Shock Flashcards
Definition of Shock
- common symptoms
- SBP under 90 or a drop of 40+ from normal
- sudden drop of blood flow through the body –> tissue hypoxia
- MAP usually under 65
- cold and clammy (or warm early on), weak and rapid pulse, irregular breathing, JVP low or high, decreased LOC, decreased urine output, low O2 sat, dilated pupils, dry mouth, delayed cap refill, hyper or hypocapnea
*SBP and pulse pressure may initially be high but will eventually drop
SIRS criteria
- two or more of:
- temperature above 38 or below 36
- HR above 90
- RR above 20, PaCO2 under 32
- WBC over 12000 or under 4000, over 10% immature neutrophils
Equations for:
- CO
- MAP
CO = HR x SVR (maintained by compensating tachycardia)
MAP = ((2xDBP)+SBP)/3
Different Types of Shock
- general treatment methods
- Cardiogenic –> MI, arrythmias, heart failure, valve disease, ischemia
- reversal of cause, inotropes
- Hypovolemic –> hemorrhage, GI loss, capillary leak, burns, trauma, dehydration
- volume infusion
- Obstructive –> PE, tension pneumothorax, tamponade, valve disease
- relieve obstruction
- Distributive –> sepsis, anaphylaxis, neurogenic (SCI), adrenal insufficiency (Addison’s), liver failure
- volume and vasopressor support
- Other –> cellular poisons (CO, methemoglobinemia, cyanide)
- antidote
Complications of Shock
- ischemia, decreased LV compliance, increased LDP
- pulmonary edema, respiratory failure
- decreased GFR, blood flow redistributing from renal cortex (oliguira)
- transaminitis, cholestasis
- ileus, mesenteric ishcemia
- delirium, encephalopathy
- hyper/hypoglycemia, hyperK
- typically metabolic acidosis with respiratory compensation
Common Diagnostic tests for Shock
- increased lactate
- low mixed and central venous O2 saturation
- increased WBCs
- altered ABGs
- high K and urea
- low sodium
- increased or decreased glucose
- also check PT/PTT/INR, BUN, Cr, liver, cultures, pregnancy, urinalysis, cortisol, etc.
- ECG, CXR, maybe CT
Pathology Pathway of Shock
- inadequate perfusion –> cell hypoxia –> lactic acid increase and pH decreases (anaerobic metabolism buffers lactic acid into lactate) –> metabolic acidosis (vasoconstriction, sphincter failure, peripheral blood pooling) –> cell membrane dysfunction and failure of Na pump –> intracellular lysozymes release digestive enzymes (K efflux, Na/H20 influx) –> toxins in circulation –> damage, cell death
- SNS increases vasoconstriction and HR, release of NE/E/dopamine/cortisol/ADH (RAAS to maintain intravascular volume)
- blood flow increases to the brain but decreases to kidneys/GI/periphery
- cellular death is what leads to the increase in K/urea/lactate
Criteria for Circulatory Shock
4 of:
- ill appearance or decreased LOC
- HR over 100
- RR over 20 or PaCO2 under 32
- urine under 0.5mL/kg/hr
- arterial hypotension for over 30 minutes
- arterial base deficit under -4mEq/L or lactate over 4mM/L
Consider these causes when bradycardia and hypotension
- inotrope overdose
- thyroid
- Addison crisis
- steroid withdrawal
Equation for O2 Delivery
O2 Delivery = CO x CaO2
*CaO2 = arterial O2 content
- Hgb bound = [Hgb] x O2 sat x 1.34
- Hgb dissolved = PaO2 x 0.003
*PaO2 = pp of dissolved O2 in arteries
Preload
- tension across ventricular wall and the end of diastole
- end diastolic volume x LV radius
- want to increase EDV to increase SV…to a point! if it increases too much SV will eventually decrease
- an optimal EDV is patient specific, evaluate via JVP/straight leg raise*/CVP/echo/fluid challenge/urine output/CO
*if you lift their leg and the MAP increases, they need fluids (and vv.)
Afterload
- tension across ventricular wall during systole
- LV SBP-intrapleural pressure x LV radius
- asthma is negative pressure –> increases afterload
- ventilation is positive pressure –> lower afterload
- increased LV SBP increases afterload and lowers SV
- decreased LV SBP decreases afterload and increases SV
Contractility
- lower contractility lowers SV and vice versa
Anaerobic Metabolism pathway to lactate
- pyruvate –> lactate –> only 2 ATP –> cell death
NORMALLY
- pyruvate –> Kreb’s cycle –> 36 ATP
Different types of shock and their effect on CO/SV/preload/afterload/contractility/HR/SVR/CVP etc.
