Critical Care Flashcards
Right/ left shift
Right shift on O2 curve – High CO2, 2.3 BPG,, low pH, methemoglobinemia
Left shift = carbon monoxide poisoning, fetal hgb
-Rightward shift of the curve indicates that hemoglobin has a decreased affinity for oxygen, thus, oxygen actively unloads
-Leftward shift: indicates increased hemoglobin affinity for oxygen and an increased reluctance to release oxygen
Sepsis Fluid Recommendations
Sepsis fluid recommendations is 30 ml/kg in the first 3 hours
Volume responsiveness
Pulse pressure variation or Stroke volume variation– If 13-15% strongly associated with volume responsiveness
Patient needs to be mechanically ventilated, on a controlled mode
No spontaneous breathes
Must be in sinus rhythm
Inferior Vena Cava – Ultrasound to assess volume responsiveness
Can be done if intubated or not
Performed in subxiphoid location
Measure IVC diameter 2 cm below hepatic veins
Diameter < 2 cm, or compressibility of 12% if intubated, 25-50 if spontaneously breathing indicates volume responsiveness
Milrinone
Milrinone inhibits cAMP phosphodiesterase
-Increases cAMP-> increases Ca -> increases myocardial contraction (inotropic) -> increases CO
-Also. is a pulmonary vasodilator
Digoxin
Inhibits Na/K transporter
Dopamine
- Low dose 1-5: renal dopamine receptors
- Medium dose 5-10: B1 and B2 (inotrope)
- High dose 10-15: A1
Phenylephrine
-Purely alpha
-Can cause reflex bradycardia when tone is lacking- worsening spinal cord injury
Norepinephrine (Levophed)
Alpha and some Beta 1
-Stimulates alpha-1, alpha-2, and beta-1 adrenergic receptors
-Increased contractility with peripheral and splanchnic vasoconstriction
Vasopressin
V1 vascular, V2 renal, V3 endothelial
Arginine
Precursor to nitric oxide, NO
Intra-Aortic Balloon Pump (IABP)
Inflates on T, deflates on R
-Increase coronary perfusion by inflating during diastole after aortic valve closure, to help propel blood into coronary ostia (perfuse stressed myocardium). CO moderately increased by unloading LV (deflates during systole to create a vacuum)
Contraindications: severe aortic regurgitation (worsens when the bloon inflates durng diastole), aortic aneurysm, aortic dissection
Hypothermia protocol
Hypothermia protocol (Targeted temperature management)
Best evidence to use with “out of hospital cardiac arrest” who show up with Vfib or Vtach
In hospital cardiac arrest is controversial
Target temperature 32 – 36 degrees Celsius for 24-72 hours then gradual rewarming
Improves neurologic outcome
Successful extubation
-Spontaneous breathing trial with pressure of 5-8 cm H2O for at least 30 minutes and max of 2 hours
-Can use noninvasive ventilation
-Steroids if negative cuff leak
Dead space
Dead space
V=ventilation, Q=perfusion
Lung ventilated but not perfused
MCC of increased dead space (increased V/Q) = excessive PEEP (due to capillary compression)
Also PE, pulm HTN
Increased dead space = increased PcO2
Shunt
Poor ventilation, good perfusion
MCC of shunt (decreased V/Q) = atelectasis
Also mucus plug, ARDS
Shunt causes Hypoxia
ARDS
Increases A-a gradient, increased pulmonary shunt Low V/Q
Conservative fluid improves ventilator free and ICU days, not mortality
Decrease barotrauma by keeping plateau pressure < 30
ARDSNET -> Permissive hypercapnia, maintaining pH > 7.20
Increase inspiratory time rather than expiratory to improve oxygenation
High frequency oscillatory ventilation, not shown to improve outcomes!! may worsen outcomes!!!!!!
