Shock: A Clinical Review

Definition

Shock is a life-threatening state of acute circulatory failure, leading to a systemic and profound imbalance between tissue oxygen delivery (DO2) and tissue oxygen consumption (VO2). This results in cellular dysoxia—a state where cells cannot utilize oxygen effectively to support aerobic metabolism, even if it is present—which, if uncorrected, initiates a devastating cascade from a reversible state of compensated shock to irreversible multi-organ failure and death (1, 2). The fundamental clinical challenge is to identify this state of cellular distress before it manifests as overt hypotension. Hypotension is often a late and ominous sign of decompensation, indicating that the body's compensatory mechanisms have failed. The astute clinician's goal is to recognize the subtle signs of "cryptic shock" (e.g., rising lactate with normal blood pressure) and intervene aggressively to restore perfusion.

Epidemiology

In Malaysia, shock represents a significant and life-threatening burden on the healthcare system, driven by the high prevalence of cardiovascular disease and severe infections. Data from the Malaysian National Cardiovascular Database (NCVD-ACS) registry between 2006 and 2013 revealed that cardiogenic shock complicates a substantial 10.6% of all ST-elevation myocardial infarctions (STEMI). The outcome is grim, with a high in-hospital mortality rate of 34.1%, a seven-fold increase in the risk of death compared to STEMI patients without shock (7). This highlights a critical "care gap," as timely reperfusion with percutaneous coronary intervention (PCI), the gold standard treatment which reduces mortality, was only performed in a third of these patients. This is often due to logistical delays in transferring patients from district hospitals to PCI-capable tertiary centres, a crucial reality for house officers working in peripheral settings (8).

Similarly, sepsis and septic shock are major challenges in our local setting. A 2019 study at Hospital Universiti Sains Malaysia (HUSM) found that sepsis accounted for nearly half (48%) of all ICU admissions, with an associated mortality rate of 26.7% (9). An even starker figure comes from a study at the University of Malaya Medical Centre (UMMC), which reported a 54% mortality rate for patients presenting to the Emergency Department with severe sepsis or septic shock, with pneumonia and urological infections being the most common sources (10). Furthermore, traumatic injuries, particularly from road traffic accidents, are a major and frequent cause of hypovolemic shock in our emergency departments, though specific national incidence data is less detailed. These local statistics are not just numbers; they represent the daily reality for Malaysian house officers and underscore the critical need for rapid diagnosis and effective, guideline-driven management to mitigate these high mortality rates.

Pathophysiology

The core of shock, regardless of its cause, is widespread cellular injury due to energy failure. This process unfolds through a common final pathway, which is met by a powerful but ultimately finite systemic compensatory response.

The Cellular Cascade of Dysoxia

When oxygen delivery fails, cells are forced to switch from efficient aerobic respiration (yielding ~36 ATP per molecule of glucose) to vastly inefficient anaerobic glycolysis (yielding only 2 ATP) to produce energy. This metabolic shift has catastrophic consequences. Firstly, it leads to the accumulation of lactic acid, causing a systemic metabolic acidosis that impairs the function of vital enzymes and directly depresses myocardial contractility, worsening the shock state (6). Secondly, the drastic reduction in ATP cripples energy-dependent cellular machinery. The Na+/K+-ATPase pump fails, causing an uncontrolled influx of sodium and water. This leads to cellular swelling, membrane disruption, mitochondrial damage from calcium influx, and eventual cell death through lysis and apoptosis (5).

Concurrently, hypoxic endothelial cells lining the blood vessels become activated. This triggers a massive inflammatory response, releasing a storm of cytokines like Tumor Necrosis Factor-alpha (TNF-α) and interleukins (IL-1, IL-6), which further fuel systemic inflammation and fever. These mediators also upregulate the production of inducible nitric oxide synthase (iNOS), which produces large amounts of nitric oxide (NO), a potent vasodilator that exacerbates hypotension, particularly in distributive shock (6). This inflammatory cascade, coupled with the activation of the coagulation system in areas of sluggish blood flow, can lead to microvascular thrombosis and the devastating syndrome of Disseminated Intravascular Coagulation (DIC), creating a vicious cycle of worsening tissue ischemia (12).

