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CCP Treatment Plans Flashcards

1
Q

acute pancreatitis treatment algorithm

A

“limit the severity of pancreatic inflammation and provide supportive care”

  1. IV fluid resuscitation (plasma-lyte or LR)
  2. correction of electrolyte and metabolic abnormalities
  3. Antiemetics
  4. Analgesia
  5. Vasopressor support for shock
  6. Nutritional support (enteral nutrition or NG feeds)
  7. Antibiotics (infected necrotizing pancreatitis or extrapancreatic infections)
  8. Management of complications (eg. EtOH withdrawal, infection, ARDS, shock)
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2
Q

acute liver failure treatment pathway

A

“WHAT’S THE DRIVER” (search for an underlying cause)

  1. IV fluid resuscitation
  2. correction of electrolyte and metabolic abnormalities (hypoglycaemia)
  3. Vasopressor support for shock (norepinephrine)
  4. Corticosteroids for refractory shock (hydrocortisone)
  5. Consider administration of N-acetylcysteine
  6. Management of complications (eg. elevated ICP secondary to hepatic encephalopathy, GIB secondary to hepatic coagulopathy)
  7. broad-spectrum ABX for signs of infection
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3
Q

massive UGIB treatment pathway

A
  1. IV/O2/Monitor
  2. Volume resuscitation (blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. promote gastric emptying (NG tube, metoclopramide)
  5. secure airway
  6. control bleeding (Blakemore/Minnesota/Linton tube, octreotide, vasopressin)
  7. prevent further complications (prophylactic ABX, PPI therapy)
  8. STAT GI consult
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4
Q

ruptured AAA treatment pathway

A
  1. IV/O2/Monitor
  2. Volume resuscitation (target SBP 70-90 mmHg with intact mental status, blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. Analgesia
  5. Arterial Line
  6. STAT vascular surgery consult
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5
Q

CCP Interventions to temporize abdominal compartment syndrome

A
  1. sedation + analgesia (Improve Abdominal Wall Compliance)
  2. head of bed elevation at 30 degrees (Improve Abdominal Wall Compliance)
  3. neuromuscular blockade (Improve Abdominal Wall Compliance)
  4. nasogastric decompression (Evacuate Intra-Luminal Contents)
  5. avoid excessive fluid (Correct Positive Fluid Balance)
  6. diuretics (Correct Positive Fluid Balance)
  7. maintain a APP > 60mmHg with vasopressors (organ support) APP = MAP - IAP
  8. optimise ventilation strategies (organ support)
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6
Q

CCP initial bundle of care for brain injury

A
  1. MAP > 80 mmHg, SBP < 110-160 mmHg
  2. Normal temp (avoid hyperthermia)
  3. PaCO2 35-40 mmHg (target normal)
  4. PaO2 80-120 mmHg (target normal)
  5. Hgb > 90 g/L
  6. HOB 30°, loosen collars/ties
  7. Optimize platelets/INR
  8. Propofol/ketamine to RASS -4
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7
Q

BP goal for an unsecured aneurysmal SAH

A

SBP < 140 mmHg

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8
Q

BP goals for ischemic CVA

A
  1. Pre lysis (r-TPA): SBP < 185 mmHg DBP <110 mmHg
  2. post lysis (r-TPA): SBP < 180 mmHg DBP <105 mmHg
  3. No lysis: SBP <220 mmHg DBP <120 mmHg
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9
Q

BP goals for acute hemorrhagic CVA

A

SBP < 140 mmHg

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10
Q

CCP treatment pathway for reducing ICP (Monroe-Kelly doctrine)

A
  1. Parenchyma (HTS, mannitol)
  2. Blood (PaCO2, BP, HOB 30 degrees, loosen collars/tube ties, OG, minimal PEEP, temperature control, sedation)
  3. CSF (EVD)
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11
Q

CCP TBI treatment plan checklist

A

A - Airway secured if needed, HOB 30 degrees, C-collar loosened, head in neutral alignment

B - PaCO2 - 35-45 (target normal), PaO2 - 80-120 (target normal), Peep <13 cmH2O

C - MAP > 80, SBP < 160 mmHg

D - Pupils, GCS, Motor exam completed and trended throughout transport.