Decreases mortality:
* Low TV usually 6 but 4-8 cc/kg is okay, of predicted body weight
* Paralytics, only if used in first 48 hours
* Prone decreases mortality in patient’s mod-severe ARDS, but not mild
Acute Respiratory Distress Syndrome (ARDS)
-Within 1 week of insult, characteristic radiographic finding, not cardiogenic
-Mild: P:F ratio = 200-300
-Moderate: P:F ratio = 100-200
-Severe: P:F ratio = <100
-Ventilator strategies for ARDS
-Lung protection ARDSNET protocol – Low tidal volume (4- 6cc/kg)
-Permissive hypercapnia
-If pH above 7.20, recommended to allow hypercapnia as long as patient is oxygenating; avoids further lung injury
-Strategies for ARDS patients that are failing
-Airway Pressure Release Ventilation (APRV)
-Long inhalation period with short extubation
-Set P-high (Pressure High) and P-Low (Pressure Low)
as well as T-high (Time High) and T-Low (Time Low)
-Want long T-high and short T-low
-Patient can breathe spontaneously throughout
-Proning
-Nitrous Oxide, NM blockade
Epinephrine
Alpha and Beta 1
Dobutamine
-Beta 1 agonist: contractility agent= increases cardiac output
-At higher doses: can also exert beta-2 agonist effect= peripheral vasodilatory effects
*used in cardiogenic shock but its side effects include increased myocardial oxygen demand and arrythmogenicity
ECMO
Consider ECMO when the PaO2/FiO2 < 150 in ARDS or bronchopleural fistula
Can do ECMO without heparinizing at all by using heparin-bonded circuitry
OK to use in trauma patients even with TBI
Trauma patients on ECMO do better than others
Outcomes of venovenous are better than venoarterial
Traditional cannulation = femoro-jugular. Now we have double lumen cannula, single site
DKA
DKA – the only absolute contraindication to starting insulin is hypokalemia of <3.3. If K is < 5.3 start insulin rip and give potassium
Spinal cord injury with bradycardia
vagally mediated and treated with atropine. Don’t use transcutaneous pacing
Mixed venous saturation (SvO2)
– measured in pulmonary artery ~75%
- Elevated SvO2 (>75%) occurs with: Shunting of blood (septic shock, cirrhosis, L->R cardiac shunt) OR decreased O2 extraction (hypothermia, paralysis, coma, cyanide poisoning)
- Decreased SvO2 (<75%) occurs with: Decreased O2 delivery (low CO, CHF, hypoxia, low Hct, low volume) OR Increased O2 extraction (malignant hyperthermia)
Distributive shock
-Anaphylactic, septic, neurogenic
-Decreased CVP and decreased SVR
-All other forms of shock SVR decreases
-Neurogenic: damage to brain, cervical spine, high thoracic spine; vasodilation, decreased peripheral resistance, brady cardia; IF fluids; dopamine, norepinephrine; extremities “well perfused” warm/pink b/c loss of sympathetic tone= widespread vasodilation= blood pooling
Air emboli from central venous catheter
Air emboli from central venous catheter – place in left lateral decubitus and Trendelenburg (head up, feet down)
- Will get abrupt rise in end tidal CO2, followed by a decrease in CO2 and hypotension
- Mill wheel murmur, JVD, right heart strain on EKG
- Most sensitive bedside test TEE!!!
Delirium
Delirium – associated with low levels of acetylcholine (control attention and consciousness) That’s why you avoid anti-cholinergic here
Once diagnosed with delirium, delirium itself as well as complications from it can last for up to ONE YEAR!!!
