16. Heart failure, shock, pulmonary oedema. Left ventricular function

Heart failure is a serious medical condition where the heart can't pump sufficient blood to meet the body's metabolic demands. This is typically due to pathological changes in the myocardium, which may be functional or structural. Globally, heart failure affects about 26 million people, representing around 1-2% of adults in developed countries, with a particularly high incidence among African Americans and Hispanics. It's prevalent among the elderly and occurs as frequently as the four major types of cancer combined (breast, lung, prostate, and colon). The leading causes of heart failure are coronary artery disease, hypertension, and diabetes mellitus. The prognosis for heart failure is poor, with a 50% mortality rate within five years.

Types of Heart Failure:

• Systolic Dysfunction: This common type involves decreased cardiac contractility, leading to a reduced ejection fraction and increased end-diastolic volume.

• Diastolic Dysfunction: Characterized by reduced myocardial compliance often due to hypertrophy. This type maintains a preserved ejection fraction while the stroke volume and end-diastolic volume are reduced.

• Right Heart Failure: Typically results from left heart failure but can also originate from pulmonary conditions such as cor pulmonale.

• Left Heart Failure: Involves dysfunction of the left ventricle.

• Biventricular Heart Failure: Often extends from left heart failure affecting both ventricles.

• Chronic Compensated Heart Failure: Patients exhibit heart failure signs on echocardiography but remain asymptomatic or symptomatically stable.

• Acute Decompensated Heart Failure: Marked by a sudden worsening of heart failure symptoms or onset following an acute cardiac event like a myocardial infarction.

Aetiology of Heart Failure

General Causes

1. Coronary Artery Disease and Myocardial Infarction: This is the most common cause of heart failure, particularly those cases involving reduced ejection fraction. Reduced blood flow due to artery blockages can damage the heart muscle, diminishing its pumping ability.

2. Arterial Hypertension: Chronic high blood pressure increases the heart's workload, leading to left ventricular hypertrophy. Over time, this can reduce the ventricular compliance and impair the heart's ability to fill properly.

3. Valvular Heart Disease: Faulty heart valves disrupt blood flow through the heart, which can lead to heart failure by forcing the heart to work harder to pump the same amount of blood.

4. Diabetes Mellitus and Obesity: These conditions are risk factors for both coronary artery disease and hypertension. They are often associated with heart failure with preserved ejection fraction, as they contribute to the heart's stiffness and affect its relaxation and filling phases.

5. Renal Disease: Kidney problems can affect heart function due to fluid overload and the accumulation of toxins that can affect heart muscle.

6. Infiltrative Diseases: Conditions like hemochromatosis and amyloidosis involve the accumulation of substances in the heart tissue, impairing its function.

Systolic Dysfunction

1. Dilated Cardiomyopathy: This condition, which may result from chronic alcohol abuse, Chagas disease, or be idiopathic, features weakened and enlarged ventricles, reducing the heart's ability to pump effectively.

2. Cardiac Arrhythmias: Irregular heartbeats can compromise the heart's efficiency, leading to or exacerbating heart failure.

3. Myocarditis: Inflammation of the heart muscle, often due to infection, which impairs the heart's ability to contract normally.

Diastolic Dysfunction

1. Restrictive Cardiomyopathy: This type of cardiomyopathy increases the rigidity of the heart walls and restricts the heart's ability to fill properly.

2. Hypertrophic Cardiomyopathy: Thickened heart muscle, which can block or reduce the flow of blood from the heart, also severely affecting the heart's ability to fill.

3. Pericardial Tamponade and Constrictive Pericarditis: These conditions involve the compression of the heart by fluid or scarred pericardial tissue, respectively, severely affecting the heart's filling and overall function.

Risk Factors

1. Obesity, Smoking, COPD: These conditions strain the heart and lungs, increasing the risk of developing heart failure.

2. Heavy Drug and Alcohol Abuse: These substances can directly damage the heart muscle, leading to heart failure.

Two Types of Heart Failure

Systolic Dysfunction

Systolic dysfunction is the inability of the heart to pump blood effectively during systole (the contraction phase of the heart cycle). This type of heart failure is marked by a reduced ejection fraction, where the heart cannot contract forcefully enough to eject a sufficient amount of blood into the circulation. The causes of systolic dysfunction include:

1. Reduced Contractility: This can result from damage to or loss of heart muscle cells (myocytes), often due to myocardial infarction or chronic myocardial ischemia.

2. Increased Afterload: High blood pressure or obstructions like aortic stenosis can increase the resistance against which the heart must pump, making it harder for the ventricles to eject blood.

3. Cardiac Arrhythmias: Irregular heart rhythms can disrupt the coordinated contraction of the heart muscle, reducing the efficiency of blood ejection.