Systemic Compensatory Response

In the face of falling perfusion, the body mounts a rapid neurohormonal defence to preserve blood flow to the most vital organs—the brain and the heart. This response is mediated primarily by the baroreceptor reflex. Carotid and aortic baroreceptors detect a drop in arterial pressure and trigger a massive activation of the sympathetic nervous system (4). This results in the release of catecholamines (epinephrine and norepinephrine), which act on adrenergic receptors to cause:

• Tachycardia and Increased Inotropy (β1 effect): To increase heart rate and contractility, thereby boosting cardiac output.

• Systemic Vasoconstriction (α1 effect): Constriction of arterioles in the skin, muscles, and splanchnic circulation to increase systemic vascular resistance (SVR) and redirect blood centrally. This is responsible for the classic cool, clammy skin and prolonged capillary refill.

Simultaneously, other hormonal systems are activated:

• The kidneys, sensing reduced blood flow, activate the Renin-Angiotensin-Aldosterone System (RAAS). This leads to the production of angiotensin II, a potent vasoconstrictor, and the release of aldosterone, which promotes renal retention of sodium and water to expand intravascular volume (4).

• The posterior pituitary releases Antidiuretic Hormone (ADH) in response to hypotension and hyperosmolarity. ADH promotes water reabsorption in the collecting ducts and also acts as a powerful vasoconstrictor at high concentrations (12).

These mechanisms are initially life-saving but become maladaptive if the underlying cause of shock is not corrected. Prolonged, intense vasoconstriction dramatically increases cardiac afterload and myocardial oxygen demand, which can overwhelm a struggling heart. Eventually, these defences fail, leading to decompensated shock and circulatory collapse (11).

Classification of Shock

Shock is classified into four main types, though it is crucial to recognise that patients frequently present with a mixed shock picture (e.g., a patient with pancreatitis may have distributive shock from inflammation and hypovolemic shock from third-spacing).

• Hypovolemic Shock: The "empty tank." Caused by a critical loss of intravascular volume. Hemorrhagic causes include trauma, GI bleeding, and ruptured aortic aneurysm. Non-hemorrhagic causes include severe diarrhea or vomiting (e.g., cholera), extensive burns, or severe dehydration from diabetic ketoacidosis (16).

• Cardiogenic Shock: The "failed pump." Results from primary cardiac pump failure. Myopathic causes include large myocardial infarction or fulminant myocarditis. Mechanical causes include acute mitral regurgitation from a ruptured papillary muscle or a ventricular septal defect post-MI. Arrhythmic causes include sustained ventricular tachycardia or complete heart block (11).

• Distributive Shock: The "leaky, dilated pipes." Characterized by profound vasodilation and increased capillary permeability. This includes septic shock (most common), anaphylactic shock, neurogenic shock (from spinal cord injury), and endocrine shock (e.g., adrenal crisis) (6).

• Obstructive Shock: The "blocked pipe." Caused by a physical obstruction to blood flow. This can be an obstruction to right ventricular outflow (e.g., massive pulmonary embolism) or an obstruction to ventricular filling (e.g., cardiac tamponade, tension pneumothorax) (13).

Clinical Presentation

The classic presentation of shock involves signs of systemic hypoperfusion. It is critical to recognize that hypotension is often a late sign; a patient can be in a state of compensated shock while remaining normotensive (1).

Diagnostic Clues

• Neurogenic Shock: The combination of hypotension and bradycardia is nearly pathognomonic. This occurs because a high spinal cord injury (above T6) disrupts sympathetic outflow, leaving unopposed vagal (parasympathetic) tone to dominate, causing both vasodilation and a slow heart rate (19).

• Cardiac Tamponade: Beck's Triad (hypotension, distended neck veins, muffled heart sounds) is a classic finding, caused by the compression of the heart by pericardial fluid, which restricts diastolic filling and reduces stroke volume (38). A pulsus paradoxus (an exaggerated drop in systolic BP >10 mmHg on inspiration) may also be present.

• Tension Pneumothorax: The triad of unilaterally absent breath sounds, tracheal deviation away from the affected side, and hypotension are key features. This is a clinical diagnosis; do not wait for a chest X-ray. The trapped air in the pleural space compresses the heart and great vessels, obstructing venous return (38).

