CVS Cardiac Week 3 Flashcards
TLO 3.1.1: Describe Capillary Structure
Capillaries are the smallest blood vessels in the body, designed to facilitate the exchange of substances between blood and tissues. Their key features include:
* Single endothelial cell layer: Very thin walls (one cell thick) to allow for efficient exchange.
* No smooth muscle: Unlike arterioles or venules, capillaries lack smooth muscle in their walls.
* Basement membrane: Surrounds the endothelium and supports the capillary structure.
* Pores or fenestrations: Depending on type (continuous, fenestrated, or sinusoidal), capillaries can have tight or leaky junctions for selective permeability
TLO 3.1.2: Describe Processes Across the Capillary Wall
Three main processes enable movement of substances:
Diffusion
* Movement of solutes (e.g., oxygen, carbon dioxide, glucose) down their concentration gradient.
* Most important mechanism for exchange across capillaries.
* Lipid-soluble substances (e.g., O₂, CO₂) pass directly through endothelial cells; water-soluble substances pass through intercellular clefts or pores.
2. Osmosis
* Movement of water across a semi-permeable membrane from a region of lower solute concentration to one of higher solute concentration.
* Driven by osmotic gradients created mainly by plasma proteins (especially albumin).
3. Bulk Flow
* Movement of large volumes of fluid (and some solutes) in or out of capillaries due to pressure differences.
* Two types:
o Filtration: Fluid moves out of the capillary into the interstitial space (usually at the arterial end).
o Reabsorption: Fluid moves back into the capillary (usually at the venous end).
TLO 3.1.3: Describe Factors Affecting Capillary Exchange
Four pressures determine the direction of fluid movement (Starling forces):
1. Capillary Hydrostatic Pressure (CHP)
* Pushes fluid out of the capillary.
* Higher at the arterial end, lower at the venous end.
* Promotes filtration.
2. Interstitial Fluid Hydrostatic Pressure (IFHP)
* Pressure exerted by fluid in the interstitial space.
* Usually low or slightly negative, so it may assist filtration.
3. Blood Colloid Osmotic Pressure (BCOP or πc)
* Created by plasma proteins, primarily albumin.
* Pulls fluid into the capillary.
* Promotes reabsorption.
4. Interstitial Fluid Colloid Osmotic Pressure (IFCOP or πi)
* Caused by proteins in the interstitial fluid.
* Pulls fluid out of the capillary.
* Promotes filtration, but normally this pressure is low.
Net Filtration Pressure (NFP) = (CHP + IFCOP) − (BCOP + IFHP)
Starling’s forces explain how fluid moves in and out of tiny blood vessels (capillaries). Two main forces are at play:
- Hydrostatic pressure: This pushes fluid out of the capillaries into surrounding tissues.
- Oncotic pressure: This pulls fluid back into the capillaries, thanks to proteins like albumin in the blood.
The balance between these forces determines whether fluid stays in the blood vessels or leaks into tissues. If this balance is disrupted, it can lead to swelling (oedema).
- Capillary Hydrostatic Pressure: Pushes fluid out of the capillaries into surrounding tissues.
- Interstitial Hydrostatic Pressure: Pushes fluid back into the capillaries from the surrounding tissues.
- Capillary Oncotic Pressure: Pulls fluid into the capillaries due to plasma proteins like albumin.
- Interstitial Oncotic Pressure: Pulls fluid out of the capillaries into the surrounding tissues due to proteins in the interstitial space.
TLO 3.1.4: Describe the Role of the Lymphatic System
The lymphatic system:
* Collects excess fluid and proteins from the interstitial space that are not reabsorbed by capillaries (~10% of filtered fluid).
* Returns this fluid to the venous circulation, maintaining fluid balance.
* Helps prevent edema (swelling due to fluid accumulation).
* Also plays roles in immune defense and fat absorption (via lacteals in the intestine).