*all result in decreased CO and decreased SV
Cardiogenic –> increased afterload, SVR, and CVP
- decreased contractility
-HR can either go up or down
Hypovolemic –> increased HR, contractility, SVR
- decreased preload and CVP
Obstructive –> increased afterload, HR, CVP, contractility, and SVR
- decreased preload
Distributive –> increased HR and contractility
- decreased afterload, preload, CVP, and SVR
*Hemorrhagic –> decreased preload, Hgb (CaO2)
These Signs Would Make You Suspicious Of…
- high JVP
- low JVP
- deviated trachea, asymmetric lung sounds
- extra heart sounds, crackles
- muffled heart sounds
- murmur
- wheeze
- distended/rigid abdomen
- cold, mottled skin
- warm skin
- high JVP –> obstructive/ cardiogenic
- low JVP –> distributive/ hypovolemic
- deviated trachea, asymmetric lung sounds –> pneumothorax
- extra heart sounds, crackles –> heart failure
- muffled heart sounds –> low contractility, tamponade
- murmur –> valvular disease
- wheeze –> anaphylaxis
- distended/rigid abdomen –> hemorrhage, acute abdo
- cold, mottled skin –> high SVR
- warm skin –> low SVR, septic early on
Early general treatment of Shock
- ABCs, determine underlying cause
- transfuse for Hgb over 70 in a non-bleeding patient
- inotropes for contractility (increase SV)
- IV fluids and vasopressors (increase preload)
- vasodilators and positive ventilation (decrease afterload)
- maintain sinus rhythm, treat tachy/bradycardia
ECG Approach
- What are the ventricles doing –> wide or narrow QRS
- What are the atria doing –> P waves? sinus rhythm?
- What is the AV junction doing –> PR interval, P and QRS relationship
- a prolonged PR interval is over 5 squares (0.2s)
- normal P waves are positive in II and negative in AvR
- if there is one normal rhythm strip, the rest could be artefact!
*axis –> want (+) lead I (right) and (+) aVF (down)
3 Mechanisms Causing Tachyarrythmias
- Automaticity –> seen in increased SNS states (funny current depolarization influenced)
- Triggered Activity –> early after depolarizations (long phase II) or delayed afterdepolarizations (abnormal Ca influx)
- Re-entry –> most common, requires a trigger (PAC)/ functional circuit/ 2 arms with different properties
- fast conduction pathway takes longer to repolarize, will travel up retrogradely once it has repolarized
- depends on speed and size of circuit
RBBB
- mostly degenerative, sometimes can be ischemic/ structural
- RV depolarizes later due to spread of electrical activity from the LV
- wide QRS complex (over 3 blocks) in V1/2/3
- see RSR rabbit ears in V1/V2 (LV depolarizes and repolarizes and then RV depolarizes)
- slurred S wave in aVL and V6 (slow conduction through RV, more negative in V6)
LBBB
- more commonly structural abnormalities of the LV
- LBV depolarizes later via spread of electrical activity from the RV
- wide QRS complex (over 3 blocks) in most leads
- see broad “M” in V5/6 (RV depolarizes and repolarizes and then LV depolarizes)
- deep S wave in V1 (more negative in V1)
Narrow vs Wide Complex QRS
Narrow –> ventricles depolarized via normal septal activation
- originating impulse is supraventricular
Wide –> ventricles depolarized abnormally
- impulse MAY be ventricular (dangerous)
Monomorphic vs Polymorphic Wide QRS
Monomorphic –> VT, SVT with aberrancy, SVT with pre-excitation
- each QRS looks the same and the rhythm is regular
Polymorphic –> really only VT or VF
- both automaticity/ triggered mechanisms
- sometimes A.fib with pre-excitation
- each QRS is wide but looks different, rhythm is irregular
Sinus Rhythm with PACs
- sinus, but can have early firing beats (regularly irregular rhythm)
- different P wave morphology
- narrow QRS complexes, all QRS complexes preceded by a P-wave
- not always tachyrhythmic
Sinus Rhythm with PVCs
- sinus, but can have early firing beats (regularly irregular rhythm)
- some wide QRS complexes with NO p wave preceding these complexes
Sinus Rhythm with PACs with aberrancy
- aberrancy are abnormalities in transmission due to refractoriness or low conductivity
- sinus, but can have early firing beats (regularly irregular rhythm)
- some wide QRS complexes and ALL have p waves preceding these complexes
Regular, monomorphic, wide QRS tachycardia (with history of MI/structural heart disease)
VT until proven otherwise (often re-entry mechanism due to scarring)
SVT with aberrancy vs. VT
- Aberrancy –> typical axis/RBBB/LBBB (atria is driving ventricle), P waves after or in QRS complexes
- may see flutter (2:1, 3:1, with LBBB pattern. etc.)
