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AMS shock/renal
| Question | Answer |
|---|---|
| Shock | syndrome characterized by decreased tissue perfusion and impaired cellular metabolism→ IMBALANCE between SUPPLY and DEMAND of oxygen and nutrients |
| in shock when a Cell experiences hypoperfusion | demand for oxygen/nutrients > supply |
| Goal to prevent shock: | • Cardiac output • Uncompromised vascular system (without HTN, vasoconstriction, atherosclerosis) • Sufficient volume of blood (no 3rd spacing) • Tissues about to extract and use O2 |
| in shock Tissues about to extract and use O2; Best measurement of this is SvO2 | allows us to measure the oxygen consumption at the cellular level. Want to keep the level above 70%. This is not always a guarantee that the cells extract the O2 they need, because sometimes the cells have trouble extracting O2 |
| in shock Widespread abnormal cellular metabolism that occurs when | oxygenation and tissue perfusion needs aren’t met to the level necessary to maintain cell function |
| “Syndrome” bc | the cellular, tissue, and organ events occur in a predictable sequence |
| in shock All body organs are affected and either | work harder to adapt and compensate for reduced oxygenation or fail to function bc of hypoxia |
| Compensation of shock | o Tissue and organ perfusion is r/t to MAP o Dilation: relaxing smooth muscle in vessel walls o Vasoconstriction: decrease in diameter by contracting the muscle |
| Factors that influence MAP | total blood volume, CO, size of vascular bed; • Increase in the size of vascular bed LOWER map and decreases raise MAP |
| When blood vessels dilate and total blood volume remains the same | BP decreases and blood flow is slower |
| When blood vessels constrict and total blood volume remains the same | BP increases and blood flow is faster |
| MAP | • the average pressure in the arterial circulation throughout the cardiac cycle (COxSVR) |
| SNS | • maintains the smooth muscle surrounding arterioles in a state of partial contraction or sympathetic tone |
| Pulse pressure | the difference between the systolic and diastolic BP is often an early indicator of shock--> narrowed |
| SV | • amount of blood pumped into the aorta with each contraction |
| Want to keep the O2 consumption | o greater than or around 70% |
| o Low Blood Flow shocks | • Cardiogenic: due to pump failure • Hypovolemic: decreased body fluid |
| Maldistribution of blood flow: | o volume isn’t lost, just misplaced – 3rd spacing • Septic • Anaphlyactic • Neurogenic: |
| • Cardiogenic shock: | • either systolic or diastolic dysfunction of the pumping action of the heart results in compromised cardiac output o Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. |
| o Hemodynamic criteria for cardiogenic shock are: | • sustained hypotension (systolic blood pressure <90 mm Hg for at least 30 min • reduced cardiac index (<2.2 L/min/m2) • elevated pulmonary artery wedge pressure (>15 mm Hg). |
| Systolic dysfunction: | o hearts inability to pump the blood forward • Primarily affects left ventricle because systolic pressure and tension are greater on the left side • When it affects the right side→ blood flow through pulmonary circulation is compromised |
| Decreased CO→ | • poor tissue perfusion→ anaerobic metabolism→ shock |
| Causes Systolic dysfunction: | • MI, cardiomyopathies, blunt cardiac injury, severe systemic/pulmonary HTN, myocardial depression from metabolic problems |
| Diastolic dysfunction: | impaired ability of the R/L ventricle to fill during diastole→ results in decreased stroke volume→ increased pulmonary pressure→ pulmonary edema→ reduced area for gas exchange→ lack of oxygen to cells→ poor tissue perfusion→ anaerobic metabolism→ shock |
| Diastolic dysfunction: Causes: | • cardiac tamponade (fluids accumulate in pericardium) and cardiomyopathy |
| o Precipitating Causes CARDIOGENIC SHOCK | • Myocardial infarction • Cardiomyopathy • Cardiac tamponade • Dysrhythmias, valve changes • Severe systemic or pulmonary hypertension • Electrolyte imbalances |