Capillary Exchange: Diagram
Arterial End Venous End
(Filtration) (Reabsorption)
—————————————————————
Blood Flow → → → → → → → → → → → → → → → → → → → → →
↑ ↑ ↑ [CHP high] [CHP lower] [BCOP constant] (push fluid out) (less push out) (pulls fluid back in)
← Interstitial Space ← ← ← ← ← ← ← ← ← ← ← ← ← ← ← ← ←
Net Movement:
➤ Filtration at arterial end (fluid leaves capillary)
➤ Reabsorption at venous end (fluid returns)
➤ Excess fluid goes to lymphatic system
📊 Starling Forces Summary Table
Force Symbol Direction Effect
Capillary Hydrostatic Pressure CHP Out of capillary Promotes filtration
Interstitial Fluid Hydrostatic Pressure IFHP Into capillary (usually) Opposes filtration
Blood Colloid Osmotic Pressure BCOP Into capillary Promotes reabsorption
Interstitial Fluid Colloid Osmotic Pressure IFCOP Out of capillary Promotes filtration
✅ Lymphatic Role (in short):
- Picks up ~10% of fluid not reabsorbed.
- Prevents swelling (edema).
- Returns fluid/proteins to blood.
- Supports immune and fat transport functions.
🧠 TLO 3.2.1: Define Oedema
Oedema is the accumulation of excess fluid in the interstitial (extracellular) space, leading to swelling of tissues.
It occurs when fluid filtration exceeds reabsorption and lymphatic drainage.
🔬 TLO 3.2.2: Describe the Pathophysiological Processes Causing Oedema
There are four main mechanisms of oedema:
There are four main mechanisms of oedema:
1. ↑ Capillary Hydrostatic Pressure (CHP)
o Too much pressure pushes fluid out of the capillaries into tissues.
o Common in heart failure, venous obstruction, or fluid overload.
2. ↓ Plasma Oncotic Pressure (↓BCOP)
o Less protein (esp. albumin) in blood means less fluid is pulled back into the capillary.
o Seen in liver failure, nephrotic syndrome, malnutrition.
3. ↑ Capillary Permeability
o Leaky capillaries let proteins and fluid escape into interstitial space.
o Occurs in inflammation, allergic reactions, burns.
4. Lymphatic Obstruction (↓Drainage)
o Lymph system fails to remove excess interstitial fluid.
o Can be caused by tumors, infections (e.g. filariasis), or surgery.
TLO 3.2.3: Identify Common Causes of the Pathological Processes
Mechanism Common Causes
↑ Capillary Hydrostatic Pressure - Congestive heart failure
- Deep vein thrombosis
- Pregnancy (compression of venous return)
- Excess IV fluids
↓ Plasma Oncotic Pressure - Liver disease (↓ albumin production)
- Nephrotic syndrome (protein loss in urine)
- Malnutrition (low protein intake)
↑ Capillary Permeability - Sepsis
- Burns
- Trauma
- Allergic reactions
Lymphatic Obstruction - Cancer (e.g. lymph node invasion)
- Lymph node removal (post-surgery)
- Parasitic infection (e.g. filariasis)
📍 TLO 3.2.4: Site-Specific Clinical Manifestations of Oedema
General Symptoms (what patients feel):
* Swelling (feet, legs, hands, face)
* Weight gain
* Abdominal discomfort/distention (due to ascites)
* Breathlessness (if pulmonary oedema)
Physical Signs (what you find on exam):
Site Manifestation
Legs/Ankles Pitting oedema (indentation when pressed)
Lungs Pulmonary oedema → breathlessness, crackles, pulmonary infiltrates on X-ray
Neck veins Raised Jugular Venous Pressure (JVP) in right heart failure
Liver Hepatomegaly (enlarged liver from congestion)
Abdomen Ascites (fluid in peritoneal cavity; tense, distended abdomen)
Flowchart: Pathophysiology of Oedema
↓↓↓ Oedema (Tissue Swelling) ↓↓↓
↓
┌─────────────────────────────────────────────────────┐
│ Causes of Oedema (4 Mechanisms) │
└─────────────────────────────────────────────────────┘
↓
┌────────────────────┬────────────────────┬────────────────────┬─────────────────────┐
│ ↑ Capillary │ ↓ Plasma │ ↑ Capillary │ ↓ Lymphatic │
│ Hydrostatic │ Oncotic Pressure │ Permeability │ Drainage │
│ Pressure (CHP) │ (↓BCOP) │ │ │
├────────────────────┼────────────────────┼────────────────────┼─────────────────────┤
│ - Heart failure │ - Liver disease │ - Inflammation │ - Tumors │
│ - DVT │ - Nephrotic │ - Allergic rxns │ - Filariasis │
│ - IV overload │ - Malnutrition │ - Burns, trauma │ - Surgery (lymph │
│ │ │ │ node removal) │
└────────────────────┴────────────────────┴────────────────────┴─────────────────────┘
🧠 Flashcards: Oedema Quick Review
Q1: What is oedema?