Common Symptoms (>50%)

• Tachycardia (Heart Rate > 100 bpm): The body's earliest and most reliable attempt to maintain cardiac output (CO = HR x SV) in the face of falling stroke volume (1).

• Tachypnea (Respiratory Rate > 22 breaths/min): A compensatory response to the underlying metabolic acidosis, as the body attempts to "blow off" CO2 to raise systemic pH (1).

• Altered Mental Status (initially anxiety or agitation, progressing to confusion and lethargy) due to cerebral hypoperfusion (1).

• Cool, pale, and clammy skin (in hypovolemic, cardiogenic, and late distributive shock) due to intense peripheral vasoconstriction orchestrated by the sympathetic nervous system (1).

• Oliguria (Urine Output < 0.5 mL/kg/hr), a very sensitive marker of reduced renal perfusion as the kidneys attempt to conserve volume (1).

Less Common Symptoms (10-50%)

• Warm, flushed skin (in early "warm" distributive shock, like sepsis) due to peripheral vasodilation from inflammatory mediators like nitric oxide (13).

• Bradycardia (in neurogenic shock or in patients on beta-blockers, which can mask the typical tachycardic response) (19).

• Wide pulse pressure (in early distributive shock) due to a low diastolic pressure from vasodilation, resulting in a "bounding" pulse (13).

⚠️ Red Flag Signs & Symptoms

• Hypotension (MAP < 65 mmHg or SBP < 90 mmHg): Indicates decompensated shock and requires immediate, aggressive intervention to prevent imminent cardiac arrest.

• Mottled skin (Livedo Reticularis): A blotchy, purplish, net-like discoloration of the skin, particularly over the knees. This indicates severe microcirculatory failure and is associated with a very poor prognosis.

• Significantly Altered Mental Status (GCS < 13): Suggests severe cerebral hypoperfusion and may herald the need for definitive airway protection via intubation.

• Anuria: Complete cessation of urine output, indicating severe acute kidney injury and profound circulatory failure.

Complications

Prolonged shock leads to a cascade of organ failure as cells die and tissues fail:

• Cardiovascular: Persistent hypotension can cause myocardial ischemia from coronary hypoperfusion, leading to life-threatening arrhythmias and ultimately, cardiac arrest.

• Neurological: Severe or prolonged cerebral hypoperfusion can result in hypoxic-anoxic brain injury, watershed strokes in the border zones between cerebral artery territories, or profound coma.

• Renal: Acute Tubular Necrosis (ATN) from severe hypoperfusion leads to Acute Kidney Injury (AKI), characterized by rising creatinine and oliguria, often requiring renal replacement therapy.

• Pulmonary: Endothelial injury in the pulmonary vasculature from the systemic inflammatory response leads to capillary leak, flooding the alveoli with protein-rich fluid and causing Acute Respiratory Distress Syndrome (ARDS).

• Gastrointestinal: Splanchnic hypoperfusion can cause ischemic bowel ("dead gut"), paralytic ileus, and "shock liver" (hypoxic hepatitis) with soaring transaminases.

• Hematological: Widespread activation of the clotting cascade leads to Disseminated Intravascular Coagulation (DIC), a consumptive coagulopathy characterized by the paradox of simultaneous microvascular thrombosis and systemic bleeding.

Prognosis

The prognosis of shock is highly dependent on the underlying cause, the severity, the patient's premorbid condition, and the timeliness of intervention. Cardiogenic shock complicating STEMI in Malaysia carries a dire 34.1% in-hospital mortality rate (7). Septic shock mortality in local Malaysian hospitals ranges from 26.7% to 54% (9, 10). Prognostic scoring systems like the SOFA (Sequential Organ Failure Assessment) score are used in the ICU to quantify the degree of organ dysfunction and predict mortality. However, for the house officer on the ward, one of the most powerful prognostic markers is lactate clearance. A failure to reduce serum lactate levels with resuscitation is a robust indicator of ongoing hypoperfusion and a very poor prognosis (1).

