Week 4 Flashcards
1
Q
what is CAD
A
- It results from damage to, and the death of, cells in the heart as a consequence of inadequate blood flow (ischaemia) and reduced oxygen delivery (hypoxia) to meet the workload of the heart
- The primary underlying cause of coronary ischaemia is atherosclerosis
- The physiological conditions that result are referred to as angina pectoris - where the myocardial cells experience a temporary ischaemic state - and myocardial infarction - when the cells experience anoxia and die
2
Q
CAD Aetiology
A
- CAD is a multifactorial condition caused by a combination of nonmodifiable and modifiable risk factors
Nonmodifiable risk factors: - Age: CAD risk increases with age, particularly in men over 45 years and women over 55 years
- Gender: Men are generally at higher risk than premenopausal women, though the risk equalises post menopause.
- Genetics and Family History: A positive family history of premature CAD (before 55 years in men and 65 years in women) increases an individual’s risk
Modifiable risk factors: - Hypertension: High blood pressure contributes to endothelial damage, accelerating atherosclerosis
- Dyslipidaemia: Elevated LDL and reduced HDL levels promote plaque formation
- Tobacco use damages blood vessels and increases oxidative stress and inflammation
- Diabetes mellitus: Chronic hyperglycaemia promotes endothelial dysfunction and accelerates atherosclerosis
- Obesity and sedentary lifestyle: Excess weight, particularly abdominal obesity, is linked to insulin resistance and lipid abnormalities
- Dietary factors: Diets high in saturated fats, cholesterol, and processed foods contribute to atherosclerosis
- Inflammatory markers: Elevated high-sensitivity C-reactive protein (hs-CRP) is associated with higher CAD risk
- Psychosocial stress: Chronic stress, depression and anxiety contribute to CAD development through neurohormonal dysregulation
3
Q
CAD Epidemiology
A
- 600,000 Australians aged 18 and over (3% of the adult population) have CAD
- CHD was the underlying cause of 18,600 deaths (9.8% of all deaths)
- Although the incidence of CAD has been declining in AUS as in other developed (high-income) nations, the overall number of coronary events is not expected to decrease due to factors like immigration and ageing
4
Q
Clinical man of CAD
A
- Stable Angina (Exertional Ischaemia)
- Predictable chest discomfort with exertion, relieved by rest or nitroglycerin - Acute Coronary Syndromes (ACS)
- Unstable Angina: Chest pain at rest or increasing in frequency
- NSTEMI: Ischemia with myocardial injury (elevated troponins) but no ST elevation
- STEMI: Complete coronary occlusion with ST elevation on ECG - Atypical Symptoms (More common in women, elderly, diabetics)
- Dyspnoea, fatigue, dizziness, epigastric pain or nausea without chest pain - Silent Ischaemia
- No symptoms; detected via ECG or stress testing in diabetics or elderly patients
5
Q
Angina what is it
A
- Angina pectoris is the term used when chest discomfort is thought to be attributable to myocardial ischemia
6
Q
Aetiology classification of Angina
A
- Stable Angina
- Atherosclerosis (main cause of stable angina) Mechanism: Accumulation of lipid-laden plaques in the coronary arteries reduces blood flow, leading to ischaemia and a predictable chest pain with exertion or stress, relieved by rest or medication such as nitroglycerin (vasodilator). - Unstable Angina
Caused by a sudden worsening of coronary blood flow
- Plaque rupture and thromboembolism. Mechanism: Clot formation (thrombosis) or embolisation leads to sudden coronary artery occlusion. Causes: Atrial fibrillation, prosthetic heart valves, endocarditis, hypercoagulable states. Symptoms occur at rest or with minimal exertion and are not relieved by usual measures.
- Sudden Coronary Artery Dissection (SCAD). Mechanism: A tear in the coronary artery wall creates a false lumen, obstructing blood flow. Common in: Young women, pregnancy, connective tissue disorders (e.g., Marfan syndrome). - Variant Angina (Prinzmetal Angina)
Caused by Coronary Vasospasm
- Mechanism: Sudden reversible spasm of the coronary arteries reduces blood flow even in the absence of significant atherosclerosis. Triggers: Cocaine use, smoking, cold exposure, emotional stress and certain medications. Occurs at rest, often at night or early morning. Often occurs at rest, particularly at night or early morning.
