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= pulmonary vascular vasodilator in areas where there is good lung ventilation= improves ventilation-perfusing matching, 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
Classes of hemorrhagic Shock
Up to 2 L of crystalloids can be used but early blood products better ou
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
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
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
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
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