E - Temp 36-37 (target normal, but prevent hyperthermia)

Labs - Na 140-150, Coag - INR < 1.5, PTT< 40, Platelets > 100, Fibrinogen > 1.0 Hemoglobin > 90

Herniation - Hypertonic, Mannitol, Hypervilation (PaCO 25-30)

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12
Q

first, second and third line options for status epilepticus

A
  1. Benzodiazepines (GABA)
  2. Anti-epileptics: Phenytoin, Keppra, valproic acid
  3. Infusion therapy: Propofol (GABA), Midazolam (GABA), Ketamine (NMDA)
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13
Q

neuro insults where the target SBP should be <140

A
  1. Subarachnoid bleed
  2. Epidural bleed
  3. Internal capsule bleed
  4. Ischemic stroke with hemorrhagic transformation
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14
Q

neuro insults where the target SBP should be <160 and MAP should be 80-90

A
  1. Undifferentiated TBI (SBP >110 <160, MAP >80)
  2. Subdural bleed (venous)
  3. Traumatic subarachnoid bleed
  4. DAI
  5. SCI (push that map >85 for cord perfusion!)
  6. IVH
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15
Q

pressors in neurogenic shock

A
  1. norepinephrine 1st line

2. Epinephrine if bradycardic

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16
Q

CCP interventions to reduce “parenchyma” volume (Monroe-Kelly)

A
  1. Osmotic therapy (mannitol/HTS)
  2. Sedation (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  3. Temperature control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  4. Seizure control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
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17
Q

CCP interventions to reduce “blood” volume (Monroe-Kelly)

A
  1. Hyperventilation (decreased PaCO2 leads to cerebral vasoconstriction)
  2. Head in neutral alignment (cerebral venous drainage)
  3. HOB 30 degrees (cerebral venous drainage)
  4. Loosen C-Collar/ETT Ties (cerebral venous drainage)
  5. Decrease intra-abdominal pressure (cerebral venous drainage)
  6. PEEP <13cmH2O (cerebral venous drainage)
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18
Q

Aneurysmal Subarachnoid Hemorrhage treatment goals

A
  1. securing the airway as needed
  2. blood pressure control (goal SBP <140 mm Hg)
  3. reversal of anticoagulation
  4. management of ICP
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19
Q

Aneurysmal Subarachnoid Hemorrhage treatment pathway

A
  1. IV/O2/Monitor
  2. Preliminary neuro exam
  3. secure the airway if req’d
  4. Art line/blood pressure control (goal SBP <140 mm Hg, labetalol and propofol)
  5. reversal of anticoagulation (VitK/FFP/PCC/Plt/TXA)
  6. management of ICP (mannitol/HTS)
  7. prevent secondary brain injury (optimize venous drainage, treat pain/fever/electrolytes/glucose, Consider seizure prophylaxis, optimize BP/PaO2/pCO2)
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20
Q

Intracerebral haemorrhage treatment goals

A
  1. securing the airway as needed
  2. blood pressure control (goal SBP <160 mmHg, MAP 80-90)
  3. reversal of anticoagulation
  4. management of ICP
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21
Q

Blood pressure targets in acute cerebrovascular syndrome patients

A
  1. Hypotension should be avoided and corrected when present to maintain optimal CPP
  2. Unless the patient is a candidate for IV rtPA, permissive HTN should be allowed up to 220/120 mmHg
  3. Patients receiving rtPA should have a blood pressure <185/110 mmHg before rtPA administration
  4. Post rtPA target BP <180/105
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22
Q

goal BP/MAP in multi system trauma with comorbid TBI

A
  1. MAP >80mmHg

2. SBP >110 <160

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23
Q

goal BP/MAP for ICH/intraparenchymal bleeds (deep brain parenchyma)

A
  1. ICH bleeds are normally venous = low pressure

2. Target SBP <160, follow normal TBI care plan (MAP >80, optimize venous drainage etc.)

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24
Q

CCP staged approach to refractory hypoxemia

A
  1. Increase FiO2 to 1.0 (increased diffusion gradient)
  2. Optimize PEEP (increased mean airway pressure)
  3. Switch to pressure control mode
  4. Increase RR (increased mean airway pressure)
  5. Recruitment manoever
  6. Increase Ti time (draw out your inspiratory time)
  7. Prone patient
  8. ECMO
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25
Q

CORE CLINICAL QUESTIONS in the CCP approach to mech vent

A
  1. Am I adequately oxygenating (PaO2)
  2. Am I ventilating appropriately (PaCO2)
  3. Am I on safe ground
  4. Current acid/base status
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26
Q

Asthma treatment pathway

A
  1. Oxygen (target SpO2 >90%)
  2. inhaled β-agonist and anticholinergic (salbutamol + ipratropium)
  3. Systemic corticosteroids (IV methylprednisolone)
  4. MgSO4 infusion
  5. BiPAP
  6. Epinephrine (first IM, then IV)
  7. Intubation
  8. Ongoing Ketamine infusion therapy for maintenance of anesthesia
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27
Q