- Related cause: Microvascular Dysfunction (Syndrome X). Mechanism: Dysfunction of the small coronary arteries impairs vasodilation, leading to ischaemia despite normal large arteries. Common in: Women, diabetics, hypertensive patients. Key Feature: Angina with normal coronary angiography (ie no atherosclerosis in coronary arteries).
(SEE IMAGE FOR HELP)
7
Q
Pathophysiology of Angina
A
Myocardial ischaemia (and consequently angina) occurs when myocardial oxygen demand exceeds oxygen supply
The mismatch between myocardial oxygen supply and demand can be due to:
- Reduced oxygen supply (e.g., atherosclerosis, vasospasm, SCAD, thromboembolism, microvascular dysfunction).
- Increased oxygen demand (e.g., tachycardia (faster heart rates reduce diastolic perfusion time), hypertension (higher SBP increases preload myocardial work), exertion (requires stronger contractions requiring more ATP, raising oxygen demand)
Biochemical & Cellular Changes in Ischaemia
When blood supply is insufficient, the heart switches to anaerobic metabolism, leading to metabolic and structural disturbances:
1. Metabolic Consequences
* Reduced ATP production → Impaired Na⁺-K⁺ pump, cellular swelling and dysfunction
* Increased lactate production → Cellular acidosis
* Accumulation of ischaemic metabolites → Bradykinin (causes vasodilation but also stimulates pain receptors), serotonin (released by platelets, promotes vasoconstriction), histamine and thromboxane A2 (which causes platelet aggregation and arterial spasm) contribute to pain and vasospasm
2. Endothelial Dysfunction
* Impaired nitric oxide (NO) release → Reduced vasodilation, worsening ischaemia
8
Q
clinical man of stable angina
A
- Classic symptoms: chest pain or discomfort, often triggered by exertion or emotional stress and relieved by rest or nitroglycerin
- Pain characteristics: Retrosternal discomfort radiating to the left arm, jaw, neck or back. The referred pain is thought to be due to ischaemia which stimulate chemoreceptors and mechanoreceptors in the myocardium. The pain signals travel via C5-T6 sympathetic afferents to the spinal cord. The signals ascend through the spinothalamic tract to the thalamus and cortex. Since these spinal levels also receive sensory input from the jaw, neck, and left arm, pain is referred to these areas.
- Atypical symptoms: Women, older adults, and diabetics may experience atypical symptoms such as dysnoea, fatigue, nausea, indigestion-like discomfort and dizziness
9
Q
clinical man of unstable angina
A
- Recent onset of chest discomfort
- One or more prolonged episodes (more than 20 minutes)
- Chest discomfort occurring with less exertion and/or at rest compared with prior episodes of stable angina
10
Q
acute coronary syndrome
A
ACS is a spectrum of conditions caused by acute myocardial ischaemia due to a sudden reduction in coronary blood flow
INCLUDES:
1. Unstable Angina (UA)
2. Non-ST-Elevation Myocardial Infraction (NSTEMI)
3. ST-Elevation Myocardial Infraction (STEMI)
11
Q
Aetiology of ACS
A
- atherosclerotic plaque rupture
- coronary vasospasm
- myocardial infraction with non-obstructive coronary arteries
- aortic dissection extending into coronary arteries
- inflam vasculitis
12
Q
ACS diagnostic criteria
A
applied to patients in whom there is suspicion or confirmation of myocardial ischaemia
- Unstable angina (UA) and acute NSTEMI differ primarily in whether the ischaemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (troponins)
1. UA considered present in patients with ischaemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischemia (eg, ST-segment depression or transient elevation or new T-wave inversion)
2. NSTEMI considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present.
- Since an elevation in troponins may not be detectable for hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation and initial medical management is the same for these two syndromes.
