RESUSCITATION AND PERFUSION

DR.MAGDY KHAMES ALY

CRITICAL CARE MEDICINE

ZMH AL BATAYEH

INTRODUCTION

Volume replacement remains the cornerstone of resuscitation in the critically ill and injured patient.

The initial therapeutic intervention in hypotensive patients, oliguricpatients, and patients with evidence of poor organ/tissue perfusion is volume resuscitation.

However, both underresuscitation and volume overload increase morbidity and mortality in critically ill patients.

Uncorrected hypovolemia, leading to inappropriate infusions of vasopressor agents, may increase organ hypoperfusion and ischemia.

Fluid management is one of the most important (and difficult) issues in the critically ill patient.

However, the volume status of each and every ICU patient needs to be assessed on an ongoing basis.

PHYSIOLOGICAL RESERVE

The human body is a complex system that adapts to a multitude of external stressors; however, senescence or illness can reduce inherent adaptive mechanisms, reducing complexity and reducing the threshold for decompensation (i.e. acute illness or injury). This theoretical critical threshold can be considered ‘physiologic reserve’.

The phenotypic expression of this process is frailty. Frailty is a condition in which small deficits accumulate which individually may be insignificant but collectively produce an overwhelming burden of disease and heightened vulnerability to adverse events.

Frail patients expend a greater proportion of their reserve simply to maintain homeostasis, and seemingly trivial insults can contribute to catastrophic decompensation.

SHOCK PATHOPHYSIOLOGY

Critically ill patients may have an expanded extracellular, extravascular compartment (tissue edema) with a contracted intravascular compartment. It is important to distinguish between these forms of volume depletion as the management may differ

VOLUME DEPLETION

Volume Depletion with Depleted Extravascular Compartment:

Acute blood loss

– Trauma

– GI bleed

Gastrointestinal tract losses (diarrhea, vomiting, fistula)

Decreased fluid intake due to acute medical conditions

Diabetic ketoacidosis

Heat exhaustion

Dehydration

VOLUME DEPLETION

Volume Depletion with Expanded Extravascular Compartment:

Sepsis

Pancreatitis

Trauma

Surgery

Burns

Liver failure

Cardiac failure

ORGAN PERFUSION

BEDSIDE ASSESSMENT:

– Mean arterial pressure

– Urine output

– Mentation

– Capillary refill

– Skin perfusion/mottling

– Cold extremities

– Pulse pressure variation (PPV) and/or stroke volume variation(SVV)

– Echocardiography

PERFUSION MARKERS:

– Blood lactate

– Arterial pH, BE, and HCO3

– Mixed venous oxygen saturation (SmvO2) or central venous

oxygen saturation (ScvO2)

– Mixed venous pCO2

– Tissue pCO2 (sublingual capnometry or equivalent)

– Gastric impedance spectroscopy

– Skeletal muscle tissue oxygenation StO2

PERFUSION ADEQUACY

PvO2 and SvO2

PvO2 of SVC and IVC

PO2 from IVC is normally higher (SO2 77%) than from SVC (SO2 71%)

=> because kidney takes 25% of cardiac output but use only 7-8% of body's O2 consumption

=> IVC receives blood more oxygen rich.

=> PO2 from SVC may be higher because of renal vasoconstriction with severe haemorrhage.

PERFUSION ADEQUACY

Fick's principle

"Amount of O2 extracted from respired gases equals the amount added to the blood that flows through the lung"

i.e. "O2 consumption per unit time = O2 taken up by pulmonary blood flow per unit time"

Fick equation

=> VO2 = Q (CaO2 - CvO2)

• VO2 = O2 consumption per minute (mL O2/time)

• Q = pulmonary blood flow (mL/time)

• CaO2 = O2 concentration in blood leaving lung (mL/100mL)

• CvO2 = O2 concentration in mixed venous blood (mL/100mL)

PERFUSION ADEQUACY

PvO2 and SvO2

A true PvO2 (normally 40 mmHg) measurement must come from a mixed venous blood sample containing venous drainage from the SVC, IVC, and the heart. Thus, the sample should be obtained from a pulmonary artery catheter. There are several factors that determine PvO2, which can be remembered using the mnemonic COALS:

Cardiac output

Oxygen consumption

Amount of hemoglobin

Loading of hemoglobin

Saturation of hemoglobin

Are PvO2 and SvO2 good markers of adequacy of perfusion?

They are easy to measure markers but may NOT always related to adequate tissue perfusion.