Differential Diagnosis

[Cardiogenic Shock]: This is a key differential in any patient with shock, especially the elderly or those with known cardiac disease. It is distinguished by signs of fluid overload and pump failure, such as a distended Jugular Venous Pressure (JVP), bilateral pulmonary crackles on auscultation, and possibly an S3 gallop. These signs are absent in hypovolemic and early distributive shock (19). A bedside echocardiogram showing poor left ventricular contractility, along with an ECG showing ischemia or arrhythmia and elevated cardiac troponins, would confirm this diagnosis.

[Hypovolemic Shock]: This should be suspected in any patient with a history of trauma, gastrointestinal bleeding, or significant fluid loss (e.g., severe diarrhea, diabetic ketoacidosis). The clinical picture is one of a "cold and empty" patient, with cool, clammy skin, tachycardia, and a flat JVP, indicating low preload (17). The absence of pulmonary edema and a rapid (though often temporary) response to a fluid challenge helps differentiate it from cardiogenic shock.

[Septic Shock]: Consider this in any patient with shock and a potential source of infection (e.g., cough, dysuria, cellulitis). The classic early presentation is "warm shock," with warm, flushed peripheries, a bounding pulse, and wide pulse pressure, distinguishing it from the vasoconstricted states of hypovolemic and cardiogenic shock (13). Fever and an elevated white cell count are supportive, but their absence does not rule out sepsis, especially in elderly or immunocompromised patients who may present with hypothermia.

[Massive Pulmonary Embolism (Obstructive Shock)]: This diagnosis should be considered in patients with acute onset of severe dyspnea, pleuritic chest pain, and signs of acute right heart strain (distended JVP with clear lungs). An ECG may show the classic S1Q3T3 pattern, a new right bundle branch block, or sinus tachycardia (16). It is differentiated from cardiogenic shock by the absence of left-sided failure (pulmonary edema) and from hypovolemic shock by the elevated JVP, reflecting the obstruction to right ventricular outflow.

Investigations

Immediate & Bedside Tests

• 12-Lead ECG: This is mandatory to immediately rule out acute myocardial infarction, the most common cause of cardiogenic shock (the action), and to detect life-threatening arrhythmias or specific clues like the S1Q3T3 pattern of pulmonary embolism that can guide therapy (the rationale) (16).

• Point-of-Care Ultrasound (POCUS): A rapid RUSH (Rapid Ultrasound in Shock) exam is essential to systematically evaluate the "Pump, Tank, and Pipes." It assesses cardiac contractility (is the heart hyperdynamic or hypodynamic?), pericardial fluid (for tamponade), and volume status via IVC size and collapsibility (the action), allowing for rapid differentiation between the main shock etiologies at the bedside without waiting for formal imaging (the rationale) (16).

• Fingerprick Blood Glucose: This is performed to rapidly exclude hypoglycemia as a reversible cause of altered mental status (the action) and to identify severe hyperglycemia that may point towards an underlying endocrine emergency like Diabetic Ketoacidosis (DKA) (the rationale).

Diagnostic Workup

• First-Line Investigations: An Arterial Blood Gas (ABG) is the most critical initial blood test. It provides an immediate, quantitative measure of global tissue hypoperfusion via the serum lactate and base deficit (the rationale), which is crucial for both diagnosis and for monitoring the response to resuscitation (the action) (16). The anion gap can also be calculated from the electrolytes to confirm the presence of significant lactic acidosis.

• Gold Standard: The definitive diagnosis often depends on the suspected etiology. For a massive pulmonary embolism, a CT Pulmonary Angiogram (CTPA) is the gold standard as it directly visualizes the clot in the pulmonary arteries (the rationale), confirming the cause of obstructive shock and guiding thrombolytic therapy (the action) (43). For cardiogenic shock due to AMI, coronary angiography is the gold standard for both diagnosis and therapeutic intervention via PCI (23).

Monitoring & Staging

• Full Blood Count: This is performed to assess for hemorrhage by checking the hemoglobin and hematocrit (the rationale) and to look for leukocytosis or leukopenia, which supports a diagnosis of sepsis (the action) (16).

• Renal Profile & Electrolytes: Serial measurement is used to monitor for the development of acute kidney injury, a common and serious complication of shock (the action), as a rising creatinine indicates worsening end-organ hypoperfusion (the rationale) (16).