| Clinical manifestations CARDIOGENIC SHOCK | tachycardia, HoTN, narrowed pulse pressure, increase in SVR, Low CO and cardiac index, tachypnea, crackles, increase PAWP and PVR, periperhal hypoperfusion--> cyanosis, pallor, cool and clammy, dec cap refill, decreased UO; anxiety, confusion, agitation |
| narrowed pulse pressure in cardiogenic shock | one of the first signs of shock |
| increase SVR in cardiogenic shock--> | • increase workload→ increase myocardial oxygen consumption |
| Increase in PAWP and pulmonary vascular resistance in cardiogenic shock --> | retention of fluid in left ventricle; eventually backs up enough to increase CVP, PA, etc. |
| Peripheral hypoperfusion in cardiogenic shock→ | cyanosis, pallor, cool and clammy skin, decreased capillary refill→ → SNS trying to redirect blood to vital organs |
| Decreased renal blood flow in cardiogenic shock → | sodium and water retention; decreased urine output(< 0.5 mL/kg/hr) |
| cerebral perfusion impaired in cardiogenic shock--> | anxiety, confusion, agitation |
| Collaborative Care: goal cardiogenic shock | o is to restore blood flow to myocardium by restoring the balance between O2 supply and demand |
| • Interventions: cardiogenic shock | • Thrombolytic therapy • Angioplasty with stenting • CABG • Valve replacement • Emergency revascularization • IABP or VAD • Hemodynamic monitoring • Circulatory assist devices(IABP, ventricular assist device) • Drug therapy |
| • Drug therapy: cardiogenic shock | o Diruetics to reduce preload o Beta blockers to reduce heart rate |
| • Hypovolemic shock | • loss of intravascular fluid volume; volume is inadequate to fill the vascular space; may be absolute or relative o Decrease in MAP of 5-10 mmHg |
| • Hypovolemic shock: ABSOLUTE | o loss of intravascular fluid volume >15% • fluid lost through hemorrhage • GI loss (V/D) • fistula drainage • diabetes insipidus • hyperglycemia • diuresis • burns(especially >25%) |
| • Hypovolemic shock: RELATIVE | o fluid into extravascular space= 3rd spacing • Increased capillary permeability→ sepsis • bowel obstruction • ascites • loss of blood volume into a fracture • burns • liver disease • pancreatitis • pleural effusion |
| pancreatitis in hypovolemic shock--> obstruction in bile duct→ | pancreas eats itself due to juices trapped inside |
| hypovolemic shock--> decreased venous return | dec cardiac output --> dec tissue perfusion -->impaired cellular metabolism --> shock |
| o Response to acute volume loss depends on: | • Extent of injury and severity of illness • Age (will respond differently to system problems) • General state of health • Rate of volume loss/treatment time |
| o Patient can compensate for a loss of up to | 15% of total blood volume |
| 15 to 30% blood volume loss | o SNS response = increased HR< CO and RR and depth; SV and PAWP decreased because of decreased circulating blood volume • anxiety • urine output decreased • if tx with crystolloids→ tissue dysfunction generally reversible |
| >30% fluid loss | o compensatory mechanisms begin to fail • tx: immediate blood or blood product replacement |
| >40% fluid loss | irreversible tissue destruction occurs |
| Hypovolemic shock Manifestations: Neuro | • anxiety, confusion agitation |
| Hypovolemic shock Manifestations: Lungs | tachypnea (the alveoli are not affected, but reducing the carrying capacity = hypoxemia) |
| Hypovolemic shock Manifestations: Cardio | increased in heart rate causes a brief increase in cardiac output. dec stroke volume, dec wedge pressure and dec urine output. |
| Hypovolemic shock Collaborative Care | o stop the loss of fluid and restore circulating volume • Fluid replacement is calculated using a 3:1 rule = 3mL of isotonic crystalloid for every 1mL of estimated blood loss. • Beta blockers to decrease HR |
| • Neurogenic shock | • hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at T5 or above and lasts up to 6 weeks |