Risk factors:
- Age!! >70 especially
- Existing cognitive impairment
- Vision impairment
- History of alcohol abuse
Using Precedex for sedation in ICU is associated with lower delirium vs other drugs
Intra-op rise in end tidal CO2
Intra-op rise in end tidal CO2 – MCC disconnected from circuit, PE, accidental extubation, obstructed airway
Decrease the risk of VAP in ICU, Ventilator bundle:
- Elevate HOB
- SBT
- Daily sedation vacation
- Oral chlorhexidine
- DVT px
- PUD px
Carbon monoxide poisoning
Left shift on O2 curve
Binds to heme to create carboxyhemoglobin, has higher affinity than O2
History: inhalation injury from fires = MCC
1st symptom is neurologic. Will see persistent metabolic acidosis
Oxygen saturation will be 100% but innacurate
Tx = 100% FIO2. High flow vs intubation
Indications for intubation hoarseness, stridor, > 40%TBSA (needs massive fluid)
- Hyperbaric oxygen indicated for impaired neurological status AND carboxyhemoglobin level >25%
Methemoglobinemia
Characterized by iron in hemoglobin becoming oxidized and unable to bind oxygen
Oxygen carrying ferrous 2+ is oxidized to form ferric 3+ forming mathemoglobin, cant bind oxygen
Chocolate brown arterial blood
O2 sat reads 85%., so pulse ox is unreliable
Tx: Methylene blue
Shock
-Swan Ganz Patterns – Less commonly used
-Hemorrhagic shock: Low CO, High Systemic vascular resistance (SVR), Low filling pressures (CVP/PWP)
-Septic shock: high CO (may be low in late septic shock), Low SVR, Low/ Normal filling pressures (CVP, PWP)
-Cardiogenic shock: Low CO, High SVR, High filling pressures (CVP, PWP), low venous O2 saturation
Septic Shock
If giving steroids give < 400mg/day of hydrocortisone (100 mg q8) for at least 5 days decreases mortality
Norepinephrine infiltrated in arm
If norepinephrine infiltrated in arm, can give phentolamine (alpha blocker) to prevent compartment syndrome and skin necrosis
Sepsis
-Old definition: focused on inflammation; SIRS criteria
-SIRS if ≥ 2 of the following 4 criteria:
-Temperature: > 38°C or < 36°C
-Heart rate: > 90/min
-Respiratory rate: > 20/min or PaCO2 < 32 mm Hg
-WBC: > 12,000/mm3, < 4000/mm3, and/or > 10% bands cells
-Sepsis: SIRS PLUS a suspected or confirmed underlying infection
-Severe sepsis: sepsis PLUS dysfunction of at least one organ or system
-Septic Shock: severe sepsis + hypotension/pressor requirement
- Vasopressors required to maintain mean arterial P ≥ 65 mm Hg.
-Persistent lactic acidosis: lactate > 2 mmol/L (18 mg/dL) despite fluids
-New definition of sepsis: organ dysfunction with infection (SOFA Score)
-SOFA = Sequential Organ Function Assessment
-Measures:
-Ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2)
-Amount of vasoactive medication necessary to avoid hypotension
-Bilirubin level
-Platelet count
-Glasgow coma score
-Serum creatinine or urine output
-Sepsis = If SOFA score inc by 2+ points, or a score of 2+ on initial presentation
-Septic Shock = Pressor requirement AND lactate of 2 or more despite resuscitation
-Diagnostic adjuncts:
-Procalcitonin – when normalizes can be a guide to stop antibiotics. Better at ruling out sepsis if negative; More sensitive than specific
-1,3 beta-d-glucan assay for fungal infections
-Mannan antigen and anti-mannan antibody for invasive candidiasis
-Management
-Within 3 hours: start antibiotic (send cultures prior), bolus with 30cc/kg crystalloid if lactate >4
-Within 6 hours: start pressors (norepinephrine/Levophed recommended over dopamine, vasopressin added as secondary) if needed to maintain MAP, repeat lactate
-Adrenal insufficiency in Septic Shock: generally do not do a stimulation test – if refractory shock and suspect adrenal insufficiency, empirically treat with hydrocortisone
-Tight glucose control associated with worse outcomes; shoot for <180
Glucose
Peri-op glucose, and surgical ICU patient glucose, and septic patient glucose should be 140-180. NOT 80-120, based on sugar trial, strict glucose was associated with worse outcomes 2/2 to hypoglycemic events
Pulmonary artery wedge pressure
Pulmonary artery wedge pressure – should be obtained at end expiration (intrathoracic pressure is lowest)
- If patient has hemoptysis after inflation possible rupture of pulm artery. Leave inflated, go to angiography
Pulmonary capillary wedge pressure estimates left atrial pressure. > 15 suggest left heart failure
Variables that effect pulse ox reading
-Nail polish that is not dark blue, brown, or black will not interfere with readings – don’t need to be removed
- Venous congestion
- Hypothermia/vasoconstriction
- Electrocautery
Nitroglycerin
– venous vasodilation. Moderate coronary vasodilator. Decreases preload, and O2 requirement of heart
Cyanide toxicity
Cyanide toxicity - disrupts electron transport chain. Gets left to right shunt.
