FCCS (FUNDAMENTALS OF CRITICAL CARE SUPPORT) LATEST WITH COMPLETE SOLUTION 2023

FCCS (FUNDAMENTALS OF CRITICAL CARE SUPPORT) LATEST WITH COMPLETE SOLUTION 2023 What isthe single most important indicatorin critical illness? {{Correct Ans- tachypnea Beck's Triad {{Correct Ans- hypotension, JVD, muffled heart sounds - a/w cardiac tamponade What is the thyromental distance? {{Correct Ans- It is the distance in finger breadths between the anterior prominence of the thyroid cartilage (adam's apple) and the tip of the mandible (chin). It is an estimate of the length of the mandible and the available space anteriorto the larynx What doesit mean when the thyromental space is 3 fingerbreadths? {{Correct Ans- - approx 6 cm - indicates the larynx might be more anterior and therefore difficult to visualize during laryngoscopy ** a more acute angulation of the stylet atthe distal end of the endotracheal tube may be helpful. Patient is apneic w/ a pulse. What do you do? {{Correct Ans- Bag them. - One handed bag compressions should be delivered 10-20 times per min. Each compression should take place over1 second. ** If patientstarts spontaneously breathing, try to be synchronous with theirrespiratory efforts. ** If/once the patient is breathing easily and adequate Vt are being inhaled, enough to produce minute ventilation,stop bagging. What is the goal of manual mask ventilation? {{Correct Ans- to provide adequate minute ventilation: the product of the tidal volume delivered during each resuscitation bag compression and the number of compressions permin. ** The total gas volume within most adultresus bagsis 1 to 1.5 LITERS Bag mask should be connected to % oxygen and flow at a rate of {{Correct Ans- 100% oxygen at a rate of 15L/min HFNC {{Correct Ans- - Uses up to 100% oxygen source - Provides higher amounts of FIO2 (0.32-1.0) in patients with high minute ventilation requirements by matching patient'sinspiratory demands andminimizing airdilution - These devices also can generate PEEP (that is difficult to measure; can cause barotrauma in theory) - Flow rates up to 60L/min - heated and humidified oxygen NRB {{Correct Ans- - AKA Reservoir Face Mask - Bag is filled with 100% oxygen from a supply source (tank) - The flow rate must be adjusted so that the bag remains completely or partially distended throughout the respiratory cycle - When the mask is properly applied, oxygen delivery can be maximized but rarely exceeds a FIO2of 0.6 to 0.9 - One way flap valves minimize entrapment of room air which dilutes FiO2 - NRB is a high oxygen high, flow device. - non humidified oxygen ** commonly used to improve oxygenation in patients with severe hypoxemia until further eval and treatments are accomplished. Aerosol Face Mask {{Correct Ans- - This mask has large side holes, the mask itself is attached to large bore tubing to a nebulize that blends 100% oxygen and room air to deliver a PRESET FIO2 level (done by dial on oxygen adapter) - If the entire aerosol mist disappears from the mask during. inhalation, the patient's inspiratory flow demands are probably exceeding the capacity of the nebulizer and room airis being entrained. - minimum flow rate = 8L/min - Max FIO2 = 40-60% - Thisis a variable oxygen, moderate-flow device. Simple Face Mask {{Correct Ans- - minimum flow rate: 6L/min (to clear CO2 from mask) - humidified O2 - Approx. concentrations L to FIO2 ratios: 6L = 40% 7L = 50% 8L = 60% Venturi Face Mask {{Correct Ans- - aka air entrainmentface mask - delivers O2 through a jet mixing device that increases the velocity of oxygen and causes a controlled entrainment - the FiO2 can be more precisely controlled from .24 to .5 (24% to 50%) at high flow rates simply my selecting the interchangeablenozzleand adjusting theO2flow rate - this is a high flow, controlled oxygen device. Nasal Cannula flow rate to FIO2 estimatesif RR and tidal volumes are normal {{Correct Ans- 1L = 24% 2L = 28% 3L = 32% 4L = 36% 5L = 40% 6L = 44% NPPV uses two levels of positive airway pressure, combining modalities of pressure support ventilation and what? {{Correct Ans- CPAP What is CPAP? {{Correct Ans- continuous positive airway pressure - Allows spontaneous breathing from a gas source at an elevated baseline system pressure (higher than atmosphericpressure) - Functionally equivalent to PEEP. By convention, PSV mode isreferred to as and CPAP isreferred to as when talking aboutNPPV/BIPAP {{Correct Ans- PSV = IPAP CPAP = EPAP The difference between these two numbers determines the tidal volume generated. Initiationof NPPV guidelines {{Correct Ans- - Do not delay intubation if needed and keep in mind the patient'sresuscitation status. - Consider ABG analysis prior to initiation. - Explain the procedure. - Keep head of bed at ≥45°. - Ensure appropriate mask or helmetsize. - Assess the patient's tolerance of the mask by applying it by hand before securing the harness. - Adjust the difference