13
Q
STEMI and NSTEMI
A
-patients who present with clinical characteristics compatible with myocardial ischaemia and who demonstrate elevated troponin levels in the blood
- which require the finding of an elevated troponin, are distinguished from each other based on ECG characteristics
- - Acute NSTEMI: ECG on presentation may show no significant abnormalities, ST-segment depression or elevation (usually transient), or T wave inversion
- Acute STEMI: ECG on presentation is characterised by hyperacute T waves, which are tall, peaked, and symmetric; elevation of the ST segment (depending upon the location of the MI - which leads the ST elevation is shown)
- The ST elevation is at first concave and then becomes convex, merging with the T wave
14
Q
Myocardial Infraction
A
MI is a clinical event caused by myocardial ischaemia in which there is evidence of myocardial Injury or necrosis
15
Q
MI Diagnosis
A
- Demonstration of cell death, by measurement of cardiac markers
- Presence of serum markers and intracellular proteins
Cardiac troponin I should not be found in the blood; signals myocardial cell damage - Morphological changes seen on an ECG
Location of event
Difference between angina and MI - Angiograms to quantify the location and severity of the lesion
16
Q
MI infraction size determinants
A
- Multifactorial
- Include the location and extent of the arterial occlusion, the duration of the occlusion, and the metabolic needs of the affected heart tissue
- Absence/presence of collateral circulation can also influence the extent of damage
17
Q
complications Arising from MI
A
- Can be severe and include heart failure, arrhythmias and even death, and the prognosis is influenced by a patient’s previous cardiovascular health, age and other co-morbidities PLUS speed of revascularisation
Mechanical complications of AMI: include rupture of the left ventricular free wall, rupture of the interventricular septum, and development of severe mitral regurgitation.
Conduction complications of AMI: caused by either autonomic imbalance or ischaemia/necrosis of the conduction system. Conduction disturbances can be based on location of the infarct location e.g., Inferior MI - conduction disturbances include sinus bradycardia and complete heart block (CHB) due to right coronary artery (RCA) involvement. Anterior MI - more serious conduction disturbances due to extensive myocardial necrosis affecting the bundle branches.
Pericardial complications: Either a peri-infarction pericarditis, post-MI pericardial effusion (common in a transmural MI) and post-cardiac injury syndrome
18
Q
Pathogenesis of MI
A
coronary thrombus –> small thromubs, partially occlusive thrombus (ST segment depression and/or T wave inversion) –> occlusive thrombus (transient ischemia or prolonged ischemia) (LOOK AT PAGE 81)
19
Q
NSTEMI
A
- Thrombus partly occuludes an artery
- Part if heart muscle being supplied by affected artery dies
- No charactersitic elevation in ST segement of ECG
- Cardiac enzymes e.g., CK-MB, Tropoinin I, Troponin T determine if NSTEMI (or just unstable angina)
20
Q
STEMI
A
- Thrombus compeltely blocks coronary artery
- Recognised by characteristic chnages it produce on the ECG
- Propmt recogintion to ensure reperfusion soon after presentation
21
Q
Troponins in MI
A
- Troponins are proteins that regulate cardiac muscle contraction and serve as biomarkers for myocardial injury
- The relevant forms are cardiac troponin I (cTnI) and cardiac troponin T (cTnT), both of which are specific to the heart and are used in diagnosing an acute MI
- The biological half-life of cTnI and cTnT is ~2 hours, but due to continuous release from necrotic myocardium, it remains elevated for 5 days (cTnI) to 10 days (cTnT)
- The image depicts the typical biphasic kinetic of cardiac troponin T kinetics for a STEMI and a NSTEMI - an initial peak due to early release of troponin from damaged myocardial cells, and a second peak due to continued leakage from necrotic myocardium or secondary cardiac injury, compared to monophasic kinetics in myocarditis, pulmonary embolism (PE), and endurance sports
- A biphasic troponin pattern indicates ongoing myocardial damage and may be linked to larger infarcts, with worse patient outcomes
22
Q
Pericardial Disorders
A
- The pericardium is a fibroelastic sac composed of visceral and parietal layers, enclosing the heart and containing a thin layer of lubricating fluid (15–50 mL)
- The pericardium serves as a protective barrier, promotes efficient cardiac function, and prohibits excessive displacement of the heart
Pericardial disorders invlove pathological changes in this strucutre and can manifest in different forms, including inflmmation, effucsion, constrction or a combination of these:
1. Acute pericarditis
2. Pericardial effusion (with or without tampondade)
3. Cardiac tamponade
4. Constrictive pericaditis
23
Q
Acute pericarditis
A
a sudden inflammation of the pericardium, the sac surrounding the heart, typically lasting less than 4 to 6 weeks
24
Q
Acute pericarditis Aetiology
A
- Infectious casues
* Viral: Coxsackievirus, adenovirus, influenza, SARS-CoV-2, HIV.