Diastolic Dysfunction

Diastolic dysfunction occurs when the heart experiences problems with filling during diastole (the relaxation phase). Unlike systolic dysfunction, diastolic dysfunction is characterized by a preserved ejection fraction. The heart chambers do not fill adequately due to increased stiffness or poor relaxation of the ventricular walls. Causes of diastolic dysfunction include:

1. Decreased Ventricular Compliance: Stiffening of the ventricular walls due to conditions like long-standing hypertension, constrictive pericarditis, or pericardial tamponade restricts the heart's ability to expand fully during diastole, leading to inadequate filling and increased diastolic pressure.

2. Increased Afterload: Conditions like pulmonary hypertension can increase the resistance the heart has to work against during systole, indirectly impacting diastolic function.

3. Increased Preload: Conditions that cause ventricular volume overload, such as tricuspid valve regurgitation or congenital heart defects with left-to-right shunts, can exacerbate the filling issues during diastole.

Consequences of Diastolic Dysfunction

The inability of the ventricles to fill properly leads to several complications:

• Pulmonary Congestion and Edema: Increased pressure in the left ventricle leads to the backflow of blood into the pulmonary circulation, causing pulmonary hypertension and edema, which manifest as orthopnea (difficulty breathing while lying flat).

• Systemic Venous Congestion: Inadequate cardiac output results in the accumulation of blood in the systemic venous system, leading to peripheral edema and congestion of internal organs such as the liver (resulting in a "nutmeg liver" appearance due to ischemia and fatty degeneration).

• Reduced Cardiac Output: Both types of dysfunction result in poor organ perfusion, contributing to overall organ dysfunction and clinical symptoms of heart failure.

Compensatory Mechanisms of Heart Failure

1. Increased Adrenergic Activity

   • The sympathetic nervous system is activated, increasing heart rate, blood pressure, and ventricular contractility. This response is designed to enhance cardiac output and maintain perfusion to vital organs.

2. Increased Renin-Angiotensin-Aldosterone System (RAAS) Activity

   • Angiotensin-II: Promotes peripheral vasoconstriction, which increases afterload and reduces renal blood flow. This maintains glomerular filtration rate (GFR) under stress but at the cost of increased cardiac workload.

   • Aldosterone: Stimulates sodium and water retention, increasing blood volume (preload), which enhances cardiac output through the Frank-Starling mechanism. This increase in preload helps to initially compensate for the reduced efficiency of the heart.

3. Secretion of Brain Natriuretic Peptide (BNP)

   • Released from ventricular tissue in response to excessive stretching, BNP causes vasodilation, which can help to reduce blood pressure and pulmonary capillary wedge pressure, easing the burden on the heart.

Clinical Features and Symptoms

General Symptoms of Heart Failure

• Fatigue and decreased exercise tolerance.

• Tachycardia and arrhythmias.

• Heart sounds: S3/S4 gallops indicate a volume overload and reduced ventricular compliance.

• Pulsus alternans: alternating strong and weak pulses, indicating severe left ventricular dysfunction.

• Cachexia: severe muscle and weight loss due to chronic illness.

Left-Sided Heart Failure Symptoms (Pulmonary congestion)

• Dyspnea on exertion progressing to rest, orthopnea (difficulty breathing while lying flat), and paroxysmal nocturnal dyspnea (waking up at night short of breath).

• Pulmonary edema and cardiac asthma, where increased pulmonary pressure causes fluid accumulation in the lungs and airway constriction.

• Physical examination may reveal rales (crackles) in the lungs, displaced apical pulse due to enlarged heart, and cool, pale extremities indicating poor circulation.

Right-Sided Heart Failure Symptoms (Systemic venous congestion)

• Peripheral edema, especially noticeable in the lower extremities.

• Hepatic congestion can lead to abdominal discomfort and jaundice.

• Physical signs include jugular venous distention, Kussmaul's sign (increase in jugular venous pressure on inspiration), and hepatojugular reflux.

NYHA Functional Classification of Heart Failure

This system categorizes patients based on the limitation of physical activity caused by symptoms of heart failure:

• Class I: No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath), or anginal pain. Symptoms only occur during heavy exertion.

• Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.

• Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.

• Class IV: Unable to carry on any physical activity without discomfort. Symptoms of heart failure are present even at rest. If any physical activity is undertaken, discomfort is increased.

AHA Staging of Heart Failure

The AHA stages of heart failure describe the evolution of the disease and are used alongside the NYHA classification to provide a more comprehensive assessment:

• Stage A: At high risk for developing heart failure due to conditions that are strongly associated with the development of heart failure (such as hypertension, diabetes, coronary artery disease, metabolic syndrome, or use of cardiotoxins) but without structural heart disease or symptoms of heart failure.

• Stage B: Structural heart disease (such as left ventricular hypertrophy, low ejection fraction, or structural valve disease) is present but without signs or symptoms of heart failure.