between EPAP and IPAP to achieve and effective VT and CO2 clearance. Adjust EPAP for alveolar recruitment in increments of 2 cm H2O per step to improve oxygenation. Depending on the ventilator, a similarincrease in IPAP may be required tomaintain the same VT. - If assist-control volume ventilation is used, begin with a VT of 6 to 8 mL/kg (depending on the underlyingpulmonary condition). - Titrate pressures, volume, and FIO2 to achieve appropriate pH, PaO2, and PaCO2 levels. Ventilator changes can be made every 15 to 30 minutes. - Follow vital signs, pulse oximetry, mentalstatus, clinical appearance, and ABG(if indicated). - Rememberthat goals of NPPV may include a respiratory rate 30 breaths/min, VT 7 mL/kg of predicted body weight, improved gas exchange, and patient comfort. - It is also importantto be cognizantthat IPAP 20 cm H2O may lead to gastric distension. What are the goals of NPPV? {{Correct Ans- The goals of NPPV may include a - respiratory rate 30 breaths/min - VT 7 mL/kg of predicted body weight - improved gas exchange - patient comfort. Initial NPPV settings {{Correct Ans- Use the following initial ventilatorsettings: - Mode: Spontaneous - Trigger: Maximum sensitivity - FIO2: 1.00 - (PEEP) EPAP: 4-5 cm H2O ** (higherlevels are poorly tolerated initially) - (PSV) IPAP: 10-15 cm H2O - Backup rate: Start at 6/min CPAP indications, pros, cons {{Correct Ans- - CPAP alone can also be delivered noninvasively but does not provide support of ventilation. - CPAP allows spontaneous breathing from a gas source at an elevated baseline system pressure (higher than atmospheric pressure) and isfunctionally equivalent to positive end-expiratory pressure (PEEP). - uncomfy - primarily used to treat OSA *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Fentanyl Dose: Benefits: Cautions: {{Correct Ans- *Fentanyl* Dose: 0.5-2ug/kg IV bolus every several minutes, titrated for analgesia. Benefits: Rapid onset,short acting,reversiblew/ naloxone Cautions: chest wall rigidity w/ rapid administration, respiratory depression, does not inhibit awareness of procedure *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Midazolam Dose: Benefits: Cautions: {{Correct Ans- *Midazolam* Dose: 0.1-0.3mg/kg bolus, titrated to sedate Benefits: Provides amnesia, rapid onset, short acting, reversible w/ fumazenil Cautions: Added respiratory depression when combined w/ narcotics *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Etomidate Dose: Benefits: Cautions: {{Correct Ans- *Etomidate* Dose: 0.1-0.3mg/kg single IV bolus Benefits: provides hypnosis, MAY be preferred in head injury, NO adverse CV effects Cautions: May induce myoclonus including mild trismus (consider pre-medicating w/ fentanyl), NO reversal agent,transient adrenalsuppression *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Lidocaine Dose: Benefits: Cautions: {{Correct Ans- *Lidocaine* Dose: 1-1.5mg/kg IV bolus 2-3 min before laryngoscopy Benefits: blunts hemodynamic and tracheal response to intubation, may reduce ICP during laryngoscopy Cautions:should not exceed 4mg/kg due to neurotoxicity (seizures) *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Ketamine Dose: Benefits: Cautions: {{Correct Ans- *Ketamine* Dose: 1-4mg/kg IV bolus Benefits: Rapid onset, no adverse CV effects (exception in severe CHF), short acting Cautions: May increase ICP, hallucinations, consider a small dose of benzo like midazolam as an adjunct. *DRUGS USED TO FACILITATE TRACHEAL INTUBATION* - Propofol Dose: Benefits: Cautions: {{Correct Ans- *Propofol* Dose: 1-2mg/kg IV bolus Benefits: rapid onset, short acting, provides amnesia Cautions: severe hypotension in volume depleted patients, does not provide analgesia, can cause respiratory depression RIP MJ NM blocking agents Dose,benefits,cautions {{Correct Ans- Succinylcholine, 1 to 1.5 mg/kg intravenous bolus: rapid onset; shortest duration, which provides an element of safety; may cause muscle fasciculations because this agent depolarizes skeletal muscle; emesis may occur if abdominal muscle fasciculations are severe; contraindicated when ocular injury is present; relatively contraindicated when head injury or hyperkalemia is present (potassium release of 0.5-1 mmol/L will occur routinely, and massive potassium release may occur in burn and crush injury, upper motor neuron lesions, or primary muscle disease); may precipitate malignant hyperthermia. Effects are prolonged in patients with atypical cholinesterase or decreased pseudocholinesterase levels. Vecuronium, 0.1to 0.3 mg/kg; rocuronium, 0.6 to 1 mg/kg; or cisatracurium, 0.1 to 0.2 mg/kg intravenous bolus: no fasciculations because these are nondepolarizing agents; slower onset of muscle paralysis; significantly longer duration of effects than with succinylcholine. When difficulty in mask ventilation or intubation is anticipated, care is advised before suppressing spontaneous ventilation with NMblocking