CCP core principles of ventilating an asthmatic

A
  1. target a lung-protective strategy while allowing for permissive hypercapnia. Hypercapnia is well tolerated in asthmatics (who tend to be young, and with good hemodynamic reserves)
  2. Permissive Hypercapnia is the core of safe ventilation in asthma. intentionally allowing the pH to fall is often safer than trying to strictly control it (which would involve more aggressive ventilation with risks of pneumothorax or barotrauma)
  3. Young patients can often tolerate respiratory acidosis with pH <7 surprisingly well. It’s nice to see the pH >7.15 if possible, but we must balance the risks-vs-benefits of more aggressive ventilation vs higher pH
  4. autoPEEP is the main problem. autoPEEP is inevitable with severe asthma. The goal is to minimize it as possible. autoPEEP management depends on increasing the expiratory time or decreasing the tidal volume.
  5. Benefits of set PEEP include the following: [1. May help stent open the airways during exhalation (otherwise the airways may tend to be compressed by adjacent lung tissue). 2. May assist with ventilator triggering. the work of triggering the ventilator is proportional to the difference between the Intrinsic PEEP and the Set PEEP. Increasing the Set PEEP a bit will make it easier for the patient to trigger the ventilator]
  6. slow respiratory rate with normal-ish tidal volumes (10-14 bpm). A slow respiratory rate is essential to avoid autoPEEP. Ideally, tidal volumes should be maintained around 6-8 cc/kg
  7. you shouldn’t need a lot of oxygen. Asthma causes impaired ventilation, but oxygenation should be intact.
    If the patient is requiring >55% FiO2, look for another process going on (e.g., pneumothorax, aspiration, pneumonia, mucus plugging, pulmonary embolism)
  8. “Sedate to compliance”. Fairly deep sedation is needed initially. Usually a combination of propofol, opioid, and ketamine. Goal is to suppress their respiration enough to synchronize well with the ventilator. In order to ventilate these patient’s effectively they must be synchronized and compliant with the ventilator. May have to paralyze
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28
Q

CCP Acute exacerbation of COPD (AECOPD) treatment algorithm

A
  1. Oxygen (Goal saturation 88-92%)
  2. Beta Adrenergic Agonist (salbutamol)
  3. Anticholinergic/bronchodilator (ipratropium)
  4. Corticosteroids (Methylprednisolone)
  5. Antibiotic coverage
  6. NIPPV (BiPAP or HFNC as tolerated)
  7. Intubation and MV
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29
Q

approach to staged dosing for labetalol

A

Labetalol is designed to be given in bolus-dose pushes q10min

  1. 5mg (wait 10)
  2. 10mg (wait 10)
  3. 20mg (wait 10)
  4. 40mg (wait 10)
  5. 80mg (wait 10)

Stop at total of 300mg and consider another vasodilator like hydralazine, phentalomine, nitroprusside or nifedipine

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30
Q

Clinical approach to “sympathetic crashing acute pulmonary edema”

A

1) Nitrates (hydralazine is also an option, but it is less titratable and less predictable)
2) PEEP/NIPPV
3) Diuretics (IV Lasix)
4) Beta blocker (if HR > 150)
5) Transition to long-term antihypertensive (ie. labetalol and hydralazine)

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31
Q

Clinical approach to “symptomatic bradycardia”

A

1) Atropine
2) Pacing (Transcutaneous or TVP)
3) Chronotropy (epinephrine, dopamine, isoproterenol)
4) Calcium (if secondary to hyper-kalemia)
5) Insulin (for beta blocker/CCB overdose)

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32
Q

Metabolic and electrolyte variables contributing to negative cardiac inotropy (aka, metabolic shit one must correct to improve cardiac inotropy…)

A
  1. Acidosis (pH <7.20)
  2. Hypoxia (PaO2 < 60mmHg)
  3. Hyperkalemia (K+ > 5.5)
  4. Hypomagnesaemia (Mg++ <0.9)
  5. Hypocalcaemia (iCa++ <1.0)
  6. Hypophosphataemia (PO4- <0.8)
  7. Thiamine deficiency
  8. Cortisol deficiency
  9. Thyroxine deficiency
  10. Alkalosis
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33
Q

Target electrolyte levels in the setting on an AMI

A
  1. Ca+ > 1.0 mmol/L (Low serum calcium is independently correlated with LV systolic dysfunction in CAD patients with and without AMI)
  2. K+ 3.5-4.5 mmol/L (in setting of ACS, hypokalemia defined as potassium levels <3.5 is associated with ventricular arrhythmias)
  3. Mg+ >1.0 mmol/L (low serum Mg levels may be associated with cardiac arrhythmias and sudden death. Magnesium has antiarrhythmic effects. Normal range for Mg is 0.7 to 1.0)
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34
Q

NSTEMI treatment pathway

A
  1. ASA
  2. P2Y12 inhibitors
  3. Statin therapy
  4. Beta blockade
  5. Nitrates
  6. Systemic anticoagulation
  7. Maintain normoxia
  8. Optimize electrolytes
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35
Q

treatment pathway for tamponade

A
  1. Fill the tank: isotonic fluid bolus
  2. Augment rate: Allow tachycardia
  3. Improve Forward flow: Levophed
  4. Remove effusion: pericardiocentesis
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36
Q

treatment pathway for Aortic stenotic disease

A
  1. increase LVEDV
  2. slow HR

The goal is to generate elevated LV pressures to facilitate LV outflow

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37
Q

treatment pathway for Aortic regurgitant disease

A
  1. Increase HR

The goal is to reduce diastolic regurgitant time into the LV. “Clear” the regurg by moving volume forward at a faster rate

