Hemodynamics and Shock Flashcards
Hemodynamic instability
hypotension, change in mental status, and signs of shock
Hypotension
mean arterial pressure (MAP)
Mean Arterial Pressure
MAP
80 – 100 mmHg
MAP =DBP + 1/3 (SBP-DBP)***
Better mesured for t
Need at least 65 in order for your organs to have adequate organ perfusiotn
Cardiac Output
4 – 7 L/min
CO
Cardiac Index (CI)
2.8 – 3.6 L/min/M2
CO/body surface area
–>corrected CO for weight
Pulmonary Artery Occlusion Pressure
a.k.a. Pulmonary capillary wedge pressure
12-15 mmHg
Measure the pressure of L ventricle at the end of diastole. The heart is filled with the maximum volume of blood. Learn patients volume status.
- indicates preload
- pressure in left ventricle
Systemic Vascular Resistance
SVR
1300 – 2100 dynes-s/cm5
SVR- constriction/dilation of blood vessels
SHOCK
An acute, generalized state of inadequate perfusion of critical organs
- Serious pathophysiological consequences, including death
- USUALLY but not always associated with hypotension (SBP
o Signs of poor/reduced perfusion:
Hypotension • Increased HR and RR • Cold extremities • Mental status change or unconscious • Reduced urine output (worsening renal function)-increase in ScR • Lactic acidosis
Shock: hypovolemic
Low vascular volume
Shock: Distributive
Septic or anaphylactic: vasodilation
Shock: Cardiogenic
poor heart function
• Vasopressors (“vasoconstrictors”)
Route and titrating frequency?
Administered via continuous infusion
Frequent dosing adjustments may be necessary
(titration) every 5-15minutes
Can Vasopressors be used in Central line?
phentolamine (antidote)
YES or else
Tissue necrosis with extravastation:
o To avoid: administer through a central line
o Treat extravasation with intradermal administration of
10-15 ml of saline and** 5-10 mg of phentolamine**
• Phentolamine: blocks alpha-adrenergic receptors causing vasodilation and minimizes necrosis
α1 - Vasoconstriction
α2- Vasoconstriction  β1 - inotropic (contractility) and chronotropic (HR)   β2- vaso-/Brocodilation  DA - Vasodialtion in the kidney, Heart, and GI
α1 - Vasoconstriction
α2- Vasoconstriction  β1 - inotropic (contractility) and chronotropic (HR)   β2- vaso-/Brocodilation  DA - Vasodialtion in the kidney, Heart, and GI
Dopamine
Central line line
DOC if low risk of arrhtymias
-Large DA and B1 activity
AE:
**Worst for Tachycardisa–>B1
peripheral vasoconstriction–>a1
Arrhythmias, tachycardia, peripheral and gut ischemia/ necrosis
Epinephrine
Catecholamines
Central line line
(Adrenaline®)
Large a1 and B activity (less B2)
AE:
hyperglycemia**
hypokalemia*
Agitation, tremor, headache, Arrhythmias, tachycardia hyperglycemia, peripheral and gut ischemia/ necrosis, “K+
Norepinephrine
Catecholamines
Central line line
(Levophed®)
often 1st line: a and b activity.
generally additive therapy to dopamine for septic shock
AE:
Hyperglycemia**
Agitation, headache, tremor–>B
peripheral/gut ischemia–>a
Hypokalemia**
Phenylephrine
Noncatecholamines
Central line line
Neosynephrine
Only alpha- a
indicated if hypotensive with tachyarrhthmia (no B1 effects)
Vasopression
Antidiuretic hormone
V1 Receptors – located in smooth muscle in blood vessels, hepatocytes, platelets, and on some cells in kidney
V2 Receptors: located in the renal collecting duct
Higher doses restricted in shock due to AEs
AE:
Decreased CO and circulation to skin and GI tract
peripheral ischemia
Hyponatremia**
May decrease CO and circulation to skin and GI tract (high doses > 0.04 units/min), decreased splanchnic circulation (high doses > 0.04 units/min), peripheral ischemia, hyponatremia
0.01-0.04 units/min (higher doses NOT recommended in shock–>Will cause auto amputee??? Vasopressors
Inotropes
Dobutamine
Milrinone
Dobutamine
2min half-life
hepatic metabolism
B and a1 activity
two isomers: (+) -> B-activity, (-) –>a
used in low CO states
- -> CI Left Ventricular dysfunction
- -> Shock
AE: Tachycardia, arrhythmias, hypotension (rarely), angina, premature ventricular beats