agents or sedatives that cannot be reversed. Video. laryngoscopy has been shown to be an effective method of airway management as both a primary intubation technique and in management of difficulty airway. Options for safe airway management that preserve spontaneous ventilation. include {{Correct Ans- - awake intubation by direct or video laryngoscopy - blind nasotracheal intubation - awake tracheostomy (expert consultation required, get an adult) What if you're trying to intubate someone but visualization of the glottis and bag mask ventilation is impossible ANDtheres no spontaneous ventilation??? {{Correct Ans- - LMA - esophageal-tracheal double lumen airway device - needle cric (get an adult) - surgical cric/trach (get an adult) - percutanoustrach (again, get an adult) Sellick Maneuver {{Correct Ans- A technique that is used with intubation in which pressure is applied on either side of the cricoid cartilage to allow better visualization of vocal cords; also called cricoid pressure. - Does not actually prevent/ reduce aspiration as previously thought. Targeted Temperature Management (TTM) {{Correct Ans- 32-36 degrees Celsius for at least 24 hours - has been recommended to improve neurologic outcome and reduce mortality in comatose patients following initial resuscitation from and arrest (ROSC) Hypoxemic from intrapulmonary shunt. What to do? {{Correct Ans- Shunt = good blood flow/ perfusion but limited ventilation becauseissue is atthe alveoli - Recruit and open alveoli = increase PEEP What is dead space? {{Correct Ans- Area w/ good ventilation at the alveoli (alveoli is open) but poor blood flow/ perfusion (likein a PE) What is Auto-PEEP? {{Correct Ans- If the expiratory time is too short to allow full exhalation, the previously delivered breath is not completely expired and the next lung inflation is superimposed upon the residual gas in the lung. This results in lung hyperinflation and PEEP above the preset level on the ventilator. This increase in end-expiratory pressure is called auto-PEEP, or intrinsic, inadvertent, or occultPEEP. - AKA air trapping Signs of a patient auto-PEEPing/breathstacking? {{Correct Ans- The physiologic effects of auto-PEEP on peak, plateau, andmean airway pressures are the same as those of preset PEEP. (Ex: barotrauma) - High levels of PEEP may decrease venous return to the heart, resulting in *hypotension* and *higher PCO2 due to increased dead space*, and adversely affect oxygenation (especially with asymmetric lung disease and COPD) Auto-PEEP may be reduced by the following interventions: {{Correct Ans- - Decrease respiratory rate by changing the set rate or sedating the patient. These interventions result in fewer inspirations per minute and thus increase the total expiratory time available; this is the most effective way of decreasing autoPEEP. - Decrease VT, which requires less time to deliver a smaller breath and allows more time for exhalation - Increase gas flow rate, delivering the VT faster and allowing more time in the cycle for exhalation. This intervention has little impact unless the initial flow rate was set at an extremely low level. It will also lead to an increase in the airway pressure. - Change the inspiratory waveform from decelerating (ramp) to constant (square), which delivers VT in a shortertime, allowingmore time forexhalation. Hypercapnia causes cerebral *VASO ? * and furtherincreases in the intracranial pressure. {{Correct Ans- vaso*dilation* As a general rule, FIO2, mean airway pressure, and PEEP affect the , whereas the respiratory rate, dead space (VD), and VT affect alveolar and . {{Correct Ans- - FIO2, mean airway pressure, andPEEP affectthe *PaO2* - respiratory rate, dead space (VD), and VT affect *alveolar minute ventilation* and *PaCO2*. Guidelines for the Initiation of Mechanical Ventilation {{Correct Ans- - Choose the ventilator mode with which you are most familiar. The primary goals of ventilatory support are adequate oxygenation/ventilation, reduced work of breathing, synchrony between patient and ventilator, and avoidance of high end-inspiration alveolarpressures. - The initial FIO2 should be *1.0.* The FIO2 thereafter can be titrated downward to maintain the SpO2 at 92% to 94%. In severe acute respiratory distress syndrome, SpO2 ≥88% may be acceptable to minimize complications of mechanical ventilation. - Initial VT = *8 to 10 mL/kg* in patients with relatively *normal lung compliance*. In patients with poor lung compliance (eg, ARDS), a target VT of 6 mL/kg by PBW is recommended to avoidoverdistension andmaintain an inspiratory plateau pressure≤30 cm H2O. - Choose a respiratory rate and minute ventilation appropriate for the particular clinical requirements. Target pH, notPaCO2. - Use PEEP in diffuse lung injury to maintain an open alveoli at end expiration. If volume is held constant, PEEP may increase peak inspiratory plateau pressure, a potentially