| • Neurogenic shock Causes | • Head injury • Trauma to spinal cord: can occur within 30 mins of injury • Insulin reaction • CNS depressant drugs • Anesthesia: one of the most common reasons for this type of shock. • Severe pain |
| • Neurogenic shock Results in | o in massive vasodilation w/o compensation due to loss of SNS vasoconstrictor tone • Leads to pooling of blood in vessels, tissue hypoperfusion→ impaired cellular metabolism |
| • Neurogenic shock and spinal anesthesia | o that blocks transmission of SNS impulses or drugs that depress the vasomotor center of medulla (benzos, opioids)→ decreased vasoconstrictor tone of the peripheral blood vessels |
| • Neurogenic shock SNS | out of operation, which gives you tone to the vessel wall |
| • Neurogenic shock PNS | will take over (via vagus nerve) and causes vasodilation and dec in heart rate, dec BP, dec stroke volume, dec cardiac output. |
| • Neurogenic shock Manifestations | • BRADYCARDIA • HoTN • Initially= warm skin due to massive dilation w/o compensation • As the heart dissipates, pt is at risk for hypothermia • Poikilothermia→ skin temp regulates to external temp • Skin is dry |
| • Neurogenic shock BRADYCARDIA | unopposed parasympathetic stimulation |
| Neurogenic shock Poikilothermia | Inability to regulate temperature + vasodilation→ heat loss |
| Neurogenic shock Collaborative care | o treat hypotension & bradycardia • Use vasopressors and atropine • Fluids used cautiously as hypotension is not related to fluid loss • Use hypertonic crystalloids to move fluid back into vascular space (e.g. D10W) • Monitor for hypothermia |
| Hypertonic per Iggy for neurogenic shock | o D10W o D5NS o D5NS o D5LR |
| Spinal shock | not the same as neurogenic shock; transient condition that is present after an acute spinal cord injury→ will have absence of all voluntary and reflex neurologic activity below the level of injury |
| • Anaphylactic shock | acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance(drug, chemical, vaccine, food, insect venom) |
| • Anaphylactic shock Immediate reaction→ | o massive vasodilation, release of vasoactive mediators and increase in capillary permeability→ leaks from vascular space into interstitial space o Loss of blood vessel tone and decreased CO |
| • Anaphylactic shock Manifestations | • respiratory distress • circulatory failure→ vasodilation • dizziness, chest pain, incontinence, swelling of the lips, tongue, wheezing, stridor • flushing of skin, pruritis, urticaria and angioedema • anxiety, confusion, impending sense of doom |
| • Anaphylactic shock: Leads to respiratory distress | laryngeal edema or severe bronchospasm |
| • Anaphylactic shock: Collaborative care | • Give epinephrine and Benadryl(diphenyhydramine) • Maintain patent airway • Aggressive fluid replacement • IV corticosteroids if significant hypotension persists after 1-2 hours of aggressive therapy |
| • Anaphylactic shock: Maintain patent airway | • Nebulized bronchodilators • ET intubation or ricothryoidotomy may be necessary |
| SIRS | physiologic response to a massive insult on the body (usually by infection-usually bacterial, but also trauma and burns). Septic shock can result from this situations |
| SIRS manifestations (patient needs to have any two or three of these): | o Fever of >100.4F (38C) or < 96.8F (36C) o Heart rate >90bpm o Respiratory rate of more than 20bpm or a PaCO2 <32mmHg o Abnormal white blood cell count - >12K or <4K o Immature WBCs >10% of bands |
| Sepsis | SIRS resulting from infection |
| Severe sepsis | sepsis + organ dysfunction |
| Septic Shock | presence of sepsis with hypotension despite adequate fluid resuscitation & inappropriate oxygenation to the tissues (poor perfusion) despite giving 100% O2 |
| MODS (multiple organ dysfunction syndrome) | is a state of physiological derangements in which organ function is not capable of maintaining homeostasis. |
| Septic shock begins with | septicemia ( bacteremia). As pathogens destroyed, ruptured cell membranes allow endotoxins to leak into the plasma. |