- VT –> weird axis and morphology
- may have AV dissociation (more QRS complexes than P waves)
- capture (normal QRS peaks amongst wide ones) and fusion beats (somewhere inbetween)
Torsades de Pointes
- specific polymorphic VT
- prolonged QT interval and alternating T wave morphologies
- triggered by a PVC that occurs during repolarization
WPW Syndrome
- bypassing Av node via accessory pathway (pre-excitation)
- wider QRS indicates more conduction via the accessory pathway
- afib can be translated to vfib –> dangerous
- do NOT give AV blockers (digoxin, BBs, CCBs), treat instead with antiarrhythmics (procainamide) or cardioversion
V fib
- irregular, chaotic deflections with no P/QRS complexes
What is typical blood pH?
How is acid produced/ excreted?
- 7.35-7.45 (acidosis is considered under 7.4, alkalosis is considered over 7.4)
- CO2, organic acids, amino acids, ketones from fat, lactic acids
- excreted by the kidneys and lungs
*glutamate, acetate, and citrate are all alkaline
Buffering Mechanisms
Bone –> acid dissolution in bone crystal (releases Ca salts and HCO3 into the ECF), can result in osteomalacia and osteoporosis overtime
Proteins –> intracellular a.a.s, Hgb in RBCs, plasma proteins i.e albumin
Bicarbonate –>
CO2 + H20 <–> H2CO3 (carbonic acid) <–>H+ + HCO3-
- lungs deal with CO2 end, kidneys with HCO3 end
Management of HCO3- by the kidneys
- causes of metabolic acidosis/ alkalosis
- proximal tubule –> tubular cells secrete H+ into fluid and reabsorb filtered HCO3- as NaHCO3 (1:1)
- carbonic anhydrase on the apical membrane and intracellularly facilitates movement of HCO3-
- distal tubule –> 10% of HCO3- reabsorption
- low HCO3- or too much acid –> metabolic acidosis
- increased acid production, loss of HCO3- from GI or kidney, kidneys unable to secrete acid (RTA)
- high HCO3- or not enough acid –> metabolic alkalosis
- loss of acid (vomiting), contraction alkalosis (more water excreted than HCO3, ECG contracts around fixed HCO3), hyperaldosteronism or hypokalemia (unable to exchange for H+)
*aldosterone itself activates the K/H symporter, resulting in lots of H excretion)
Management of CO2 by the lungs
- causes of respiratory alkalosis/acidosis
- CO2 excretion is directly paired to ventilation
- low CO2 (high resp rate) –> respiratory alkalosis
- pain, anxiety, ASA overdose, pregnancy, liver failure, sepsis, pneumonia initially, PE initially, heart failure initially
- high CO2 (low resp rate) –> respiratory acidosis
- CNS depression (drugs, trauma), myasthenia gravis, ALS, upper airway obstruction, asthma, COPD, pneumonia, Pneumothorax, heart failure, ILD
Le Chatelier’s Principle
- if low CO2
- if low HCO3-
If low CO2 –> equation will shift to the left and both HCO3- and H+ will decrease
If low HCO3- –> equation will shift to the right and CO2 will decrease while H+ increases
Compensation
- metabolic acidosis –> CO2 will decrease (hypervent)
- metabolic alkalosis –> CO2 will increase (hypovent)
- respiratory acidosis –> HCO3- will increase (kidneys increase reabsorption and generation)
- respiratory alkalosis –> HCO3- will decrease (kidneys decrease reabsorption and generation)
*lungs work in minutes, kidneys work in days
* if the AG is high, compensation should be by the same number
*if the compensation is small, it’s likely an acute process
*however, if one value dropped a shit load and the other only slightly compensated, there’s likely a secondary pathology at play
Anion Gap
- correcting for albumin
AG = unmeasured anions - unmeasured cations
AG = Na - Cl - HCO3
- a normal AG is under 12
- low AG indicates an increase in UC (hypercalcemia, myeloma, Li overdose)
- high AG indicates an increase in UA (alcohol, poor nutrition, lactate, ethanol, ASA, renal failure, ketoacidosis)
- for every 10g/L decrease in albumin (- charged), lower the AG by 2.5
Osmolar Gap (do if AG)
- used as a screening tool for toxins
= measured osmoles - calculated osmoles
calculated osmolality = (2*Na)+glucose+urea (BUN) - under 10 is considered normal
- consider toxic ingestion if high with metabolic acidosis (etoh, methanol, ethylene or propylene glycol)
Delta/Delta (do if AG)
- compare the change in AG to the change in HCO3
= (AG-12)/(24-HCO3-)
<0.4 –> hyperchloremic NAGMA
0.4-0.8 –> HAGMA and NAGMA
1-2 –> uncomplicated HAGMA
>2 –> metabolic acidosis with pre-existing elevated HCO3- (M.alkalosis or R.acidosis)
If NAGMA (non AG metabolic acidosis)
- causes
- follow up test
- different types of RTA
- GI (diarrhea, ureteral diversions), RTA, CKD, normal saline IV, acetazolamide, cholestyramine
- urine anion gap –> is it a kidney or GI problem?