• Stage C: Structural heart disease with prior or current symptoms of heart failure (similar to NYHA Class II to III).

• Stage D: Refractory heart failure requiring specialized interventions, representing advanced disease where conventional heart failure therapy is no longer sufficient (similar to NYHA Class IV).

Diagnostics of Heart Failure

1. Laboratory Tests

• BNP and NT-proBNP: Elevated levels of B-type Natriuretic Peptide (BNP) and its N-terminal prohormone (NT-proBNP) are markers of cardiac stretch and stress, commonly elevated in heart failure. Values above 400-500 ng/L suggest heart failure is likely.

• ANP: Atrial Natriuretic Peptide, another heart failure marker, increases with atrial pressure.

• Electrolytes: Hyponatremia (low sodium) can indicate poor heart failure prognosis due to advanced disease affecting renal function and fluid balance.

• Renal Function: Elevated creatinine levels can indicate renal impairment secondary to reduced cardiac output.

• Urine Analysis: Assesses renal function and detects proteinuria or other abnormalities that could contribute to or result from heart failure.

• Blood Glucose and Lipid Profile: To assess additional cardiovascular risk factors.

2. Electrocardiogram (ECG)

• Left Ventricular Hypertrophy: Indicated by increased QRS voltage and duration. Left bundle branch block (LBBB) and left axis deviation are common findings.

• Signs of Past or Acute Myocardial Infarction: Such as Q waves.

• Arrhythmias: Common in heart failure due to altered electrical pathways.

• Low Voltage ECG: Can indicate pericardial effusion or tamponade.

3. Chest X-ray

• Cardiothoracic Index: A ratio greater than 0.5 is indicative of cardiomegaly.

• Boot-shaped Heart: Often seen in right ventricular enlargement.

• Pulmonary Congestion: Manifests as Kerley B lines, peribronchial cuffing, and pleural effusions, indicating fluid backup.

4. Transthoracic Echocardiography (TTE)

• Assessment of Heart Chambers: Size, function, and wall motion.

• Ejection Fraction: Key measure of left ventricular function.

• Valvular Function: Any regurgitation or stenosis.

• Pulmonary Pressures: Elevated in cases of pulmonary hypertension secondary to left heart failure.

5. Cardiac Stress Test

• Evaluates the heart's response to stress and can help identify ischemic heart disease.

6. Coronary Angiography

• Essential for detecting coronary artery disease that may cause or contribute to heart failure. Can lead to interventional procedures if significant blockages are found.

7. CT Angiography

• Used for detailed visualization of heart and coronary vessels, particularly in patients with suspected coronary artery disease.

8. Cardiac MRI

• Provides detailed images of cardiac structures and function. It can differentiate between ischemic heart damage and other cardiomyopathies, and assess myocardial fibrosis.

TREATMENT OF HEART FAILURE

1. Lifestyle Modifications

• Salt Restriction: Less than 3 grams per day to decrease fluid retention.

• Fluid Restriction: Generally recommended to be between 1.5 to 2 liters per day to prevent fluid overload.

• Weight Management and Exercise: Regular exercise improves cardiovascular health but should be avoided during periods of acute decompensation.

• Smoking and Alcohol Cessation: Both are risk factors for worsening heart function.

• Vaccinations: Pneumococcal and influenza vaccines are recommended to prevent respiratory infections that could worsen heart failure.

2. Pharmacological Treatment - First Line

• ACE Inhibitors: Such as enalapril, captopril, and perindopril. They reduce the progression of heart failure and decrease mortality by inhibiting the renin-angiotensin system, which controls blood pressure and fluid balance.

• Angiotensin Receptor Blockers (ARBs): Such as losartan and valsartan. Used as an alternative to ACE inhibitors, especially in patients who experience side effects like cough from ACE inhibitors.

• Beta-blockers: Such as carvedilol and metoprolol. These drugs decrease the heart rate and reduce myocardial demand. They are particularly beneficial after a myocardial infarction and in chronic heart failure.

• Aldosterone Antagonists: Such as spironolactone and eplerenone, reduce mortality in patients with severe heart failure or heart failure following a heart attack.

• Diuretics: Such as furosemide, are used to relieve symptoms of volume overload but do not improve long-term survival.

3. Pharmacological Treatment - Second Line

• Digoxin: Helps by decreasing the heart rate and increasing contractility but is generally used when symptoms continue despite first-line therapy.

• Angiotensin Receptor-Neprilysin Inhibitors (ARNI): Such as valsartan-sacubitril, provide a more comprehensive inhibition of the neurohormonal systems that worsen heart failure.

• SGLT2 Inhibitors: Such as dapagliflozin and empagliflozin, originally used to treat diabetes, have been shown to significantly reduce hospitalization and mortality in heart failure patients.

4. Device Therapy

• Implantable Cardiac Defibrillator (ICD): Prevents sudden cardiac death in patients with severely reduced heart function by automatically treating life-threatening arrhythmias.

