week 4 Flashcards
Coronary artery disease CAD
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.
angina pectoris
where the myocardial cells experience a temporary ischaemic state
myocardial infarction
when the cells experience anoxia and die.
aeitology of CAD
multifactorial condition caused by a combination of nonmodifiable and modifiable risk factors
Nonmodifiable Risk Factors for CAD
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 postmenopause.
Genetics and Family History: A positive family history of premature CAD increases an individual’s risk
Modifiable Risk Factors of CAD
HTN- contributes to endothelial damage
Dyslipidaemia: Elevated LDL and reduced HDL levels promote plaque formation
Tobacco use damages blood vessels and increases oxidative stress and inflammation
Obesity and sedentary lifestyle
diabetes
dietary factors
inflammatory markers
psychological stress
Epidemiology of CAD
estimated 600,000Links to an external site. Australians aged 18 and over (3.0% of the adult population) have CAD.
types of CAD/Clinical Manifestations of CAD
Stable Angina (Exertional Ischaemia)
Acute Coronary Syndromes (ACS)
Atypical Symptoms (More common in women, elderly, diabetics)
Silent Ischaemia
Silent Ischaemia
No symptoms; detected via ECG or stress testing in diabetics or elderly patients
- 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) of cad
Dyspnoea (SOB), fatigue, dizziness, epigastric pain or nausea without chest pain
- Stable Angina (Exertional Ischaemia)
Predictable chest discomfort with exertion, relieved by rest or nitroglycerin
chest discomfort is thought to be attributable to?
myocardial ischaemia.
Stable Angina pathophysiology
(atherosclerosis) 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
Unstable Angina caused by
Caused by a sudden worsening of coronary blood flow.
Plaque rupture and thromboembolism (unstable angina) mechanism and cause
Mechanism: Clot formation (thrombosis) or embolisation leads to sudden coronary artery occlusion. Causes: Atrial fibrillation
Sudden Coronary Artery Dissection (SCAD) mechanism and common in who
Mechanism: A tear in the coronary artery wall creates a false lumen, obstructing blood flow. Common in: Young women, pregnancy, connective tissue disorders
Variant Angina (Prinzmetal Angina) caused by
Caused by Coronary Vasospasm.
Pathophysiology of angina
myocardial oxygen demand exceeds oxygen supply
Biochemical & Cellular Changes in Ischaemia
When blood supply is insufficient, the heart switches to anaerobic metabolism eg:
reduced ATP production
increase lactate,
Accumulation of ischaemic metabolites
Impaired nitric oxide (NO) release → Reduced vasodilation, worsening ischaemia
Clinical manifestations of stable angina
chest pain or discomfort, often triggered by exertion or emotional stress and relieved by rest or nitroglycerin
where is pain w stable angina
Retrosternal discomfort radiating to the left arm, jaw, neck or back
Clinical manifestations of unstable angina
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
Acute coronary syndrome
spectrum of conditions caused by acute myocardial ischaemia due to a sudden reduction in coronary blood flow. It includes:
Unstable Angina (UA)
Non-ST-Elevation Myocardial Infarction (NSTEMI)
ST-Elevation Myocardial Infarction (STEMI)
Coronary Vasospasm primary mechanism
Transient coronary artery spasm reduces blood flow, causing ischaemia
Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA) primary mechanism
Diverse causes such as microvascular dysfunction, embolism, or SCAD
Aortic Dissection Extending into Coronary Arteries primary mechanism
Aortic tear extends into coronary arteries, causing acute ischaemia.
Inflammatory Vasculitis (e.g., Kawasaki, Takayasu) primary mechanisms
Inflammation and endothelial dysfunction cause thrombosis and vascular damage
unstable angina dx criteria
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)
NSTEMI Dx crieteria
considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present
STEMI Dx criteria
myocardial ischaemia and who demonstrate elevated troponin levels in the blood they are distingusished from NSTEMI by ECG characteristics
Acute NSTEMI: ECG
no significant abnormalities, ST-segment depression or elevation (usually transient), or T wave inversion.
Acute STEMI: ECG
characterised by hyperacute T waves, which are tall, peaked, and symmetric; elevation of the ST segment. The ST elevation is at first concave and then becomes convex, merging with the T wave.