• Sepsis Workup: In suspected septic shock, obtaining at least two sets of blood cultures from different sites before administering antibiotics is crucial. This is done to identify the causative organism and its antibiotic sensitivities (the rationale), which allows for the de-escalation of broad-spectrum antibiotics to targeted therapy later, a key principle of antimicrobial stewardship (the action) (16).

• Advanced Hemodynamic Monitoring: While not routine, a Central Venous Catheter (CVC) can be placed to monitor Central Venous Pressure (CVP) and central venous oxygen saturation (ScvO2). While a single CVP value is a poor predictor of fluid status, the trend in response to fluid challenges can be informative. An ScvO2 < 70% indicates that systemic oxygen delivery is inadequate to meet tissue demands, signaling a need for further resuscitation.

Management

Management Principles

The management of shock focuses on the simultaneous restoration of adequate tissue perfusion through resuscitation (the "fix the numbers" phase) and the prompt diagnosis and treatment of the underlying cause (the "fix the problem" phase).

Acute Stabilisation (The First Hour)

• Airway/Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to maximize arterial oxygen content and improve oxygen delivery to ischemic tissues (the rationale) (16). Have a low threshold for early endotracheal intubation in patients with altered mental status (GCS < 8), severe respiratory distress, or hemodynamic instability, as the work of breathing itself consumes significant oxygen.

• Circulation: Secure two large-bore IV cannulas (14-16G) and administer a stat fluid bolus of a balanced isotonic crystalloid like Hartmann's solution 20-30mL/kg over 15-30 minutes for most forms of shock (the action) to rapidly expand intravascular volume, increase preload, and improve cardiac output and organ perfusion (the rationale) (16). Use fluids with extreme caution in suspected cardiogenic shock, where a smaller bolus (250mL) may be trialed while observing for signs of worsening pulmonary edema.

• Disability: Rapidly assess neurological status with the GCS and check blood glucose to rule out hypoglycemia.

Definitive Therapy

Hypovolemic Shock

The absolute priority is to stop the volume loss (e.g., direct pressure, urgent endoscopy, emergency surgery) and replace lost volume. For hemorrhagic shock, activate the Massive Transfusion Protocol (MTP), providing packed red blood cells, fresh frozen plasma, and platelets in a balanced 1:1:1 ratio to mimic whole blood and prevent the lethal triad of trauma: acidosis, hypothermia, and coagulopathy (16). Administer Tranexamic Acid (TXA) 1g IV if within 3 hours of traumatic injury, as it has been shown to reduce mortality from bleeding by inhibiting fibrinolysis (49).

Cardiogenic Shock

The definitive treatment is urgent coronary revascularization for AMI. The Malaysian STEMI CPG recommends primary PCI as the preferred strategy. If transfer time to a PCI-capable centre is >120 minutes, a pharmaco-invasive strategy with immediate fibrinolysis followed by transfer is indicated (23). Noradrenaline is the first-line vasopressor to restore a MAP ≥65 mmHg. If signs of hypoperfusion persist despite an adequate MAP, an inotrope like Dobutamine should be added to improve cardiac contractility (23). In refractory cases, advanced mechanical circulatory support like an Intra-Aortic Balloon Pump (IABP) or Extracorporeal Membrane Oxygenation (ECMO) may be required at specialized tertiary centres.

Distributive Shock

• Septic Shock: Management is dictated by the "Hour-1 Bundle" (48). After obtaining blood cultures, administer appropriate broad-spectrum antibiotics immediately (within one hour). Continue fluid resuscitation with 30mL/kg of crystalloid for hypotension. Start Noradrenaline if hypotension persists to maintain a MAP ≥65 mmHg. Crucially, pursue early source control (e.g., draining an abscess, removing an infected catheter, debriding necrotic tissue) as this is essential for reversing the septic process.

• Anaphylactic Shock: The cornerstone of treatment is immediate intramuscular (IM) Adrenaline 0.5mg (0.5mL of 1:1000) into the anterolateral thigh. This can be repeated every 5-15 minutes. Adrenaline is the only therapy that reverses all life-threatening features (bronchospasm, vasodilation, laryngeal edema) (19). All other treatments—IV fluids, antihistamines (H1/H2 blockers), and corticosteroids—are secondary and must never delay the administration of adrenaline.

