Shock and cardiovascular emergencies

By the end of this note, the student will be able to define, classify, and explain the pathophysiological mechanisms of shock and cardiovascular emergencies encountered in Kenyan clinical practice; all drug dosages and protocols must be verified against current Kenya Ministry of Health guidelines and local institutional formularies.

Definition

Shock is a state of systemic hypoperfusion resulting in acute cellular hypoxia due to an imbalance between oxygen delivery ($DO_2$) and systemic oxygen demand ($VO_2$). Left untreated, this cellular energy crisis leads to irreversible organ damage and death. A normal blood pressure does not rule out shock; hypotension (systolic blood pressure

Anatomy and physiology you need

Tissue perfusion depends on Mean Arterial Pressure ($MAP$), calculated as: $MAP = \text{Cardiac Output } (CO) \times \text{Systemic Vascular Resistance } (SVR)$

Cardiac output is the product of Stroke Volume ($SV$) and Heart Rate ($HR$). Stroke volume is governed by three physiological variables:

• Preload: The end-diastolic wall tension of the ventricles, governed by venous return and intravascular volume.
• Contractility (Inotropy): The intrinsic myocardial force generated at a given sarcomere length, dependent on myocardial perfusion, calcium flux, and sympathetic stimulation.
• Afterload: The resistance against which the ventricles must contract to eject blood, primarily determined by arteriolar tone ($SVR$) and aortic elastance.

Oxygen delivery ($DO_2$) is the product of $CO$ and arterial oxygen content ($CaO_2$): $DO_2 = CO \times [ (1.34 \times \text{Haemoglobin} \times SaO_2) + (0.003 \times PaO_2) ]$

In the microcirculation, inadequate capillary hydrostatic pressure and cellular hypoxia shift metabolism from the mitochondrial Krebs cycle to anaerobic glycolysis, producing lactic acid, reducing adenosine triphosphate ($ATP$) synthesis, and impairing the $Na^+/K^+$ ATPase pump.

Causes and risk factors

The etiologies of shock are categorized into four broad classes, with distinct regional drivers in East Africa:

Region-Specific Risk Factors

• Tuberculosis: A primary driver of obstructive shock via massive pericardial effusion (cardiac tamponade) or constrictive pericarditis.
• HIV/AIDS: Increases vulnerability to opportunistic polymicrobial sepsis, tuberculous pericarditis, pulmonary arterial hypertension, and dilated cardiomyopathy.
• **Severe Malaria (P. falciparum):** Induces distributive shock and microvascular obstruction via cytoadherence and sequestration of parasitized red blood cells.
• Rheumatic Heart Disease (RHD): Prevalent in young adults, predisposing to cardiogenic shock through acute valvular failure (e.g., mitral regurgitation), infective endocarditis, or atrial arrhythmias.
• Sickle Cell Disease: Precipitates hypovolemic shock (splenic sequestration crisis in children) or obstructive shock (acute chest syndrome with cor pulmonale).

Pathophysiology

Hypovolemic Shock

Loss of whole blood or plasma $\rightarrow$ Decreased venous return to the heart $\rightarrow$ Reduced ventricular end-diastolic volume (decreased preload) $\rightarrow$ Decreased stroke volume and cardiac output $\rightarrow$ Baroreceptor uncoupling and sympathetic activation $\rightarrow$ Peripheral vasoconstriction and compensatory tachycardia $\rightarrow$ Prolonged hypoperfusion exhausts compensation $\rightarrow$ Microcirculatory collapse and tissue ischemia.

Cardiogenic Shock

Primary myocardial or valvular insult $\rightarrow$ Impaired systolic ejection or diastolic filling $\rightarrow$ Profound drop in stroke volume $\rightarrow$ Elevation of left ventricular end-diastolic pressure $\rightarrow$ Backward transmission of hydrostatic pressure to pulmonary capillaries $\rightarrow$ Acute cardiogenic pulmonary edema $\rightarrow$ Concomitant systemic hypoperfusion triggers compensatory vasoconstriction $\rightarrow$ Increased afterload further impedes the failing ventricle.

Distributive Shock (Sepsis/Malaria)

Endotoxins, exotoxins, or parasitic sequestrations $\rightarrow$ Systemic release of pro-inflammatory cytokines (TNF-$\alpha$, IL-1, IL-6) and nitric oxide $\rightarrow$ Pathological peripheral arterial and venous dilation (profoundly decreased $SVR$) $\rightarrow$ Endothelial injury and increased microvascular permeability $\rightarrow$ Plasma extravasation into interstitial space (relative hypovolemia) $\rightarrow$ Microvascular thrombus formation and mitochondrial dysfunction $\rightarrow$ Cytopathic hypoxia despite preserved or elevated cardiac output.