* Bacterial: Tuberculosis (TB), pneumococcus, staphylococcus, streptococcus.
* Fungal: Histoplasmosis, aspergillosis.
* Parasitic: Trypanosoma cruzi - Non-Infectious causes
* Autoimmune Diseases: Systemic lupus erythematosus (SLE), rheumatoid arthritis, scleroderma, sarcoidosis
* Post-cardiac Injury Syndromes: Post-myocardial infarction), post-cardiac surgery, post-trauma or invasive procedures
* Neoplastic Causes: Metastatic lung, breast cancer, lymphoma, leukaemia
* Uremic Pericarditis: Seen in chronic kidney disease and dialysis patients
* Radiation-Induced: Post-radiotherapy for thoracic malignancies
* Drug-Induced: Hydralazine, isoniazid, procainamide
25
Acute pericarditis Pathogenesis
- The pathogenesis of pericardial disorders depends on the underlying aetiology
- In general, inflammation of the pericardial layers leads to increased vascular permeability and pericardial fluid accumulation
- If persistent, fibrosis and calcification may develop, potentially leading to constrictive pericarditis
Infectious Pericarditis: Direct invasion by pathogens leading to pericardial inflammation and exudate formation
COVID-19 Pericarditis: Combination of direct viral injury, immune-mediated inflammation, and microvascular thrombosis
Immune-Mediated Pericarditis: Autoantibody formation and immune complex deposition
Post-Cardiac Injury Pericarditis: Inflammatory response to myocardial injury, with pericardial immune activation
Neoplastic Pericarditis: Direct tumuor infiltration or metastatic spread causing pericardial thickening and effusion
Uremic Pericarditis: Accumulation of metabolic toxins in patients with renal failure leading to fibrinous exudate formation
Radiation-Induced Pericarditis: Fibrotic changes in the pericardium following radiation exposure
26
Pericardial Effusion what is it
the buildup of excess fluid in the space surrounding the heart, known as the pericardial space
27
Pericardial Effusion Aetiology
- Idiopathic (most common in developed countries)
- Infectious Causes: Viral: Coxsackievirus, COVID-19; Bacterial: Tuberculosis, purulent pericarditis; Fungal & parasitic: Histoplasmosis, Candida, Toxoplasmosis
- Non-Infectious Causes:
Post-myocardial infarction
Post-cardiac surgery and trauma
Malignancy-associated pericardial effusion: Lung cancer, breast cancer, leukaemia, lymphoma, mesothelioma
- Autoimmune diseases: SLE, rheumatoid arthritis, scleroderma
- Uremia and dialysis-associated pericarditis
- Hypothyroidism
- Aortic dissection extending into the pericardium
28
Pericardial Effusion Pathogenesis
- Increased pericardial fluid production (due to inflammation, malignancy, or infection)
- Decreased pericardial fluid drainage (due to lymphatic obstruction, malignancy)
- Rapid accumulation can lead to cardiac tamponade (compression of the heart, impairing filling)
29
Constructive Pericarditis what is it
a condition where the pericardium, the sac surrounding the heart, becomes thickened and rigid, restricting the heart's ability to fill with blood during diastole (relaxation)
30
Constructive Pericarditis Aetiology
- Chronic pericarditis leading to fibrosis and calcification
- Tuberculosis (most common cause in developing countries)
- Post-cardiac surgery or radiation exposure
- Chronic inflammatory conditions (autoimmune, post-viral pericarditis)
31
Constructive Pericarditis Pathogenesis
- Fibrotic pericardium restricts diastolic filling, leading to elevated venous pressures and reduced cardiac output
32
CLINICAL MAN OF ALL PERICARDIUM
AP - chest pain, ECH changes, fever, fatigue
PE - muffled heart sounds, small medium and large effusions,
CT - hypotension, tachy, muffled heart sounds
CP - signs of right heart failure
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disorders of cardiac conduction
Dysrhythmias - TACHY, FIBRILLATIONS, BRADY, CONDUCTION BLOCKS
Arhthymias
34
Dysrhythmias
- Disturbance of the rhythm of the heart
- Reflect an alternation of the electrical activity of the heart, either at the level of the conduction network of the heart or because of an altered electrical stability of the myocytes
4 types:
1. Tachycardias: can be restricted to either the upper chambers (atria), the lower chambers (ventricular), can be generalisable (sinus tachycardia) or can originate in the atria and spread to the ventricles (supraventricular tachycardia). Despite the many variations, the root cause of a tachycardia is due to re-entry, early after-depolarisation or delayed after-depolarisation
