Chapter 4 - Critical Care Concepts and Complex Health Issues Flashcards
What is right atrial (RA) pressure?
- preload
- the pressure in the RA reflects the amount of blood returning to the heart and the ability of the heart to pump blood into the arterial system
- normal range: 2-6 mmHg
What is the central venous pressure (CVP)?
- preload
- reflects the amount of blood returning to the heart; a good approximation of RA pressure
- normal range: 2-6 mmHg
What is right ventricle (RV) pressure?
- indicates right ventricular function and general fluid status
- increased RVP may indicate pulmonary HTN, RV failure, CHF
- normal range: 15-30 mmHg (systolic); 2-6 mmHg (diastolic)
What is pulmonary artery (PA) pressure?
- reflects the BP in the pulmonary artery
- increased PA pressure can indicate a left-to-right shunt, PA HTN, COPD, PE, pulmonary edema
- normal range: 20-30 mmHg (systolic); 5-10 mmHg (diastolic); mean 10-20 mmHg
What is pulmonary capillary wedge pressure (PCWP/PAW)?
- preload
- measures the LV pressure when mitral valve is open
- high wedge pressure can indicate LV failure, mitral valve pathology, cardiac insufficiency
- normal range: 8-12 mmHg
What is systemic vascular resistance (SVR)?
- afterload
- measures resistance of the systemic vascular bed to blood flow
- increased SVR can be caused by vasopressors, hypovolemia, or late septic shock
- decreased SVR can be caused by early septic shock, vasodilators, morphine, nitrates
- normal range: 900-1400
What is cardiac output (CO)?
- contractility
- the volume of blood pumped by the heart in 1 minute
- increased CO indicates high circulating volume
- decreased CO means a decrease in circulating volume or a decreased in the strength of ventricular contraction
- normal range: 4.8-6.4 L/min
What is cardiac index (CI)?
- contractility
- the amount of blood pumped per minute per meter square of body surface area
- normal range: 2.5-4.2 L/min
What is saturation of mixed venous oxygen (SvO2)?
- the estimate of the amount of oxygen returning to the cardiopulmonary circulation
- reflective of the patient’s ability to balance O2 supply and demand at the tissue level
- normal range: 70-75% (60-80%)
Hypovolemic shock - pathophysiology
- nothing to fill up the vessels
- most common form of shock in trauma
- multiple organ failure d/t inadequate circulating volume leading to inadequate tissue perfusion
Hypovolemic shock - common causes
- acute hemorrhage
- severe dehydration
- severe burns
Hypovolemic shock - cardiac pressures
- SBP: < 90 mmHg
- CVP: ↓ (not a lot of fluid returning to heart)
- PAOP: ↓ (nothing to fill up vessels & ventricles)
- CO/CI: ↓ (no fluid to circulate = no fluid to put out)
- SVR: ↑ (vasoconstriction as compensatory mechanism)
- SvO2: ↓ (not enough fluid to circulate and oxygenate)
Hypovolemic shock - treatment
- treat underlying cause
- volume replacement
- transfuse PRN
Cardiogenic shock - pathophysiology
- have enough fluid, just the pump isn’t working
- inadequate tissue perfusion secondary to a loss of contractile function; “pump failure”
Cardiogenic shock – common causes
- Acute MI
- Acute heart failure
- Dysrhythmia
Cardiogenic shock – cardiac pressures
- SBP: < 90 mmHg
- CVP: ↑ (fluid backs up)
- PAOP: ↑ (fluid backs up)
- CO/CI: ↓ (pump not working effectively)
- SVR: ↑ (not d/t vasoconstriction! Due to fluid backing up and putting pressure on vessels)
- SvO2: ↓ (not enough blood returning because you can’t pump it out and circulate it)
Cardiogenic shock – treatment
- Treat underlying cause
- Support cardiac output with inotropic agents
- Support oxygenation
Distributive shock – pathophysiology
- Vasodilation!