A1: Oedema is the excess accumulation of fluid in the interstitial space, causing tissue swelling.
________________________________________
Q2: Name the 4 main mechanisms of oedema.
A2:
1. ↑ Capillary hydrostatic pressure
2. ↓ Plasma oncotic pressure
3. ↑ Capillary permeability
4. ↓ Lymphatic drainage
________________________________________
Q3: What are 2 conditions that lower plasma oncotic pressure?
A3:
* Liver disease (↓ albumin production)
* Nephrotic syndrome (protein loss in urine)
________________________________________
Q4: What are common signs of pulmonary oedema?
A4:
* Breathlessness
* Crackles on auscultation
* Pulmonary infiltrates on chest X-ray
________________________________________
Q5: What causes pitting oedema?
A5: Increased interstitial fluid compresses tissue when pressed, leaving a visible dent.
________________________________________
Q6: What is ascites, and what can cause it?
A6: Ascites is fluid buildup in the abdominal cavity; causes include liver cirrhosis and right heart failure.
TLO 3.3.1: Define Heart Failure
Heart failure (HF) is a clinical syndrome where the heart is unable to pump blood effectively to meet the metabolic demands of the body, or it can only do so at the cost of increased filling pressures.
* May involve systolic dysfunction (↓ contractility) or diastolic dysfunction (↓ filling).
* Also known as congestive heart failure (CHF) when fluid accumulation is prominent.
⚠️ TLO 3.3.2: Risk Factors & Aetiology of Heart Failure
Major Risk Factors:
Major Risk Factors:
* Hypertension
* Coronary artery disease (CAD)
* Diabetes mellitus
* Valvular heart disease
* Obesity
* Smoking
* Sedentary lifestyle
* Family history of cardiomyopathy
Common Aetiologies:
Cause Mechanism
Ischemic heart disease MI leads to scarred myocardium → systolic failure
Hypertension Chronic ↑ afterload → LV hypertrophy → dysfunction
Valvular disease Volume/pressure overload (e.g., aortic stenosis)
Cardiomyopathies Dilated, hypertrophic, or restrictive types
Arrhythmias Impaired cardiac output (e.g., AF)
Infections (e.g., viral myocarditis) Direct myocardial damage
📊 TLO 3.3.3: Stages and Classification of Heart Failure
A. AHA/ACC Stages of HF (focuses on disease progression):
Stage Description
A At risk (e.g., HTN, diabetes), no structural disease
B Structural heart disease, no symptoms
C Structural disease + prior/current symptoms
D Refractory HF needing advanced interventions
B. NYHA Functional Classification (focuses on symptoms):
Class Symptoms
I No limitation of physical activity
II Slight limitation (comfortable at rest)
III Marked limitation (less than ordinary activity causes symptoms)
IV Symptoms at rest
❤️🩹 TLO 3.3.4: Pathophysiology & Clinical Features of Left Heart Failure
Pathophysiology:
* Left ventricle can’t effectively pump blood → blood backs up into lungs → pulmonary congestion.