2. Fibrillations: whether they occur in the atria or ventricles, represent a type of electrical storm in the heart. Individual myocytes contract independently instead of a coordinated whole. Atrial fibrillation can usually be tolerated by a healthy adult with a healthy heart, ventricular fibrillation is a medical emergency as the myocytes fail to contract in a coordinated fashion. Thus, there is no stroke volume and no cardiac output
3. Bradycardias: Sinus bradycardia can occur normally, particularly during sleep or at rest and in well-conditioned athletes. Sinus bradycardia can also be seen in a variety of pathophysiologic settings, most commonly due to medication effects/toxicities or primary sinoatrial disease
4. Conduction Block: abnormalities that occur at any part of the conduction system
35
Arrythmia
- Any heart rhythm that is not normal sinus rhythm with normal atrioventricular conduction
36
Normal heart beat
- Normal sinus rhythm originates from the sinus node in the upper portion of the right atrium
- During sinus rhythm, the heart rate is in the normal range, the P waves are normal on the ECG and the rate is stable
- By definition, a sinus tachycardia is a heart rate >100 bpm, whilst a sinus bradycardia is a rate <60 bpm in an adult; in both the sinoatrial (SA) node must control the rhythm
- Sinus bradycardia or tachycardia may be physiologic (i.e., normal) or nonphysiologic (i.e., abnormal)
37
Tachycardias and Fibrillations aetiology
Can arise from structural, electrical, metabolic, or autonomic abnormalities in the atria or ventricle:
- Structural heart disease: MI, cardiomyopathy, valvular heart disease are common reasons for re-entry circuits due to scar formation and conduction heterogeneity
- Ion channelopathies (Inherited): Long QT syndrome, Brugada syndrome, and familial AV block are due to genetic defects in ion channel subunits
- Acquired electrolyte and metabolic disorders: Hypokalaemia, acidosis and ischaemia disrupt normal action potential propagation and recovery
- Drug-induced proarrhythmic: Antiarrhythmics, digoxin and QT-prolonging agents
- Autonomic nervous system imbalance: High sympathetic tone increases risk of tachyarrhythmias via enhanced automaticity
38
Tachycardias and Fibrillations Pathogenesis
- An electrical impulse reactivates same region of heart tissue, forming a loop that fires repeatedly, causing rapid and often dangerous heart rhythms
How It Happens:
- Normally, impulses die out after depolarising all cells
- In re-entry, a transient block (due to ischaemia, scar tissue, or electrolyte imbalance) delays conduction
- The impulse loops around an anatomical or functional obstacle (e.g., scar, blood vessel)
- The previously depolarised area is now ready to depolarise again, sustaining the circuit e.g., ventricular tachycardia in ischaemic heart disease
39
Early After Depolarisation (EADs) what is it
The ECG pattern is characterized by an elevation of the J-point (the point where the QRS complex meets the ST segment)
40
Early After Depolarisation (EADs) Aetiology
Prolonged action potential duration due to:
- Inherited long QT syndrome (LQTS)
- Medications, macrolide antibiotics
- Electrolyte disturbances e.g., hypokalaemia
41
Early After Depolarisation (EADs) Pathogenesis
- It occurs during repolarisation – a prolonged action potential allows calcium channels to reopen, leading to an early inward calcium current
- This triggers a secondary depolarisation before the cell has fully reset
- If this reaches threshold, it initiates a new action potential
42
Early After Depolarisation (EADs) Clinical Man
- Palpitations
- Dizziness or light-headedness
- Syncope or near-syncope
- May lead to Torsades de Pointes (a polymorphic ventricular tachycardia)
43
Delayed after depolarisation (DADs)
what is it
are brief, transient depolarizations that occur in the diastolic phase of the heart's electrical cycle, after repolarization is complete
44
Delayed after depolarisation (DADs) Aetiology
- Intracellular calcium overload, often due to digoxin toxicity, high sympathetic tone (e.g., stress, catecholamines)
- Rapid heart rates
- Myocardial ischaemia
45
Delayed after depolarisation (DADs) Pathogenesis
- Occur after repolarisation is complete. Excess calcium leaks from the sarcoplasmic reticulum. This activates the Na⁺/Ca²⁺ exchanger, which brings sodium in, causing a net inward current.