- Systemic event causes the loss of the normal responses of vascular smooth muscle to physiologic vasoconstrictive agents coupled with direct vasodilating effect
Distributive shock – common causes
- Septic shock
- Anaphylactic shock
- Neurogenic shock
Distributive shock – cardiac pressures
- SBP: < 90 mmHg
- CVP: ↓ (plenty of fluid but vessels are wide open so they seem empty)
- PAOP: ↓ (vessels don’t fill up)
- CO/CI: ↓ (fluid not returning back to heart because vessels are too wide)
- SVR: ↓ (vessels are wide open)
- SvO2: ↓ or ↑
Distributive shock – treatment of septic
• See later slides for full treatment
Distributive shock – treatment of anaphylactic
- Volume replacement
- Epinephrine (terminates anaphylaxis)
- Glucocorticoids (IV or PO) (extends life of Epi and suppresses inflammatory response)
- Antihistamines (suppresses inflammatory response)
Distributive shock – treatment of neurogenic
• Volume replacement followed by alpha antagonists
Septic Shock – pathophysiology
• A dysregulated response to infection resulting in severe vasodilation and a critical reduction in tissue perfusion leading to organ dysfunction
Septic Shock Hemodynamic Parameters – Hyperdynamic Shock/”Warm Shock”
- CVP: INCREASED or decreased
- PAOP: normal
- CO/CI: increased
- SVR: decreased
- SvO2: increased
- As compensatory mechanisms begin to fail, move from warm to cold shock
Septic Shock Hemodynamic Parameters – Hypodynamic Shock/”Cold Shock”
- CVP: increased or DECREASED
- PAOP: decreased
- CO/CI: decreased
- SVR: decreased
- SvO2: increased or decreased
Surviving Sepsis Management of Septic Shock – within 3 hours…
- Measure lactate level
- Obtain blood cultures prior to administration of antibiotics
- Administer broad-spectrum antibiotics (narrow coverage later based on cultures)
- Administer 30 ml/kg crystalloid for hypotension or lactate ≥ 4 mmol/L
Surviving Sepsis Management of Septic Shock – within 6 hours….
- Apply vasopressors (Levophed) (for hypotension that doesn’t respond to initial fluid resuscitation) to maintain a MAP ≥ 65 mmHg
- In the event of persistent hypotension after initial fluid bolus (MAP < 65) or if initial lactate was > 4, reassess volume status and tissue perfusion and document findings
- Re-measure lactate if initially elevated
Evaluation and Follow-Up of Septic Shock
Option #1
o Repeat focused exam (after initial fluid resuscitation) including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings
Option #2 – more of an ICU follow-up
o Measure CVP, ScvO2, bedside cardiovascular ultrasound, and dynamic assessment of fluid responsiveness with passive leg raise or fluid challenges
Overall Goals of Septic Treatment
- CVP 8-12 mmHg
- MAP ≥ 65 mmHg
- Urine output ≥ 0.5 ml/kg/hr
- ScvO2 > 70%
ABG Interpretation with normal levels
pH: 7.35-7.45
o ↑ = alkalosis state; ↓ acidosis state
PaCO2: 35-45 mmHg
o ↑ = respiratory acidosis; ↓ respiratory alkalosis HCO3: 22-26 mEq/L
o ↑ = metabolic alkalosis; ↓ metabolic acidosis
- Full compensation means normal pH
- Partial compensation means abnormal pH + PaCO2 and HCO3 will also be abnormal
ABG Example: pH 7.3, PaCO2 68, HCO3 28, PaO2 60
• Respiratory acidosis, partially compensated
ABG Example: pH 7.0, PaO2 90, PaCO2 23, HCO3 12
• Metabolic acidosis, partially compensated
ABG Example: pH 7.6, PaO2 120, PaCO2 31, HCO3 25
• Respiratory alkalosis, uncompensated
ABG Examples: pH 7.5, PaO2 85, PaCO2 40, HCO3 34
• Metabolic alkalosis, uncompensated
Burn Sources/Types of Burns
- Thermal – caused by heat source such as a hot item, steam, smoke, etc.