Occurs in smoke inhalation injury, fires = MCC
Also, sodium nitroprusside can cause this
Severe lactic acidosis = hallmark of cyanide toxicity.
High SVO2
Dx: Can check thiocyanate level
Tx: Best one to give is hydroxocobalamin Or can try inhaled Amyl nitrite + intravenous sodium nitrite
Risk of OSA
- Loud snoring, BMI > 35, age > 50, male gender, HTN
Patients with open abdomen for damage control surgery
feed them enterically with TF immediately enteral nutrition increases chance of primary abdominal closure and decreases risk of pneumonia
-Oxygenation vs Ventilation:
-Oxygenation affected by: Fi02, PEEP, Mean Airway Pressure
-Ventilation affected by: RR x Tidal Volume= Minute Ventilation
Ventilator Settings and Management
-Peak pressure: pressure in large airways
-Plateau pressure: must do inspiratory pause -> pressures equilibrate, better reflects alveolar pressure
-Large differential between peak and plateau pressure (e.g. Peak 50, Plateau 30):
-Large airway obstruction, bronchospasm
-Peak and plateau both high: Alveolar lung disease (e.g. ARDS)
-Negative inspiratory Force (NIF): must do expiratory pause to check
Continuous mandatory ventilation (CMV)/Assist Control (AC)
-Respiratory Rate (RR) and Volume set
-Every breath is fully supported
-Problems:
-Volume set regardless of P-> barotrauma
-Hyperventilation if patient RR high
Pressure Support (PS)
-Pressure set
-Limits barotrauma but hypoventilation
Synchronized Intermittent Mandatory Ventilations (SIMV)
-RR and Volume set
-Spontaneous breaths above set rate not fully supported
-Delivered breaths synchronized= more comfortable
-Patients can tire out
Cardiovascular physiology
-Central Venous Pressure (CVP): surrogate for end diastolic right ventricular volume
-Pulmonary Wedge Pressure (PWP): surrogate for end diastolic left ventricular volume
-Cardiac Output (CO)= Stroke volume x Heart Rate
-Cardiac index (CI)= Cardiac Output/Body Surface Area
Oxygen delivery/ consumption
-Oxygen Delivery = CO x [Hb x 02 Saturation x 1.34 + (Pa02 x 0.003)]
-Oxygen Consumption = CO x (Arterial-Venous 02 difference)
-Extraction Ratio = O2 Consumption/O2 Delivery
-Decreased by: sepsis, cardiac failure, anemia/hypoxia, fever, seizure
Hemoptysis after Swan Ganz Balloon Inflation?
-Ruptured pulmonary artery
-Tx: Angioembolization
Tachyarrhythmia, Torsades de Pointes on EKG?
-IV Magnesium
-No brainstem reflexes, fixed and dilated pupils, normotensive,
normothermic. What’s next to declare brain death?
-Apnea Test
Post Op Day 2 CABG patient with decreased chest tube output followed by PEA?
-Cardiac Tamponade
-Tx: Cut wires and open chest in ICU
-Frequent IV Haldol doses for ETOH withdrawal followed by arrhythmia?
-Prolonged QT
-Patient with positive UA with MAP of 60 and lactate of 4.5?