| endotoxins leak out and | they trigger immune and inflammatory response, disrupt the vascular system and coagulation mechanism. |
| Endotoxins damage | the endothelial lining of small blood vessels and cellular damage activates coagulation factor XII resulting in multiple intravascular clots. |
| in septic shock Capillary permeability and vasodilation leads to | fluid shift. Hypovolemia and intravascular coagulation lead to anaerobic metabolism, lactic acidosis and cellular death. |
| Disseminated Intravascular Coagulation | a generalized response to injury is manifested by simultaneous bleeding and clotting . Clotting slows circulation while stimulating fibrinolysis. This depletes clotting factors leading to generalized bleeding. |
| • Septic shock/sepsis Manifestations: | o Tachypnea & tachycardia o Temperature dysregulation o dec Urine output o Altered neurologic status o GI dysfunction (blood shifting to more vital organs) o Respiratory failure is common o Abnormal WBC > 12,0000 or <4,000; or >10% bands |
| • Early phase/Hyperdynamic: (warm):septic shock | o Increased CO and decreased SVR – first 24 hours o Vasodilation o Respiratory alkalosis develops (with tachypnea), and with respiratory tiring, the RR rate is reduces, anaerobic metabolism – respiratory and metabolic acidosis. |
| vasodilate in hyperdynamic state septic shock | results in weakness, and warm, flushed skin and septicemia causes fever→ chills |
| • Late phase/Hypodynamic (cold): septic shock | o hypovolemia and activity of the compensatory mechanisms result in decreased CO, cold, ashy, pale, moist skin, oliguria and LOC changes. |
| Labs septic shock | • show abnormal CBC: leukocytosis or leukopenia and elevated liver enzymes, C-reactive protein, alteration in clotting factor, creatinine levels. |
| SNS septic shock | • SNS response and blood shift from less important organs |
| Septic shock Collaborative care FIRST THING | Culture and then start broad spectrum antibiotics (within the first 3 hours) |
| Septic shock Collaborative care Fluid replacement | 6-10L of isotonic crystalloids and 2-4L of colloids to restore perfusion |
| Septic shock Collaborative care | o Hemodynamic monitoring o Vasopressor drug therapy o Vasopressin for patients refractory to vasopressor therapy o Glucose levels should be <150mg/dL |
| Septic shock Collaborative care IV corticosteroids | o for patients who require vasopressor therapy, despite fluid resuscitation to maintain adequate BP • Corticosteroids will stabilize cellular membrane and will help prevent fluid shift (ideally given in the first 8 hours) |
| Septic shock Collaborative care Stress ulcer prophylaxis | o with proton pump inhibitors or H2 receptor blockers |
| Septic shock Collaborative care DVT prophylaxis | o with low dose low-molecular weight heparin • many ICU patients on low dose lovenox to help with DVTs and DIC |
| Septic shock Collaborative care Drotregogin alfa (Xigris) | for activated protein C; major BLEEDING SIDE EFFECT, withdrawn from use; not used anymore |
| Initial Stage of shock | • usually not clinically apparent – changes are at the cellular level o Metabolism changes from aerobic to anaerobic • Process requires unavailable O2 o Patient’s baseline MAP decreases by 10mmHg o SNS starts to kick in |
| Initial Stage of shock Lactic acid | • accumulates and must be removed by blood and broken down by liver→but lack of O2 in the blood will prevent liver from breaking lactic acid down. • Lab draw will show lactic acid > 4 if in sepsis |
| Initial Stage of shock SNS | • Increase HR and contractility= increased CO • Increased vasoconstriction→ increased SVR and arterial pressure |
| Initial Stage of shock Manifestations: | HR and RR are increased from the patient’s baseline level or a SLIGHT INCREASE n diastolic blood pressure may be the ONLY OBJECTIVE manifestation of this early stage |
