week 5 Flashcards
Mitral (bicuspid) valve location
Between left atrium and left ventricle
Mitral (bicuspid valve Leaflets/Cusps
2 leaflets
Mitral (bicuspid) function
Prevents backflow from LV to LA during systole
Tricuspid valve location
Between right atrium and right ventricle
Tricuspid Leaflets/Cusps
3 leaflets
Tricuspid valve function
Prevents backflow from RV to RA during systole
aortic Valve location
Between LV and aorta
aortic valve Leaflets/Cusps
3 semilunar cusps
aortic valve function
Prevents backflow from aorta to LV during diastole
Pulmonary valve location
Between RV and pulmonary artery
Pulmonary valve Leaflets/Cusps
3 semilunar cusps
how to remember what side the tricupspid vavle is on
tri to be right
Pulmonary valve function
Prevents backflow from pulmonary artery to RV during diastole
afterload is what
is the resistance the ventricle must overcome to eject blood during systole. It corresponds to the wall stress that the myocardial fibres experience during contraction
preload
refers to the initial stretch of myocardial fibres at the end of diastoleI
nfluenced by the volume of blood returning to the heart (venous return), left ventricular (LV) compliance and left atrial filling
Contractility
is the intrinsic ability of cardiac muscle fibres to generate force at a given preload
what is afterload influenced by
Aortic pressure
Ventricular chamber size
Wall thickness
Aetiology Aortic Regurgitation (AR) ACUTE
Infective endocarditis
Aortic dissection
Chest trauma
Congenital cusp rupture
Iatrogenic injury
Chronic Aortic Regurgitation is typically due to (aeitology)
Bicuspid aortic valve
Chronic aortic root dilation
Degenerative or calcific disease
Rheumatic heart disease (RHD)
Prosthetic valve failure
Epidemiology Aortic Regurgitation in Low- and Middle-Income Countries (LMICs)
RHD dominant cause of aortic valve disease
Commonly affects young people, often leading to early valve damage
sub-Saharan Africa, South Asia, Oceania and among Indigenous populations in high-income countries
Epidemiology Aortic Regurgitation High-Income Countries (HICs)
Degenerative calcific aortic stenosis (AS) is the most prevalent form.
Affects older populations (>80yo) often alongside comorbidities.
Driven by population ageing and atherosclerotic risk factors (e.g., hypertension, high cholesterol, smoking)
Pathogenesis Aortic Regurgitation (AR) ACUTE
. The non-compliant LV is unable to accommodate sudden regurgitant volume, causing elevated LV end-diastolic pressure, decreased cardiac output, and pulmonary edema.
Pathogenesis Aortic Regurgitation (AR) CHRONIC
The LV adapts through eccentric hypertrophy and dilation, preserving forward flow for years. Eventually, increased wall stress and subendocardial ischemia lead to systolic dysfunction and heart failure
Pathogenesis of Aortic Stenosis (AS)
AS imposes pressure overload on the LV due to a fixed obstruction at the valve. The LV undergoes concentric hypertrophy to maintain cardiac output despite increased afterload
acute aortic regurgitation clinical manifestation
sudden onsent of dyspnoea, orthopnea, hypotension.
Signs of cardiogenic shock: cool extremities, tachycardia, and poor perfusion
Low-pitched early diastolic murmur
Pulmonary oedema on auscultation and chest radiograph
chronic Aortic Regurgitation Clinical manifestations
Often asymptomatic for years
When symptoms appear: exertional dyspnoea, palpitations or angina
High-pitched diastolic murmur at left sternal border
Aortic Stenosis (AS) clinical manifestations
Dyspnoea on exertion: due to diastolic dysfunction and inability to increase output
Mitral valve prolapse (MVP) Aetiology
Degenerative MV disease
Genetic predisposition
Connective tissue disorders
Rheumatic heart disease
Infective endocarditis
Trauma
Mitral valve prolapse (MVP) Epidemiology
2–3% in the general population. MVP is more common in women, but men with MVP are more likely to develop complications such as severe MR, atrial fibrillation, and heart failure.
Mitral valve prolapse (MVP) Pathophysiology
Leaflet Degeneration
Elongated or Ruptured Chordae Tendineae
Elongated or Ruptured Chordae Tendineae
the chordae tendineae may stretch excessively, reducing tension needed to keep the valve shut or rupture, causing a flail leaflet.