• Cardiac Resynchronization Therapy (CRT): A specialized pacemaker for patients with heart failure who have an abnormality in the electrical conduction system of their hearts (such as a bundle branch block).

5. Surgical Options

• Cardiac Transplantation: Considered for patients with end-stage heart failure who do not respond to other treatments. It involves replacing the failing heart with a healthy heart from a donor.

Contraindicated Drugs in Heart Failure:

1. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs): These medications can worsen renal perfusion, counteract the effects of diuretics, and may trigger acute cardiac decompensation by increasing fluid retention and worsening hypertension.

2. Calcium Channel Blockers (non-dihydropyridines like verapamil and diltiazem): They have a negative inotropic effect, which can worsen symptoms and prognosis in patients with heart failure by reducing heart muscle contractility.

3. Inhalation Anesthetics: These agents can induce myocardial depression, peripheral vasodilation, and decrease sympathetic activity, potentially leading to a dangerous drop in blood pressure and heart function during surgery.

4. Citalopram (a type of SSRI): At higher doses, it can cause dose-dependent QT-prolongation, increasing the risk of ventricular arrhythmias.

Complications of Heart Failure:

1. Acute Decompensated Heart Failure: Characterized by a rapid exacerbation of symptoms such as severe dyspnea, frothing at the mouth, blood-tinged sputum, cyanosis, rales, and wheezing. Diagnostic X-rays may show a constellation of signs known as ABCDE, indicative of congestive heart failure.

2. Cardiorenal Syndrome: Deterioration of renal function as a direct result of heart failure, driven by inadequate renal perfusion and congestion due to an ineffective heart pump and venous congestion.

3. Cardiac Arrhythmias: Increased incidence of rhythm problems, including potentially fatal tachyarrhythmias and stroke risk with atrial fibrillation due to clot formation in the left atrium.

4. Central Sleep Apnea: Breathing irregularities during sleep, caused by impaired breathing control that stems from heart dysfunction.

5. Cardiogenic Shock: A severe medical condition where the heart suddenly can't pump enough blood to meet the body's needs.

6. Chronic Kidney Disease: Often develops secondary to prolonged cardiac dysfunction and poor circulation.

7. Cardiac Cirrhosis: Liver damage and fibrosis caused by chronic congestion of the liver in cases of prolonged right-sided heart failure.

8. Venostasis: Sluggish blood flow in the veins, typically in the legs, leading to swelling and increased risk for deep vein thrombosis.

Prognosis:

• The prognosis varies greatly depending on the stage of heart failure, measured by the NYHA functional classification:

  • NYHA Class I: Minimal symptoms and high 1-year survival rate (95%).

  • NYHA Class II-III: Moderate to marked limitation of physical activity with a slightly lower survival rate (85%).

  • NYHA Class IV: Severe limitations with symptoms even at rest, significantly reduced 1-year survival rate (35%).

Treatment and Management:

• The LMNOP acronym provides a mnemonic for managing acute decompensated heart failure:

  • Lasix (furosemide) for diuresis to reduce fluid overload.

  • Morphine to relieve pain and anxiety, which can reduce the workload on the heart.

  • Nitrates to dilate blood vessels and decrease preload.

  • Oxygen to improve tissue oxygenation.

  • Positioning (elevated upper body) to reduce pulmonary congestion and make breathing easier.

SHOCK

Shock is a critical condition that significantly impairs the body's ability to circulate blood and deliver oxygen to tissues, leading to severe and potentially fatal complications. The progression of shock can be understood through its three distinct phases:

1. Compensatory Phase:

   • Sympathetic Activation: In response to decreased blood flow and oxygen delivery, the body activates the sympathetic nervous system. This results in increased heart rate (tachycardia), enhanced cardiac output, and peripheral vasoconstriction. These responses are aimed at maintaining blood pressure and prioritizing blood flow to vital organs.

   • Renin-Angiotensin-Aldosterone System (RAAS) Activation: This system further aids in maintaining blood pressure by conserving sodium and water, which helps increase blood volume.

   • Oliguria: Reduced urine output occurs as the kidneys receive less blood flow and focus on conserving fluids to support the circulatory system.

2. Progressive Phase:

   • Sympathetic System Failure: The initial compensatory mechanisms become overwhelmed, leading to a failure in maintaining adequate blood pressure and circulation.

   • Worsening Hypotension and Hypoperfusion: As blood pressure continues to drop, blood flow to the peripheral tissues decreases significantly, resulting in the buildup of lactic acid (lactic acidosis) due to anaerobic metabolism.

   • Microcirculatory Changes: These contribute to further reduction in tissue perfusion and oxygenation, exacerbating cellular injury and dysfunction.