undesirable effect in ARDS. PEEP levels 15 cm H2O are rarely necessary. - Set the triggersensitivity to allow minimal patient effort to initiate inspiration. Beware of auto cycling if the triggersetting istoo sensitive. - In patients at risk of obstructive airway disease, avoid choosing ventilator settings that limit expiratory time and cause or worsen auto-PEEP. - Call the critical care consultant or other appropriate consultant for assistance. What respiratory conditions are likely to respond to Noninvasive Positive Pressure Ventilation? {{Correct Ans- HypoxemicRespiratory Failure: - Cardiogenic pulmonary edema without hemodynamic instability - Respiratory failure in patients with mild to moderate Pneumocystis pneumonia - Respiratory failure in immunocompromised patients (especially in hematologic malignancies and transplant patients) Hypercapnic Respiratory Failure: - Acute exacerbation of chronic obstructive pulmonary disease - Acute exacerbation of asthma - Respiratory failure in patients with cystic fibrosis Use the following initial ventilator settings for BiPAP: {{Correct Ans- Mode: Spontaneous Trigger:Maximumsensitivity FIO2: 1.00 EPAP: 4-5 cm H2O (higherlevels are poorly tolerated initially) IPAP: 10-15 cm H2O Backup rate: Start at 6/min IPAP 20 cm H2O may lead to {{Correct Ans- gastric distension Contraindications to Use of Noninvasive Positive Pressure Ventilation: {{Correct Ans- - Cardiac or respiratory arrest - Hemodynamic instability - Myocardial ischemia or arrhythmias - Patient who is unable to cooperate - Inability to protect the airway - High risk for aspiration - Active upper gastrointestinal hemorrhage - Severe hypoxemia - Severe encephalopathy - Facial trauma, recentsurgery, and/or burns - Significant agitation Measurements of global oxygen balance that may be useful in monitoring the seriously ill patient include and {{Correct Ans- central venous oxyhemoglobin saturation (*ScvO2*) and *lactate* concentrations. How do you measure ScvO2? {{Correct Ans- ScvO2 can be obtained continuously or intermittentlyfrom a catheterplaced in the internal jugularorsubclavian vein ScvO2 correlates with the mixed venous oxyhemoglobin saturation (SVO2) obtained from a pulmonary artery catheterin the pulmonary artery. How do you measure SvO2? {{Correct Ans- PA catheterin pulmonary artery - this is a mixed venoussample The SVO2 measures the oxyhemoglobin saturation of blood from the superior vena cava and the inferior vena cava that has been mixed in the right ventricle. These measures of venous oxyhemoglobin saturation represent the amount of oxygen still bound to hemoglobin after traversing the tissue capillaries and returning to the right heart; the decrease from the SaO2 estimates the amount of oxygen utilized In normal individuals, the SVO2is % and the ScvO2 is 2% to 3% lower. However, in patients with shock and/or hypoperfusion, the ScvO2 may be 5% to 7% higher than the SVO2 due to greater desaturation of venous blood from the gastrointestinal tract contributing to SVO2 {{Correct Ans- 65% Low values of ScvO2 suggest an imbalance in the oxygen supply and demand. This imbalance may be due to decreasesin: - - - Patients may have more than one abnormality contributing to oxygen imbalance. {{Correct Ans- - cardiac output - hemoglobin concentration, or SaO2, - increases in tissue oxygen consumption.(fever/sepsis) A normal ScvO2 may still be associated with tissue hypoxia in conditions such as severe sepsis and certain poisonings (eg, ). Further evaluations of lactate concentration and organ function are needed to assess oxygen balance in the seriously ill patient when the ScvO2 is normal. {{Correct Anscyanide Lactate is another indicator of the overall oxygen balance. It is produced during anaerobic metabolism when cellular occurs. The elevation of blood lactate in shock and hypoperfusion may be due to inadequate oxygen supply to tissue but also may be affected by altered hepatic metabolism, use of vasoactive drugs, andotherfactors. {{CorrectAns- hypoxiaoccurs Passive leg raising (PLR) is another technique that may be used at the bedside with less-invasive monitoring techniques to determine if additional fluid is beneficial. This maneuver is performed by {{Correct Ans- by placing the head of the bed flat from the semi-recumbent position and then raising both legssimultaneously to a 45° angle. - This action results in a gravitational transfer of approximately 300 mL of blood from the lower limbs and splanchnic compartmenttoward the right heart. - No fluid is infused and the clinical effects are completely reversible. - If a significant increase in cardiac output or stroke volume is noted within 30 to 60 seconds of PLR, the patientis determined to be fluid responsive. Hyponatremia flow chart {{Correct AnsFor hyponatremia, the serum sodium increase should be limited to approximately to mmol/L in the first 24 hours.