Myocardial Infarction definition
defined as a clinical event caused by myocardial ischaemia in which there is evidence of myocardial injury or necrosis
Determinants of infarct size
include the location and extent of the arterial occlusion, the duration of the occlusion, and the metabolic needs of the affected heart tissue
Complications arising from MI
Conduction complications
include rupture of the left ventricular free wall, rupture of the interventricular septum, and development of severe mitral regurgitation.
what is a pericardium
fibroelastic sac composed of visceral and parietal layers, enclosing the heart and containing a thin layer of lubricating fluid
pericardium function
protective barrier, promotes efficient cardiac function, and prohibits excessive displacement of the heart
Acute pericarditis aetiology
classified based on their underlying causes
Acute pericarditis Infectious Causes
Viral: Coxsackievirus, adenovirus, influenza, HIV.
Bacterial: Tuberculosis (TB), pneumococcus, staphylococcus, streptococcus.
Fungal: Histoplasmosis, aspergillosis.
Parasitic: Trypanosoma cruz
Acute pericarditis Non-Infectious Causes
Autoimmune Diseases
Post-cardiac Injury Syndromes
Neoplastic Causes
Uremic Pericarditis
Radiation-Induced
Drug-Induced
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
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
Pericardial Effusion aetiology
idiopathic hw can have infectious causes (viral, bacterial, fungal and parasitic) and non infectious causes (post MI, post cardiac surgery and trauma, malignancy-assosiated pericardial effusion)
in addition can have contributuions from Autoimmune diseases
Uremia and dialysis-associated pericarditis
Hypothyroidism
Aortic dissection extending into the pericardium
Pathogenesis of Pericardial Effusion
Increased pericardial fluid production
Decreased pericardial fluid drainage
Rapid accumulation can lead to cardiac tamponade
Cardiac Tamponade Aetiology
Rapidly accumulating pericardial effusion from trauma, aortic dissection, malignancy, infection
Cardiac Tamponade Pathogenesis
Pericardial pressure exceeds right atrial and ventricular diastolic pressures
Impaired cardiac filling leads to decreased stroke volume and cardiac output
Constrictive 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
Constrictive Pericarditis Pathogenesis
Fibrotic pericardium restricts diastolic filling, leading to elevated venous pressures and reduced cardiac output
Acute Pericarditis clinical features
sharp chest pain, improved when sitting up and leaning forward
Pericardial Friction Rub
ECG Changes: Diffuse ST elevation, PR segment depression
Pericardial Effusion
fever, Fatigue, Myalgia
Pericardial Effusion clinical features
Muffled heart sounds
Small Effusions- Often asymptomatic if mild
Moderate Effusions: Chest discomfort/ pressure
Large Effusions: Can lead to cardiac tamponade
Constrictive Pericarditis clinical manifestations
Chronic pericardial inflammation
Signs of right heart failure
Kussmaul’s sign: Jugular venous distention that does not decrease with inspiration
Cardiac Tamponade clinical manifestations
Hypotension, tachycardia, pulsus paradoxus
Elevated jugular venous pressure
Muffled heart sounds
Which investigation is most sensitive and specific for detecting a pericardial effusion
Transthoracic echocardiogram (TTE)
What is the typical volume of fluid found in a normal pericardial cavity
15–50 mL
Which of the following is a common cause of pericardial effusion
Viral infection
What is the pathophysiological hallmark of constrictive pericarditis?