• Neurogenic Shock: After judicious fluid resuscitation to ensure euvolemia, vasopressors are the mainstay of treatment to restore vascular tone. Noradrenaline is often preferred as its α-agonist effects counter the vasodilation and its β-agonist effects can counter the associated bradycardia (19).

Obstructive Shock

Treatment is the immediate relief of the physical obstruction, as this is the only way to restore circulation.

• Tension Pneumothorax: Immediate needle thoracostomy in the 2nd intercostal space (mid-clavicular line) or 5th intercostal space (anterior axillary line), followed by definitive chest tube insertion (22).

• Cardiac Tamponade: Urgent pericardiocentesis (needle drainage of the pericardial sac), ideally under ultrasound guidance, or a surgical pericardial window (22).

• Massive Pulmonary Embolism: For the unstable patient, systemic thrombolysis (e.g., with Alteplase) should be administered if there are no absolute contraindications. Catheter-directed thrombolysis or surgical embolectomy are alternatives available at specialized centres (22).

Supportive & Symptomatic Care

• Provide adequate analgesia (e.g., morphine, fentanyl) to reduce pain and the associated detrimental sympathetic stress.

• Administer antiemetics to prevent vomiting and the risk of aspiration in a patient with a compromised airway.

• Initiate stress ulcer prophylaxis (e.g., with a proton pump inhibitor) and VTE prophylaxis (e.g., with low molecular weight heparin) as per local ICU protocols, once any active bleeding is controlled.

• Maintain normoglycemia with an insulin infusion if necessary, as both hyperglycemia and hypoglycemia are associated with poor outcomes.

• Consider early nutritional support (enteral feeding is preferred) once the patient is hemodynamically stabilized to prevent catabolism and support immune function.

Key Nursing & Monitoring Instructions

• Continuous cardiac monitoring and pulse oximetry.

• Insert an arterial line for continuous, accurate beat-to-beat blood pressure monitoring and to allow for frequent, painless ABG sampling.

• Insert an indwelling urinary catheter and monitor urine output hourly as a key indicator of renal perfusion.

• Maintain a strict input/output chart.

• Inform medical staff immediately if MAP drops below 65 mmHg, urine output is <0.5mL/kg/hr for two consecutive hours, or if there is any new neurological change.

• Perform serial lactate measurements (e.g., 2-4 hourly) to guide the resuscitation effort; a falling lactate is a robust sign of success.

Long-Term Plan & Patient Education

Follow-up will be dictated by the underlying cause of shock. For survivors of septic shock, education should focus on the signs of recurring infection and the potential for Post-Sepsis Syndrome. For patients post-MI, education on aggressive secondary prevention, including strict medication compliance (aspirin, statins, beta-blockers, ACE inhibitors) and comprehensive lifestyle modification, is critical. All patients and their families should be educated on the reason for the critical illness, the expected (and often prolonged) recovery pathway, and the potential long-term physical and cognitive sequelae of surviving critical illness (Post-ICU Syndrome).

When to Escalate

Call Your Senior (MO/Specialist) if:

• The patient remains hypotensive (MAP < 65 mmHg) despite an initial 30mL/kg fluid bolus and initiation of vasopressors (e.g., noradrenaline > 0.2 mcg/kg/min).

• The patient develops any new neurological signs or a drop in GCS of ≥2 points.

• Serum lactate fails to clear by at least 10-20% or continues to rise after 2 hours of active resuscitation.

• The patient requires escalating doses of vasopressors or the addition of a second agent (e.g., vasopressin).

• You are considering intubation, as this procedure can itself cause hemodynamic collapse and should be performed by an experienced operator.

• Urine output remains <0.5mL/kg/hr despite adequate MAP and fluid resuscitation.

Referral Criteria:

• Refer to the Cardiology team immediately for any patient with suspected cardiogenic shock for consideration of urgent revascularization or advanced mechanical circulatory support.

• Refer to the General Surgery or Trauma team for any patient with non-compressible hemorrhagic shock requiring urgent surgical or endovascular source control.

• Refer to the Intensive Care Unit (ICU) team for any patient requiring vasopressor support, mechanical ventilation, or advanced hemodynamic monitoring. The Malaysian Society of Intensive Care provides guidelines on admission criteria, which also include considerations for futility and palliative care pathways (60).

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8. Ibid.

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