* Decreased cardiac output → ↓ perfusion to tissues.
Clinical Features:
Symptoms (what patient feels):
* Dyspnoea (especially on exertion)
* Orthopnoea (needs to sit up to breathe)
* Paroxysmal nocturnal dyspnoea (wakes up gasping)
* Fatigue
* Exercise intolerance
Signs (what you find on exam/investigations):
* Pulmonary crackles
* Tachypnoea
* S3 gallop
* Pulmonary oedema on chest X-ray
* Elevated BNP or NT-proBNP
💙 TLO 3.3.5: Pathophysiology & Clinical Features of Right Heart Failure
Pathophysiology:
* Right ventricle fails → blood backs up into systemic circulation
* Often secondary to left-sided failure or pulmonary disease (cor pulmonale)
Clinical Features:
Symptoms:
* Swelling of feet/ankles
* Abdominal discomfort (due to ascites or hepatomegaly)
* Fatigue
* Weight gain (fluid retention)
Signs:
* Raised jugular venous pressure (JVP)
* Pitting peripheral oedema
* Hepatomegaly
* Ascites
* Right ventricular heave
TLO 3.4.1: Define Cardiac Remodeling
Cardiac remodeling is the structural and functional change in the size, shape, and function of the heart after stress or injury, such as myocardial infarction, hypertension, or volume overload.
* It involves changes at the cellular and molecular level (e.g., hypertrophy, fibrosis).
* Remodeling can be adaptive at first but becomes maladaptive over time, leading to heart failure.
🧠 TLO 3.4.2: Causes of Cardiac Remodeling
Cause Mechanism
Hypertension Pressure overload → LV hypertrophy
Myocardial infarction (MI) Loss of contractile tissue → dilation
Valvular heart disease Pressure or volume overload (e.g., AS, MR)
Cardiomyopathies Genetic or acquired changes in heart muscle
Chronic sympathetic stimulation ↑ Catecholamines → hypertrophy, fibrosis
Neurohormonal activation RAAS, natriuretic peptides → volume changes
Inflammation or infection Viral myocarditis or autoimmune responses
📘 TLO 3.4.3: Concentric Remodeling & Its Complications
🔁 What is Concentric Remodeling?
What is Concentric Remodeling?
* Occurs in pressure overload states (e.g., chronic hypertension, aortic stenosis).
* Characterized by:
o Increased wall thickness
o No change or reduction in chamber size
o ↑ Relative wall thickness
o Sarcomeres added in parallel
⚠️ Complications:
* ↓ Diastolic compliance → diastolic heart failure (HFpEF)
* Increased risk of arrhythmias
* Myocardial ischemia (due to impaired coronary perfusion)
* Progression to eccentric hypertrophy if pressure overload persists
📗 TLO 3.4.4: Eccentric Remodeling & Its Complications
🔄 What is Eccentric Remodeling?
What is Eccentric Remodeling?