-Septic Shock
-5yo trauma patient with bradycardia during attempted intubation?
-Atropine
-Post Op CABG patient with hypotension with CVP and wedge pressure of 20?
-Cardiac Tamponade
-Critically ill patient in sudden drop in end tidal CO2?
-Decreased cardiac output or cardiac arrest
-Large volume paracentesis for ascites in a cirrhotic patient followed by oliguria and elevated Cr, Urine Na is less than 10?
-Hepatorenal syndrome
-Tx: Albumin and vasopressin; transplant
Classes of hemorrhagic Shock
Up to 2 L of crystalloids can be used but early blood products better ou
Acute heart failure post op
Chest pain, respiratory failure, bilateral pulmonary congestion, EKG changes (ST depression in anterior leads)
Tension pneumothorax
-Intrathoracic pressure (normally negative) becomes increasingly positive as air accumulates in pleural space
-Positive pressure shifts thoracic and mediastinal structures= diminished venous return= decreased stroke volume= decreased CO
-Sx: respiratory distress, tachycardia, hypotension, tracheal deviation, absence of breath sounds, neck vein distention
-differentiate from cardiac tamponade: hyperressonance, absence of breath sounds on affected sounds
-Dullness on percusion= hemothorax
Occult tension PNX on ventilator: high peak airway pressure (> 30 cm H2O), high PEEP (> 15 cm)
Over fluid resucitation with heart failure
Frank-Starling relationship: increased left ventricular end-diastolic volume (preload) = increased force and volume of contraction during systole
systolic heart failure: impaired contractility of left ventricle leads to decrease in cardiac output
Frank-starling curve flattens at high end-diastolic volume= further reduces CO because of decrease in cardiac contractility
Tx of systolic heart failure in setting of fluid overload= inotropic drugs (dobutamine), diuretics
Transcutaneous pacing
-Indicated in the setting of unstable and symptomatic bradycardia until patient is stabilized and either an adequate rhythm has returned or a transvenous pacemaker is inserted
-Initiated without delay wehn there is impairment in the conduction system resulting in high-degree block (Mobitz type II second-degree block or third-degree AV block)
-Third-degree AV block: complete lack of conduction between the atrium and ventricles; EKG= no association betwee P and QRS waves
Senile calcification
Most common etiology of acquired aortic stenosis
-Normal leaflets become calcified as a result of normal leaflet stress at flexion points= leaflet immobility
Any symptoms related to aortic stenosis requrie replacement of the aortic valve (e.g. angina, syncope)
Normal valve area 3-4 cm2
symptomatic when aortic valve less than/equal to 1 cm 2
VAP empiric antibiotic therapy
-Should cover gram-negative bacilli, pseudomonas aeruginosa, and staphyloccoccus aureus
-Zosyn + vancomycin/linezolid
-Meropenem + vancomycin/linezolid
-Cefepime + vancomycin/ linezolid
-most common: pseudomonas or MRSA
Abdominal compartment syndrome
-Intra-abdominal HTN leading to multiorgan dysfunction (e.g. third-spacing from IV fluids due to inflammatory cytokines released in pancreatitis)
-Increased intracranial P (> 15 mmHg)
-Impaired oxygenation with elevated peak inspiratory pressures (> 40 cmH2O) 2/2 decreased lung and chest wall compliance
-Cardiac failure as a result of decreased preaload, elevated intrathoracic pressure
-Oliguric renal faiure: direct effects on renal parenchyma/veins and decreased cardiac output and increased SVR (> 1,500 dynes/sec/cm^-5)
-GI ischemia due to decreased splanchnic perfusion
-Abdominal wall musculocutaneous ischemia
Most common cause of mortalit for cardiac transplants 1 year after surgery
sudden cardiac death suspected to be due to graft vasculopathy
also infection
Pre-renal azotemia
