Shock

by Maryam AlBadwawi

Introduction

Shock, in simple terms, is a reduced circulatory blood flow state within the body. The inadequate circulation deprives the tissues of its oxygen and essential nutrients. Mitochondria are the first cellular structure to be affected by hypoxia. As a result of anaerobic respiration, they start to produce lactate, leading to lactic acidosis. Initially, the shock is reversible. Extended shock state leads to cellular and organ dysfunction and ultimately death.

The shock is a life-threatening medical emergency with a mortality rate up to 20%. The primary goal of resuscitation is to optimize organ perfusion. It may result from a variety of causes. It is divided into four categories according to the mechanism of the disease and treatment (See Table 1). Differentiating the type facilitates treatment, however, all categories of shock lead to the same result.

Table 1: Shock Types

Case presentation

A 61-year-old male with fever, shortness of breath and vomiting was brought to the ED by ambulance. He also complained of dizziness, malaise, and reduced urination. His symptoms started one week earlier and got progressively worse in time. However, he did not seek any medical assistance before. His medical history includes diabetes mellitus and hypertension.

On examination, he appeared ill. His vital signs were: BP: 80/50 mmHg, HR: 140 bpm, T: 38.6°C, RR: 30 bpm, SPO2: 90% on room air. His blood sugar was 5.3 mmol/dL, and capillary refill was four seconds. He responds to verbal comments on the AVPU score. On auscultation, coarse crackles were heard on the right side. Heart sounds were normal. There was 1+ pitting edema on bilateral legs. Abdominal examination was unremarkable, and there was no focal neurological deficit.

The pre-diagnosis was the septic shock. He needed emergent resuscitation and antibiotics administration.

Two large bore IV cannulas were inserted. CBC, urea, electrolytes, creatinine, LFT, cardiac enzymes, lactate, and ABG were ordered. Bedside US scan revealed a collapsing inferior vena cava. A urinary catheter was placed for urinalysis and to monitor the output.

While waiting for the results, one liter of isotonic saline, one dose of Vancomycin (15-20 mg/kg) and Piperacillin-Tazobactam ( 80-100 mg/kg) were administered. His BP did not improve. After the second liter of isotonic saline, his HR settled to 120, but his mean arterial pressure (MAP) remained below 60 mmHg. A central line was inserted, and epinephrine (2-10 mcg/min) started. His MAP improved to 65 and remained stable. He was transferred to the ICU.

Critical Bedside Actions and General Approach

Early and accurate management is essential as it reduces mortality significantly in certain types of shock. Heart rate, blood pressure, and partial oxygen saturation must be continuously monitored. Optimizing airway, breathing, and circulation (ABC) is the priority. Check the airway of the patient, and consider intubation in case of inadequate oxygenation and ventilation. Maximizing arterial oxygen saturation through proper oxygenation is crucial. Central venous oxygenation should be monitored with a target of minimum 70%. Reducing the work of breathing lessens the metabolic load.

History and Physical Examination Hints

Common features of the shock include hypotension, altered mental status, and oliguria, regardless of the etiology. The patient history is significant to diagnose the type of shock and accurately treat the patient.

• Hypovolemic shock might have a history of trauma, pregnancy, gastrointestinal losses or burn. Initially, heart rate and force of contraction increase. Vasoconstriction causes elevated diastolic BP, and pulse pressure (the difference between systolic and diastolic BP) narrows. The blood flow to the noncritical organs decreases so that cells produce lactic acid. As bleeding continues, ventricular filling and cardiac output (CO) decrease, resulting in decreased BP. Hypotension is a late sign of shock.
• Cardiogenic shock occurs when more than 40% of the myocardium undergoes necrosis from ischemia, inflammation, toxins or immune destruction. It induces the same impairment as hemorrhagic shock. Patients have evidence of ventricular dysfunction earlier in the disease.
• Obstructive shock should be considered in patients with chest pain, shortness of breath, and altered mental status. The physical examination may reveal jugular venous distention, muffled heart sounds, pulsus paradoxus, tachypnea, tachycardia, cold extremities, friction rub, new murmur, and signs of deep vein thrombosis.
• Distributive shock findings depend on the cause. Sepsis and septic shock cause signs of infection. Other symptoms and signs include hypo/hyperthermia, tachycardia, tachypnea, wide pulse pressure, warm extremities, altered mental status, oliguria, and skin rash. Anaphylactic shock is characterized by skin and mucosa manifestation such as urticaria, flushing, pruritis, and angioedema. Respiratory symptoms may include rhinitis, bronchospasm, dyspnea, and stridor (pharyngeal/laryngeal edema). The patient may experience dysrhythmias, hypotension, presyncope, and syncope. Additionally, GI symptoms such as nausea, vomiting, and diarrhea may be present.
• Blood pressure may be normal or even high in the early course of shock; however, if left untreated, it may proceed to tachycardia and hypotension. Shock Index (heart rate divided by systolic blood pressure), may reveal obscure shock. The normal shock index ranges from 0.5 to 0.7. A value of >0.9 is considered abnormal and associated with higher mortality.