{{CorrectAns- 6 to 8 mmol/L Hypertonic saline is indicated fortreatment in the presence hyponatremia w/ severe symptoms, such as {{Correct Ans- seizures, coma, orimpending respiratory arrest. The goal of therapy in this situation is to remove free water and not sodium. The increase in serum sodium should be controlled, and although the precise rate of increase is controversial, the serum sodiumincrease should be limited to approximately 6to 8 mmol/L in the first 24 hours. - When hypertonic saline is used in symptomatic patients, 1 mmol/kg sodium chloride should be infused initially (3% saline contains ~0.5 mmol/mL). The same amount can be administered in incremental doses to a maximumof 3 to 5 mmol/kg or untilsymptomsresolve. When serumsodium is greaterthan 125 to 130 mmol/L, alone allows for slower return of the sodiumlevel to normal.{{Correct Ans-restrictionof free water Correction of the serum sodium level that is too rapid may result in CNS injury called , particularly in the setting of chronic hyponatremia. {{Correct Ans- osmotic demyelinating syndrome - Osmotic demyelinating syndrome rarely occurs in patients whose serum sodium is greater than 120 mmol/L. - Symptoms of demyelination are typically seen after initial improvement in mentation. In 1 to 7 days following a hasty reversal of chronic hyponatremia, patients may develop focal motor deficits, respiratory insufficiency, and progressive loss of consciousness. Who is at risk for osmotic demyelinating syndromes? {{Correct Ans- those with malnutrition or hypokalemia, alcohol abusers, elderly women, and burnpatients. MOA of Vaptans {{Correct Ans- They inhibit resorption of water via their action on the V2 receptor of the kidney and resultin a slow rise in the serumsodiumlevel. - conivaptan - tolvaptan ** To prevent over-correction, avoid using vasopressin antagonists in combination with hypertonic saline. - Once an increase of 6 to 8 mmol/L is achieved, consider replacing free water (orally or intravenously) to match urine output and prevent an excessiverise in sodiumlevels After a vasopressin receptor antagonist (vaptan) is administered, serum sodium levels should be monitored frequently every hr due to concerns for rapid sodium correction and neurological sequelae (specifically, demyelination).{{CorrectAns- every 4hours Sodium contents of infusions {{Correct AnsAdministration of intravenous recombinant tissue plasminogen activator during the hours following the known onset of ischemic stroke substantially improves outcome in one -third of patients{{CorrectAns- first3to 4.5 Ischemic stroke: For those who are not candidates for thrombolysis, emergency administration of antihypertensive agents is not indicated unlessthe diastolic blood pressure is mm Hg, systolic blood pressure is 220 mm Hg, or there is evidence of end-organ injury (eg, pulmonary edema). {{Correct Ans- 120 mm Hg - If treatment is indicated, the blood pressure should be lowered cautiously with a reasonable goal of lowering the pressure approximately 15% in the first 24 hours afterstroke onset. Urgent anticoagulation with unfractionated orlow-molecular-weight heparin is in acute stroke.{{CorrectAns- notindicated - Prophylactic heparin should be administered to immobilized patients to prevent venous thromboembolism, butthe ideal time to startthistherapy is not known. - Aspirin administration within 24 to 48 hours of stroke onset is recommended for most patients after hemorrhage is excluded, but clopidogrel administration is not recommended. Significant edema formation, typically within the first 72 hours, or extensive hemorrhage within the ischemic zone may indicate emergent hemicraniectomy tPA and Blood Pressure Goals/Options/Doses{{Correct AnsPrinciples of TBI management: {{Correct Ans- - Ensure the ABCs of resuscitation are performed - Avoid hypotension and maintain systolic blood pressure 90 mm Hg. It may be valuable to maintain mean arterial pressure higher than the mean arterial pressure associated with a systolic blood pressure of 90 mmHg. Optimal mean arterial pressureisunknown. - Avoid hypoxemia (PaO260 mm Hg [8.0 kPa] or oxygen saturation 90%) while adequate oxygenation ismaintained. - Maintain alignment between head and trunk to avoid jugular compression. - Keep the head of the bed at 30° to 45°elevation unless the patient is hypotensive. Elevation of the head promotes venous drainage and cerebrospinal fluid displacement to the spinal compartment. Adjust any devicesthatmay constrictthe neck, including cervical collars. - Maintain the PaCO2 at 35 to 40 mm Hg (4.7-5.3 kPa). Prophylactic hyperventilation is not recommended. Hyperventilation is recommended as a temporizing measure for reduction of elevated intracranial pressure. Cerebral blood flow is often reduced in the first 24 hours after head trauma, and hyperventilation should be avoided in this period to preventfurtherreductions. - Use normal saline as the primary maintenance