Chapter 16: Critical Care Flashcards
Normal value: cardiac output (CO) (L/min)
4-8
Normal value: cardiac index (CI) (L/min)
2.5 - 4
Normal value: systemic vascular resistance (SVR)
800 - 1,400
Normal value: pulmonary capillary wedge pressure (PCWP)
11 +/- 4
Normal value: central venous pressure
7 +/- 2
Normal value: pulmonary artery pressure (PAP)
25/10 +/- 5
Normal value: mixed venous oxygen saturation (SvO2)
75 +/- 5
MAP?
MAP = CO x SVR
CI?
CI = CO/BSA
% Cardiac output:
- Kidney
- Brain
- Heart
- Kidney: 25%
- Brain: 15%
- Heart: 5%
Left ventricular end-diastolic length, linearly related to left ventricular end-diastolic volume (LVEDV) and filling pressure
Preload
Resistance against the ventricle contracting (SVR)
Afterload
What determines stroke volume?
LVEDV, contractility and afterload
Stroke volume?
Stroke volume = LVEDV - LVESV
Ejection fracture?
EF = SV / LVEDV
What determines EDV (end-diastolic volume)?
Preload and distensibility of the ventricle
What determines ESV (end-systolic volume)?
Determined by contractility and after load
Why does cardiac output start to decreased with HR 120-150?
Decreased diastolic filled time
Accounts for 20% of LVEDV
Atrial kick
Automatic increase in contractility secondary to increased afterload
Anrep effect
Automatic increase in contractility secondary to increased afterload
Anrep effect
Automatic increased in contractility secondary to increased heart rate
Bowditch effect
Equation: arterial oxygen content
CaO2 = HgB x 1.34 x O2 saturation + (Po2 x 0.003)
Equation: oxygen delivery
oxygen delivery = CO x arterial oxygen content (caO2) x 10
Equation: oxygen consumption
(VO2) = CO x (CaO2 - CvO2); CvO2 = venous O2 content
Normal oxygen delivery-to-consumption ratio
5: 1. CO increases to keep this ratio constant.
- Oxygen consumption is usually supply dependent (consumption does not change until low levels of delivery are reached)
Causes of right shift on oxygen-hemoglobin dissociation curve (oxygen unloading)
Increased CO2, increased temperature, increased ATP production, increased 2,3-DPG, decreased pH
Normal p50 (O2 at which 50% of oxygen receptors are saturated)
27 mmHg
What causes increased SvO2?
Increased shunting of blood or decreased oxygen extraction (e.g., sepsis, cirrhosis, cyanide toxicity, hyperbaric oxygen, hypothermia, paralysis, coma, sedation)
What causes decreased SvO2?
Increased oxygen extraction or decreased oxygen delivery (e.g., decreased O2 saturation, decreased CO, malignant hyperthermia)
What can throw off the PCWP?
May be thrown off by pulmonary hypertension, aortic regurgitation, mitral stenosis, mitral regurgitation, high PEEP, poor LV compliance
Where should Swan-Ganz catheter be placed?
Zone III (lower lung)
Treatment: hemoptysis after flushing Swan-Ganz catheter
Increase PEEP, which will tamponade the pulmonary artery bleed, mainstem intubate non-affected side; can try to place Fogarty balloon down mainstem on affected side; may need thoracotomy and lobectomy
Relative contraindications to Swan-Ganz catheter placement
Previous pneumonectomy, left bundle branch block
Approximate Swan-Ganz catheter distance to wedge
- R SCV
- R IJ
- L SCV
- L IJ
- R SCV: 45 cm
- R IJ: 50 cm
- L SCV: 55 cm
- L IJ : 60 cm
How can you measure the pulmonary vascular resistance (PVR)?
PVR can be measured only by using a Swan-Ganz catheter (ECHO does not measure PVR)
When should wedge pressure be taken?
At end-expiration (for both ventilated and non ventilated patients)
Primary determinants of myocardial oxygen consumption (can lead to myocardial ischemia)
Increased ventricular wall tension (#1) and HR
Why is LV blood 5mmHg (PO2) lower than pulmonary capillaries?
Unsaturated bronchial blood empties into pulmonary veins
Normal alveolar-arterial gradient
10 - 15 mmHg in a normal nonventilated patient
Blood with the lowest venous oxygen saturation
Coronary sinus blood (30%)
Most basic definition of shock
Inadequate tissue oxygenation
When do you see tachypnea and mental status changes in shock?
Tachypnea and mental status changes occur with progressive shock
MCC adrenal insufficiency
Withdrawal of exogenous steroids
Cardiovascular collapse; characteristically unresponsive to fluids and pressers; nausea and vomiting, abdominal pain, fever, lethargy, decreased glucose, increased potassium
Adrenal insufficiency
Tx: adrenal insufficiency
Dexamethasone
Steroid potency:
1x?
5x?
30x?
