SHOCK Complications & Approach to Patient Dr.Mohammed Sharique Ahmed Quadri Assistant Prof.Physiology Almaarefa College

Complications of Shock Acute respiratory distress syndrome Acute renal failure Gastrointestinal complications Disseminated intravascular coagulation Multiple organ dysfunction syndrome

Acute Respiratory Distress Syndrome (ARDS) Potentially life threatening form of lung injury Characterized by Severe dyspnea of rapid onset Respiratory rate increases Profound hypoxemia (cyanosis) refractory to supplemental oxygen Results from greatly reduced diffusion of gases across the thickened alveolar membranes. Pulmonary infiltration ( x-ray chest) Exact cause is unknown

Pathophysiology of (ARDS) cytokines Accumulates in pulmonary vasculature Activation of neutrophils Injury to endothelial cells Leakage of fluid and plasma proteins in alveolar spaces Atelectasis Impaired gas exchange Decrease compliance (stiffness) Decrease surfactant

X-ray chest (ARDS)- GROUND GLASS APPEARANCE

Clinical features OF ARDS Tachypnea, tachycardia, hypoxia, and respiratory alkalosis are typical early clinical manifestations Usually followed by the appearance of diffuse pulmonary infiltrates and respiratory failure within 48 hours.

Acute Renal Failure (ARF) Renal vasoconstriction cuts off urine production Results in Acute renal failure Continued vasoconstriction cuts off renal oxygen supply Renal tubular cells die leading to Acute tubular necrosis

Acute Renal Failure (ARF) Frequent monitoring of urine out put provided a means of assesing renal blood flow.(urine out put of 20 ml/hr or less indicate impaired renal perfusion) Serum creatinine and blood urea nitrogen levels provided valuable information regarding renal status

G.I Complication Constriction of vessels supplying GIT for redistribution of blood flow Severe Decrease mucosal perfusion GIT ulceration Bleeding

Disseminated Intravascular Coagulation (DIC) pathways activated clots in platelets many and small clotting blood proteins vessels used up ORAGAN FAILURE microinfarcts, bleeding ischemia problems

Multiple Organ Dysfunction Syndrome (MODS) The most frequent cause of death in the noncoronary intensive care unit Affects multiple organ system (kidney, heart lungs, liver & brain. Mortality rates vary from 30% to 100% Pathogenesis not clearly understood

Major risk factor for development of MODS are Severe trauma Sepsis Prolonged periods of hypotension Hepatic dysfunction Infarcted bowel Advanced age Alcohol abuse

Approach to the Patient in Shock

Avoid over reliance on invasive haemodynamic monitoring Pulse rate Capillary fill time temperature Blood pressure Level of consciousness Blood-gas estimation Assess Intervene RE-assess Seek help

Practically Speaking…. Keep eye on these patients Frequent vitals signs: Monitor success of therapies Watch for decompensated shock Let your nurses know that these patients are sick!

Is this the appropriate environment?

Approach to the Patient in Shock ABCs Cardiorespiratory monitor Pulse oximetry Supplemental oxygen IV access ABG, labs Foley catheter Vital signs

Diagnosis Physical exam (Vital Signs, mental status, skin color, temperature, pulses, etc.) Surveillance for Infectious source Labs: CBC Chemistries ( urea, creatinin ,etc) Lactate Coagulation studies Cultures ABG ( arterial blood gas analysis)

Further Evaluation CVP( central venous pressure)and PCWP(pulmonary capillary wedge pressure) CT of head/sinuses Lumbar puncture Wound cultures Abdominal/pelvic CT or USG Cortisol level Fibrinogen, FDPs(fibrin degradation product), D-dimer D-dimer is a fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two crosslinked D fragments of the fibrin protein. D-dimer concentration may be determined to help diagnose thrombosis Its main use, therefore, is to exclude thromboembolic disease where the probability is low. In addition, it is used in the diagnosis of the blood disorder disseminated intravascular coagulation, Deep vein thrombosis (DVT) ,Pulmonary embolism (PE) ,Strokes CVP = 0-6 mmHg Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left ... value that is very similar to left atrial pressure (normally about 8-10 mmHg). The jugular venous pressure is usually assessed by observing the right side of the patient's neck. The normal mean jugular venous pressure, determined as the vertical distance above the midpoint of the right atrium, is 6 to 8 cm H2O .

Approach to the Patient in Shock Physical examination Vital Signs CNS – mental status Skin – color, temp, rashes, sores CV – JVP, heart sounds Resp – lung sounds, RR, oxygen sat, ABG GI – tenderness , rigidity, guarding, rebound Renal – urine output History Recent illness Fever Chest pain, SOB Abdominal pain Comorbidities Medications Toxins/Ingestions Recent hospitalization or surgery Baseline mental status

Is This Patient in Shock? Patient looks ill Altered mental status Skin cool and mottled or hot and flushed Weak or absent peripheral pulses SBP <110 Tachycardia Yes! These are all signs and symptoms of shock

Shock Do you remember how to quickly estimate blood pressure by pulse? 60 by palpating a pulse, you know SBP is at least this number 70 80 90

Goals of Treatment ABCDE Airway control work of Breathing optimize Circulation assure adequate oxygen Delivery achieve End points of resuscitation