If PvO2 or SvO2 are become normal, does it mean that the patient adequately resuscitated? NO because may be the patient’s tissue can’t extract the O2 (cytotoxic hypoxia).

In the other hand if SvO2 is decreased, does it mean that the patient not resuscitated? No because SvO2 depends on many changeable variables during resuscitation e.g: Hb% which may be diluted by resuscitation fluids

PERFUSION ADEQUACY

A-V PCO2 Gradient (DPCO2)

Similar to Fick's principle

Production of CO2 = Elimination of CO2

VCO2 = Q (CaCO2-CvCO2)

CvCO2 = CaCO2 - VCO2/Q

When CO2 dissociation curve is fixed

CvCO2 is increased when

CaCO2 is increased => heavily influenced by alveolar ventilation

CO2 output is decreased

Cardiac output is increased

NB. CO2 output and production are the same in steady state, but different in dynamic state because much of CO2 produced is diverted into body stores.

DPCO2 = PvCO2 – PaCO2

PERFUSION ADEQUACY

A-V PCO2 Gradient (DPCO2)

Can the PCO2 gradient between arterial and venous blood gas samples (DPCO2) represent adequacy of perfusion?

In healthy tissues, decreases in oxygen delivery (QO2 = cardiac output X arterial O2 content) do not lower oxygen consumption (VO2) because tissue O2 extraction increases proportionately. When delivery is reduced below a critical threshold, VO2 falls because tissue extraction exceeds a critical threshold, and cannot compensate for the reduction in delivery.

The critical oxygen delivery point is when consumption (VO2) is dependent on delivery (DO2)

The DPCO2 is an index to identify the critical oxygen delivery point (VO2/DO2).

PERFUSION ADEQUACY

A-V PCO2 Gradient (DPCO2)

critical oxygen delivery point is associated with an abrupt increase of blood lactate levels and a significant widening in DPCO2.

PERFUSION ADEQUACY

A-V PCO2 Gradient (DPCO2)

It is logical that DPCO2 may serve as an excellent measurement of adequacy of perfusion.

PERFUSION ADEQUACY

Lactate

Lactate

PATHWAYS OF LACTATE PRODUCTION AND HYPERLACTATEMIA :

IN TISSUE HYPOXIA, lactate is overproduced and underutilized because of impaired mitochondrial oxidation, largely through anaerobic glycolysis.

Hyperlactatemia can also result from aerobic glycolysis, independent of tissue hypoxia.

In the hyperdynamic stage of sepsis, epinephrine-dependent stimulation of the b2-adrenoceptor augments glycolytic flux both directly and through enhancement of sarcolemmal Na+/K+-ATPase.

Other conditions associated with elevated epinephrine levels, such as severe trauma and cardiogenic shock, can cause hyperlactatemia through this mechanism.

In inflammatory states, aerobic glycolysis can also be driven by cytokine-dependent stimulation of cellular glucose uptake

Lactate

Lactic acidosis refractory to standard resuscitation is frequently caused by increased aerobic glycolysis in skeletal muscle instead of anaerobic glycolysis from hypoperfusion. Continued resuscitation attempts targeting lactate levels may thus lead to unnecessary blood transfusion and use of inotropic agents.

Lactate

LACTATE AND ITS CLEARANCE ARE USEFUL PROGNOSTIC MARKERS:

The clinical relevance of lactate and its clearance have been repetitively evaluated. Lactate clearance greater than 10% from the initial value is predictive of survival from septic shock, and targeting 10% clearance provided similar survival rates to targeting central venous oxygen saturation

In patients with sepsis, lactate clearance greater than 20% during the initial 8 h showed a 22% decline in mortality risk relative to clearances less than 20%

LACTATE

CONCLUSIONS REGARDING LACTATE:

Because hyperlactatemia can be simultaneously related to,and unrelated to, tissue hypoxia, physicians should recognize that resuscitation to normalize plasma lactate levels could be over-resuscitation and worsen the physiological status.

Thus, lactate is a reliable indicator of sepsis severity and a marker of resuscitation, but is not a reliable marker of tissue hypoxia/hypoperfusion.

KEY POINTES

It is important to distinguish between the forms of volume depletion as the management may differ.

PvO2 and SvO2 they are easy to measure markers but may NOT always related to adequate tissue perfusion.

A-V PCO2 Gradient (DPCO2) It is logical that DPCO2 may serve as an excellent measurement of adequacy of perfusion.

lactate is a reliable indicator of sepsis severity and a marker of resuscitation, but is not a reliable marker of tissue hypoxia/hypoperfusion

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