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38
Q

treatment pathway for aortic stenosis

A
  1. preload-dependent
  2. judicial fluids
  3. Avoid preload-decreasing drugs
  4. Vasopressors for cardiogenic shock (Phenylephrine, norepinephrine)
  5. sensitive to both bradyarrhythmia and tachydysrhythmias (Treat both aggressively)
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39
Q

treatment pathway for aortic regurgitation

A
  1. treat underlying cause (dissection, endocarditis)
  2. emergency surgical valve repair or replacement
  3. Inotropes (dobutamine)
  4. Correct pulmonary edema (nitrates/lasix/CPAP)
  5. Afterload reduction
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40
Q

treatment pathway for mitral regurgitation

A
  1. treat underlying cause (ischemic MR vs non-ischemic MR)
  2. emergency surgical valve repair or replacement
  3. Inotropes (dobutamine)
  4. Correct pulmonary edema (nitrates/lasix/CPAP)
  5. Afterload reduction
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41
Q

ACS treatment pathway

A
  1. Dual antiplatelet therapy (Aspirin + P2Y12 inhibitor)
  2. Anticoagulant (UFH/enoxaparin/fondaparinux)
  3. Oxygen (sats >90%)
  4. Rate control (Metoprolol)
  5. Analgesia (NTG, opioids)
  6. Statin therapy
  7. Reperfusion (TnK or PCI)
  8. Angiotensin-converting enzyme inhibitors
42
Q

PULMONARY EDEMA + LOW BP (“wet and cold” Cardiogenic Shock) treatment algorithm

A
  1. IV/O2/Monitor
  2. differentiate shock (contractility vs structural)
  3. optimize the MAP (norepinephrine)
  4. fix the lungs (CPAP/NIPPV/Intubation)
  5. optimize volume status (fluid bolus vs lasix)
  6. consider inotrope for HFrEF (dobutamine)
  7. treat underlying etiology
  8. mechanical circulatory support (ECMO)
43
Q

treatment goals for acute cardiogenic shock

A
  1. Address the underlying cause of shock
  2. If shock is from pump failure, patients are frequently extravascularly fluid-overloaded but intravascularly volume-depleted
  3. Fluid challenges in 250-mL isotonic crystalloid boluses with frequent re-assessment if intravascular volume status
  4. if patient is still hypotensive post fluids, start an adrenergic agonist (norepinephrine)
  5. Dobutamine is a good option for inotropy when the primary mechanism of shock is poor cardiac contractility. Patients may still require levo for hemodynamic support
44
Q

treatment for heart failure patients who are “warm and wet”

A
  1. volume removal and/or vasodilation to reduce their afterload (vasodilation shifts fluid out of the lungs without affecting the total body volume)
45
Q

Acute HF treatment goals

A
  1. fix the lungs (effusion + pulm edema)
  2. optimize the MAP
  3. optimize volume status
  4. consider inotrope for HFrEF
  5. treat underlying etiology
  6. mechanical circulatory support
46
Q

CCP principals of blood pressure management in acute aortic dissection

A

CCP treatment consists of reducing the pulse pressure-related shear force (Δp/Δt) through pharmacologic rate control followed by blood pressure control

  1. Treat the pain. The most common presenting symptom of AD is pain. Pain is classically described as sudden in onset and severe. Ongoing pain leads to sympathetic stimulation causing tachycardia and worsening shear stress. Use IV opioids to treat the pain
  2. Following adequate analgesia, a Class I recommendation based on expert consensus is to initiate intravenous β-blockade and titrate to an HR of 60 beats per minute or less. Use labetalol
  3. If the SBP remains >120 mm Hg following the initiation of β-blockade, an intravenous vasodilatory agent should be initiated to reduce the SBP to <120 mm Hg while maintaining adequate end-organ perfusion. Use hydralazine

don’t forget ongoing analgesia. start an a-line and watch your BP closely

47
Q

Clinical approach to “symptomatic bradycardia”

A

1) Atropine
2) Pacing (Transcutaneous or TVP)
3) Chronotropy (epinephrine, dopamine, isoproterenol)
4) Calcium (if secondary to hyper-kalemia)
5) Insulin (for beta blocker/CCB overdose)

48
Q

treatment pathway in acute mitral regurgitation

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
49
Q

treatment pathway for acute aortic regurgitation

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
50
Q

Sequential approach to refractory hypoxemia

A
  1. Increase FiO2
  2. Increase PEEP
  3. Paralyze patient
  4. Pressure control (square waveform)
  5. Lengthen out I-time
  6. Recruitment maneuver
  7. Prone positioning

*Don’t forget to consider a fluid bolus to improve West Zone physiology

51
Q

process for performing a recruitment maneuver

A
  1. Paralyze
  2. Switch to pressure control
  3. Prolong I-time
  4. Increase PIP to desired level
  5. Clamp tube on end-inspiration and hold for desired timeframe
  6. Dial in new vent settings with increased PEEP
  7. Monitor for changes
52
Q