Milrinone
Half-life: 1-2hours
Renal (need lower in renal dysfunction)
PDE-3 inhibitor to enhance contractility
AE: Hypotension, arrhythmias
Hypovolemic Shock: Causes
Blood loss (shot wounds)
Fluid sequestered within a compartment of the body due to loss of oncotic pressure or increased capillary permeability
Fluid lost from urine, diarrhea/vomiting, skin (burns) o Hemodynamic effects
Hypovolemic Shock: Hemodynamic effects
Decreased: MAP, CVP, PCWP, CO, SVR
Increased: SVR
Hypovolemic Shock: Treatment
Plasma expanders - 1st line
- -> NSS or Lactated ringer (isotonic crystalloid)
- ->albumin (colloids)
- ->Blood: if caused by blood loss
Vasopressor–Last line
–>vessel are already contracted to compensate for loss of BP
Hypovolemic Shock: Monitoring
HR, BP, lactate, and Scr
Distributive Shock: Septic Shock
Cause
Infection - Gram (+) most common
Distributive Shock: Septic Shock
Risk factors
Elderly
Immunosuppressed states (AIDS, cancer, transplant, chronic immunosuppressing medications)
Malnutrition
Alcoholism
Chronic organ failure
Definition of Systemic inflammatory response syndrome (SIRS)
Patient must have two or more of the following:
WBC ≥ 12,000 or WBC ≤ 4,000 or bands > 10%
Hyperthermia (≥38°C or 100.4°F) or hypothermia (≤36°C or 96.8°F)
(PaCO2 ≤32 mmHg)
RR ≥20
Mechanical ventilation for an acute respiratory process
Heart rate ≥ 90 beats/min
Sepsis
SIRS + infection
Severe Sepsis
Sepsis + organ dysfunction
Septic Shock
1 or 2 or 3 + Fluid refractory hypotension
Distributive Shock: Septic Shock
Pathophysiology
(1) Bacteria toxins cause-->Macrophages recognize the infection and (over)react and release inflammatory mediators. --> TNF-α --> IL-1 --> IL-6
- Vasodilation
- Vascular endothelial injury resulting in activation of the coagulation cascade
- o Fluid to leak out of vasculature and into tissues
Distributive Shock: Septic Shock
Hemodynamic Effects
Decreased: MAP, CVP, PCWP, SVR
Increased: CO
S/S
Early sepsis
Fever or hypothermia Rigors or chiles Tachycardia Tachypnea Hypoxia Hyperglycermia Myalgias
S/S
Late sepsis (evidence of organ failure
Increase Lactate*
Increase LFTs*
Pulmonary failure*
Decrease urine output/increase Scr
Hypotension
Thrombocytopenia
COMA
Treatment (Surviving Sepsis Guidelines)
Prompt diagnosis and identification of pathogen causing infection
Early administration of antibiotics
Adequate organ perfusion (CVP > 8 and MAP > 65,
lactate
Distributive Shock: Septic Shock
Antimicrobial therapy
Blood cultures should be sent before antimicrobial therapy is initiated as well as cultures from any other site that is suspected as causing the infection
–Blood must be sent immediately; start antimicrobial empirically within 1 hour*** (IV therapy)
Distributive Shock: Septic Shock
(1) Fluids
Fluide challenge:
Administer 30 ml/kg of NNS or Lactated Ringers
–>Continue giving until goals met or signs of volume overload
Albumin - 2nd line
Blood due to loss
Monitoring: Sodium/chloride (crystalloids only), BP, HR, CVP, lactate, urine output, pulmonary edema, heart failure, edema
(2)Vasopressors/inotropes
Noreperienpherine: 1st line for hypotension in septic shock
Dopamine: alternative if at low risk of arrhythmias–> low dose not useful. “Renal-dose dopamine” not useful (
(2) Vasopressors/inotropes
Goals and Monitor
MAP>65
BP, HR, potassium, glucose,
peripheral/splanchnic vasoconstriction
(3) Steroids
Adminstration (period) And Monitoring and Goals
Recommended to administer intravenous hydrocortisone in septic shock patients refractory to (1) fluids and (2) vasopressors
–> (Hydrocortisone 50mg IV)** every 6 hours or as continuous at 8 mg/hr
Goals: MAP > 65, avoid adverse effects, discontinuation of vasopressors
Monitoring: BP, glucose, mental status, fluid retention, infection, GI ulceration
(4) Insulin
Goal and monitor
Glucose elevate by EPI–> (precaution)
Continuous infusion with short-acting insulin
(regular or lispro)
***Goal: blood glucose