UAG = Na+K-Cl - if (-) –> diarrhea (GI loss), RTA II (proximal)
- if (+) –> RTA I or IV, renal failure
RTA I (distal) –> cannot excrete H+ distally
RTA II (proximal) –> fanconi’s (HCO3- loss), myeloma
RTA IV (hypoaldosteronism) –> DM, NSAIDs, adrenal
What is typically used for fluid resuscitation?
- balanced crystalloid and blood products
Vasoactive Agent Targets
- a1 –> peripheral vasoconstriction
- B1 –> inotropy, dromotropy, chronotropy
- B2 –> inotropy, bronchodilation
Noradrenaline (Norepinephrine)
- S/E
- mainly a1, some B1
- increases BP/CO/HR
- recommended first line in most patients with shock
- S/E - decreased renal perfusion, increased afterload can decrease SV and increase O2 demand
Adrenaline (Epinephrine)
- S/E
- B1 at low dose, A1 at high dose (some B2)
- increases HR/CO/BP
- good for anaphylaxis (stabilizes mast cells and prevents degranulation)
- good for MI?
- S/E –> tachyarrythmia, increased myocardial oxygen demand, can decrease CO if too much
Dobutamine
- S/E
- B1 and B2
- increases CO and slightly HR, peripherally and pulmonary vasodilates (lowers SVR)
- good for septic shock and renal failure
- S/E –> tachyarrythmia, hypotension, increase myocardial oxygen consumption, cardiomyopathy
Dopamine
- S/E
- B1 at medium dose, A1 at high dose
- increases contractility, SV, CO, afterload, PVR, mAP
- S/E –> tachyarrythmia
Vasopressin (ADH)
- osmoreceptors detect increased osmotic pressure, baroreceptors in the aortic arch and carotid sinus detect lowered BP –> release of ADH from posterior pituitary
- V1 receptor in sm increases intracellular Ca –> vasoconstriction
- V2 receptor in renal collecting duct –> anti-diuresis
- V3 receptors in pituitary gland (release of ACTH)
- increased water reabsorption in the kidneys
- increases BP
Which drugs are inotropes vs vasopressors?