Mech Vent strategy for obstructive lung disease

A
  1. High Flow (80-100lpm)
  2. Prolonged expiratory time (I:E of at least 1:3)
  3. Lower RR (10 to 14 frequency, monitor capnographic waveform)
  4. Lower Vt (Keep tidal volumes below 8mL/kg)
  5. Allow permissive hypercapnia; target pH instead
  6. Lung protection (Keep Pplat <30cmH2O)
  7. Monitor autoPEEP carefully
  8. Ongoing bronchodilator therapy
53
Q

initial settings for BiPAP in COPD

A
  1. IPAP 12 cmH2O and EPAP 6 cmH2O.
  2. Wean FiO2 to maintain saturation 88-92%.
  3. Titrate IPAP and EPAP while maintaining at least 5 cmH2O ∆
  4. Titrate up 2 cmH2O q5min prn
  5. If there is no improvement after approximately 1 h, the patient requires intubation
54
Q

initial settings for IPPV in COPD

A
  1. AC-Volume
  2. RR: 8-10 breaths/min
  3. Tidal volume: 6-8 mL/kg IBW
  4. FiO2: 40%.
  5. PEEP: 0-5 cm H2O
  6. Prolonged I:E ratio with permissive hypercapnia (prolonged expiratory time)
  7. Can increase I:E by decreasing tidal volume, increasing flow, and decreasing respiratory rate
55
Q

initial settings for NIPPV in Acute cardiogenic pulmonary edema

A
  1. CPAP 5-10 cmH2O or BiPAP 12/6
  2. Titrate PEEP/FiO2 to maintain saturation >92%
  3. Titrate by 2 cmH2O q5min prn (as tolerated based on patient comfort, vital signs, and respiratory difficulty)
  4. maintain at least 5 cmH2O ∆ if on BiPAP
56
Q

initial settings for IPPV in Acute cardiogenic pulmonary edema

A
  1. AC-Volume
  2. RR: 15-18 bpm
  3. Tidal volume: 6-8 mL/kg IBW
  4. FiO2: 100%
  5. PEEP 5 cmH2O
  6. Inspiratory flow of 60 L/min as a starting point; can increase to 80-100 L/min and titrate prn based on patient comfort
  7. Titrate PEEP per ARDSnet protocol
57
Q

initial approach to potassium balance in DKA

A
  1. If K+ is ≥3.3 mmol/L, start insulin infusion
  2. If K+ is <3.3 mmol/L, replenish potassium before initiating insulin infusion

be smart though. like, if the dude’s potassium is 3.4, and you’re pumping in like 4L of fluid, there’s probably gonna be some element of dilutional hypokalemia and you should probably put a couple bags of K+ in before you start the insulin. like this isn’t a hard and fast thing

58
Q

main tenets of DKA management

A
  1. Airway, breathing, circulation
  2. Commence fluid resuscitation (plasma-lyte or LR)
  3. Treat potassium
  4. Replace insulin (blood glucose should not be corrected by >3 mmol/L per hour)
  5. Acidosis management (bicarb for pH <6.9)
  6. Prevent complications (too fast a reversal of the hyperglycaemia/osmolarity)
59
Q

thyroid storm treatment algorithm

A
  1. ABC’s
  2. Beta blockers
  3. Anti-thyroid medications
  4. Iodine
  5. Hydrocortisone
  6. prevent hyperthermia with passive cooling and tylenol
60
Q

3 basic tenets of treating thyroid storm

A
  1. Block the effects of thyroid hormone
  2. Decrease the levels of circulating thyroid hormone
  3. Treating the inciting event and providing supportive care
61
Q

myxoedema coma treatment algorithm

A
  1. ABC’s
  2. IV thyroid hormone (Levothyroxine)
  3. High dose Hydrocortisone
  4. Vasopressors for shock
  5. Electrolyte replacement
  6. Passive warming
62
Q

Sepsis treatment pathway

A
  1. Cultures and source control (ie. drain abscess)
  2. Early Antibiotics
  3. Restore Perfusion (fluid loading)
  4. Adjuncts (ie. vasopressors, steroids, electrolytes)
63
Q

Surviving sepsis campaign sepsis bundle

A

1) Measure lactate
2) Obtain cultures
3) Begin broad-spectrum ABx
4) Isotonic 30mL/kg bolus if MAP < 65 or Lactate > 4
5) Vasopressor if MAP <65 (following fluid admin)

64
Q

refractory septic shock treatment pathway

A

1) Optimize DO2 (Preload, afterload, contractility)
2) Source control (remove infected lines)
3) Correct profound metabolic acidosis (pH <7.0)
4) Correct hypocalcemia (serum ionized Ca++ < 1.0)
5) Adjunctive therapies (corticosteroids)

