shock & monitoring

8/9/2019 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

shock & monitoring

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