Inflammatory thickening and fibrosis of the pericardium
Conduction block
abnormalities that occur at any part of the conduction system
Common Causes of Conduction Disorders
Ischaemic heart disease
Electrolyte imbalances
Degenerative changes
Medications
Congenital conditions
Infectious or inflammatory diseases
Surgical injury
what causes tachycardias and fibrillations aetiology
can arise from structural, electrical, metabolic or autonomic abnormalities in the atria or ventricle
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
transient block steps
- A temporary block affects a region of myocardial cells
- cells either do not receive any inflow of positive ions, or receive a reduced ionic current -> cells do not depolarise when the impulse fires
- After the transient block resolves, ions begin to enter the previously blocked cells HW cells are now functionally impaired and conduct slowly
- Re-entry loop forms - if conduction through the blocked cells is slow enough, by the time the signal exits this region, the surrounding “healthy” cells have repolarised and become excitable again (i.e., they are out of their refractory period)
- continue to loop activating cells again and again, creating extra beats. If this loop continues fast enough and for long enough, the person will experience tachycardia
Early After-depolarisations EADs Aetiology
Prolonged action potential duration due to:
Inherited long QT syndrome (LQTS)
Medications
Electrolyte disturbance
Early After-depolarisations (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
Early After-depolarisations clinical manifestations (EADs)
Palpitations
Dizziness or light-headedness
Syncope or near-syncope
May lead to Torsades de Pointes
Delayed After-depolarisations (DADs) aetiology
Intracellular calcium overload, often due to digoxin toxicity, high sympathetic tone (e.g., stress, catecholamines)
Rapid heart rates
Myocardial ischaemia
Delayed After-depolarisations (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
Delayed After-depolarisations (DADs) CM
Palpitations
Dizziness or light-headedness
Syncope or near-syncope
Can cause premature beats, ventricular tachycardia or bidirectional VT (classic in digoxin toxicity)
Narrow QRS complex tachyarrhythmias millisecond duration
<120 milliseconds
Wide QRS complex tachyarrhythmias millisecond duration
≥120 milliseconds
Bradycardias Aetiology
sinus node dysfunction, leads to inability of the SA node to produce an adequate heart rate that meets the physiologic needs of the individual
Bradycardias Pathogenesis common causes
drugs such as beta-blocker, Sinus node dysfunction, Ischaemia
Bradycardias Clinical manifestations
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
Conduction blocks Aetiology
The conduction disturbance can be transient or permanent, and it can have many causes
First-degree atrioventricular block
every electrical impulse from the atria reaches the ventricles, but each is slowed as it moves through the atrioventricular node
Second-degree atrioventricular block
only some electrical impulses reach the ventricles. The heart may beat slowly, irregularly, or both
Third-degree atrioventricular block
no impulses from the atria reach ven the tricles, and the ventricular rate and rhythm are controlled by the atrioventricular node, bundle of His or the ventricles themselves
Pathogenesis
Congenital AV Block
Often immune-mediated: maternal antibodies cross the placenta, which damage foetal cardiac cells by disrupting calcium metabolism → leads to cell death and fibrosis of the conduction system.
Acquired AV Block Pathogenesis
most common cause of AV block- Idiopathic: caused by fibrosis and sclerosis of the conduction system
Ischaemic heart disease: conduction can be disturbed
Iatrogenic AV block, which can result from either medications or invasive procedures
Conduction blocks clinical manifestations
bradycardia
an irregular pulse
hypotension
Bundle Branch Blocks is and how is this shown on an ECG
a type of conduction block involving partial or complete interruption of the flow of electrical impulses through the right or left bundle branches
defined by variations in QRS duration compared to normal.
Left Bundle Branch Block (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.
LBBB aeitology
Structural heart disease, especially hypertension, CAD, cardiomyopathies, valvular heart disease, acute MI, myocarditis
Iatrogenic e.g., post-cardiac surgery
LBBB Pathogenesis
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
LBBB Clinical Manifestations
often asymptomatic, especially if no heart disease.
may cause worsening heart failure symptoms, syncope
Right Bundle Branch Block (RBBB) is and how is this shown on an ECG
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.
RBBB aeitology
Can be normal in healthy individuals.
Structural causes: Pulmonary embolism,
congenital heart disease,
iatrogenic (e.g., catheter trauma)
Age-related conduction disease
RBBB Pathogenesis
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.
RBBB Clinical Manifestations
often asymptomatic; may be found incidentally on ECG
permanent pacemaker insertion for those with symptoms
Atrial Tachyarrhythmias clinical manifesations
Often presents with palpitations, dyspnoea, fatigue
Atrial Bradyarrhythmias clinical manifestations
Symptoms include fatigue, lightheadedness, syncope.
Ventricular Tachyarrhythmias clinical manifestations
Often life-threatening; may cause syncope, cardiac arrest.
requires urgent intervention
Ventricular Bradyarrhythmias clinical manifestations
Usually a sign of severe conduction system failure or dying myocardium
May be transient or terminal; pacemaker may be needed
varient angina mechanisms
Mechanism: Sudden reversible spasm of the coronary arteries reduces blood flow even in the absence of significant atherosclerosis
varient angina triggers
Triggers: Cocaine use, smoking, cold exposure, emotional stress and certain medications.