65
Q

sepsis initial treatment pathway

A
  1. Early investigations to determine infectious source
  2. Early source control with appropriate antibiotics
  3. Ongoing crystalloid resuscitation (Plasmalyte or LR preferred) as long as fluid responsive (passive leg raise, IVC ultrasound, PulsePressure variability on art line)
  4. First line vasopressor NORepinephrine 2 to 200 mcg/min for MAP goal of 65 mmHg
  5. consider EPInephrine 2 to 50mcg/min if bradycardic
  6. consider vasopressin 0.03-0.04 units/min when NORepinephrine >15mcg/min
  7. foley/central line/invasive arterial monitoring
  8. trend lactate and fluid responsiveness
  9. If lactate fails to improve on subsequent readings consider septic-induced cardiomyopathy or other source of hyperlactatemia
  10. adjunctive agents such as corticosteroids if refractory shock
66
Q

Treatment goals for salicylate toxicity

A

“Alkalinize and dialyze”

67
Q

primary treatment modality for digoxin toxicity

A
  1. digoxin-specific antibody fragments (digoxin-Fab)

2. also known as “Digi-bind”

68
Q

rescue therapy for acetaminophen toxicity

A

N-acetylcysteine (NAC)

69
Q

plan for intubating a salicylate toxicity patient

A
  1. Don’t do it
  2. Don’t do it
  3. If intubating maintain or exceed minute ventilation requirements
  4. pursue aggressive bag-valve mask procedures (higher RR + Vt)
  5. ensure adequate fluid loading and hydration prior to induction. these patients are usually dry
  6. use amps of bicarb peri intubation
  7. RSI with most experienced intubator and get the tube in quick
  8. adjust vent settings to maximize minute ventilation (e.g. 8-10 cc/kg breaths, high RR)
70
Q

primary treatment for toxic alcohol poisoning

A
  1. Inhibition of alcohol dehydrogenase through either fomepizole or ethanol
  2. this prevents the development of toxic acid metabolites
71
Q

first-line treatment for cyanide poisoning

A
  1. Hydroxocobalamin
  2. 5 g IV over 30 min (may repeat dose × 1)
  3. Forms cyanocobalamin (vitamin B12)
72
Q

treatment plan for Emergency reversal of anticoagulation from warfarin for life-threatening hemorrhage in adults

A

In descending order of efficacy

  1. 4-factor PCC + Vitamin K
  2. 3-factor PCC + Factor VIIA + Vitamin K
  3. 3-factor PCC + FFP + Vitamin K
  4. FFP + Vitamin K
73
Q

treatment plan targets for correcting anticoagulation in traumatic brain injury

A
  1. Platelets >100
  2. INR <1.5 (If supratherapeutic INR consider octaplex)
  3. Target PTT <40 (If PTT too high, consider FFP)
  4. If patient is heparinized consider protamine sulphate
  5. Fibrinogen >1 (if fibrinogen <1 consider cryoprecipitate)
  6. Target Hgb >90 (transfuse PRBC if necessary)
  7. Consider TXA in low pressure bleed (such as SDH)
74
Q

CCP treatment goals for a 🔥🔥L I T🔥🔥 hemostatic resuscitation in trauma

A
  1. Minimal administration of crystalloid
  2. Prevention of acidemia
  3. Reduce coagulopathy of trauma
  4. prevent hypothermia
  5. Early transfusion of blood
75
Q

initial ventilator settings for post drowning

A

use lung protective strategy
initial settings per ARDS protocol

  1. Tidal volume 6-8 mL/kg
  2. Plateau pressure <30 mmHg
  3. PaO2 80-100 mmHg
  4. escalating PEEP
  5. gastric tube to decompress stomach and increase lung ventilation
76
Q

VGH/BC Burn Network burn resuscitation guidelines 2020

A
  1. fluid resuscitation for major burns should start at 3cc/kg/%TBSA.
  2. Perform hourly calculation of “ins” and “outs”. Titrate fluid resuscitation hour-by-hour, especially in the early phase of major burns trauma. Clinical endpoints include responses in blood pressure, heart rate, and lactate clearance.
  3. Titrate urine output to 30-50cc/hr for major burns (50-100cc/hr in electrical burns to facilitate clearance of myoglobin and decrease the risk of acute kidney injury).
  4. Use warmed, balanced crystalloids (Ringer’s Lactate or Plasmalyte-A) in major burns
  5. Keep the patient warm
77
Q

treatment pathway for hyperkalemia

A
  1. Stabilize cardiac cell membrane (Calcium)
  2. Shift potassium intracellularly (dextrose, insulin, bicarb, ventolin, MgSO4)
  3. Remove potassium from body (IV fluids, lasix, dialysis, GI binding agents [kayexalate])
78
Q

treatment pathway for severe metabolic acidosis

A
  1. Support perfusion
  2. Support ventilation
  3. Bicarb IV
  4. Hemodialysis
79
Q

treatment pathway for volume overload

A
  1. Positive pressure ventilation
  2. Nitrates
  3. Lasix
  4. hemodialysis
80
Q

acute pancreatitis treatment algorithm

A

“limit the severity of pancreatic inflammation and provide supportive care”