Pre-renal azotemia: rise in creatinine, decreased urinary output, fractional excretion of sodium < 1%; clinical improvement with fluids (e.g. dehyrdation)
Acute tubular necrosis: “muddy brown casts” epithelial cells; lack of improvement with fluid bolusing
Rhabdomylosis: elevated creatinine kynase and myoglobinuria
CSW
-Cause of hyponatremia in CNS disease especially aneurysmal subarachnoid hemorrhage
-Hyponatremia and extrcellular fluid depletion due to inappropriate sodium wasting in urine; elevated urine output
=Tx: isotonic or hypertonic fluid +/- sodium supplementation =/- fludrocortisone
-Avoid correcting sodium more than 10 mEq/L over 24 hours to avoid central pontine myelinosis
Difference between SIADH: euvolemic or hypervolemic; tx= demeclocycline
CSW=hypovolemic, dehydrated
Bleeding noted on either side of transected sternum after clamshell thoracotomy
-Internal mammary (internal thoracic) branch of subclavian artery commonly injured in clamshell thoracotomy; must identify and ligate
Elective surgery after DES
-Should be postponed at least 6 months after DES implanation
-Can be safely shortned to 3-6 months if needed
Aortic insufficiency
-High pitched decrescendo diastolic murmur, best heard along left sternal border
-Angina when sleeping= heart rate slows= decreased diastolic pressure (cardiac cycle when myocardium receives oxygenated blood flow)=decreased coronary perfusion
Supraventricular tachycardia: narrow, regular QRS complex without P-waves
Stable patient: vagal maneuvers, IV adenosine
-6 mg IV adenoside as a rapid IVP bolus, followed by 20 mL normal saline flush; if initial dose unsuccessful can give second dose of 12 mg
Unstable: synchronized cardioversion
Emergent surgery for cirrhotic
-Give FFP and vitamin K
-high PT/high INR
Treatment for aspergillosis
Voriconazole
-In immunocompromised; risk factors= neutropenia, glucocorticoid use
Thoracentesis position
-Insert needle along superior edge of rib to avoid injury to intercostal vessels and nerves
Postcardiotomy syndrome
-Pleuritic chest pain and fever within a few weeks after pericardial injury/invasion (e.g. CABG)
-Elevated: WBC, ESR, CRP
-EKG: diffuse ST-segment elevation in association with PR depressions
-1st line treatment: NSAIDS +/- colchicine
Atrial fibrillation
-Stable: beta blockers or calcium channels; amiodarone in CHF or if AV nodal blockade failed
-Unstable: synchronized cardioversion
Isoproterenol
-Inotropic and chronotropic agent; increases heart rate and cardiac contracility; causes peripheral vasodilation.
-Used diagnostically to provoke arrhythmias and latent ventricular outflow gradients in symptomatic hypertrophic cardiomyopathy without sings of obstruction
Berlin criteria
Example: PaO2 60% on a FiO2 of 80%= 60/0.8=75= Severe
Ventilator dyssynchrony
-Reverse triggering (breath stacking) due to respiratory muscle effort triggered by reflex mechanisms (diaphragmatic contractions triggered by ventillator insufflation) resulting from ventilator-delivered breath during pressure-controlled ventilation
-Dyssynchrony usually observed in deep sedation and resolves with light sedation and paralytic agent
HFpEF
Blood pressure controll with beta blockers, angiotensin-converting enzyme inhibitors, or hydralazine
Central diabetes insipidus
-ADH produced by hypothalamic neurons in supraoptic and paraventricular nuclei; migrates to posterior pituitary gland= stored
-ADH acts on vasopressin receptors; 3 subtypes= V1a, V1b, V2; increases water absorption in distal nephron via stimulation of V2 receptors that increase aquaporin on surface of collecting duct (concentrating urine)
-Central diabetes inspidus= decrease in activation v2 receptors on distal nephrons= hypotonic polyuria, hypernatremia; tx= desmopressin
-Trauma, tumors
Nephrogenic insipidus: vasopressin resistant; tx= thiazide diuretic