- If strong enough, this depolarisation reaches threshold and triggers an extra action potential
46
Delayed after depolarisation (DADs) clinical man
- Palpitations
- Dizziness or light-headedness
- Syncope or near-syncope
- Can cause premature beats, ventricular tachycardia or bidirectional VT (classic in digoxin toxicity)
47
Treatment of any Tachyarrhymias
- Treatment of any tachyarrhythmias depend on a variety of clinical factors
- However, most treatment decisions are made based on the width, morphology, and regularity of the QRS complex
- In most patients, the differentiation between narrow and wide QRS complex tachyarrhythmias requires only a surface ECG
Narrow QRS complex tachyarrhythmias have a QRS complex <120 milliseconds in duration e.g., sinus tachycardia, atrial flutter, atrial fibrillation
Wide QRS complex tachyarrhythmias have a QRS complex ≥120 milliseconds in duration e.g., ventricular tachycardia
48
Bradycardias what is it
a heart condition where the heart beats slower than normal
49
Bradycardias Aetiology and Pathogenesis
- Common cause: drugs such as beta-blocker, which alter the balance between the parasympathetic and sympathetic nervous systems in the control of the intrinsic heart rate, to favour a reduced heart rate.
- Sinus node dysfunction, also known by its historical name sick sinus syndrome: due to a dysfunction of SA node secondary to senescence of the SA node and surrounding atrial myocardium. Usually occurs in people aged >70 years. The most common cause is the replacement of sinus node tissue by fibrous tissue
- Ischaemia: sinus node is perfused by sinoatrial nodal artery from the right coronary artery/left circumflex artery. Narrowing of these arteries (e.g., from atherosclerosis) can lead to impairment of the sinus node function
50
Bradycardias Clinical Man
- Many patients tolerate heart rates of 40 beats/min surprisingly well
- At lower rates symptoms can include dizziness, near syncope, syncope, ischaemic chest pain and hypoxic seizures
51
Conduction Blocks what is it
a disruption in the heart's electrical system, which can cause the heart to beat slowly or irregularly
CLASSIFIED TO: AV block or Bundle Branch block
52
Conduction Blocks Aetiology
- Atrioventricular (AV) conduction can be delayed, intermittently blocked or completely blocked—classified correspondingly as first, second-, or third-degree block. The conduction disturbance can be transient or permanent, and it can have many causes
53
Atrioventricular Block Aetiology
- Can result from physiologic slowing of cardiac conduction in response to increased parasympathetic nervous system output.
- Represents a delay or disturbance in the transmission of an impulse from the atria to the ventricles.
- Can be due to an anatomical or functional impairment in the heart's conduction system, temporary or permanent.
First-degree atrioventricular block: every electrical impulse from the atria reaches the ventricles, but each is slowed as it moves through the atrioventricular node. Common among well-trained athletes, young adults and people with a highly active vagus nerve. This disorder rarely causes symptoms and does not require treatment
Second-degree atrioventricular block: only some electrical impulses reach the ventricles. The heart may beat slowly, irregularly, or both. Type 1 second degree AV block may be present in young, athletic people; Type 2 always indicates heart disease is present.