  1. IV fluid resuscitation (plasma-lyte or LR)
  2. correction of electrolyte and metabolic abnormalities
  3. Antiemetics
  4. Analgesia
  5. Vasopressor support for shock
  6. Nutritional support (enteral nutrition or NG feeds)
  7. Antibiotics (infected necrotizing pancreatitis or extrapancreatic infections)
  8. Management of complications (eg. EtOH withdrawal, infection, ARDS, shock)
81
Q

treatment pathway for toxic megacolon

A

primarily supportive therapy

  1. ICU monitoring
  2. fluid resuscitation
  3. correction of electrolyte and metabolic derangements, 4. broad-spectrum ABX
  4. steroids
  5. complete bowel rest
  6. surgical consult for colonic perf, necrosis, full-thickness ischemia, intra-abdominal HTN, ACS, peritonitis
82
Q

acute liver failure treatment pathway

A
  1. IV fluid resuscitation
  2. correction of electrolyte and metabolic abnormalities (hypoglycaemia)
  3. Vasopressor support for shock (norepinephrine)
  4. Corticosteroids for refractory shock (hydrocortisone)
  5. Consider administration of N-acetylcysteine
  6. Management of complications (eg. elevated ICP secondary to hepatic encephalopathy, GIB secondary to hepatic coagulopathy)
  7. broad-spectrum ABX for signs of infection
83
Q

massive UGIB treatment pathway

A
  1. IV/O2/Monitor
  2. Volume resuscitation (blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. promote gastric emptying (NG tube, metoclopramide)
  5. secure airway (see lit fluid airway algorithm card)
  6. control bleeding (Blakemore/Minnesota/Linton tube, octreotide, vasopressin)
  7. prevent further complications (prophylactic ABX, PPI therapy)
  8. STAT GI consult
84
Q

ruptured AAA treatment pathway

A
  1. IV/O2/Monitor
  2. Volume resuscitation (target SBP 70-90 mmHg with intact mental status, blood products preferred)
  3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets)
  4. Analgesia
  5. Arterial Line
  6. STAT vascular surgery consult
85
Q

CCP Interventions to correct abdominal compartment syndrome

A
  1. sedation + analgesia (Improve Abdominal Wall Compliance)
  2. head of bed elevation at 30 degrees (Improve Abdominal Wall Compliance)
  3. neuromuscular blockade (Improve Abdominal Wall Compliance)
  4. nasogastric decompression (Evacuate Intra-Luminal Contents)
  5. avoid excessive fluid (Correct Positive Fluid Balance)
  6. diuretics (Correct Positive Fluid Balance)
  7. maintain a APP > 60mmHg with vasopressors (organ support) APP = MAP - IAP
  8. optimise ventilation strategies (organ support)
86
Q

CCP principals of blood pressure management in acute aortic dissection

A
  1. ↓ pulse pressure-related shear force (Δp/Δt) through HR rate control + BP control
  2. ↓ sympathetic outflow via treating pain. AD patients has ++ pain/discomfort → sympathetic stimulation → tachycardia + worsening shear stress. Use opioids
  3. initiate IV β-blockade (labetalol). target HR of ≤60
  4. target SBP to ≤120 mmHg while maintaining adequate end-organ perfusion (stack hydralazine onto labetalol if need be)

start an A-line for titrating your vasoactives

87
Q

hemodynamic strategies and targets in aortic dissection

A

Hemodynamic goals:

  1. Heart rate (HR) <60 beats/min.
  2. Systolic blood pressure (SBP) <120 mm Hg
  3. arterial line for accurate titration of antihypertensive agents
  4. In the event of blood pressure discrepancy among extremities, dose the antihypertensive medication based on the extremity with the higher SBP
  5. Labetalol IV 10-20 mg bolus over 2 min, then 20-80 mg bolus every 10-15 min to a max of 300 mg, or initiate labetalol continuous infusion at 0.5-2 mg/min, titrate up by 0.5 mg/min every 10 min to a max of 10 mg/min.

Note: Labetalol IV has 7 times more beta blocker activity than alpha blocker activity; therefore, labetalol is often inadequate for blood pressure control

might have to stack hydralazine on top of your labetalol to hit the alpha reduction

88
Q

treatment for patients who are “cold and wet”