Obstructive Shock (Tamponade/Tension Pneumothorax)

Mechanical obstruction within the thorax $\rightarrow$ Elevated intrapericardial or intrathoracic pressure exceeding intracardiac chamber filling pressures $\rightarrow$ Restriction of ventricular diastolic filling $\rightarrow$ Precipitous collapse of cardiac preload $\rightarrow$ Acute drop in stroke volume $\rightarrow$ Inability to augment cardiac output despite maximal systemic vasoconstriction $\rightarrow$ Sudden cardiovascular collapse.

Clinical features

History questions that matter

• Onset and tempo: Did collapse occur instantaneously (arrhythmia, massive pulmonary embolism, aortic dissection) or evolve over days (worsening heart failure, occult sepsis, dehydration)?
• Fluid losses: Enquire about severe diarrhoea, vomiting, overt gastrointestinal bleeding (haematemesis, melaena), or reduced intake in hot weather.
• Chest symptoms: Is there acute, tearing chest pain radiating to the back (dissection), crushing substernal pressure (myocardial infarction), or pleuritic pain with breathlessness (pulmonary embolism)?
• Infection cues: Inquire about fever, cough with hemoptysis or night sweats (tuberculosis), dysuria, skin breaks, or animal contacts (leptospirosis).
• Underlying disease and drugs: History of rheumatic fever, advanced HIV, sickle cell crises, antiretroviral therapy, recent broad-spectrum antibiotics, or abrupt cessation of long-term steroids (adrenal crisis).

Examination findings and mechanisms

• Altered mental state: Restlessness, confusion, or coma results from impaired cerebral perfusion once mean arterial pressure drops below the cerebral autoregulation threshold.
• Tachycardia: Compensatory sympathetic activation attempts to maintain cardiac output ($CO = HR \times SV$) via beta-1 adrenergic stimulation. Bradycardia may occur in complete heart block, terminal shock, or beta-blocker overdose.
• Hypotension: Systolic blood pressure
  lt;90\text{ mmHg}$ or mean arterial pressure
  lt;65\text{ mmHg}$ indicates failure of compensatory vasoconstriction to offset low stroke volume or vasodilation.
• Tachypnoea: Increased respiratory rate occurs to blow off carbon dioxide, producing a respiratory alkalosis to compensate for systemic lactic acidosis.
• Oliguria: Urine output
  lt;0.5\text{ mL/kg/h}$ due to reduced renal perfusion pressure and compensatory aldosterone and antidiuretic hormone release to conserve volume.
• Cold, clammy peripheries and delayed capillary refill (
  gt;2\text{ seconds}$): Alpha-1 mediated peripheral vasoconstriction diverts blood from skin and skeletal muscle to vital core organs (classic in hypovolaemic, cardiogenic, and obstructive shock).
• Warm, flushed peripheries and flash capillary refill: Systemic vasodilation and reduced systemic vascular resistance in early distributive (septic, anaphylactic) shock.
• Elevated jugular venous pulse (JVP): Reflects high right-atrial pressure, seen in cardiogenic shock (RV failure), cardiac tamponade, tension pneumothorax, and massive pulmonary embolism. Flat neck veins indicate hypovolaemia or early distributive shock.
• Beck's triad (hypotension, elevated JVP, muffled heart sounds): Mechanical restriction of ventricular filling due to pericardial fluid accumulation under tension.
• Bilateral basal crackles and third heart sound ($S_3$): Indicates elevated left-ventricular end-diastolic pressure and acute pulmonary edema (cardiogenic shock).
• Unilateral absent breath sounds with hyper-resonance and tracheal deviation: Air trapped in the pleural space displacing mediastinal structures, causing kinking of the vena cava and obstructive shock.

Differential diagnosis

Investigations

Diagnosis and severity

Diagnostic synthesis

Diagnosis requires demonstrating systemic tissue hypoperfusion through the "triad of shock":

1. Haemodynamic: Mean arterial pressure
   lt;65\text{ mmHg}$ or systolic blood pressure
   lt;90\text{ mmHg}$ (or a drop
   gt;40\text{ mmHg}$ from baseline).
2. Clinical signs: Cutaneous (mottling, prolonged capillary refill, cold skin), renal (oliguria
   lt;0.5\text{ mL/kg/h}$), and neurological (encephalopathy, confusion).
3. Biochemical: Elevated blood lactate (
   gt;2\text{ mmol/L}$, typically
   gt;4\text{ mmol/L}$ in severe shock), reflecting anaerobic glycolysis.

Identify the shock phenotype via volume status and JVP: elevated JVP denotes cardiogenic or obstructive shock; low JVP denotes hypovolaemic or distributive shock.