- Electrical – caused by a form of electrical current such as AC or DC current
- Chemical – caused by a chemical agent such as acid or alkali chemical substance
- Radiation – caused by a form of radiation such as sun exposure or cancer treatments
Common Complications of Burns
- Pulmonary injury
- Capillary leak syndrome (third-spacing)
- Mechanical obstruction (esp. with circumferential burns)
- Loss of skin integrity
- Loss of temperature control
- Other forms of trauma/injury
Treatment of Burns
- Safety of patient and provider
- Stop the burning process – wipe chemical away, deactivate chemical, remove hot items (ex: jewelry)
- Pain control – typically with opioids, but dictated by extent, degree of burn, and other comorbidities
- Fluid replacement – Parkland formula (if > 15-20% TBSA)
- Maintain urinary output of 0.5 mg/kg/hr
Parkland Formula
- 24-hour fluid replacement = 4 ml/kg/%TBSA
* ½ volume in 8 hours from time of burn and remaining ½ in the remaining 16 hours
How to figure out protein status?
- Serum albumin – reflects nutritional status for previous 1-2 months
- Serum transferrin – reflects nutritional status for previous weeks
- Serum pre-albumin – reflects nutritional status for previous week
- Nitrogen balance – an estimate of nitrogen in vs. nitrogen out; reflects immediate nutritional status
Nitrogen Balance – what does it mean?
- Neutral balance – burning off all protein that goes in
- Negative balance – burning off more than going in, in a malnourished state
- Positive balance – burning off less than going in, have protein reserve
Basic way to calculate caloric needs in acute illness
- All patients: 25-30 kcal/kg/day
- Moderate illness, injury, or malnutrition: 30-35 kcal/kg/day
- Critical illness or injury: 35-40 kcal/kg/day
Nutritional support – can use the gut
If > 6 weeks – use endostomal tube
If < 6 weeks – need to assess risk for aspiration
o If risk for aspiration – duodenal tube
o If no risk for aspiration – nasogastric tube
Nutritional support – cannot use the gut
- If > 2 weeks – use central venous access and TPN
* If < 2 weeks – use peripheral vein (PPN)
Normal BMP levels – Na, K, Ca, Mg
- Na: 135-145
- K: 3.5-5
- Ca: 8.5-10.5
- Mg: 1.7-2.2
Pathophysiology of Hyponatremia
• Most common electrolyte disturbance in acute care. There are 3 main types of hyponatremia and each have their own pathophysiologic basis
Initial diagnostic workup of hyponatremia
- Step 1: obtain a serum sodium value
* Step 2: obtain a serum osmolality value (normal is 270-290 mOsm/L)
Pathophysiology of isotonic hyponatremia
- “Normal serum”; serum osmo is 270-290 mOsm/L
- Typically r/t a chronic process, where sodium is chronically displaced. An increase in one of the indissolvable solutes displaces the sodium and plasma water. The most common cause is HLD
Additional workup for isotonic hyponatremia
• None typically needed
Potential consequences of isotonic hyponatremia
• No risk of fluid shift and no risk of neurologic complications
Treatment for isotonic hyponatremia
- Sodium replacement is not necessary in this solution
* Correct the indissolvable solute
Pathophysiology of hypertonic hyponatremia
- “Thick serum”; serum osmo > 290 mOsm/L
- Typically r/t to acute increase in another dissolvable solute, which causes the kidney to acutely dump sodium – there is too much of another solute (like another electrolyte) so the kidneys make room for it. Since Na is most abundant, Na usually is the one that gets kicked out
Additional workup for hypertonic hyponatremia
• None typically needed
Potential consequences of hypertonic hyponatremia
- Risk of fluid shift from intracellular space to intravascular space, resulting in cellular shrinkage
- Fluid will move from inside the cell to outside to try and dilute the serum – risk of neurologic complications
Treatment for hypertonic hyponatremia
- Sodium replacement is typically not acutely necessary
* Correct the underlying cause (remove the excess dissolvable solute)
Pathophysiology of hypotonic hyponatremia
- “Thin serum”; serum osmo < 270 mOsm/L
* Typically r/t volume overload or volume depletion, resulting in a change in ADH secretion from an acute process
Additional workup for hypotonic hyponatremia
- Step 1 – assess patient’s volume status
* Step 2 – obtain a urine sodium level (if volume depleted) (normal urine Na is 10-20)