A
  1. Systemic hypoperfusion due to low cardiac output (cold)
  2. Filling pressures are elevated (wet)
  3. Giving volume will worsen their pulmonary congestion (making them wetter)
  4. Removing volume will worsen their systemic hypoperfusion (making them colder)
  5. Management of cold and wet cardiogenic shock usually requires interventions to improve cardiac function (e.g., inotropic medications, revascularization, or a mechanical support device)
89
Q

treatment goals for acute cardiogenic shock

A
  1. Address the underlying cause of shock
  2. If shock is from pump failure, patients are frequently extravascularly fluid-overloaded but intravascularly volume-depleted
  3. Fluid challenges in 250-mL isotonic crystalloid boluses with frequent re-assessment if intravascular volume status
  4. if patient is still hypotensive post fluids, start an adrenergic agonist (norepinephrine)
  5. Dobutamine is a good option for inotropy when the primary mechanism of shock is poor cardiac contractility. Patients may still require levo for hemodynamic support
90
Q

treatment goals for Hypertensive acute decompensated HF

A
  1. target preload + afterload reduction
  2. ↓ Preload and Afterload w/ NTG
  3. loop Diuretics (Lasix) for preload reduction
  4. respiratory support with NIPPV or ETI
  5. Check and replenish electrolytes, particularly magnesium and potassium (arrhythmias)
91
Q

PULMONARY EDEMA + LOW BP (“wet and cold” Cardiogenic Shock) treatment algorithm

A
  1. IV/O2/Monitor
  2. Differentiating the shock (pump failure vs mechanical complications)
  3. optimize the MAP (vasopressors)
  4. fix the lungs (CPAP/NIPPV/Intubation)
  5. optimize volume status (fluid bolus vs lasix)
  6. consider inotrope for HFrEF (dobutamine)
  7. treat underlying etiology
  8. mechanical circulatory support
92
Q

treatment pathway for aortic stenosis

A
  1. preload-dependent
  2. give fluids
  3. Avoid preload-decreasing drugs
  4. Vasopressors for cardiogenic shock (Phenylephrine, norepinephrine)
  5. sensitive to both bradyarrhythmia and tachydysrhythmias (Treat both aggressively)
93
Q

treatment pathway in acute mitral regurgitation

(rupture of chordae tendinae or papillary muscles from ischemia)

aka how to augment your CO equation to optimize forward flow (DO2) in mitral regurgitation

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
94
Q

treatment pathway in acute mitral stenosis

aka how to augment your CO equation to optimize forward flow (DO2) in mitral stenosis.

A
  1. preload normal
  2. afterload normal
  3. HR low (prevent pulmonary edema/back flow)
  4. contractility normal
95
Q

treatment pathway for acute aortic regurgitation

aka how to augment your CO equation to optimize forward flow (DO2) in aortic regurgitation

these guys are fucked and the AR is usually due to either a dissection or a savage endocarditis

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
96
Q

CO goals in aortic stenosis

aka how to augment your CO equation to optimize forward flow (DO2) in aortic stenosis.

A
  1. preload high (force blood through the tiny little hole)
  2. afterload normal
  3. HR low (prevent pulmonary edema/back flow)
  4. contractility high (force blood out)
97
Q

Metabolic variables to augment to increase cardiac inotropy

A
  1. Acidosis (pH <7.20)
  2. Hypoxia (PaO2 < 60mmHg)
  3. Hyperkalemia (K+ > 5.5)
  4. Hypomagnesaemia (Mg++ <0.9)
  5. Hypocalcaemia (iCa++ <1.0)
  6. Hypophosphataemia (PO4- <0.8)
  7. Thiamine deficiency
  8. Cortisol deficiency
  9. Thyroxine deficiency
  10. Alkalosis
98
Q

treatment pathway for tamponade

A
  1. Optimize preload with a fluid bolus (remember that tamponade is OBSTRUCTIVE and not cardiogenic shock. obstructive shock patients are preload dependent d/t elevated RV afterload
  2. Augment rate: Allow tachycardia (in your CO equation your preload/afterload/contractility are all fucked so if you want to maintain MAP you’ll have to keep the HR a little bit higher)
  3. Improve Forward flow: Levophed (if they are in shock you’ll have to support their hemodynamics with vasopressors. levy is 1st line)
  4. Remove effusion: pericardiocentesis
99
Q

NSTEMI treatment pathway

A
  1. “Dual anti platelet therapy” (ASA + P2Y12 inhibitors)
  2. Statin therapy (atorvastatin)
  3. Beta blockade (metoprolol)
  4. Nitrates (NTG)
  5. Systemic anticoagulation (heparin/LMWH)
  6. Maintain normoxia (SpO2 >90%)
  7. Optimize electrolytes (target normal range)
100
Q

Clinical approach to “symptomatic bradycardia”

A

1) Atropine
2) Pacing (Transcutaneous or TVP)
3) Chronotropy (epinephrine, dopamine, isoproterenol)
4) Calcium (if secondary to hyper-kalemia)
5) Insulin (for beta blocker/CCB overdose)

101
Q

Clinical approach to “sympathetic crashing acute pulmonary edema”

A

1) Nitrates (hydralazine is also an option, but it is less titratable and less predictable)
2) PEEP/NIPPV
3) Diuretics (IV Lasix)
4) Beta blocker (if HR > 150)
5) Transition to long-term antihypertensive (ie. labetalol and hydralazine)

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