3. Irreversible Phase:

   • Multi-Organ Dysfunction: By this stage, the lack of effective perfusion results in severe damage across multiple organ systems:

     • Cerebral Hypoxia: Leads to impaired neurological function and potential brain damage.

     • Myocardial Ischemia: The heart muscle itself suffers from inadequate blood supply, risking acute coronary syndromes and further weakening cardiac output.

     • Acute Kidney Failure: Characterized by acute tubular necrosis due to severe renal hypoperfusion.

     • Liver Failure: Hypoperfusion leads to hepatic cell death and potential liver failure.

     • Acute Respiratory Distress Syndrome (ARDS): Lung function is compromised, often requiring mechanical ventilation.

     • Gastrointestinal Complications: Such as ischemic bowel, leading to risk of sepsis and further inflammatory responses.

     • Disseminated Intravascular Coagulation (DIC): A severe complication involving widespread activation of clotting in the small blood vessels, leading to microthrombi and multiple organ dysfunction.

     • Adrenal Insufficiency: Can manifest as acute adrenal crisis due to stress-related adrenal exhaustion.

     • Dermatologic and Soft Tissue Damage: Including necrosis and severe infections like necrotizing fasciitis.

Cardiogenic Shock: Cardiogenic shock is a critical condition caused primarily by the heart's inability to pump sufficient blood, often following severe cardiac events.

• Aetiology of cardiogenic shock :

  • Primary Cause: Myocardial infarction (MI) is the most common cause.

  • Other Causes: Arrhythmias, advanced heart failure, various forms of cardiomyopathy, myocarditis, and mechanical complications such as ventricular septal defects.

  • Medication Induced: Negative inotropic effects from beta-blockers or calcium channel blockers can exacerbate or precipitate the condition.

• Pathophysiology of cardiogenic shock:

  • Heart's pumping action is compromised, leading to inadequate cardiac output.

  • This triggers a stress response including the release of catecholamines and activation of the renin-angiotensin-aldosterone system (RAAS).

  • The result is systemic vasoconstriction, increased myocardial oxygen demand, and fluid retention, all exacerbating the heart's workload and further impairing tissue perfusion.

• Symptoms of cardiogenic shock:

  • Tachycardia, low blood pressure (hypotension), and difficulty breathing (dyspnea).

  • Mental status changes due to reduced cerebral perfusion.

• Physical Examination of cardiogenic shock:

  • Cold, clammy skin, poor capillary refill, indicating poor perfusion.

  • Heart sounds may include third and fourth heart sounds (S3 and S4).

  • Signs of pulmonary congestion like pulmonary edema and diffuse lung crackles.

  • Elevated jugular venous pressure and distended neck veins reflect right-sided heart strain.

• Diagnostic Tools of cardiogenic shock:

  • ECG and cardiac biomarkers to assess for myocardial infarction.

  • Echocardiography to evaluate cardiac function and structure.

• Treatment of cardiogenic shock:

  • Immediate Care: CPR if the patient is unresponsive or has no pulse.

  • Inotropic Support: Dopamine for low blood pressure or dobutamine for cardiac support without causing further hypertension.

  • Vasoconstrictors: Noradrenaline to improve coronary and cerebral perfusion.

  • Fluid Management: Judicious use of fluids or diuretics depending on the patient’s fluid status.

Hypovolemic Shock: Hypovolemic shock occurs due to a significant loss of body fluids.

• Aetiology of hypovolemic shock :

  • Primary Causes: Severe blood loss (hemorrhage), extensive vomiting, diarrhea, burns, or significant third space fluid shifts.

  • Secondary Causes: Conditions leading to excessive renal fluid loss.

• Pathophysiology of hypovolemic shock :

  • Fluid loss leads to decreased venous return and cardiac output.

  • Compensatory mechanisms include systemic vasoconstriction and increased heart rate to maintain blood flow to vital organs.

• Symptoms of hypovolemic shock :

  • Rapid pulse (tachycardia), fast breathing (tachypnea), and low blood pressure.

• Physical Examination of hypovolemic shock :

  • Cool, pale, and moist skin.

  • Delayed capillary refill and decreased skin turgor.

  • Dry mucous membranes.

  • Typically, jugular venous pressure is not elevated due to the reduced blood volume.

• Treatment of hypovolemic shock :

  • Fluid Resuscitation: Rapid administration of crystalloids or colloids to restore circulating volume.

  • Blood Products: Transfusions may be necessary if blood loss is significant.

  • Control of Hemorrhage: Immediate actions to stop ongoing blood loss.

Obstructive Shock: Obstructive shock occurs when there is a physical blockage in the heart or major blood vessels, significantly impairing the heart’s ability to pump effectively.

• Aetiology of Obstructive Shock:

  • Impaired Right Ventricular (RV) Diastolic Filling: Caused by conditions that compress or restrict the heart, such as cardiac tamponade, constrictive pericarditis, or restrictive cardiomyopathy.

