Week 4 Module 2 - Disorders of Cardiac Function

Coronary heart disease - chronic coronary syndromes (e.g. stable anginga)

Disease is present and symptoms are predictable

Coronary heart disease - acute coronary syndromes (ACS)

Represents a sudden, acute worsening of disease - unstable angina or myocardial infarction

Stable angina vs unstable angina (trigger)

Predictable and occurs with physical exertion or emotional stress vs unpredictable and occurs at rest or with minimal exertion

Stable angina vs unstable angina (symptom pattern)

Consistent over time and typical for patient vs accelerating symptoms and new onset symptoms present for less than two weeks

Stable angina vs unstable angina (duration)

Generally relieved by rest or nitroglycerin within 15-20 minutes vs symptoms often persistent and may not be relieved by rest or standard meds

Stable angina (cause)

Stable plaque with thick fibrous cap - fixed narrowing due to atherosclerosis, microvascular dysfunction or predictable vasospasms - non-atherosclerosis

Unable angina (cause)

Unstable atherosclerotic plaque - ruptured or eroded) or non-occlusive thrombus, acute vasospasm, coronary embolism or early stage SCAD - non-atherosclerosis

Stable angina vs unstable angina (cardiac troponin)

Normal with no cell necrosis vs no cell necrosis - differentiates from myocardial infarction

Stable angina vs unstable angina (ECG findings)

Usually normal at rest but transient changes may occur during pain vs ischaemic changes - ST depression or T wave inversion but no ST elevation

Clinical manifestations of stable angina - trigger

predictable, triggered by physical exertion or emotional stress

Clinical manifestations of stable angina - symptom pattern

Consistent, pain follows typical known pattern for patient

Clinical manifestations of stable angina - subjective symptoms

Pressure, tightness, squeezing, radiation to jaw neck or left arm

Clinical manifestations of stable angina - objective signs

Usually absent at rest

Clinical manifestations of stable angina - relief

Relieved within minutes by rest or GTN

Clinical manifestations of unstable angina - trigger

Unpredictable, occurs at rest or with minimal exertion

Clinical manifestations of unstable angina - symptom pattern

Accelerating, increasing in frequency, duration or intensity

Clinical manifestations of unstable angina - subjective symptoms

Severe crushing pain, intense nausea, sense of impending doom

Clinical manifestations of unstable angina - objective signs

Diaphoresis, tachycardia

Clinical manifestations of unstable angina - relief

Persistent, pain not fully relieved by rest or standard medications

Coronary heart disease aetiology

Inadequate supply of oxygenated blood to myocardium due to obstruction or dysfunction of coronary arteries, atherosclerotic or non-atherosclerotic

Atherosclerotic aetiology for CHD - process

Chronic inflammation and lipid accumulation within intimal layer of epicardial arteries

Atherosclerotic aetiology for CHD- acute event

Typically triggered by plaque rupture or erosion, exposes necrotic core to blood

Atherosclerotic aetiology for CHD - response

Formation of intraluminal thrombus, results in partial or complete occlusion of vessel

Non-atherosclerotic aetiologies for MI - functional disorders

Coronary vasospasm, coronary microvascular dysfunction

Non-atherosclerotic aetiologies for MI - anatomical and structural disruption

Spontaneous coronary artery dissection (SCAD), coronary embolisation, coronary artery abnormalities

Non-atherosclerotic aetiologies for MI - inflammatory, infectious and infiltrative aetiologies

Systemic vasculitis and coronary arteritis and infectious triggers

Coronary vasospasm

Transient reduction in coronary lumen that restricts blood flow enough to cause ischaemia and injury

Coronary microvascular dysfunction

Disease of small resistance vessels that fail to dilate to meet myocardial demand

Spontaneous coronary artery dissection (SCAD)

Separation of arterial wall that creates a false lumen, blocks blood flow

Coronary embolisation

Blood clots that travel through blood stream and lodge into coronary artery

Coronary artery abnormalites

Congenital issues where segment of a coronary artery is buried, leads to mechanical compression

Systemic vasculitis and coronary arteritis

Inflammation of vessel wall due to systemic vasculitis

Infectious triggers

Infections causes pro-thrombotic effects, inflammation-induced plaque vulnerability or direct vessel inflammation

Pathophysiology of myocardial ischaemia and MI

Metabolic state where myocardial oxygen demand exceeds oxygen supply, causes primary reduction in flow e.g. thrombus or excessive increase in demand e.g. extreme tachycardia

Consequences of ischaemia = metabolic shift

Heart switches from aerobic or anaerobic metabolism

Consequences of ischaemia - lactic acidosis

Accumulation of lactate and hydrogen ions

Consequences of ischaemia - mechanical dysfunction

Tissue contracts less effectively - drop in CO

Consequences of ischaemia - electrophysical changes

Altered ion gradients lead to ECG changes

Consequences of ischaemia if flow is restored

Damage is reversible with no permanent cell death

Consequences of MI

If ischaemia is prolonged usually for greater than 20-30 minutes it progresses into irreversible myocardial necrosis

Myocardial necrosis

Death of cardiac muscle cells due to prolonged ischaemia, necrosis within 20-30 minutes of total occlusion

What determines the damage of ischaemia / MI

Specific coronary artery determines location, duration or ischaemic time, collaterals, metabolic demand