Severity stratification

• Compensated shock: Normal blood pressure maintained by tachycardia, tachypnoea, and peripheral vasoconstriction. Mild elevation in serum lactate. Highly reversible if managed immediately.
• Decompensated shock: Compensatory mechanisms fail. Frank hypotension, severe oliguria, altered consciousness, and worsening metabolic acidosis (lactate
  gt;4\text{ mmol/L}$).
• Irreversible (refractory) shock: Persistent hypotension and profound tissue hypoperfusion despite high-dose vasopressors, inotropes, and appropriate volume resuscitation. Leads to Multiple Organ Dysfunction Syndrome (MODS): anuria, acute respiratory distress syndrome (ARDS), hepatic necrosis, and disseminated intravascular coagulation (DIC). High mortality risk.

Management

Immediate Stabilisation

• Airway and Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain oxygen saturation above ninety-two percent; intubate early if the patient has altered consciousness, severe exhaustion, or refractory hypoxaemia.
• Circulation: Secure two wide-bore peripheral intravenous cannulae. Rapidly infuse warmed crystalloids (Ringer's lactate or normal saline) in hypovolaemic, septic, or anaphylactic shock.
• Vasopressors: Start peripheral or central vasopressors if mean arterial pressure remains inadequate despite volume resuscitation. Noradrenaline is the primary agent to restore vascular tone without causing excessive tachycardia.
• Inotropes: Initiate dobutamine in cardiogenic shock with persistent hypoperfusion despite adequate intravascular filling pressures to improve myocardial contractility.
• Bedside Decompression: Immediately perform needle thoracostomy for tension pneumothorax or emergent pericardiocentesis for cardiac tamponade before awaiting imaging.
• Anaphylaxis Protocol: Administer intramuscular adrenaline immediately into the anterolateral thigh; avoid intravenous boluses unless trained and cardiac monitoring is attached.

Definitive Management

• Empiric Antimicrobials: Administer within the first hour of suspected sepsis (e.g., intravenous ceftriaxone plus metronidazole, with blood-film guided antimalarials such as artesunate if indicated in endemic zones).
• Cardiovascular Emergencies: Dual antiplatelet therapy and anticoagulation for acute coronary syndromes; intravenous labetalol or hydralazine for hypertensive emergencies with end-organ damage (aim to lower mean arterial pressure by no more than twenty-five percent in the first hour).

Monitoring, Follow-up, and Safety

• Hemodynamic Targets: Monitor urine output hourly via an indwelling catheter (target above zero-point-five millilitres per kilogram per hour), serial blood lactate clearance, and continuous pulse oximetry and telemetry.
• Fluid Safety: Continuously auscultate lung bases and evaluate the jugular venous pulse during fluid challenges; stop immediately if pulmonary crackles appear or the gallop rhythm worsens.
• Vasopressor Safety: Monitor peripheral infusion sites closely for extravasation, which causes severe local tissue ischaemia and necrosis.

Complications and Prognosis

• Multiorgan Dysfunction Syndrome (MODS): Prolonged tissue hypoperfusion precipitates acute kidney injury (acute tubular necrosis), ischaemic hepatitis ("shock liver"), stress ulceration, and disseminated intravascular coagulation.
• Acute Respiratory Distress Syndrome (ARDS): Endothelial injury and alveolar leak secondary to systemic inflammation or aggressive fluid administration.
• Prognosis: Mortality correlates directly with the duration of uncorrected hypotension, peak serum lactate levels, and pre-existing comorbidities such as advanced HIV disease, severe malnutrition, or rheumatic heart disease.

High-Yield Exam Points

• The Fluid Overload Trap: The commonest wrong first step in a hypotensive patient with elevated jugular venous pressure and crackles is giving a fluid bolus. Recognize cardiogenic shock early and choose inotropes or vasopressors over volume.
• Tamponade vs. Tension Pneumothorax: Both present with hypotension, elevated jugular venous pulse, and tachycardia. Auscultation separates them: unilateral absent breath sounds and tracheal deviation indicate tension pneumothorax; bilateral normal breath sounds and muffled heart sounds indicate tamponade.
• Adrenaline Route: Intramuscular injection into the mid-anterolateral thigh provides faster and higher peak plasma concentrations than subcutaneous administration or intravenous boluses in non-arrested anaphylactic patients.
• Bedside Examiner Question: "Why must you avoid reducing blood pressure rapidly to normal limits in a hypertensive emergency?" Answer: Autoregulatory curves in vital organs (brain, kidneys) are shifted rightward; rapid normalization causes critical hypoperfusion, leading to cerebral infarction or acute renal failure.

