shock & monitoring
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ShockDifferential Diagnosis and Hemodynamic
Monitoring
Andrew Watt
SICU CONFERENCE
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Shock
Shock is a Cardiovascular Derangement.
1. Deliver Oxygen and Metabolic Substrates
2. Remove Products of Cellular Metabolism
3. Thermoregulation
Definition:
A physiological state characterized by a significant,systemic reduction in tissue perfusion, resulting indecreased tissue oxygen delivery and insufficientremoval of cellular metabolic products, resulting intissue injury.
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Clinical Markers of Shock
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Brachial systolic blood pressure: 90 beats/min
Respiratory rate: 29 breaths/min
Urine Output:
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Etiology & Hemodynamic Changes
in Shock
Etiology of
shock
example CVP CO SVR VO2 sat
preload hypovolemic low low high low
contractilitycardiogenic high low high low
afterload distributive
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Etiology & Hemodynamic Changes
in Shock (Afterload)ETIOLOGY
OF SHOCK
EXAMPLE CVP CO SVR VO2 SAT
AFTERLOAD DISTRIBUTIVE
Hyperdynamic Septic Low/High High Low High
Hypodynamic
Septic
Low/High Low High Low/High
Neurogenic Low Low Low Low
Anaphylactic Low Low Low Low
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Hypovolemic Shock
Decreased preload->small ventricular end-diastolicvolumes -> inadequate cardiac generation of pressureand flow
Causes:
-- bleeding: trauma, GI bleeding, ruptured aneurysms,hemorrhagic pancreatitis
-- protracted vomiting or diarrhea
-- adrenal insufficiency; diabetes insipidus
-- dehydration
-- third spacing: intestinal obstruction, pancreatitis,cirrhosis
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Hypovolemic Shock
Signs & Symptoms: Hypotension, Tachycardia,MS change, Oliguria, Deminished Pulses.
Markers: monitor UOP,CVP, BP, HR, Hct, MS,
CO, lactic acid and PCWP
Treatment: ABCs, IVF (crystalloid), Trasfusion
Stem ongoing Blood Loss
Patients on -blockers, w/ spinal shock &
athletes may not be tachycardic
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Septic/Inflammatory Shock
Mechanism: release of inflammatory mediators leading to
1. Disruption of the microvascular endothelium
2. Cutaneous arteriolar dilation and sequestration of blood incutaneous venules and small veins
Causes:
1. Anaphylaxis, drug, toxin reactions
2. Trauma: crush injuries, major fractures, major burns.
3. infection/sepsis: G(-/+ ) speticemia, pneumonia,peritonitis, meningitis, cholangitis, pyelonephritis,necrotic tissue, pancreatitis, wet gangrene, toxic shock
syndrome, etc.
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Septic/Inflammatory ShockSigns: Early warm w/ vasodilation, often adequate urine
output, febrile, tachypneic.
Late-- vasoconstriction, hypotension, oliguria,
altered mental status.
Monitor/findings: Earlyhyperglycemia, respiratoryalkylosis, hemoconcentration,
WBC typically normal or low.
Late Leukocytosis, lactic acidosis
Very Late Disseminated Intravascular
Coagulation & Multi-OrganSystem Failure.
Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)
pressors.
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Cardiogenic Shock
Mechanism: Intrinsic abnormality ofheart -> inability todeliver blood into the vasculature with adequate power
Causes:
1. Cardiomyopathies: myocardial ischemia, myocardial infarction,
cardiomyopathy, myocardiditis, myocardial contusion
2. Mechanical: cardiac valvular insufficiency, papillary musclerupture, septal defects, aortic stenosis
3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias
(atrial fibrillation, atrial flutter, ventricular fibrillation)4. Obstructive disorders: PE, tension peneumothorax, pericardial
tamponade, constrictive pericaditis, severe pulmonaryhypertension
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Cardiogenic Shock
Characterized by high preload (CVP) with low CO
Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP,oliguria
Monitor/findings: CXR pulm venous congestion, elevatedCVP, Low CO.
Tx: CHF diuretics & vasodilators +/- pressors.
LV failure pressors, decrease afterload,
intraaortic ballon pump &
ventricular assist device.
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Neurogenic Shock
Causes:
1. Spinal cord injury
2. Regional anesthesia3. Drugs
4. Neurological disorders
Mechanism: Loss of autonomic innervation of thecardiovascular system (arterioles, venules, smallveins, including the heart)
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Monitoring Adjuncts in Shock
Sphyngomanometry
Pulse Oximeter
Arterial Line
Central Venous Line (Cordice, Triple Lumen,Pulmonary Artery Catheter)
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Pulmonary Artery
Catheterization
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Allows for accurate and continuous hemodynamic monitoringin shock patients
1. Evaluate Fluid Resuscitation
2. Titration of Vasoactive Medications
3. Allows for Assessment of Cardiovascular
Performance.
4. Monitor the Effects of Changes in Mechanical
Ventilation.
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Pulmonary Artery
Catheterization
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Pulmonary Artery
Catheterization: cardiovascular
performance
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Central Venous Pressure (CVP):
CVP = right atrial pressure (RAP) = right-ventricularend-diastolic pressure (RVEDP) (Right VentricularPreload)
Pulmonary Capillary Wedge Pressure (PCWP)
PCWP = left atrial pressure (LAP) = left-ventricularend-diastolic pressure (LVEDP) (Left VentricularPreload)
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Cardiovascular Performance
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Cardiac Output (CO) = HR x SV (L/min)Normal CO = 4 to 8 L/min
Cardiac Index (CI) = CO/BSA (L/min/m2)
Normal CI = 2.5-4.2 L/min/m2
Stroke Volume Index (SVI): CI/HR (ml/beat/m2)
Normal SVI = 40-85 ml/beat/m2
Systemic Vascular Resistance = MAP CVP / CO x 80
Normal SVR = 900-1600 dynes/sec/cm-5
Systemic Vascular Resistance Index = MAP CVP / CI x 80
Normal SVRI = 1970-2390 dynes/sec/cm-5
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Hemodynamic Profiles
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PCWP CVP CO/CI SVR/I
Hypovolemic Low Low Low High
Cardiogenic High High Low High
Inflammatory Low / N Low/N High Low
Neurogenic Low Low Low Low
Shock
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