Diagnosis of MI

Cardiac troponin cTn, high sensitivity hs-cTn, rise and/or fall requirement over serial blood tests, 99th percentile

Diagnostic triad for MI

Elevated troponin plus one of the following - clinical manifestations of ischaemia, ECG changes, imaging via echocardiogram or invasive angiography

Angina vs MI

Angina stable or unstable = ischaemia with no cell death (normal troponin), MI = prolonged ischaemia with irreversible necrosis (elevated troponin)

Clinical manifestations of MI

Chest pain or pain in other areas such as arm, shoulders, back, jaw or stomach, coughing or choking sensation when breathing, syncope, nausea or vomiting, sweating or a cold sweat, palpitations

Clinical manifestations for MI specifically in females

Pain in back, neck, jaw or both arms, shortness of breath or nausea, feeling very tired, pressure or tight feeling in chest

Clinical manifestations for MI specific in older age (>75 years)

Shortness of breath, fatigue, dizziness rather than chest pain

STEMI (ST elevation myocardial infarction)

Time-critical presentation type of ACOMI - acute coronary occlusion myocardial infarction

STEMI pathophysiology

Complete persistent occlusion of major coronary artery

STEMI injury

Results in transmural necrosis - cell during occuring through full thickness of heart muscle wall

STEMI ECG

New ST segment elevation at least 1mm in most leads

STEMI clinical priority

Emergency reperfusion via primary percutaneous coronary intervention or thormbolysis

Non-STEMI (non ST elevation myocardial infarction) pathophysiology

Partial or transient occlusion, blood flow severely restricted but still present

NSTEMI injury

Results in subendocardial necrosis - innermost layer of heart muscle

NSTEMI ECG

No ST elevation, may show ST depression, T wave inversion or normal

NSTEMI clinical priority

Stabilisation, prevent vessel from closing - antiplatelets and anticoagulants, followed by angiogram

Complications of MI

Embolism, cardiogenic shock, arrhythmias, congestive heart failure, pericarditis, cardiac tamponade

Cardiomyopathies aetiology

Diseases of myocardium associated with mechanical and or electrical dysfunction, leads to heart failure and progressive disability

Aetiology of dilated cardiomyopathies

Genetics viral, inflammatory toxins, alcohol factors

Clinical manifestations of dilated cardiomyopathies

Fatigue, light headedness, exertional dyspnoea - shortness of breath, pulmonary or venous congestion, peripheral oedema

Aetiology of hypertrophic cardiomyopathies

Genetically determined heart muscle disease, primary disease, characterised by left ventricular hypertrophy and disproportionate thickening of interventricular septum

Pathogenesis of hypertrophic cardiomyopathies

Diastolic failure - thick stiff muscle cannot relax to receive blood, low stroke volume due to small ventricular cavity, left ventricular outflow tract obstruction due to thickened septum and mitral valve

Clinical manifestations of hypertrophic cardiomyopathies (vary)

Dyspnoea - elevated diastolic lv pressure backing up into lungs, angina and syncope - reduced co and LVOT obstruction, arrhythmias - myocyte disarray

Percardium

Double layered fibro-elastic sac of visceral and parietal layers separated by pericardial cavity, contains 15-50 ml of ultrafiltrate of plasma in healthly individuals

Functions of percardium

Isolates heart from other thoracic structures, maintains position in thorax, prevents it from overfilling, contributes to coupling distensibility between two ventricles during diastole

Cardiac tamponade pathophys and clinical manifestations

Life threatening compression of heart - rapid fluid or blood build up, severe dyspnoea, hypotension and muffled heart sounds

Acute pericarditis aetiology

Infectious - viral, or traumatic / iatrogenic

Acute pericarditis pathophys

Acute inflammatory response of visceral and or parietal pericardium, trigger causes local vasodilation and increased capillary permeability, inflamed surfaces of pericardium rub against each other

Acute pericarditis clinical manifestations

Chest pain from pericardial friction rub, fever, dyspnoea, ECG changes

Pericardial effusion aetiology

Fluid accumulates in pericardial sac, can occur due to acute pericarditis, cardiac surgery or MI

Pericardial effusion pathophys

Rate of fluid production exceeds pericardium’s ability to reabsorb, stretch to accommodate large volumes if accumulates slowly, if accumulates rapidly = small amount can cause life threatening spike in pressure

Pericardial effusion clinical manifestations

Asymptomatic, dull constant ache in left side of chest, dysphagia, dyspnoea, hoarseness or hiccups, severe = cardiac tamponade signs and symptoms

Constrictive pericarditis aetiology

Associated with acute pericarditis, long standing inflammation due to mediastinal radiation, cardiac surgery or infection

Constrictive pericarditis pathophys

End stage of chronic inflammation where pericardium loses its elasticity, ventricles cannot expand to receive blood, pressure rises in atria and venous system

Constrictive pericarditis pathophys - rigid remodelling

Visceral and parietal layers fuse together

Constrictive pericarditis pathophys - diastolic limitation

Filling halted once heart hits rigid pericardium

Constrictive pericarditis clinical manifestations

Ascites, oedema, dyspnoea, fatigue, exercise intolerance, muscle wasting, weight loss, hypotension, arrhythmias