inotropes (increase contractility) –> epinephrine, dobutamine, milrinone
vasopressors (vasoconstriction) –> norepinephrine, vasopressin, phenylephrine (A1)
Milrinone
- PDE3 inhibtor
- increases CO and HR
Infective Endocarditis
- risk factors
- L sided vs R sided
- 60+, male, IV drug use, poor dentition, structural heart disease (valve/ congenital), prosthetic valves, ICDs, catheters or procedures, chronic hemodialysis, history of IE
- L –> MV or AV, more common (90%)
- higher pressure on the left leads to turbulence across the MV and AV –> endothelial damage
- higher oxygenation on the left supports bacterial growth
- congenital and acquired valve defects are more common on the left
- R –> TV or PV, most common in IDU (almost always S. aureus)
- disproportionate damage to the TV with injection of foreign material and diluent in presence of high grade, frequent bacteremia
Symptoms of Infective Endocarditis
- L vs R side
- fever in 90%, murmur in 85%
- chills, weight loss, night sweats, malaise, headache, arthralgias, splinter hemorrhages, Janeway lesions, Osler’s nodes, petechiae, conjunctival hemorrhage, roth spots
- perivalvular abscess (infection breaks through annulus and spreads into nearby tissues), most common in AV and prosthetic valves
L side –> cerebral emboli (most MCA), meningitis, brain abscess, IC hemorrhage (all highest risk with anterior leaflet MV vegetations of s.aureus)
R side –> pulmonary emboli
Dx of infective endocarditis
Modified Duke Criteria (2 major OR 1 major and 3 minor OR 5 minor)
- major –> at least 2 positive blood cultures in absence of primary focus, single positive blood culture for Coxiella burnetti or antiphase1 IgG over 1:800, echo consistent with IE
- minor –> predisposing heart condition or IDU, vascular phenomenon, immune phenomenon, (+) cultures that dont meet major criteria, (+) serology for organism associated with IE
*blood cultures are most important, done every 48-72 hours until negative
* 20% of IE will be (-) –> fastidious/ unculturable organisms
*ECG should be done in all patients (new AV block may cause abscess)
Imaging for Infective Endocarditis
- on echo –> oscillating intracardial mass or vegetation, annular abscess, prosthetic valve dehiscence, new valvular regurgitation
- transesophageal is #1 (more sensitive, can use with prosthetic valves, better for high risk patients with CHD, murmur, etc.)
- transthoracic may be better for R-sided, less complicated, lower risk patients
Treatment of Infective Endocarditis
- Coagulase (-) Staph
- MSSA
- MRSA
- Viridans and Group D Strep (2nd most common)
- Enterococcus (faecalis/ faecium) (3rd most common)
- Dental Prophylaxis
- surgery done in some situations (unresponsive to meds, perivalvular extensions with new heart block, annular or aortic abscess, candida, mobile vegetation over 10mm)
- vegetations –> high bacterial density causes inoculum effect and thus B-lactams and vanco are less effective
- prosthetic valves are worse as they often form biofilms
- S. aureus is the most common cause
- Coagulase (-) Staph –> PV, most resistant to B-lactams
- treat with vancomycin
- MSSA –> cloxacillin/ cefazolin for 6 weeks or 2-4 weeks in R-sided IDUs
- if prosthetic –> cloxacillin + rifampin + gentamycin (2w) for 6 weeks
- MRSA –> vancomycin/ daptomycin for 6 weeks
- if prosthetic –> vancomycin+ rifampin + gentamycin (2w) for 6 weeks
- Viridans/ Group D Strep –> Penicillin G/ ceftriaxone 4 weeks
- if prosthetic –> Penicillin G/ ceftriaxone and gentamicin (2w) for 6 weeks
- Enterococcus –> Pen G or ampicillin to disrupt cell wall, aminoglycoside (gentamycin) to penetrate and kill bacteria for 6 weeks
- can be 4-6 weeks if no prosthetic/ otherwise healthy
Dental Prophylaxis –> amoxicillin
- only if prosthetic valves, previous IE, CHD, transplants
Common Causes and Treatments of:
- Native valve non-IDU IE
- Native valve IDU IE
- Prosthetic valve IE
- Culture negative IE
- s. aureus (MSSA), VGS, entero
- cloxacillin and Pen G OR ampicillin and gentamycin
- wait for culture results if not critically ill
- S. aureus (MSSA and MRSA)
- vancomycin
- S. aureus, CONS, VGS, entero
- vancomycin and gentamicin and rifampin
- Coxiella –> doxycycline and hydroxychloroquine
- Bartonella –> ceftriaxone and doxycycline and gentamycin
Cardiac Ap Stages vs. Pacemaker Ap Stages
Cardiac
0 - fast Na channels open (Ina)
I - Na channels close, K channels open (Ito)
II - Ca channels open (Ical), K channels open (Iks, Ikr)
III - Ca channels close, K still open
IV - resting potential restored, Na/K and Na/Ca exchange
Pacemaker
IV - If channels self-depolarize (Na)
0 - L-type Ca channels open
III - K channels open
* no stable resting potential due to If
Class Ia Antirhythmics
- moderate Na blockade
- decrease the slope of phase 0 (slowed speed of propagation and conduction velocity)
- increase refractoriness via K channel blockade (increased QT interval)
- procainamide
- give procainamide for WPW
Class Ib Antirhythmics
- mild Na blockade
- mild slowing of speed of propagation and conduction velocity
- shorter AP duration (shorter QT interval)
- exclusive for ventricular tissue, best for diseased states at risk for K leak
- lidocaine, phenytoin, mexilitine
Class Ic Antirhythmics
- contraindicated in?