  • Obstruction of Venous Return: Conditions like tension pneumothorax or large intrathoracic tumors can impede blood flow back to the heart.

  • Increased Ventricular Afterload: Severe conditions such as massive pulmonary embolism, aortic dissection, or severe pulmonary hypertension increase the workload on the heart, making it difficult for the ventricles to eject blood.

• Pathophysiology of Obstructive Shock:

  • These obstructions prevent normal filling or outflow of blood, leading to a critical drop in cardiac output despite normal blood volume.

  • The body compensates through vasoconstriction and tachycardia, similar to responses seen in hypovolemic shock.

• Symptoms of Obstructive Shock:

  • Initially, symptoms may mirror those of hypovolemic shock, including tachycardia and hypotension.

• Treatment of Obstructive Shock:

  • Cardiac Tamponade: Emergency pericardiocentesis to remove fluid from the pericardial space.

  • Pulmonary Embolism: Thrombolytic therapy to dissolve the clot.

  • Tension Pneumothorax: Immediate needle decompression followed by chest tube placement to relieve the pressure.

Septic Shock: Septic shock is a severe and life-threatening condition caused by a widespread infection leading to systemic inflammation and circulatory collapse.

• Aetiology of Septic Shock:

  • Primarily caused by widespread infection with gram-negative bacteria, but gram-positive bacteria and other pathogens can also induce sepsis.

• Pathophysiology of Septic Shock:

  • The body’s response to the infection includes the release of immune mediators that cause widespread vasodilation, increased capillary permeability, and fluid leakage from the vascular system into tissues, resulting in profound hypotension and reduced blood flow to organs.

• Symptoms of Septic Shock:

  • Early signs include fever or hypothermia, tachycardia, and possibly chills or confusion.

  • As shock progresses, blood pressure drops, and major organs may begin to fail.

• Physical Examination of Septic Shock:

  • Early stage: Patient’s skin may be warm and flushed due to vasodilation.

  • Later stage: Skin becomes cold, pale, and clammy as shock progresses, with prolonged capillary refill time indicating poor blood flow.

• Treatment of Septic Shock:

  • Fluid Resuscitation: Aggressive administration of fluids to counteract the effects of vasodilation and maintain blood volume.

  • Vasoconstrictors: Noradrenaline (norepinephrine) is commonly used to increase vascular tone and improve blood pressure.

  • Antibiotics: Prompt initiation of broad-spectrum antibiotics to treat the underlying infection, adjusted based on culture results and sensitivity.

Anaphylactic Shock: Anaphylactic shock is an extreme, life-threatening allergic reaction that affects multiple body systems.

• Aetiology of Anaphylactic Shock:

  • Triggered by allergens that induce a systemic hypersensitivity reaction. Common triggers include certain foods (like peanuts), insect stings, medications (such as penicillin or sulfa drugs), and contrast agents used in imaging procedures.

• Pathophysiology of Anaphylactic Shock:

  • Exposure to the allergen leads to an IgE-mediated immune response, causing mast cells and basophils to release large amounts of histamine and other inflammatory mediators.

  • This release triggers widespread vasodilation, increased vascular permeability, and smooth muscle contraction.

• Symptoms of Anaphylactic Shock:

  • Rapid onset of symptoms, usually within minutes to hours after exposure to the allergen.

  • Signs include severe hypotension, tachycardia, respiratory distress due to bronchospasm, laryngeal edema, extensive skin hives, facial and oral angioedema, gastrointestinal symptoms like vomiting and diarrhea.

• Treatment of Anaphylactic Shock:

  • Immediate administration of intramuscular epinephrine is critical to counteract the reaction.

  • Volume resuscitation with intravenous fluids to manage hypotension.

  • Additional treatments include antihistamines and corticosteroids to reduce inflammation and stabilize vascular permeability. Vasopressors may be needed if hypotension persists despite fluid resuscitation.

Neurogenic Shock: Neurogenic shock results from disruption of autonomic pathways due to nervous system damage.

• Aetiology of Neurogenic Shock:

  • Typically follows severe central nervous system injuries such as spinal cord injury (especially high cervical injuries), traumatic brain injury, or major insults to the brain like cerebral hemorrhage. It can also occur after severe neural anesthesia.

• Pathophysiology of Neurogenic Shock:

  • Damage to the spinal cord or brain disrupts sympathetic nervous system output, which is responsible for maintaining vascular tone.

  • The loss of sympathetic tone leads to unopposed parasympathetic activity, resulting in systemic vasodilation and a significant reduction in blood pressure.

• Symptoms of Neurogenic Shock:

  • Characterized by bradycardia and hypotension, contrary to other forms of shock that typically present with tachycardia.

  • Patients often exhibit warm, flushed skin due to vasodilation, unlike the cold, clammy skin seen in hypovolemic or septic shock.