| • Compensatory stage SNS involvement | • including release of catecholamines (to try to bring more oxygen to the cells and overcome anaerobic metabolism |
| • Compensatory stage RAAS | the kidneys and Baroreceptors since the decrease in MAP and trigger the RAAS as well as ADG, aldosterone, epi, and norepi. Kidney compensation begins with RAAS and there is a decrease in urine output and increase in Sodium retention and vasoconstriction. |
| • Compensatory stage ADH | this is secreted by the posterior pituitary gland to increase water reabsorption in the kidney. This causes less output as well as vasoconstriction in skin and other less vital organs like the gut. |
| • Compensatory stage Hormonal | The adaptive mechanisms are initiated here because cardiovascular adjustments alone are not enough to help maintain our MAP now. |
| • Compensatory stage | o Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis. o Begins after MAP drops 10-15 mmHg below patient’s baseline. |
| • Compensatory stage: mechanisms | can maintain MAP for only a short period of time. If effective treatment is provided, the process is arrested and no permanent damage occurs. Underlying cause of shock must be reversed |
| • Compensatory stage Manifestations FIRST SIGN | • drop in BP and narrowing of pulse pressure, due to cardiac output (then SNS kicks in after sensing this change) |
| • Compensatory stage Manifestations | • Tachycardia • Tachypnea • cold, clammy, pale skin • dec urine output • dec bowel sounds • inc heart rate and contractility • High V/Q mismatch |
| inc heart rate and contractility compensatory stage | temporarily, since this increases oxygen consumption and its already difficult to get oxygen to the cells |
| Progression compensatory stage | • Baroreceptors in the carotid and aorta activate SNS in response to dec BP --> vasoconstriction while blood to vital organs is maintained --> dec blood to kidneys activates RAAS --> inc venous return to the heart, cardiac output and BP |
| If perfusion deficit corrected in compensatory stage | patient recovers with no residual sequelae |
| • Progressive Stage | o Begins when compensatory mechanisms fail o Aggressive interventions to prevent MODS o MAP falls of 20mmHg or more, fluid loss is 35-50% o organs are already damaged, much harder to bring pt back to normal state. |
| • Progressive Stage Anasarca | 3rd spacing, generalized – therefore less fluid to the organs |
| • Progressive Stage | o Hallmarks of decreased cellular perfusion and altered capillary permeability • Leakage of protein into interstitial space • Increase systemic interstitial edema |
| • Progressive Stage: Pulmonary | • Arterioles are constricted, Decreased blood flow and further aggrevate the VQ mismatch. • Fluid is moved into alveoli dec gas exchange. • dec surfactant production- atelectasis. • Pulm edema, bronchoconstriction, dec residual capacity |
| • Progressive Stage Cardio | dec blood pressure; falling CO; High wedge pressure(>12) because CO is reduced;• BP will be low→ not pumping to periphery and it will drop; Myocardial dysfunction |
| • Progressive Stage With falling CO --> | • dec peripheral perfusion, hypotension, weak peripheral pulses, ischemia of distal extremities • High wedge pressure(>12) because CO is reduced o If no intervention→ eventually will be low because no more fluid to be pumped or to back up |
| • Progressive Stage PAC would show dec blood pressure | • pressure (no matter how hard the SNS is trying to constrict the vessels, inc wedge pressure initially (because cardiac output is reduced), then will eventually become low (since you won’t have any fluid return), inc PA pressure |
| • Progressive Stage Myocardial dysfunction results in | • Dysrhythmias, ischemia, MI --> end result is complete deterioration of cardiovascular system |
| • Progressive Stage Neuro | confusion, anxiety, irritability, LOC changes, obtundation, coma |
| • Progressive Stage Renal: | o acute renal failure – drop in urine output, increased BUN and Creat. Metabolic acidosis • Acute tubular necrosis/acute renal failure |