* Occurs in volume overload states (e.g., mitral or aortic regurgitation, post-MI)
* Characterized by:
o Dilated chamber
o Thinner walls relative to chamber size
o Sarcomeres added in series
⚠️ Complications:
* Systolic dysfunction → HFrEF (Heart Failure with Reduced Ejection Fraction)
* Progressive ventricular dilation
* Functional mitral regurgitation
* ↑ Wall stress and oxygen demand
* Ventricular arrhythmias, especially in dilated ventricles
________________________________________
🧠 Mnemonic Tip:
“C” for Concentric = “Contracted walls”
“E” for Eccentric = “Enlarged chamber”
TLO 3.5.1: Steps to Diagnose Heart Failure
TLO 3.5.1: Steps to Diagnose Heart Failure
1. History
Look for symptoms suggestive of heart failure:
* Dyspnoea (especially on exertion, orthopnoea, PND)
* Fatigue, weakness
* Swelling in ankles/legs
* Weight gain (fluid retention)
* Nocturia, palpitations, or chest discomfort
2. Clinical Examination
Look for signs:
* Raised JVP
* Pulmonary crackles (basal)
* S3 gallop
* Peripheral oedema
* Hepatomegaly, ascites
* Tachycardia, hypotension, or cool peripheries
3. Diagnostic Tests
🧪 TLO 3.5.2: Diagnostic Modalities for Heart Failure
Test Use/Findings
ECG May show LVH, past MI, atrial fibrillation, bundle branch blocks
BNP / NT-proBNP Elevated in heart failure due to ventricular stretch (helps differentiate dyspnoea causes)
Troponin Rules out/ischaemia or myocardial infarction
Chest X-ray (CXR) Detects signs of pulmonary congestion or cardiomegaly
Echocardiogram Gold standard to assess EF (ejection fraction), wall motion, valve function
Bloods U&Es, LFTs, FBC, TSH – check for contributing causes or complications (e.g., anaemia, CKD)
🩻 TLO 3.5.3: Relevant CXR Pathological Findings
CXR Feature Interpretation
Alveolar oedema “Batwing” perihilar pattern – indicates pulmonary oedema
Upper lobe diversion Redistribution of blood flow to upper lobes (CHF sign)
Cardiomegaly Cardiothoracic ratio >50%
Pleural effusions Usually bilateral, more on the right
Kerley B lines Short horizontal lines at lung bases – indicate interstitial oedema
⚠️ TLO 3.5.4: Complications of Heart Failure
Acute Complications
* Acute pulmonary oedema
* Cardiogenic shock
* Arrhythmias (e.g., AF, VT/VF)
* Renal dysfunction
Chronic Complications
* Progressive decline in EF
* Thromboembolism
* Liver congestion → cardiac cirrhosis
* Cachexia and muscle wasting
* Anemia and hyponatraemia
TLO 3.6.1: Management and Pharmacology of Acute Decompensated Heart Failure (ADHF)
Initial Management of ADHF:
1. Oxygen Therapy:
o Administer oxygen if hypoxemia is present.
o Non-invasive ventilation (NIV), such as CPAP (Continuous Positive Airway Pressure) or BiPAP (Bilevel Positive Airway Pressure), is often used in acute pulmonary oedema to improve oxygenation and reduce preload.
2. Diuretics:
o Frusemide (Furosemide) – Loop diuretic:
Mechanism: Inhibits sodium and chloride reabsorption in the loop of Henle, leading to increased urine output.
Indication: Relieves pulmonary congestion and peripheral oedema.
Dose: Initial bolus, followed by continuous infusion or repeated bolus, depending on severity.
Monitor: Electrolytes, renal function, and fluid status.
3. Vasodilators:
o Nitrates (e.g., nitroglycerin):
Mechanism: Venodilation (reduces preload) and arterial dilation (reduces afterload), leading to reduced myocardial oxygen demand.
Indication: Severe pulmonary oedema and when BP allows for vasodilation.
Administration: Sublingual or IV.
4. Inotropic Support (if necessary):
o Dobutamine (Beta-1 agonist):
Mechanism: Increases myocardial contractility and cardiac output.
Indication: Used in cases of cardiogenic shock with severe hypotension.
o Milrinone (Phosphodiesterase inhibitor):
Mechanism: Increases cardiac contractility and vasodilation.
Indication: Often used when dobutamine is ineffective or contraindicated.
5. Monitoring:
o Regular assessment: Monitor vital signs, oxygenation, urine output, electrolytes, and acid-base status.
🏥 TLO 3.6.2: Management and Pharmacology of Chronic Heart Failure
Pharmacologic Management of Chronic Heart Failure:
1. ACE Inhibitors (e.g., Enalapril, Lisinopril):
o Mechanism: Inhibits conversion of angiotensin I to angiotensin II → vasodilation, reduced preload/afterload, and improved renal perfusion.
o Indication: Standard treatment for systolic heart failure to reduce symptoms and mortality.
o Monitor: Renal function, potassium levels (risk of hyperkalemia), blood pressure.