Emergency Diagnostic Tests and Interpretation

The suspected cause of shock, attributed from the history and physical examination, should guide diagnostic testing. The goal is to determine the involvement of organ hypoperfusion and damage. The following are helpful investigations in shock:

• Complete blood count and coagulation profile
  • Anemia, infection, hypo-coagulopathy related abnormalities can be seen
• Electrolytes
  • Some of the cases may show electrolyte disturbance because of their comorbidities or continuous medical problems affecting their nutrition or metabolism.
• Renal function tests
  • Blood urea nitrogen/creatinine
    • Renal functions impair because of low perfusion. High blood urea nitrogen compared to creatinine may provide information about prerenal causes showing a volume or blood loss.
  • Urinalysis
    • Urosepsis is one of the common sepsis causes.
• Hepatic function tests
  • Hepatic functions impair because of low perfusion.
• Lactate
  • Lactate gives an opinion about the hypoperfusion status. Its levels considered normal between 0.5-1 mmol/L. Lactate levels more than 2 considered as abnormal in the critically ill patients. Levels more than 4 shows increased the risk of mortality and morbidity. Therefore, those levels are used for some institutions to decide ICU admission.
• Urine pregnancy test
  • Considering every female patient in childbearing age as a pregnant patient is essential thinking in the ED.
• Chest x-ray
  • For pneumonia, pleural effusion, and other possible shock causes such as cardiac tamponade, aortic dissection, pneumothorax (tension).

What are your diagnoses in hypotensive patients with below chest x-rays?

• ECG
  • For arrhythmias, MI, cardiomyopathy and other findings
• US (RUSH protocol to find the cause of the shock

• Other invasive tests:
  • Arterial blood gas analysis for O2 pressure and pH level,
  • Some centers may prefer to measure systemic vascular resistance, central venous oxygen, and cardiac output in the ED.
• Certain etiologies of shock will require additional investigations:
  • SIRS and sepsis: Cultures (blood, sputum, urine, or wound), head CT and lumbar puncture
  • Cardiogenic: ECG, cardiac enzymes, and echocardiography
  • Obstructive: CT or V/Q scan for PE, echocardiography for cardiac tamponade

In any ill-appearing patient with tachycardia and hypotension or high shock index, the shock must be considered. The mentioned signs, symptoms and relevant diagnostic tests often help to arrive at a diagnosis and initiate appropriate treatment. However, certain disease processes can complicate the picture and lead to an alternate diagnosis. Therefore, understanding the shock physiology is important (Table 2). The labs should be completed, but it is important not to wait for the results before initiating treatment.

Table 2: Important Physiological Changes in Shock

 

Using certain criteria to help make the diagnosis and point to specific types of shock is more beneficial.

Septic shock

• SIRS (Systemic Immun Response Syndrome) – Two or more of the following:
  1. Temperature >38°C or <36°C
  2. Heart rate >90 beats/min
  3. Respiratory rate >20 breaths/min or PaCO2 <32 mmHg
  4. WBC >12,000/mm3, <4,000/mm3, or >10% band neutrophilia
• Sepsis
  • SIRS with finding the source of infection and associated with organ damage or hypoperfusion.
  • Sequential Organ Failure Assessment (S.O.F.A. or sofa) was recently described and created multiple discussions in emergency and critical care journals. q (Quick) sofa score includes Hypotension: systolic blood pressure less than or equal to 100 mmHg, Altered mental status, and Tachypnoea: respiratory rate greater than or equal to 22 breath per minute. 2 or more criteria violation in Q sofa score is considered the poor outcome predictor.
• Septic shock
  • Sepsis and hypotension despite adequate fluid resuscitation.

Hemorrhagic shock

• Simple hemorrhage
  • Suspected bleeding with normal vitals and normal base deficit
• Hemorrhage with hypoperfusion
  • Suspected bleeding with base deficit <-4 mEq/L or persistent pulse >100 beats/min
• Hemorrhagic shock
  • Suspected bleeding with at least four of the following criteria:
    1. Ill appearance or altered mental status
    2. Heart rate >100 beats/min
    3. Respiratory rate >20 breaths/min or PaCO2 <32 mmHg
    4. Arterial base deficit <-4 mEq/L or lactate >4 mmol/L
    5. Urine output <0.5 mL/kg/hr
    6. Arterial hypotension > 30 continuous minutes

Cardiogenic shock

• Cardiac failure
  • Clinical evidence of impaired forward flow of heart, including presence of dyspnea, tachycardia, pulmonary edema, peripheral edema, or cyanosis.
• Cardiogenic shock
  • Cardiac failure and at least four criteria of that similar to hemorrhagic shock.

