Transcript Circulatory Shock and Vasopressors

Circulatory shock
Vasopressors
Shock: definition
Shock is the physiologic state characterized by significant
reduction of systemic tissue perfusion, resulting in
decreased tissue oxygen delivery.
This creates an imbalance between oxygen delivery and
oxygen consumption.
Prolonged oxygen deprivation leads to cellular hypoxia and
derangement of critical biochemical processes at the
cellular level, which can progress to the systemic level
Shock: Stages
Preshock = warm or compensated shock: rapid
compensation for diminished tissue perfusion by various
homeostatic mechanisms (↑HR, peripheral
vasoconstriction, ↑or↓ in BP)
Shock: the compensatory mechanisms become
overwhelmed and signs and symptoms of organ
dysfunction appear (↑HR, dyspnea, oliguria, acidosis).
End-organ dysfunction: progressive end-organ
dysfunction leads to irreversible organ damage and patient
death.
Pathogenesis
Impairment in tissue perfusion and vasomotor paralysis that
could become irreversible
Mechanisms for the vasodilatation
1. Opening of ATP-Sensitive Potassium Channels→
hyperpolarization of Vascular Smooth Muscle→↓Ca entry
→persistent vasodilation
2. Increased Synthesis of Nitric Oxide
3. Generation of free radicals
4. Deficiency of Vasopressin due to exhaustion of
hypophyseal stores and rapid degradation of vasopressin in
plasma
Classification of Circulatory Shock
HYPOVOLEMIC
Hemorrhagic
• Trauma
• Gastrointestinal
• Retroperitoneal
Fluid depletion (nonhemorrhagic)
• External fluid loss
- Dehydration
- Vomiting
- Diarrhea
- Polyuria
Classification of Circulatory Shock
CARDIOGENIC
Myopathic (myocardial infarction, nonischemic
cardiomyopathy, septic or pharmacologic myocardial
depression)
Mechanical (valvular failure, hypertropic cardiomyopathy
ventricular septal defect)
Arrhythmic
Classification of Circulatory Shock
EXTRACARDIAC OBSTRUCTIVE
Impaired Diastolic Filling
Direct venous obstruction (obstructive tumor)
Increased intrathoracic pressure(tension
pneumothorax, status asthmaticus)
Decreased cardiac compliance (constrictive
pericarditis, cardiac tamponade)
Impaired Systolic Contraction
Right ventricle ( massive PE, acute PAH)
Left Ventricle ( aortic dissection)
Classification of Circulatory Shock
DISTRIBUTIVE
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic( Adrenal crisis, thyroid storm)
Toxic (nitroprusside, bretylium)
Shock: Clinical presentation
Cardinal findings
- hypotension
- oliguria
- cool and clammy skin
- abnormal mental status
- metabolic acidosis
Suggestive findings suggest a particular type of shock
Shock: Evaluation
History: including medications, allergies, procedures,
comorbidities, immunocompromised state
Physical examination: JVP, left S3, S4, gallop, new
murmurs, arrhythmia, rub, pulsus paradoxus,peripheral
edema, fever, rigors, infection focus, abdominal tenderness,
GI bleeding, neurological exam, rashes
Laboratory data: Blood work (CBC, Chem, LFT,
Amylase/lipase, coags, lactate, ABG), EKG, imaging
(Chest/abdominal Xray, CT, Echo), toxicology
Pulmonary artery catheter
Diagnosis
PCWP =
preload
CO
Tissue perf
= sVO2
↓
SVR =
afterload
↑
Hypovolemic
↓
Cardiogenic
↑
↓
↑
↓
Distributive
↓or↔
↑or↔
↓
↑
Obstructive
↔or↓
↓
↑PVR
↓
↓
A Clinical Approach to Shock
Diagnosis and Management
Immediate Goals in Shock
Hemodynamic support
MAP > 60mmHg
PAOP = 12 - 18 mmHg
Cardiac Index > 2.2 L/min/m2
Maintain oxygen delivery
Hemoglobin > 9 g/dL
Arterial saturation > 92%
Supplemental oxygen and
mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L)
Maintain urine output
Reverse encephalopathy
Improving renal, liver function