- 1x: cortisone, hydrocortisone
- 5x: prednisone, prednisolone, methylprenisolone
- 30x: dexamethasone
- Loss of sympathetic tone; usually associated with spine or head injury
- Usually have decreased heart rate, decreased blood pressure, warm skin
Neurogenic shock
Tx: neurogenic shock
Give volume first, then phenylephrine after resuscitation
Initial alteration in hemorrhagic shock
Increased diastolic pressure
Beck’s triad
Cardiac tamponade
- Hypotension
- JVD
- Muffled heart sounds
Mechanism of hypotension in cardiac tamponade
Decreased ventricular filling due to fluid in the pericardial sac around the heart
Echo: cardiac tamponade
Impaired diastolic filling of right atrium initially (first sign)
Does pericardiocentesis blood in cardiac tamponade form a clot?
No. Pericardiocentesis blood does not form clot.
Tx: cardiac tamponade
Fluid resuscitation to temporize situation; need pericardial window or pericardiocentesis
Hemorrhagic shock:
- CVP and PCWP
- CO
- SVR
Hemorrhagic shock:
- CVP and PCWP: decreased
- CO: decreased
- SVR: increased
Septic shock (hyperdynamic):
- CVP and PCWP
- CO
- SVR
Septic shock (hyperdynamic):
- CVP and PCWP: decreased (usually)
- CO: increased
- SVR : decreased
Cardiogenic shock:
- CVP and PCWP
- CO
- SVR
Cardiogenic shock:
- CVP and PCWP: increased
- CO: decreased
- SVR: increased
Neurogenic shock:
- CVP and PCWP
- CO
- SVR
Neurogenic shock:
- CVP and PCWP: decreased
- CO: decreased
- SVR: decreased
Adrenal insufficiency:
- CVP and PCWP
- CO
- SVR
Adrenal insufficiency:
- CVP and PCWP: decreased (usually)
- CO: decreased
- SVR: decreased
Early sepsis triad
Hyperventilation
Confusion
Hypotension
Early gram-negative sepsis
Decreased insulin, increased glucose (impaired utilization)
Late gram-negative sepsis
Increased insulin, increased glucose (secondary to insulin resistance)
When does hyperglycemia occur in sepsis?
Hyperglycemia often occurs just before the patient becomes clinically septic
Neurohormonal response to hypovolemia
- Rapid: epi and norepi release (adrenergic release; results in vasoconstriction and increased cardiac activity)
- Sustained: renin (from kidney; renin-angiotensin pathway activated resulting in vasoconstriction and water resorption); ADH (from pituitary; reabsorption of water) and ACTH release (from pituitary; increases cortisol)
Hormones involved in rapid neurohormonal response to hypovolemia
Epinephrine and norepinephrine
Hormones involved in sustained neurohormonal response to hypovolemia
Renin, ADH, ACTH
Petechiae, hypoxia and confusion
- MC with lower extremity (hip, femur) fractures / orthopedic procedures
Fat emboli
Stain: may show fat in sputum and urine
Sudan red stain
Chest pain and dyspnea; decreased PO2 and PCO2; respiratory alkalosis; increased heart rate and increased respiratory rate; hypotension and shock if massive
Pulmonary emboli
Where do most PE’s arise from?
Iliofemoral region
Tx: Pulmonary embolism
Heparin, coumadin; consider open or percutaneous (suction catheter) embolectomy if patient is in shock despite massive pressers and inotropes
Treatment: air emboli
Place patient head down and roll to the left (keeps air in RV and RA) then aspirate air out with central line or PA catheter to RA/RV
When does intra-aoritc balloon pump inflate and deflate?
Inflates on T wave (diastole) and deflates on P wave (systole)
Contraindication to IABP
Aortic regurgitation
Where does tip of IABP sit?
Place tip of catheter just distal to left subclavian (1-2 cm below the top of the arch)
What is IABP used for?
Used for cardiogenic shock (after CABG or MI) or in patients with refractory angina awaiting revascularization
Advantages of intra-aortic balloon pump (IABP)
- Decreased after load (deflation during ventricular systole)
- Improves diastolic BP (inflation during ventricular diastole), which improves diastolic coronary perfusion
Receptor: vascular smooth muscle constriction, gluconeogenesis, and glycogenolysis
Alpha-1
Receptor: venous smooth muscle constriction
Alpha-2
Receptor: myocardial contraction and rate
Beta-1
Receptor: relaxes bronchial smooth muscle, relaxes vascular smooth muscle; increases insulin, glucagon, and renin
Beta-2
Receptor: Relax renal and splanchnic smooth muscle
Dopamine receptors
Dopamine
- 2-5 ug/kg/min
- 6-10 ug/kg/min
- > 10 ug/kg/min
Dopamine
- 2-5 ug/kg/min: dopamine receptors (renal)
- 6-10 ug/kg/min: beta-adrenergic (heart contractility)
- > 10 ug/kg/min: alpha-adrenergic (vasoconstriction and increased BP)