2. Angiotensin Receptor Blockers (ARBs) (e.g., Losartan, Valsartan):
o Mechanism: Block angiotensin II receptors, providing similar benefits as ACE inhibitors with less risk of cough.
o Indication: For patients intolerant to ACE inhibitors.
3. Angiotensin Receptor-Neprilysin Inhibitors (ARNI) (e.g., Sacubitril/Valsartan):
o Mechanism: Combines ARB (Valsartan) with neprilysin inhibitor (Sacubitril) to reduce vasoconstriction, sodium retention, and myocardial fibrosis.
o Indication: Standard therapy for patients with HFrEF (Heart Failure with Reduced Ejection Fraction).
4. Beta-blockers (e.g., Metoprolol, Carvedilol, Bisoprolol):
o Mechanism: Reduce sympathetic nervous system activation, decreasing heart rate, blood pressure, and myocardial oxygen demand.
o Indication: First-line for chronic heart failure to improve symptoms, prevent hospitalization, and prolong survival.
o Monitor: Heart rate, blood pressure, and signs of fluid retention.
5. Mineralocorticoid Receptor Antagonists (MRAs) (e.g., Spironolactone, Eplerenone):
o Mechanism: Block aldosterone effects → reduces sodium and water retention, and prevents myocardial fibrosis.
o Indication: Beneficial in HFrEF, improves survival, and reduces hospitalizations.
o Monitor: Renal function, potassium levels (risk of hyperkalemia).
6. SGLT2 Inhibitors (e.g., Dapagliflozin, Empagliflozin):
o Mechanism: Inhibit sodium-glucose co-transporter 2, reducing glucose reabsorption in the kidneys and promoting natriuresis.
o Indication: Shown to improve outcomes in both diabetic and non-diabetic patients with heart failure.
o Monitor: Renal function, electrolytes, and risk of dehydration.
7. Digoxin:
o Mechanism: Increases myocardial contractility and decreases heart rate through inhibition of Na+/K+ ATPase.
o Indication: Used for rate control in atrial fibrillation and in severe heart failure for symptom relief.
o Monitor: Serum digoxin levels, renal function, and electrolytes (especially potassium).
- Non-Pharmacologic Management of Chronic Heart Failure:
- Lifestyle modification: Weight management, low-sodium diet, fluid restriction.
- Exercise: Regular, moderate activity as tolerated.
- Device therapy:
o Implantable cardioverter-defibrillator (ICD) for prevention of sudden cardiac death in high-risk patients.
o Cardiac resynchronization therapy (CRT) for patients with intraventricular conduction delay (e.g., wide QRS).
🩺 TLO 3.7.1: Define and Enumerate the Types of Shock
Shock is a syndrome characterized by impaired tissue perfusion, resulting in cellular hypoxia and potential organ failure. It is usually classified based on its etiology:
Types of Shock:
Types of Shock:
1. Hypovolemic Shock:
o Caused by decreased blood volume (e.g., hemorrhage, dehydration, fluid loss).
2. Cardiogenic Shock:
o Caused by impaired cardiac function leading to inadequate cardiac output (e.g., acute myocardial infarction, heart failure).
3. Distributive Shock (e.g., septic shock, neurogenic shock, anaphylactic shock):
o Caused by vasodilation and abnormal distribution of blood flow.
4. Obstructive Shock:
o Caused by physical obstruction of blood flow (e.g., massive pulmonary embolism, cardiac tamponade, tension pneumothorax).
🧠 TLO 3.7.2: Stages of Shock
There are typically four stages of shock based on severity and clinical progression:
1. Compensated Shock (Non-progressive stage):
* Body compensates for reduced perfusion using mechanisms like vasoconstriction, tachycardia, and fluid retention to maintain blood pressure and perfusion.
