CCP Treatment Plans Flashcards

Question

CORE CLINICAL QUESTIONS in the CCP approach to mech vent

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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)

Answer 7

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)

Answer 8

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

Answer 9

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)

Answer 10

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

Answer 11

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

Answer 12

1. increase LVEDV 2. slow HR The goal is to generate elevated LV pressures to facilitate LV outflow

Answer 13

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

Answer 14

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)

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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)

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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

Answer 23

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)

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

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

Answer 34

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)

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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)

Answer 40

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)

Answer 41

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

Answer 42

“Alkalinize and dialyze"

Answer 43

1. digoxin-specific antibody fragments (digoxin-Fab) | 2. also known as "Digi-bind"

Answer 44

N-acetylcysteine (NAC)

Answer 45

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)

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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)

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

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])

Answer 54

1. Support perfusion 2. Support ventilation 3. Bicarb IV 4. Hemodialysis

Answer 55

1. Positive pressure ventilation 2. Nitrates 3. Lasix 4. hemodialysis

Answer 56

"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 4. Antiemetics 5. Analgesia 6. Vasopressor support for shock 7. Nutritional support (enteral nutrition or NG feeds) 8. Antibiotics (infected necrotizing pancreatitis or extrapancreatic infections) 9. Management of complications (eg. EtOH withdrawal, infection, ARDS, shock)

Answer 57

primarily supportive therapy 1. ICU monitoring 2. fluid resuscitation 3. correction of electrolyte and metabolic derangements, 4. broad-spectrum ABX 5. steroids 6. complete bowel rest 7. surgical consult for colonic perf, necrosis, full-thickness ischemia, intra-abdominal HTN, ACS, peritonitis

Answer 58

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

Answer 59

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

Answer 60

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

Answer 61

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)

Answer 62

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

Answer 63

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

Answer 64

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)

Answer 65

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

Answer 66

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)

Answer 67

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

Answer 68

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)

Answer 69

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

Answer 70

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

Answer 71

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

Answer 72

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)

Answer 73

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

Answer 74

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

Answer 75

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)

Answer 76

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)

Answer 77

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)