Emergency Treatment Options

Fluid Resuscitation

Two large bore IV access should be obtained to support the circulatory system. A central line is also very beneficial in delivering fluid and medication, especially inotropes. Crystalloid fluids (normal saline or Ringer’s lactate) should be used in boluses (2-3 L bolus in 5-20 min – 20ml/kg in neonates and pediatrics). Pay close attention to patients in cardiogenic shock. Do not administer I.V. fluids rapidly to patients with signs of pulmonary congestion. Small fluid boluses such as 250 mL should be preferred in those cases.

Blood Products Resuscitation

Blood transfusion is considered if there is no response to two liters of fluid boluses, ongoing hemorrhage, or impending cardiovascular collapse. O-negative blood is standard for child-bearing women and O-positive in men is acceptable. Additionally, controlling the source of bleeding is critical. In special cases like hereditary or acquired bleeding diathesis, platelet transfusion is indicated if platelet count <50,000/μL. FFP transfusion is indicated for patients on warfarin with an elevated INR and significant bleeding, liver failure, or massive transfusion (>10 units PRBC in 24 hours). PCC is used for warfarin reversal (FFP, if not available). In a massive transfusion, plasma, platelets, and red blood cells should be given in 1:1:1 ratio.

Inotropes

If volume resuscitation does not improve the patient’s hemodynamic status and MAP remains below 65, inotropes may be used. Inotropes are also used in cardiogenic shock for depressed LV function. Norepinephrine (2-10 mcg/min) stimulates alpha and beta-adrenergic receptors, increasing peripheral vascular tone. Dobutamine (2.5-15 mcg/kg/min) may improve myocardial contractility and augment diastolic coronary blood flow through beta-1 adrenergic agonist effect, and it may cause mild peripheral vasodilation through beta-2 adrenergic agonist effect. Dopamine at moderate doses (5-10 μg/kg/min) has alpha and beta-1 adrenergic effects.

Treatment Success

Monitoring fluid status is encouraged by using a urinary catheter, intra-arterial blood pressure measurements, and central venous pressure monitoring.

When patients’ hemodynamic status become normal (blood pressure, heart rate and urine out put) and necessary volume restored. These help to maximize tissue oxygenation, resolution of acidosis and decrease lactate levels. These are the findings of successful resuscitation.

Medications

• Distributive shock
  • The treatment depends on the specific cause of shock.
  • In septic shock, it is important to start early broad-spectrum antibiotics:
    • Neonates: Ampicillin (150-200 mg/kg) with Cefotaxime (150-200 mg/kg)
    • Children: Vancomycin (15-20 mg/kg) and Cefotaxime (150-200 mg/kg)
    • Adult: Vancomycin (15-20 mg/kg) with Piperacillin-Tazobactam ( 80-100 mg/kg)
    • Consider low-dose corticosteroids to treat relative adrenal suppression if refractory hypotension is present despite fluids and inotropes.
• Anaphylactic shock
  • Epinephrine is the first line of treatment.
    • Adults: 0.3-0.5 mg of 1:1000 solution IM q5-10 minutes
    • Pediatrics: 0.01 mg/kg, max 0.3 mg of 1:1000 solution IM q5-10 minutes
    • Histamine blockers.
      • Diphenhydramine (H1 blocker): (25-50 mg IM/IV, pediatric 1 mg/kg IM/IV)
      • Cimetidine or ranitidine (H2 blockers).
    • Aerosolized albuterol and ipratropium are important in anaphylactic shock.
    • Steroids should be considered

Procedures

In the management of obstructive shock, it is essential to remove obstruction by pericardiocentesis in cardiac tamponade tamponade, by needle thoracocentesis followed by tube thoracostomy in tension pneumothorax, by thrombolysis in massive P.E., and afterload reduction until definitive treatment in aortic dissection.

Chest X-ray shows position of the chest tube in a patient with pneumothorax.

An intra-aortic balloon pump decreases afterload and increases diastolic BP and bridge to revascularization or valvular repair. Also, cardiogenic shock may necessitate emergent angiography or surgical procedures such as bypass or valve repair.

Disposition Decisions

Despite proper treatment, the mortality rates from severe shock can exceed 50 percent. Even after aggressive treatment in the ED, ICU admission is required.

References and Further Reading

• Marx, J. A., Hockberger, R. S., & Rosen, P. (2014). Rosen’s emergency medicine: Concepts and clinical practice (8th ed., Vol. 1). Philadelphia, PA: Mosby Elsevier.
• Blok, B. K., Cheung, D. S., & Platts-Mills, T. F. (2012). First aid for the emergency medicine boards (2nd ed.).
• Avegno, J., MD. (n.d.). CDEM Self-Study Modules. The approach to shock. Retrieved May 11, 2016, from http://www.cdemcurriculum.org/ssm/approach_to/shock.php – link
• Shock – 2017 Chris Nickson – Lifeinthefastlane – Link
• Shock – 2017 Josh Farkas – EMCrit Project – Link