Leaflet Degeneration
leaflets become thickened, redundant, and floppy due to accumulation of proteoglycans and disruption of the normal collagen-elastin structure
Mitral valve prolapse (MVP) Clinical Manifestations
Asymptomatic in majority
When symptomatic: Atypical chest pain, palpitations ± arrhythmias (e.g., PVCs, AF), fatigue, dyspnoea (with MR), autonomic symptoms (e.g., dizziness)
Mitral valve prolapse (MVP) complications
Complications: MR (most common), infective endocarditis, AF, cerebrovascular embolism (stroke), sudden cardiac death (rare).
Mitral Regurgitation (MR) Aetiology
Primary - due to structural abnormalities of the valve
Degenerative – most common in developed countries
Rheumatic heart disease – globally significant
Infective endocarditis
Trauma
Congenital
Drug-induced
Cardiac amyloidosis – valve thickening, MR
Mitral annular calcification – in elderly
Secondary (Functional) Mitral Regurgitation — due to ventricular or atrial remodeling (MR)Aetiology
Ischaemic heart disease – post-MI, papillary muscle dysfunction
Dilated cardiomyopathy – annular dilation and leaflet tethering
Right ventricular pacing
Atrial functional MR
Epidemiology of Mitral Regurgitation
most common specific type of heart valve disease in Australia.
Prevalence: 1–2% in people aged <60 years, 9–11% in people aged >70 years
MR is more common in men than women and is strongly associated with cardiovascular risk factors and ageing
Pathogenesis Primary MR
Valve leaflet/chordal degeneration → incomplete closure → retrograde flow into LA
Over time: LA and LV volume overload, compensatory dilation, eccentric hypertrophy
Chronic overload → LV dysfunction and elevated LA pressure
Pathogenesis Secondary MR:
Normal leaflets, but abnormal ventricular geometry causes:
Papillary muscle displacement
Annular dilation
Impaired coaptation (“tenting”)
MR severity may fluctuate with haemodynamic condition
Clinical Manifestations of MR
Can be asymtomatic hw symptomatic =
Exertional dyspnoea
Paroxysmal nocturnal dyspnoea, orthopnoea
Pulmonary oedema
Right-sided HF signs
Sudden worsening
Tricuspid regurgitation (TR)
TR disrupts the forward flow of blood from the right ventricle (RV) to the pulmonary circulation during systole, leading to a backward volume overload into the right atrium (RA) and systemic venous system.
Tricuspid regurgitation (TR) Aetiology primary
Congenital anomalies eg Ebstein anomaly
Fibrosis
Leaflet destruction from infective endocarditis
Device-related: leaflet damage from pacemaker or ICD lead
Prolapse or flail
Chordal rupture
Papillary muscle infarction or fibrosis
Valve Perforation or Impingement: pacemaker/ICD leads may perforate or entangle leaflets or chordae
Direct trauma
Tricuspid regurgitation (TR) Aetiology secondary
1.Ventricular STR due to RV dilation, due to:
Left-sided heart disease (e.g., MR, AS)
Pulmonary hypertension
RV infarction or cardiomyopathy
2.Atrial STR due to atrial fibrillation and right atrial enlargement
3.Cardiac implantable electronic device related STR: Due to lead impingement or induced dyssynchrony
Right Heart Remodelling
Chronic volume overload leads to RA dilation, RV dilation, and eventually RV systolic dysfunction
This further impairs leaflet coaptation and worsens TR
Often accompanied by pulmonary hypertension, worsening RV afterload.
Epidemiology of TR
Mild TR is seen in ~75–80% of adults on echocardiography
Moderate to severe TR affects ~4–5% of Australians over 75
particularly among women
Pathogenesis of TR
TR results in systolic backflow of blood into the right atrium, leading to:
Right atrial pressure overload
Chronic venous congestion
Progressive right ventricular (RV) dilation and dysfunction
chronically can lead to
RV systolic dysfunction
Decreased forward output
Symptoms of right-sided heart failure
TR clinical manifestations
Fatigue, exertional dyspnoea (due to low cardiac output)
Peripheral oedema, ascites, weight gain
Abdominal discomfort, hepatomegaly
Neck pulsations (from jugular venous distension)
Chest x-ray: Pleural effusions, cardiomegaly (RA and RV enlargement)
Dilated azygos vein or pulmonary arteries
Pulmonary stenosis (PS)
refers to an obstruction of blood flow from the right ventricle (RV) to the pulmonary artery. Pulmonary regurgitation (PR) is incompetency of the pulmonary valve, which results in leakage of blood from the pulmonary artery back into the right ventricle.