Third-degree atrioventricular block: no impulses from the atria reach the ventricles, and the ventricular rate and rhythm are controlled by the atrioventricular node, bundle of His or the ventricles themselves. These substitute pacemakers are slower than the sinoatrial node, and are often irregular and unreliable. Thus, the ventricles beat very slowly (30-50 bpm), and is a serious arrhythmia
54
Congenital AV block pathogenesis
- Often immune-mediated: maternal anti-Ro and anti-La antibodies cross the placenta, which damage foetal cardiac cells by disrupting calcium metabolism → leads to cell death and fibrosis of the conduction system.
- In congenital structural heart disease, AV block results from maldevelopment or disruption of conduction pathways (e.g., central fibrous body)
55
Acquired AV Block Pathogenesis
- Idiopathic: caused by fibrosis and sclerosis of the conduction system; most common cause of AV block
- Ischaemic heart disease: conduction can be disturbed with either chronic ischaemic heart disease or during an acute MI
- Iatrogenic AV block, which can result from either medications or invasive procedures e.g., cardiac surgery or transcatheter aortic valve replacement can cause AV block through mechanical injury to conduction tissue
56
Clinical Man of conduction block
- Bradycardia
- An irregular pulse
- Hypotension
57
bundle branch blocks what is it
- Bundle branch block is a type of conduction block involving partial or complete interruption of the flow of electrical impulses through the right or left bundle branches
- Bundle branch and fascicular blocks are usually defined by variations in QRS duration compared to normal
58
left BBB
- LBBB results when normal electrical activity in the His-Purkinje system is interrupted altering the normal sequence of activation, resulting in the characteristic ECG appearance of a widened QRS complex
59
LBBB Aetiology
- Structural heart disease, especially hypertension, CAD, cardiomyopathies, valvular heart disease, acute MI, myocarditis
- Iatrogenic e.g., post-cardiac surgery, or age-related degeneration of the conduction system
60
Pathogenesis of LBBB
- Block in the left bundle → Impulse can't travel normally; right ventricle activates first, then delayed left ventricle; causes dyssynchronous contraction of the ventricles; may lead to inefficient LV contraction
61
Clinical man of LBBB
- Often asymptomatic, especially if no heart disease
- May cause worsening heart failure symptoms, syncope
62
Right BBB
- RBBB results when normal electrical activity in the His-Purkinje system is interrupted altering the normal sequence of activation, resulting in the characteristic ECG appearance of a widened QRS complex
63
Aetiology of RBBB
- Can be normal in healthy individuals.
- Structural causes: Pulmonary embolism, pulmonary hypertension, MI, myocarditis, congenital heart disease, iatrogenic (e.g., catheter trauma)
- Age-related conduction disease
64
Pathogenesis of RBBB
- Block in the right bundle → Right ventricle depolarises late; left ventricle activates normally, then impulse spreads slowly to right ventricle; usually has minimal impact on ventricular contraction
65
Clinical man of RBBB
- Often asymptomatic; may be found incidentally on ECG
- Permanent pacemaker insertion for those with symptoms
66
Atrial Arrhythmias
- Can be either tachycardias or bradycardias – but most are tachyarrhythmias
67
Aetiology of both Atrial Tachy and Atrial Brady
AT - over 100bpm, hypertension, VHD, pulmonary disease, hyperthyroidism,
AB - under 60bpm, Ischemia heart disease, hypothyroidism, drugs
68
Ventricular arrhythmias
- Abnormal heart rhythms originating from the ventricles, ranging from benign escape rhythms (ventricular bradycardia) to life-threatening tachyarrhythmias (like ventricular tachycardia and fibrillation)
- Typically caused by ischaemic heart disease, cardiomyopathies, electrolyte imbalances or inherited conditions, and can present with palpations, syncope, or sudden cardiac arrest
69
VentricularTachy and Brady Aetiology
VT - ischemia heart disease, cardiomyopathies, heart failure
VB - Complete AV block, SA and AV node failure, severe myocardial ischemia or infraction
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