- strong Na blockade
- major decrease in speed of propagation and conduction velocity
- widens QRS
- primarily for suppressing atrial arrythmias
- contraindicated in structural/ischemic disease (i.e. cannot give for VT if due to MI)
- flecainide, propafenone
*if giving for flutter MUST also give with a AV node blocker (otherwise too many beats may actually get through to the ventricles)
Class III Antirhythmics
- K channel blockers
- prolong the AP (and thus QT)
- amiodarone (also Na/Ca blocker and a/b antiadrenergic)
- sotalol (also B-blocker)
Class II and IV Antirhythmics
- B-blockers and L-type Ca channel blockers
- decrease automaticity (BBs), re-entry (CCBs), and triggered activity
- Verapamil and Diltiazem
Class V Antirhythmics
- Digoxin –> PNS-mimetic
- narrow TI so rarely used, may cause arrythmias
Adenosine –> most potent inhibitor of the AV node (some SA activity)
- short acting, acts in all phases
- decreases duration of AP
Agents that act on:
- SA and AV node
- atrial myocardium
- ventricular myocardium
- Adenosine, B-blockers, Calcium channel blockers, Digoxin
- procainamide, flecainide, propafenone, sotalol, amiodarone, BBs and CCBs
- procainamide, lidocaine, mexilitine, sotalol, amiodarone, BBs and CCBs
S/E of antiarrhythmics
- Na blockers (Class I) and K blockers (Class III) can actually be pro-arrhythmic
Procainamide –> lupus
Lidocaine –> neuropathy
Flecainide –> ischemic death
Sotalol –> torsades de pointes
Amiodarone –> a million things
Digoxin –> arrythmias, colour vision issues
Signs and Symptoms of Pericardial Tamponade
- quiet heart sounds
- increased JVP
- reflex tachycardia
- pulsus paradoxus (SBP decreases on inspiration)
- increased cardiac silhouette
- echo confirmation (diastolic collapse of RA/RV)
Consequences of Malnutrition
- pressure ulcers, poor wound healing, lowered immunity
- higher rates of mechanical ventilation, readmission
Malnutrition
- 60-75% of ICU patients (stress, inadequate nutrition, fever, tachycardia)
- with stress, the primary fuel is glucose –> glycogen depleted rapidly –> loss of skeletal muscle and lean body mass
Enteral vs. Parenteral Nutrition
Enteral –> via GI (NG tube is most common)
- better! 1st pass metabolism, fewer infections, cheaper, GI structure and function
- start ASAP
- contraindicated if bowel obstruction, GI bleed, hemodynamically unstable, GI ischemia
Parenteral –> via IV (a.a.s, lipids, dextrose, lytes)
- infections, cholestasis, cirrhosis, steatosis, fluid overload, lyte disturbances
- start ASAP if patient is already malnourished
- only if enteral cannot be used
Refeeding Syndrome
- risk factors
- symptoms when nutrition is suddenly given to malnourished patients
- drop in phosphate/K/Mg/thiamine
- increase in fluid, Na, CHF, arrythmias, neuro and resp issues
- insulin secretion promotes uptake of glucose/lytes/thiamine
- start low and go slow! monitor lytes/thiamine/supplementation for 7 days
- risks –> ED, SUD, weight loss, CF, dysphagia, COPD
*well nourished patients can receive their target energy right away
Circulatory vs. Neurological Death
Circulatory –> no cardiac or respiratory activity
Neurological –> no cortical or brain stem activity, trickier ethics wise
Palliative Care
- opioids and benzos for dyspnea (midazolam)
- antipsychotics (haloperidol) for delirium
Uses of a Swan-Ganz (PA) Catheter
- continuous CO monitoring
- temp/RA/RV pressure/venous sat measurement
- estimation of L diastolic filling
What are normal values for an ABG?
pH –> 7.4
pCO2 –> 40
HCO3 –> 24
pO2 –> 100
- can have both respiratory alkalosis and metabolic alkalosis (or acidemia)… it’s just a mixed pathology!
Diabetic Ketoacidosis
- will likely see Kussmaul breathing (hyperventilation to try and blow off CO2 to compensate for metabolic acidosis)