fluid. Do not use hypotonic fluids. - Actively treat fever to maintain body temperature at normal levels. - Control harmful agitation with sedation if necessary. - Use medications with a relatively short half-life to facilitate reliable and ongoing neurologic assessments. (Ex: Haldol is better,shorter half life, than Ativan for agitation) - Maintain the usual electrolyte homeostasis and treat hyperglycemia/hypoglycemia. - Assess and treat coagulation defects. - Provide nutrition to attain full caloric replacements astolerated. - Prophylactic anticonvulsants are appropriate during the first week aftertraumatic brain injury. - Give mannitol (0.25-1 g/kg IV push) or hypertonic saline (eg, 5-10 mL/kg of 3% NaCl as rapidly as possible) for signs of herniation or for neurologic deterioration not attributable to other factors. Expert consultation should be obtained if thistype of hyperosmolartherapy is considered. - Avoid steroid use. These agents are contraindicated in patients with head trauma - Maintain the lowest cerebral perfusion pressure compatible with adequate cerebral blood flow. The target cerebral perfusion pressure is in the range of 50 to 70 mm Hg, although patients with intact autoregulation may tolerate higher values. The ideal is the pressure that provides adequate cerebral perfusion and oxygenation whileintracranial pressure ismaintained 20 mmHg. Initiate appropriate intracranial pressure monitoring: {{Correct Ans- 1. For a patient with a GCS between 3-8 afterresuscitation or a score between 9-12with an abnormal computed tomography scan 2. For a patient who has a normal computed tomography scan but at leasttwo of the following factors: -- Age 40 years -- Systolic blood pressure 90mm Hg -- Unilateral or bilateral motor posturing (decerebrate/decorticate) Hypotension w/ initiation of ventilator support can be caused by: {{Correct Ans- 1. Tension PTX: when hypotension occurs immediately after initiation of mechanical ventilation, tension pneumothorax should be one of the first considerations. This diagnosis is based on a physical examination that finds decreased or absent breath sounds and tympany to percussion on the side of the pneumothorax. Tracheal deviation away from the side of the pneumothorax may be observed, although it is uncommon after placementof an endotracheal tube. 2. Conversion from Negative to Positive Intrathoracic Pressure: when positive pressure ventilation is initiated, intrathoracic pressure becomes positive. As intrathoracic pressure rises, right atrial pressure rises and the intravascular pressure gradient for return of blood from the large extrathoracic veins into the right heart decreases. As a result, blood return to the heart may be reduced. Left ventricular preload, stroke volume, cardiac output, and blood pressure then may decrease in sequence. Underlying intravascular volume depletion exacerbates the deleterious effects of the increased intrathoracic pressure on cardiac output and blood pressure. 3. Auto-PEEP: occurs when the combination of ventilator settings and patient physiology results in an inadequate expiratory time. Excessive end-expiratory pressure may increase intrathoracic pressure and cause hypotension due to decreased venous return to the heart. Although auto-PEEP may occur in any patient, those with obstructive airway disease are particularly predisposed to this condition because of the need fora prolonged expiratory phase. 4. Myocardial Ischemia/Infarction: Stress from the cause of acute respiratory failure, as well as the stress of intubation itself, may lead to increased myocardial oxygen demand and to acute myocardial ischemia, infarction, and subsequent hypotension. Patients at high risk should be evaluated with serial electrocardiograms andmyocardial markers of injury Classes of Hemorrhagic Shock {{Correct Ans- ATLS/FCCS chart combined Example of nSTEMI {{Correct Ans- The ST-segment depression in lead V6 is characteristic of non-STelevation acute coronary syndrome What is a GRACE score? {{Correct Ans- Several risk stratification scores have been developed and validated to assist in predicting the risk of death and ischemic events in NSTE-ACS. The GRACE 2.0 (Global Registry forAcute CardiacEvents) - An APP/ website: TIMI score can also be used AKA Thrombolysis in Myocardial Infarction risk score can be easily determined at the bedside What isthe make up of the TIMI score? {{Correct Ans- 1 pointfor each: - Age ≥65 y - Known coronary artery disease (coronary stenosis ≥50%) - ST-segment deviation of at least 0.5 mm - At least 2 angina events in prior 24 hours - Use of aspirin in prior 7 days - At least 3 risk factors for coronary artery disease (family history of premature coronary artery disease, hypertension, hyperlipidemia, diabetes,smoking) - Elevated serum cardiac markers ACS and oxygen supplementation {{Correct Ans- Oxygen (2-4 L/min by nasal cannula) should be administered to