Airway Determine need for intubation but remember: intubation can worsen hypotension Sedatives can lower blood pressure Positive pressure ventilation decreases preload May need volume resuscitation prior to intubation to avoid hemodynamic collapse

Control Work of Breathing Respiratory muscles consume a significant amount of oxygen Mechanical ventilation and sedation decrease WOB and improves survival

Optimizing Circulation Isotonic crystalloids Titrated to:(aims to achieve) CVP 8-12 mm Hg Urine output 0.5 ml/kg/hr (30 ml/hr) Improving heart rate May require 4-6 L of fluids Crystalloids passed readily through the membrane, whereas colloids (from the Greek word for glue) did not. Intravenous fluids are similarly classified based on their ability to pass through barriers separating body fluid compartments, particularly the one between intravascular and extravascular (interstitial) fluid compartments The principal component of crystalloid fluids is the inorganic salt sodium chloride (NaCl). The prototype crystalloid fluid is 0.9% sodium chloride (NaCl), also called isotonic saline or normal saline. The latter term is inappropriate because a one normal (1 N) NaCl solution contains 58 g NaCl per liter Other crystalloids are , R.L and dextrose solutions As mentioned earlier, colloids are large molecules that do not pass across diffusional barriers as readily as crystalloids. Colloid fluids infused into the vascular space therefore have a greater tendency to stay put and enhance the plasma volume than do crystalloid fluids( albumin, dextrans etc )

Maintaining Oxygen Delivery Decrease oxygen demands Provide analgesia and anxiolytics to relax muscles and avoid shivering Maintain arterial oxygen saturation/content Give supplemental oxygen Maintain Hemoglobin > 10 g/dL Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction SmvO

End Points of Resuscitation Goal of resuscitation is to maximize survival and minimize morbidity Use objective hemodynamic and physiologic values to guide therapy Goal directed approach Urine output > 0.5 mL/kg/hr CVP 8-12 mmHg MAP 65 to 90 mmHg Central venous oxygen concentration > 70%

Treatment objectives Specific treatment will depend on the underlying cause ABC approach Volume replacement: Hypovolemic or septic Inotropes: Cardiogenic Vasopressors: Septic Adrenaline: Anaphylactic

Break !!

What Type of Shock is This? 68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive Hypovolemic Shock

Hypovolemic Shock ABCs Establish 2 large bore IVs or a central line Crystalloids Normal Saline or Lactate Ringers Up to 3 liters PRBCs O negative or cross matched Control, if any bleeding Arrange definitive treatment

What Type of Shock is This? An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.40C, hypotensive with a widened pulse pressure, tachycardia, with warm extremities Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive Septic

Sepsis Two or more of SIRS criteria Temp > 380C or < 360C HR > 90 beats /min RR > 20 /min WBC > 12,000 or < 4,000 / mm3 Plus the presumed existence of infection Blood pressure can be normal!

Treatment of Septic Shock 2 large bore IVs NS IVF bolus- 1-2 L wide open (if no contraindications) Supplemental oxygen Empiric antibiotics, based on suspected source, as soon as possible

Persistent Hypotension If no response after 2-3 L IVF, start a vasopressor (norepinephrine, dopamine, etc) and titrate to effect Goal: MAP > 60 Consider adrenal insufficiency: hydrocortisone 100 mg IV

What Type of Shock is This? A 55 yo M with hx of HTN, DM presents with “crushing” sub sternal Chest Pain, diaphoresis, hypotension, tachycardia and cool, clammy extremities Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive Cardiogenic

Cardiogenic Shock Signs: Defined as: Cool, mottled skin Tachypnea Hypotension Altered mental status Narrowed pulse pressure Rales, murmur Defined as: SBP < 90 mmHg CI < 2.2 L/m/m2 PCWP > 18 mmHg Normal value for PCWP 8-10 mmHg CI = 3.2 L/m/m2

Ancillary Tests ECG Chest X-Ray CBC, Chemistry , cardiac enzymes, coagulation studies Echocardiogram

Treatment of Cardiogenic Shock Goals- Airway stability and improving myocardial pump function Cardiac monitor, pulse oximetry Supplemental oxygen, IV access Intubation may decrease preload and result in hypotension Be prepared to give fluid bolus

What Type of Shock is This? A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing. Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive Anaphylactic

Anaphylactic Shock- Diagnosis Clinical diagnosis Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems Look for exposure to drug, food, or insect Labs have no role

Anaphylactic Shock- Treatment ABC’s Angioedema and respiratory compromise require immediate intubation IV line , cardiac monitor, pulse oximetry IVFs, oxygen Epinephrine Second line Corticosteriods H1 and H2 blockers Epi – the single most important step in treatment

What Type of Shock is This? Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive A 41 yo M presents to the ER after an RTA complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities Neurogenic

Neurogenic Shock- Treatment A,B,Cs Remember c-spine precautions Fluid resuscitation Keep MAP at 85-90 mm Hg If crystalloid is insufficient use vasopressors Search for other causes of hypotension For bradycardia Atropine Pacemaker

What Type of Shock is This? A 24 yo M presents to the ED after an RTA c/o chest pain and difficulty breathing. On Physical examination, you note the patient to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive Obstructive

Any Questions?