Shock & Monitoring.ppt

8/10/2019 Shock & Monitoring.ppt

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Shock

Differential Diagnosis and HemodynamicMonitoring

Andrew Watt

SICU CONFERENCE


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Classification of Shock

Hypovolemic

Septic/Inflammatory

Cardiogenic (Intrinsic, compressive &Obstructive)

NeurogenicAnaphylactic


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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 ofshock

example CVP CO SVR VO2 sat

preload hypovolemic low low high low

contractility cardiogenic 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 in

cutaneous 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 shocksyndrome, etc.


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Septic/Inflammatory ShockSigns: Earlywarm w/ vasodilation, often adequate urine

output, febrile, tachypneic.Late-- vasoconstriction, hypotension, oliguria,

altered mental status.

Monitor/findings: Earlyhyperglycemia, respiratory

alkylosis, hemoconcentration,

WBC typically normal or low.

LateLeukocytosis, lactic acidosis

Very LateDisseminated Intravascular

Coagulation & Multi-OrganSystem Failure.

Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)

pressors.


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Cardiogenic ShockMechanism: Intrinsic abnormality of heart -> inability to

deliver blood into the vasculature with adequate power

Causes:

1. Cardiomyopathies: myocardial ischemia, myocardial infarction,

cardiomyopathy, myocardiditis, myocardial contusion2. Mechanical: cardiac valvular insufficiency, papillary muscle

rupture, septal defects, aortic stenosis

3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias

(atrial fibrillation, atrial flutter, ventricular fibrillation)

4. Obstructive disorders: PE, tension peneumothorax, pericardialtamponade, 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, elevated

CVP, Low CO. Tx: CHFdiuretics & vasodilators +/- pressors.

LV failurepressors, decrease afterload,

intraaortic ballon pump &

ventricular assist device.


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Neurogenic Shock

Causes:

1. Spinal cord injury

2. Regional anesthesia

3. Drugs

4. Neurological disorders

Mechanism: Loss of autonomic innervation of thecardiovascular system (arterioles, venules, smallveins, including the heart)


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Neurogenic Shock

Characterized by loss of vascular tone & reflexes.

Signs: Hypotension, Bradycardia, Accompanying

Neurological deficits.

Monitor/findings: hemodynamic instability, test bulbo-

carvernous reflex

Tx: IVF, vasoactive medications if refractory


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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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Pulmonary Artery

Catheterization: systemic oxygen

transport

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Oxygen Delivery (DO2) [520-570 mL/min x m2]: rate

of oxygen transport in arterial blood

DO2= CI x 13.4 x Hb x SaO2

Oxygen Uptake (VO2) [110-160 ml/min x m2]: rate of

oxygen taken up from the systemic microcirculation

VO2= CI x 13.4 x Hb x (SaO2SvO2)


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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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Shock & Monitoring.ppt