patients with dyspnea, hypoxemia (oxygen saturation measured by pulse oximetry 90% on room air), or evidence of heartfailure orshock - Emerging data suggest that routine use of supplemental oxygen in cardiac patients with normal oxygenation may have untoward effects, including increased coronary vascular resistance, reduced coronary blood flow, and an increased risk of death. Nitroglycerin tx and NSTEMI {{Correct Ans- Patients with ongoing ischemic discomfort should receive up to three doses ofsublingual orspray nitroglycerin. -The dose of IV nitrates should be tapered and discontinued when ischemic manifestations have resolved for12 to 24 hours. - Nitrates should not be administered if the SBP measures 90 mm Hg or ≥30 mm Hg below the patient's baseline blood pressure. - Additional contraindications to nitrate administration are: - HR 50 beats/min - tachycardia 100 beats/min in the absence of heart failure symptoms - in suspected right ventricular infarction orsevere aortic stenosis. - Use of phosphodiesterase inhibitors in the last 24hr (erectile dysfunction pills) [48hr for Tadalafil] Morphine dose forACS {{Correct Ans- 1-5 mg every 5-30 min as needed forpain Nitroglycerine not helping w/ NSTEMI pain. What to use? {{Correct Ans- Morphine sulfate is a reasonable analgesic formanagement of pain refractory to initial antianginal therapy. - NSAIDs, other than aspirin, and COX-2 inhibitors should not be initiated and should be discontinued during hospitalization because of the potentially increased risk for major adverse cardiac events, especially with long-termuse When to start BBs in NSTEMI? {{Correct Ans- within first 24hr if there are no contraindications - Routine use of IV β-blockers in the initial management of patients with suspected NSTE-ACS is not supported by current evidence, but may be considered in patients with ongoing chest pain, especially with concomitant hypertension ortachycardia; IV dosing should be followed by oral administration. - Caution is advised with the use of IV β-blockers in patients with risk factors for shock (age 70 years, heartrate 110 beats/min,systolicblood pressure 120 mmHg, or late presentation). improves survival and reduces the incidence of MI. {{Correct Ans- Aspirin What antiPLT drugs benefit in MI? {{Correct Ans- - aspirin - adenosine diphosphate inhibitors (eg, clopidogrel, prasugrel, and ticagrelor) - glycoprotein (GP) IIb/IIIa inhibitors - Non−enteric-coated ASA at a dose of 162 to 325 mg should be chewed as soon as possible to all patients with NSTE-ACS (including those in the prehospital setting) if no aspirin allergy is suspected. ASA should be administered indefinitely. - Clopidogrel or ticagrelor should be considered as an alternative antiplatelet agent if aspirin is contraindicated. - If an early invasive strategy or noninterventional conservative approach is planned, clopidogrel or ticagrelorshould be added to ASA to decrease the risk of cardiovascular death, MI, and stroke. - Clopidogrel, prasugrel, or ticagrelor should be administered in patients undergoing percutaneous coronary interventions (PCIs), but prasugrel is contraindicated in those with a prior history of stroke or transientischemic attack and is associatedwith an increased risk of bleeding. - The choice of a specific adenosine diphosphate inhibitor should be discussed with the cardiologist when possible. Therapy with an adenosine diphosphate inhibitor is recommended for at least 12 months. In ACS patients treated with a conservative ischemia-guided approach, what drugs would be given? {{Correct Ans- low-molecular-weight heparin, unfractionated heparin, bivalirudin, or fondaparinux should administered assoon as possible unlessthere are significant contraindications. Patients w/ ACS managed with fondaparinux require to prevent if a PCI is subsequently performed. {{Correct Ans- an additional anticoagulant to prevent catheterthrombosis - Unfractionated heparin is continued at least 48 hours, and enoxaparin orfondaparinux forthe duration of the hospital stay (up to 8 days), in patients managed with medical therapy or until PCI is performed. If an early invasive strategy is planned, unfractionated heparin, enoxaparin, or bivalirudin should be initiated assoon as possible. Serial counts are required to monitor for heparin-induced thrombocytopenia. {{Correct AnsPLT Argatroban is an alternative anticoagulant in patients with known . {{Correct Ans- heparin-induced thrombocytopenia Patients who are adequately anticoagulated with warfarin who have ACS stillrequire but anticoagulation with heparin or alternative agents is generally not needed unless the international normalized ratio islessthan 2.0. {{Correct Ans- antiplatelettherapy ACE inhibitors and NSTEMI {{Correct Ans- An angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker should be administered in the first 24 hours to patients with NSTE-ACS and evidence of pulmonary congestion