* Clinical signs: Cold extremities, mild tachycardia, low-normal blood pressure, increased respiratory rate.
2. Progressive Shock:
* The compensatory mechanisms begin to fail as the body is unable to maintain adequate perfusion.
* Clinical signs: Hypotension, marked tachycardia, oliguria, altered mental status (confusion, lethargy).
3. Irreversible Shock:
* Organ damage becomes irreversible; cells undergo necrosis, leading to multi-organ failure.
* Clinical signs: Severe hypotension, bradycardia, severe metabolic acidosis, loss of consciousness, and multi-organ failure.
🧬 TLO 3.7.3: Pathophysiology of Cardiogenic Shock
Pathophysiology:
1. Reduced Cardiac Output:
o A fall in stroke volume (SV) and heart rate results in decreased cardiac output.
2. Compensatory Mechanisms:
o Activation of sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) to increase heart rate and vasoconstrict.
3. Increased Preload:
o Venous congestion occurs due to backward failure (blood accumulates in the venous system), causing pulmonary edema or systemic edema.
4. Impaired Oxygen Delivery:
o Decreased cardiac output leads to tissue hypoxia, organ dysfunction, and metabolic acidosis.
5. Metabolic Derangements:
o Lactate accumulation and acidosis occur as cells switch to anaerobic metabolism.
🩺 TLO 3.7.4: Stages of Cardiogenic Shock and Clinical Manifestations
Stages of Cardiogenic Shock:
- Stage 1 (Initial Stage):
o Clinical Manifestations: Mild hypotension, increased heart rate, mild tachypnea.
o Compensatory Mechanisms: SNS and RAAS activation maintain blood pressure. - Stage 2 (Progressive Stage):
o Clinical Manifestations: Severe hypotension (< 90 mmHg), rapid tachycardia, cold extremities, oliguria, restlessness.
o Pathophysiology: Decreased perfusion to organs, worsening metabolic acidosis, and impaired oxygen delivery. - Stage 3 (Irreversible Stage):
o Clinical Manifestations: Severe hypotension, bradycardia, altered consciousness, multi-organ failure.
o Pathophysiology: Extensive tissue damage, irreversible cell death, and failure of compensatory mechanisms.
🏥 TLO 3.7.5: Management of Cardiogenic Shock
General Measures:
* Oxygen therapy: To improve tissue oxygenation.
* Monitoring: Continuous monitoring of vital signs, urine output, and central venous pressure (CVP).
* Intensive care: Most patients require ICU admission.
2. Pharmacologic Treatment:
* Inotropes (e.g., dobutamine, milrinone):
o Mechanism: Increase myocardial contractility and cardiac output.
* Vasopressors (e.g., norepinephrine, dopamine):
o Mechanism: Vasoconstriction to improve systemic vascular resistance and raise blood pressure.
* Diuretics (e.g., furosemide):
o Mechanism: Reduce pulmonary edema and venous congestion by promoting fluid excretion.
3. Mechanical Support:
* Intra-aortic balloon pump (IABP):
o Mechanism: Increases coronary perfusion and reduces afterload by inflating during diastole and deflating during systole.
* Left ventricular assist device (LVAD):
o Used in refractory cases of cardiogenic shock when other treatments are ineffective.
4. Treatment of Underlying Cause:
* Revascularization: Percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in cases of acute myocardial infarction.
* Valve repair/replacement: In cases of valvular heart disease.
5. Fluid Management:
* Careful fluid resuscitation: Use judiciously to avoid fluid overload, which can worsen pulmonary congestion.
Summary of Key Management Points for Cardiogenic Shock:
Summary of Key Management Points for Cardiogenic Shock:
* Inotropes and vasopressors to maintain cardiac output and blood pressure.
* Oxygen therapy to prevent tissue hypoxia.
* Diuretics for fluid management, avoiding volume overload.
* Mechanical support devices (IABP, LVAD) in refractory cases.
* Revascularization or surgery to treat the underlying cardiac condition.