tests
Shock: Management
Hypovolemic
Cardiogenic
Rapid volume
replacement
(saline, blood
products)
Idenify source
of loss
-Endoscopy
-Angiography
-MRI/CTscan
LV infarct
-IABP
-revascularize
RV infarct
-fluids/inotropes
Valve
problem
-surgery
Distributive
Septic
Obstructive
Pericardial
tamponade
-Antibiotics
pericardiocentesis
- Fluids,
surgical drainage
pressors,
inotropes
Pulmonary
embolism
- Goals:
Heparin
SV02 > 70%
improving organ VQ scan/CTA
function
Consider
tPA/embolectomy
decreasing
lactate levels
Shock: Management
Fluids
▪Crystalloids, isotonic (NS)
▪20 mL/kg fluid challenge in hypovolemic or septic
shock with re-challenges of 5 - 10 mL/kg
▪100 - 200 mL challenges in cardiogenic shock
Vasopressors
induce vasoconstriction and elevate mean arterial pressure
few controlled clinical trials have directly compared these or
documented improved outcomes
adrenergic receptors relevant to vasopressor activity
▪ ά-1 in vascular walls, induces vasoconstriction. Also in the
heart and can ↑ the duration of contraction but no ↑ chronotropy
▪ β-1 in the heart, mediate ↑ in inotropy and chronotropy with
minimal vasoconstriction
▪ β-2 in blood vessels induce vasodilation
▪ dopa in renal, splanchnic, coronary, and cerebral vascular
beds; stimulation leads to vasodilation. A second subtype causes
vasoconstriction by inducing norepinephrine release (high doses of
medication)
Dopamine
Precursor of norepinephrine and epinephrine
Increases MAP and CO due to increase in SV and to a
lesser extent to a HR. Increases CI
Increases oxygen delivery but effects on oxygen
consumption mixed (microcirculatory flow)
Dose dependent effects
<5 mcg/kg/min→dopa receptors →vasodilation in renal
and mesenteric beds
5-10 mcg/kg/min →β1 receptors →increase in cardiac
contractility and heart rate
>10 mcg/kg/min →ά1 receptors→vasoconstriction and
increase in BP
Norepinephrine
Potent ά-adrenergic agent with less pronounced β-agonist effect
Increases MAP by vasoconstriction, 10-15% increase in CO and
SV
More potent than Dopamine
Dose range: start with 0.5-1 mcg/min, increase up to 30
mcg/min
Improves tissue oxygenation
Effect on renal hemodynamics- !adequate volume resuscitation
prior to norepi start
Effect on splanchnic blood flow - mixed results
Phenylephrine
Selective ά-1 adrenergic agonist, increases BP by
vasoconstriction.
Rapid onset of action, short duration, primary vascular effect
Concerns for potential reduction in CO
Dose range: start with 40-60 mcg/min and increase to 100-180
mcg/min until BP stable.
Second line agent
Consider in tachyarrhythmias limiting therapy with other
vasopressors.
Vasopressin
Peptide hormone, synthesized in the hypothalamus, stored in
pituitary gland. Released in response to decreased
intravascular volume, increased osmolarity
Constricts vascular smooth muscle via V1 receptors
Increases vessel responsiveness to catecholamines
Low steady dose vasopressin 0.01-0.04 Units/min
Vasopressin (0.03 Units/min) + Norepinephrine safe
No effect on mortality
Drug
ά1
β1
β2 dopa Dominant clinical effect
Phenylephrine
+++
0
0
0
SVR ↑↑, CO↔/↑
Norepinephrine
+++
++
0
0
SVR ↑↑, CO↔/↑
Epinephrine
+++
+++
++
0
CO↑↑, SVR↓(low dose),
SVR ↑ (higher dose)
0.5-2.0mcg/kg/min
0
+
0
++
CO
5-10 mcg/kg/min
+
++
0
++
CO↑, SVR ↑
10-20mcg/kg/min
++
++
0
++
SVR ↑↑
Dobutamine
0/+
+++
++
0
CO↑, SVR↓
Isoproterenol
0
+++
+++ 0
CO↑, SVR↓
Vasopressin
+++
0
0
SVR ↑↑, CO↔
Dopamine
0
Vasopressors: complications of use
Hypoperfusion
Dysrhythmias
Myocardial ischemia
Local effects
Hyperglycemia
NO STUDY HAS DEMONSTRATED A SURVIVAL
BENEFIT DUE TO ONE VASOPRESSOR COMPARED
TO ANOTHER