or left ventricular ejection fraction 40% unless contraindications are present. Statin and NSTEMI {{Correct Ans- A statin should be initiated or continued after consideration of contraindications. Aldosterone blockade and NSTEMI {{Correct Ans- This is an option in patients receiving an ACE inhibitor and β-blocker who have an ejection fraction 40%, diabetes or heart failure, and no contraindications. Patients with STEMI have a high likelihood that a thrombus occludes a coronary artery, resulting in a wave front of myocardial necrosis that begins at the endocardial surface within 15 minutes. The infarction progresses outward to the epicardium over approximately hours unless collateral flow, spontaneous reperfusion, or reperfusion via an intervention is established. {{Correct Ans- SIX HOURS The most common finding in patients w/ STEMI in NSR is indicating decreased left ventricular complianceatthe end of ventricularfilling {{Correct Ans- S4heartsound A right-sided ECGis indicated in patients with an to determine if ST-segment elevation suggesting right ventricularinfarction is present.{{Correct Ans- - inferior STEMI - II,III, aVF - supplied by RCA II, III, aVF {{Correct Ans- Inferior wall leads (RCA) Therapy for STEMI {{Correct Ans- 1. Aspirin should be administered immediately. 2. The addition of a loading dose and subsequent maintenance doses of clopidogrel or ticagrelor as part of dual antiplatelettherapy decreasesthe rates of mortality andmajor vascular events. 3. An anticoagulant agent, unfractionated heparin or bivalirudin, should also be administered to patients undergoingPCI. 4. Intravenous nitroglycerin may be useful in patients with STEMI and ongoing chest pain, hypertension, or heart failure, unlessthe systolicblood pressure is below 90mm Hg. 5. Intravenous β-blockers are not routinely administered but may be considered at presentation if hypertension orongoing ischemia is present and there are no contraindications. *6.* Prompt restoration of flow can be achieved by primary PCI, fibrinolysis, orsurgical intervention What is PCI? {{Correct Ans- - PCIs = angioplasty, usually with deployment of an intracoronary bare-metal or drug-eluting stent, alongwith pharmacologicmeasuresto preventthrombosis. - Primary PCI results in higher patency rates of the infarct-related coronary artery and lower rates of recurrentischemia,reinfarction, and death. - Primary PCI is the preferred reperfusion technique if the procedure can be performed by experienced personnel within 12hoursof symptomonset. - It is also preferred with clinical or electrocardiographic evidence of ongoing ischemia, even if more than 12 hours have elapsed since symptomonset. *** A goal of 90 minutes or less from hospital presentation to balloon inflation is optimal Fibrinolysis vs PCI {{Correct Ans- PCI is preferred over Fibrinolysis with the following considerations: - In general, the higher the patient's mortality risk (as with large infarctions, heart failure or hemodynamic instability, previous infarctions, or acute left bundle branch block), the more primary PCI is preferred. Similarly, the higherthe risk of fibrinolysis, the more primary PCI is preferred. - Transfer for PCI is preferred over fibrinolysis in patients who present 3 to 12 hours after onset of symptoms if transfer can be accomplished in a timely manner. For patients who fail to reperfuse after fibrinolytic therapy, PCI isrecommended, even if itrequires transferto anotherinstitution. HOWEVER: - Patients presenting within 3 hours of the onset of symptoms who have a low risk of bleeding appear to derive particularbenefitfrompromptreperfusionwith fibrinolytic therapy Is PCI is contraindicated by the presence of coma or a need for targeted temperature management after cardiac arrest? {{CorrectAns-NO! If PCI is not available or cannot be performed within 120minutes of arrival, should be considered{{CorrectAns- fibrinolytic therapy Is the fibrinolysis for STEMI working? How to check? {{Correct Ans- Findings that suggest reperfusion include - relief of symptoms - maintenance orrestoration of hemodynamic and/or electrical stability - reduction of at least 50% of the initial ST-segment elevation injury pattern on a follow-up ECG performed 6-90minutes afterthe initiation oftherapy After Fibrinolysis for ACS {{Correct Ans- - heparin should be used to maintain vessel patency for at least 48 hours. - Enoxaparin is preferred over unfractionated heparin following fibrinolysis. - Infusion rates of unfractionated heparin should be adjusted to keep the aPTT at 1.5 to 2 times the control value. - Heparin anticoagulation after use of streptokinase is not necessary; fondaparinux, a factor Xa inhibitor, can be considered in thesesituations. - Aspirin (81-325 mg/day) should be continued. - Clopidogrel is the antiplatelet agent of choice in patients treated with fibrinolytics who undergo delayed invasivereperfusion interventions