• Treatment of Neurogenic Shock:

  • Management focuses on fluid resuscitation to improve blood pressure and maintain organ perfusion.

  • Atropine may be administered to address bradycardia.

  • Vasopressors are often necessary if fluid therapy alone is insufficient to restore and maintain adequate blood pressure.

PULMONARY EDEMA
Pulmonary edema is a condition where fluid accumulates in the lungs, leading to impaired gas exchange and potentially severe respiratory distress. Here's a breakdown of its causes and associated risk factors:

Risk Factors of pulmonary edema

• Heart Disease: Particularly conditions affecting the left side of the heart such as left ventricular dysfunction or valvular heart disease.

• Acute Respiratory Distress Syndrome (ARDS): A severe form of lung injury that leads to widespread inflammation and capillary damage.

• Inhalation of Toxic Gases: Exposure to substances like ammonia or chlorine that directly irritate or damage pulmonary tissues.

Causes of pulmonary edema

1. Left-Sided Heart Disease:

   • The most common cause of pulmonary edema.

   • Failure of the left ventricle leads to increased pressure in the left atrium and pulmonary veins, resulting in transudation of fluid from the pulmonary capillaries into the interstitial space and alveoli.

   • Conditions such as myocardial infarction, cardiomyopathy, and hypertension-induced heart failure are typical culprits.

2. Capillary Injury:

   • Occurs in conditions like ARDS or due to the inhalation of toxic gases, which damage the alveolar-capillary membrane.

   • This damage increases the permeability of the capillaries, allowing protein-rich fluid to leak into the alveolar spaces, further pulling in fluid by osmotic force.

   • The presence of protein in the alveoli disrupts the normal balance of hydrostatic and oncotic pressures, exacerbating the edema.

3. Lymphatic Obstruction:

   • When the lymphatic system, which helps drain excess fluid from tissues, is obstructed by tumors, fibrosis, or external pressure, it can lead to a backlog of fluid.

   • Increased systemic venous pressure can also contribute to this condition by hindering the flow of fluid through the lymphatic system.

Pathophysiology of pulmonary edema

• Pulmonary edema involves the accumulation of fluid within the alveoli and lung interstitium.

• Normally, the balance between hydrostatic pressure (pushing fluid out of capillaries) and oncotic pressure (pulling fluid into capillaries), along with an intact capillary membrane and effective lymphatic drainage, prevents lung fluid accumulation.

• Disruption in any of these mechanisms can lead to the onset of pulmonary edema, severely affecting oxygen exchange and leading to symptoms such as shortness of breath, coughing, and extreme respiratory distress.

Clinical Manifestations of pulmonary edema

• Dyspnea: Patients experience shortness of breath, which initially occurs during exertion but can worsen to occur at rest as the condition progresses.

• Increased Work of Breathing: Due to fluid in the alveoli, the lungs become stiffer, making breathing efforts more laborious.

• Inspiratory Crackles: These are heard during lung auscultation and are caused by the popping open of small airways and alveoli collapsed by fluid.

• Dullness on Percussion: This occurs over the lung bases and is indicative of fluid accumulation within the lung parenchyma.

• Hypoxemia: A mismatch between ventilation (air reaching the alveoli) and perfusion (blood reaching the alveoli) leads to inadequate oxygenation of blood.

• Severe Edema: In advanced cases, patients may cough up pink, frothy sputum, a sign of significant fluid accumulation. This condition also leads to decreased lung compliance and potentially to hypercapnia (excessive carbon dioxide in the bloodstream).

Treatment of pulmonary edema

The treatment for pulmonary edema depends largely on the underlying cause and the severity of the symptoms:

1. For Increased Hydrostatic Pressure:

   • Diuretics: These medications help reduce fluid volume in the body, thus decreasing the pressure forcing fluid into the alveoli.

   • Vasodilators: These help to reduce the workload on the heart by dilating blood vessels, lowering blood pressure, and thus reducing hydrostatic pressure across the pulmonary capillaries.

   • Positive Inotropes: Medications like digoxin increase the force of heart contractions, improving cardiac output and reducing the volume of blood backing up into the lungs.

2. For Increased Capillary Permeability:

   • Removal of Offending Agent: For example, if a toxin or drug has induced pulmonary edema, stopping exposure to the toxin or drug is crucial.

   • Steroids and Other Anti-Inflammatory Agents: These can be used to reduce inflammation in the capillaries.

   • Antibiotics: If an infection is the cause, antibiotics are necessary to treat the underlying infection.

3. Supportive Care:

   • Oxygen Therapy: To address hypoxemia and ease the work of breathing.

   • Mechanical Ventilation: In cases where breathing is severely compromised, mechanical ventilation may be required to ensure adequate oxygenation and carbon dioxide removal.