| • Progressive Stage GI | o ulcers, bleeding, dec ability to absorb nutrients, ischemia, loss of protective barrier which will cause translocation of bacteria into abdominal cavity, resulting in peritonitis • METABOLIC ACIDOSIS |
| • Progressive Stage Liver | o unable to process ammonia, and lactic acid, increased ALT, decreased Kupffer cells (patient becomes more susceptible to other type of infection), jaundice, risk for DIC and bleeding • Decreased ability for liver to put out Kupffer cells→ |
| Kupffer cells | helps with immunity process→ further decrease in the immune system and ability to fight off infection |
| • Progressive Stage | |
| DIC from septic shock labs | • dec Fibrinogen (will be used up with the clots) • dec Platelets • inc PT, PTT, INR (normal ranges – PT= PTT= INR=) • inc D-Dimer (fragments of broken down fibren) |
| • Refractory Stage | patients will not survive if they reach this stage, despite interventions |
| • Refractory Stage cardio | o Tachycardia worsens o dec coronary blood flow |
| • Refractory Stage | o Tissue anoxia o Exacerbation of anaerobic metabolism o Accumulation of lactic acid o Inc capillary permeability o Profound hypotension and hypoxemia o Cerebral ischemia o Failure of one organ system affects others |
| Profound hypotension and hypoxemia in refractory stage | despite fluid resusicitation and other efforts→ body unable to respond |
| elevated neutrophils | • indicate an acute infection |
| • monocytes | indicate a bacterial infection |
| • eosinophils | indicate an allergic response |
| Always try ____ first | • crystaolloids first and then move to colloids after |
| Crystalloids | these contain no protein substances like salt, minerals and sugars. These are given to maintain an adequate fluid and electrolyte imbalance; NS, LR |
| Normal Saline | which is 0.9 % sodium chloride in water and is used to replace plasma volume also infused with blood products. |
| Ringers lactate | has sodium, chloride, calcium, potassium, and lactate dissolved in water. NOT WITH BLOOD products because the calcium induces clotting of the infusing blood. |
| Colloid | contain large molecules like proteins and starches. help restore the osmotic pressure used when blood is lost. Whole blood is for large fluid loss to help improve oxygen carrying capacity. PRC are given for moderate so we don’t fluid overload them. |
| Human plasma | has clotting factors given to restore our osmotic pressure when the hct and hg level are with in normal limits. |
| Surgical management | Surgery is need to stop the CAUSE OF SHOCK after it has been found. This includes Vascular repair, wound change, ulcer |
| For septic, hypovolemic and anaphylactic shock | volume expansion; isotonic crystalloids(NS); rapid infusion; central line benefit |
| Complications of fluid resuscitation | hypothermia or coagulopathy |
| Anytime you give large volumes | • you will also need to give diuretics, vasodilators (nitros), and vasopressors (epinephrine)→ to manage/maintain BP and renal function |
| Nitroglycerin is better for | • cardiogenic |
| nitropresside is better for | • non-cardio shock. |
| • Nutrition shock | o Enteral feedings to start in first 24 hours o Parenteral if enteral are contraindicated o If patient is on TPN, check blood glucose o weigh the patient daily; check labs for total protein and albumin o Nitrogen balance o BUN o electrolytes |
| shock patient | may have high levels of protein because the patient is in hypermetabolic state |
| nitrogen balance indicates | • Check that respiratory muscles have enough strength to be taken off the vent |
| When DIC develops, | give heparin! |
| Activated protein C | low level in sepsis. helps prevent inappropriate clot formation and activates when it binds to healthy endothelial cells on the blood vessels and whey they are injured due to toxins can t activate it, 1000s of small clots are formed. first sign of sepsis |
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