Pulmonary stenosis (PS) Aetiology congenital causes (most common)
Congenital Causes
Isolated Valvular PS: Accounts for 7% to 12% of congenital heart disease (CHD).
Associated with Other CHDs: Tetralogy of Fallot, tricuspid atresia, transposition of the great arteries (TGA), double outlet right ventricle (DORV).
Genetic Syndromes
Pulmonary stenosis (PS) aquired causes aeitology
Rheumatic heart disease
Carcinoid heart disease
Cardiothoracic tumors (e.g., teratoma, thymoma)
Postsurgical or post-catheterisation complications
Pathophysiology of pulmonary stenosis
- Obstruction to Outflow:
The narrowed valve or tract increases resistance to blood ejection
Increased RV Pressure:
The RV must generate higher pressure to overcome the outflow obstruction
This leads to right ventricular hypertrophy (RVH) over time
Impaired RV Compliance:
Chronic pressure overload causes the RV to stiffen, reducing its ability to fill properly during diastole
Post-stenotic Dilatation:
Turbulent blood flow may cause dilatation of the pulmonary artery distal to the stenosis
Clinical Manifestations of pulmonary stenosis
Mild PS: Typically asymptomatic; heart sounds - normal S1, ejection click
Moderate PS: Dyspnoea on exertion, fatigue, ejection click close to S1, systolic murmur
Severe/Critical PS: Cyanosis (especially in neonates), chest pain, syncope, sudden death (rare
Pulmonary Regurgitation Aetiology
Pulmonary hypertension
Post-surgical repair of congenital heart defects
Iatrogenic: Post-valvotomy/valvectomy or balloon valvuloplasty
Carcinoid heart disease
Rheumatic heart disease
Endocarditis
Drug-induced
Pulmonary Regurgitation Pathophysiology
Retrograde Flow:
instead of blood staying in the pulmonary artery, some flows backward into the RV
RV Dilation and Hypertrophy:
The RV adapts to the increased volume by dilating, and over time, hypertrophy may develop to maintain cardiac output
Progressive RV Dysfunction
Tricuspid Regurgitation:
RV dilatation stretches the tricuspid annulus resulting in functional tricuspid regurgitation
Arrhythmias and Heart Failure
Pulmonary Hypertension-Associated PR
Clinical manifestations of pulmonary regurgitation
Early/Moderate PR:
Often asymptomatic
Mild exertional dyspnoea or reduced exercise tolerance
Severe PR:
Symptoms of RV failure: peripheral oedema, hepatic congestion, ascites
Palpitations, lightheadedness due to arrhythmias
Stage A: At Risk for Heart Failure
At risk for HF but without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury
Stage B: Pre-Heart Failure
Stage B: Pre-HF
No symptoms or signs of HF and evidence of 1 of the following:
Structural heart disease
Evidence for increased filling pressures
Evidence for increased filling pressures eg, from echocardiography Patients with risk factors + increased levels of BNPs or persistently elevated cardiac troponin
Stage C: Symptomatic Heart Failure
Structural heart disease with current or previous symptoms of HF.
Stage D: Advanced Heart Failure
Marked HF symptoms that interfere with daily life and with recurrent hospitalisations despite attempts to optimize medical therapy
heart failure aeitology
HF is caused by a number of conditions including LV dysfunction, RV dysfunction, valvular heart disease, pericardial disease or obstructive lesions in the heart or great vessels
heart functions
moves deO2 blood from venous system into pulmonary circulation
moves O2 blood from pulmonary circ into arterial system
right and left heart maintain equal output to function properly
Epidemiology of heart failure
64 million people with HF worldwide
144,000 Australians aged 18+ have HF
Pathophysiology heart failure
sob, tired, swollen ankles, loss of appetite, coughing, dizziness, abnormal bloating,sleep disturbances
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) is
A clinical syndrome where the heart, particularly the left ventricle (LV), cannot contract effectively. This leads to insufficient blood ejection during systole and an ejection fraction
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Haemodynamic Changes
Contractility ↓
Stroke Volume ↓
Preload ↑
Afterload ↑
LV end-diastolic pressure ↑
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Pressure-Volume Relationship:
the pressure-volume loop shifts rightward (LV is dilated), becomes flatter (contractility is impaired), shows an elevated end-diastolic volume and pressure but lower stroke volume. This reflects both systolic dysfunction and later diastolic impairment as the heart becomes stiffer.