LEFT VENTRICULAR DYSFUNCTION

Left ventricular dysfunction is a critical cardiac condition that significantly impairs the heart's ability to pump blood efficiently, which can lead to heart failure. It can be divided into two main types based on the function that is affected: systolic dysfunction, where there is impaired contraction of the left ventricle, and diastolic dysfunction, where there is impaired relaxation and filling of the left ventricle.

Systolic Dysfunction

In systolic dysfunction, the heart's ability to contract and pump out blood is diminished. This typically results in a decreased ejection fraction, which is the percentage of blood that is pumped out of the left ventricle during each contraction.

Diastolic Dysfunction

Diastolic dysfunction involves problems with the heart's ability to relax and fill with blood during the rest period between heartbeats. This type of dysfunction can occur even if the contraction strength is normal. In diastolic dysfunction, despite normal ejection fraction, the heart cannot fill properly, leading to increased pressure in the left ventricle.

Ventricular Filling Pressure

• Normal Values: For the left ventricle, normal filling pressure is less than 12 mmHg, and for the right ventricle, it is less than 6 mmHg.

• Frank-Starling Mechanism: This principle states that the heart's force of contraction is directly related to the initial length of the cardiac muscle fibers (end-diastolic volume). However, beyond a certain point (e.g., 18 mmHg in the left ventricle), further increases in filling pressure do not enhance contraction, which can instead lead to congestion and pulmonary edema.

• Measurement: Ventricular filling pressures can be indirectly measured using a pulmonary artery catheter to assess pulmonary capillary wedge pressure, which reflects left ventricular end-diastolic pressure. Direct measurement involves inserting a catheter into the left ventricle, though this is more invasive.

Causes of Left Ventricular Dysfunction

• Coronary Artery Disease and Myocardial Infarction: Blockages in different coronary arteries can affect specific regions of the left ventricle, such as the anterior wall, posterolateral wall, or inferobasal wall.

• Arterial Hypertension: High blood pressure makes the heart work harder, leading to hypertrophy and eventually dysfunction.

• Valvular Heart Disease: Problems with heart valves can lead to either overload or inadequate filling of the heart.

• Diabetic Cardiomyopathy: Diabetes can cause changes in the heart muscle, leading to dysfunction.

• Renal Disease: Chronic kidney disease can affect heart function due to fluid overload and metabolic derangements.

• Cardiomyopathies: These are diseases of the heart muscle that can be caused by genetic factors, alcohol abuse, infections, and more.

• Myocarditis: Inflammation of the heart muscle, often due to viral infections, can impair its ability to function.

• Arrhythmias: Irregular heartbeats can disrupt the effective pumping of the heart.

• Infiltrative Diseases: Conditions like amyloidosis can deposit abnormal substances in the heart muscle, impairing its function.

Diagnostics of Left Ventricular Dysfunction

1. Echocardiography

Echocardiography is the primary imaging modality used to evaluate left ventricular function. It helps in assessing:

• Wall Motion Abnormalities:

  • Hypokinesia: Reduced movement of the ventricular wall, indicative of decreased muscle function.

  • Akinesia: Absence of movement in areas of the ventricular wall, typically seen after myocardial infarction where the muscle is scarred.

  • Dyskinesia: Abnormal movement, such as paradoxical bulging of a segment during systole, often seen in cases of previous myocardial damage.

  • Hyperkinesia: Increased movement, usually observed in unaffected areas compensating for the weakened parts of the heart.

• Ejection Fraction (EF): This quantifies how much blood the left ventricle ejects with each contraction and is a key measure of systolic function. Normal EF is greater than 55%. An EF below 35% indicates severe dysfunction, and EF in the range of 10-20% is often seen in cardiogenic shock.

2. Measurement of Blood Flow

• Cardiac Output and Cardiac Index: These measurements reflect the volume of blood the heart pumps in a minute. Cardiac output is adjusted for body surface area to derive the cardiac index. These are crucial in assessing the overall performance of the heart and can be measured using techniques such as thermodilution or Doppler ultrasound.

3. Measurement of Pressures

• LV Filling Pressure: Indicates the pressure in the left ventricle at the end of diastole (just before the heart contracts). High filling pressures suggest diastolic dysfunction.

• LV Systolic Pressure: The pressure during the peak of contraction of the left ventricle.

• Pulmonary Capillary Wedge Pressure: An indirect measure of the left atrial pressure, typically measured via right heart catheterization, providing insights into left ventricular end-diastolic pressure and function.

4. Additional Diagnostic Tools

• Electrocardiogram (ECG): Can indicate underlying ischemic heart disease, previous myocardial infarction, and arrhythmias.

• Cardiac MRI: Offers detailed images of the heart’s structure and function, useful for assessing myocardial scarring and differentiation between ischemic and non-ischemic causes of heart failure.

• Cardiac Catheterization: Invasive but very accurate, used for measuring intracardiac pressures, evaluating coronary arteries, and precise assessment of heart muscle performance.