Clinical Case

A 24-year-old female presents with severe dizziness, lethargy, and breathlessness for two days. She has a history of rheumatic mitral stenosis. On examination, blood pressure is 78/48 mmHg, pulse is 138 beats per minute and irregularly irregular, respiratory rate is 32 breaths per minute, jugular venous pressure is elevated, and bilateral coarse crackles are present across the lower lung zones.

Question 1: What type of shock does this patient have, and what triggered it?
Answer: Cardiogenic shock, triggered by new-onset rapid atrial fibrillation leading to loss of atrial kick and shortened diastolic filling time across the stenosed mitral valve.

Question 2: Why are rapid intravenous crystalloid boluses contraindicated in this patient?
Answer: Left atrial and pulmonary venous pressures are already severely elevated; additional volume worsens hydrostatic pulmonary oedema without improving left ventricular filling.

Question 3: What is the immediate definitive stabilization step if she remains unstable?
Answer: Synchronised direct-current cardioversion to restore sinus rhythm, alongside respiratory support and inotropic or vasopressor infusions.

Practice Questions

Question 1

A 32-year-old male with pulmonary tuberculosis presents with a blood pressure of 80/50 mmHg, pulse of 124 beats per minute, elevated jugular venous pressure, clear breath sounds bilaterally, and soft heart sounds. Pulsus paradoxus is noted. What is the immediate management step?

A. Administer a rapid infusion of normal saline and start broad-spectrum antibiotics
B. Perform urgent needle thoracostomy in the second intercostal space
C. Perform emergency bedside pericardiocentesis
D. Administer intravenous furosemide to reduce venous congestion

Answer: C. Perform emergency bedside pericardiocentesis
Explanation: Beck's triad (hypotension, elevated JVP, muffled heart sounds) and pulsus paradoxus in a patient with tuberculosis point to cardiac tamponade from tuberculous pericardial effusion, which requires immediate fluid evacuation to relieve obstructive shock.

Question 2

A 45-year-old female presents with fever, productive cough, confusion, and a blood pressure of 82/40 mmHg. Despite receiving a full crystalloid fluid challenge, her mean arterial pressure remains 55 mmHg. What is the preferred next step to restore vascular tone?

A. Dobutamine infusion
B. Noradrenaline infusion
C. Adrenaline bolus intravenously
D. Intravenous hydrocortisone bolus

Answer: B. Noradrenaline infusion
Explanation: Septic shock unresponsive to adequate volume resuscitation requires noradrenaline as the first-line vasopressor to restore vascular tone and organ perfusion via alpha-1 adrenergic vasoconstriction.

Question 3

A 60-year-old known hypertensive male presents with a headache and blood pressure of 220/130 mmHg. Fundoscopy reveals bilateral flame-shaped haemorrhages and papilloedema. Which of the following describes the correct initial therapeutic approach?

A. Lower blood pressure immediately to normal levels within thirty minutes using sublingual nifedipine
B. Lower the mean arterial pressure by no more than twenty-five percent in the first hour using titratable intravenous therapy
C. Delay treatment until magnetic resonance imaging of the brain excludes acute infarction
D. Administer high-volume crystalloids to maintain cerebral perfusion pressure

Answer: B. Lower the mean arterial pressure by no more than twenty-five percent in the first hour using titratable intravenous therapy
Explanation: In a hypertensive emergency, rapid overcorrection causes watershed cerebral and renal ischaemia due to altered autoregulation; blood pressure should be reduced gradually using controlled intravenous agents like labetalol.

Question 4

A 28-year-old male receives an intramuscular injection of an antibiotic and suddenly develops urticaria, wheezing, stridor, and a blood pressure of 74/40 mmHg. What is the most important initial medication and route?

A. Intravenous hydrocortisone
B. Intravenous chlorphenamine
C. Intramuscular adrenaline into the anterolateral thigh
D. Subcutaneous adrenaline into the deltoid

Answer: C. Intramuscular adrenaline into the anterolateral thigh
Explanation: Intramuscular adrenaline in the anterolateral thigh is the first-line lifesaving therapy for anaphylactic shock because it rapidly reverses bronchoconstriction, mucosal oedema, and vasodilation.

Question 5

A 68-year-old male with an acute inferior myocardial infarction develops hypotension and oliguria. On examination, the chest is clear to auscultation, but the jugular venous pulse is markedly elevated. Which medication must be strictly avoided?

A. Intravenous normal saline
B. Intravenous glyceryl trinitrate
C. Noradrenaline
D. Dobutamine

Answer: B. Intravenous glyceryl trinitrate
Explanation: Inferior myocardial infarction complicated by right ventricular infarction produces profound preload dependence; nitrates cause venodilation and sudden drops in preload, precipitating catastrophic hemodynamic collapse.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.