine output Diagnostics Cardiac enzymes CBC Electrolytes Coagulation profile EKG Echo Management ABCs MI – treat with ASA and heparin Vasopressors – Dopamine and Dobutamine (used more for CHF manifestations) NE for severe cases NTG once BP is controlled Intra-aortic balloon pump – decreases afterload, increases cardiac output and coronary perfusions Prognosis 80% will result in death Distributive Shock Distributive shock is abnormal distribution of vascular volume due to changes in vascular resistance or permeability. Decreased vascular tone leads to vasodilation. Leads to decreased ventricular filling and inadequate cardiac output. Includes septic shock, anaphylaxis, and neurogenic shock Septic Shock Sepsis usually starts as bacteremia from gram -/+ bacteria. Bacteria release exogenous toxins which result in peripheral vasodilation and loss of vascular tone. Might not respond to volume replacement. SIRS(sepsis(septic shock(MOSF Clinical Manifestations Warm/flushed extremities Specific manifestations depend on underlying etiology Fever/afebrile Hypotension, oliguria, and lactic acidosis Cardiac output – normal or increased Can lead to ARDS, DIC, and organ failure SIRS – fever >38, hyperventilation, tachycardia, increased WBC Sepsis – SIRS with positive blood culture Diagnostics Neutropenia, thrombocytopenia, DIC – more common to have DIC with gram negative sepsis Hyperglycemia – catecholamines release sugar Culture for CSF, sputum, blood, urine, and wounds – find underlying etiology CT for occult infection Management Broad spectrum IV antibiotics Surgical drainage if abscess Fluid administration Vasopressors – Dopamine and NE Prognosis #1 reason for ICU deaths Neurogenic Shock Neurogenic shock is failure of sympathetic nervous system to maintain vascular tone. Leads to pooling of blood with no actual blood loss. Etiology is spinal cord injury, spinal anesthesia, severe head injury, and sympatholytics. Clinical Manifestations Warm skin Decreased urine output Bradycardia, hypotension, normal cardiac output Management IV fluids Vasoconstrictors cautiously Elevate feet to increase preload Obstructive Shock Obstructive shock is due to extra-cardiac obstruction of blood flow. Leads to decreased preload. There is a problem in filling the right or left ventricle, leading to decreased cardiac output. Includes systemic circulation obstruction (vena cava), pulmonary obstruction (pulmonary embolism), and pericardial disease (tamponade, tension pneumothorax). Management Pulmonary embolism – thrombolytics Pericardial tamponade – IV fluids, pericardiocentesis Tension pneumothorax – immediate chest decompression Pulmonary HTN - vasodilators Psychogenic Shock Psychogenic shock is dilation of blood vessels leading to disruption of blood flow to the brain and syncope. Usually due to fear, bad news, or disturbing sights. Self-resolving. Acute Coronary Syndromes In acute coronary syndromes (ACS), O2 supply does not meet demand, which is determined by preload, afterload, HR, BP, and contractility. CAD is the leading cause of death among adults in USA and inadequate blood flow to myocardium. Leads to ischemia Risk Factors HTN High LDL Low HDL Smoking DM Family history of MI <55 years Elderly Males Cocaine Types Unstable angina – irregular atherosclerotic plaque ruptures leading to thrombus formation, increased platelet activity, and vasospasm. Leads to occlusion. Usually progresses to MI. AMI is injury and necrosis to heart muscle second to prolonged ischemia. ST elevation MI is full thickness or transmural necrosis (Q wave infarcts). Non-ST elevation MI is incomplete coronary artery occlusion. Ischemia to the innermost layers of the myocardium (non-Q wave MI) Thrombus or plaque breaks off and enters coronary artery – MC is right coronary Clinical Manifestations Angina pectoris – substernal chest pain/epigastric that occurs during exertion and relieved by rest or nitrates. Described as pressure/squeezing/tightness Unstable angina/MI – new onset of chest pain, episodes of angina more frequent, last longer, not relieved by meds, chest pain while at rest, SOB, diaphoresis, Levine’s sign, n/v, and back pain Arrhythmias – tachy/bradyarrhythmias, VT/VF HTN or hypotension Systolic murmur, S3/S4 CHF – rales bilaterally. 40% loss of LV function presents with cardiogenic shock Right ventricle MI – JVD Anterior injury – tachyarrhythmia, Mobitz II, and complete heart block Inferior injury – increased vagal tone, first degree and 2nd type I blocks Diagnostics EKG – ischemia is ST depression and T wave inversion. Injury is ST elevation >1mm Cardiac enzymes – CK-MB should be monitored over 8-12 hours. Troponin I stays elevated longest. Myoglobin is not effective because it is present in all tissue Echo, coronary angiography CBC, electrolytes, CXR Management ABCs IV access/monitor vitals/oxygen Aspirin or other antiplatelet drugs Heparin – prevent progression. Use LMWH NTG if BP >8 – dilate coronary arteries and dilates veins as well as decrease preload Morphine post 3 NTG – provides analgesia ACE-I Beta-blockers – propranolol, Atenolol Revascularization – ST elevation should receive revascularization Thrombolytics – convert plasminogen to plasmin. TPA is mainly used. Must use within 4-6 hours of symptoms. 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„„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ5o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţ5o()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ „€„˜ţĆ€^„€`„˜ţ‡hˆH.‚ „P„L˙ĆP^„P`„L˙‡hˆH.„Đ„˜ţĆĐ^„Đ`„˜ţo()€ „ „˜ţĆ ^„ `„˜ţ‡hˆH.‚ „p„L˙Ćp^„p`„L˙‡hˆH.€ „@ „˜ţĆ@ ^„@ `„˜ţ‡hˆH.€ „„˜ţĆ^„`„˜ţ‡hˆH.‚ „ŕ„L˙Ćŕ^„ŕ`„L˙‡hˆH.€ „°„˜ţĆ°^„°`„˜ţ‡hˆH.€ 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