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Sympathetic Nervous System (SNS)
It is activated due to low perfusion (due to ↓ cardiac output) triggers baroreceptors to stimulate SNS → ↑ norepinephrine (NE).
Initial effect: ↑ heart rate and contractility help maintain output
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Renin-Angiotensin-Aldosterone System (RAAS)
It is activated due to ↓ renal perfusion → renin release → angiotensin II → aldosterone.
Effects:
Sodium and water retention
Vasoconstriction → ↑ afterload → harder for the LV to eject blood
Remodeling effects
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Antidiuretic Hormone (ADH / Vasopressin)
It is activated due to low BP and CO stimulate release from the posterior pituitary.
Effect: Increases free water reabsorption
Contributes to hyponatraemia and volume overload
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) Natriuretic Peptides (BNP, ANP
Ventricular stretch → myocytes release BNP and ANP.
Effect:
Promote natriuresis, vasodilation, and RAAS inhibition
Counteract RAAS and SNS effects
Left Ventricular Failure with Reduced Ejection Fraction (HFrEF) ventricular Remodelling
structural:
Sarcomeres added in series → LV dilation.
Walls may thin over time → reduced efficiency
cellular:
Myocyte apoptosis
Hypertrophy of surviving cells
nterstitial fibrosis from aldosterone and angiotensin II → stiffens the heart
Functional Impact
LV shape changes from elliptical (normal) to spherical (dilated) → less effective contraction
Systolic reserve ↓ and heart becomes less responsive to stress or exertion
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) Pathophysiology
HFpEF occurs when the heart fails to meet the body’s demands despite a normal ejection fraction main problem lies in diastolic dysfunction—the heart becomes stiff and does not relax or fill properly
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) . Diastolic Dysfunction due to
Relaxation is slowed
A stiff ventricle: The LV resists filling
Atrial dependence dependent on the atrial kick (late diastolic filling) to maintain preload
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) Haemodynamic Abnormalities
↑ LV diastolic pressure at rest and especially during exercise
↑ Left atrial and pulmonary venous pressures, leading to dyspnoea and pulmonary oedema
Reduced LV distensibility shifts the pressure-volume curve upward and to the left - this reflects increased stiffness
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) Structural Remodelling
Concentric hypertrophy: Chronic pressure overload (e.g., hypertension) causes sarcomeres to be added in parallel, thickening the wall without increasing chamber size
↑ Wall thickness / cavity ratio
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) . Exercise Response Abnormalities
In HFpEF, this recoil is blunted, and LV relaxation cannot accelerate → so LA pressure must rise to maintain output → leading to pulmonary congestion
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) Systolic Dysfunction in HFpEF
Less recoil = worse filling → The LV’s “suction” effect during early diastole is reduced → further compromises preload and exacerbates dyspnoea.
Left Ventricular Failure with Preserved Ejection Fraction (HFpEF) Right Heart & Pulmonary Circulation
Chronically elevated LA pressure is transmitted backward to pulmonary veins and arteries → causes post-capillary PH. Over time, pulmonary vasculature stiffens (pre-capillary PH).
RV dysfunction: The RV is thin-walled and sensitive to afterload. Chronic PH leads to RV hypertrophy, dilation, and failure—especially with AF or severe PH.
Cardiomyopathies
a group of myocardial disorders in which the heart muscle is structurally and/or functionally abnormal, in the absence of any other cardiovasular pathologies
Dilated Cardiomyopathies Pathophysiology
Characterised by ventricular chamber enlargement and impaired systolic function due to a primary insult In response, the heart dilates to maintain stroke volume
Cardiomyopathies Ventricular dilation
stretches the myocardium beyond optimal sarcomere length, reducing contractile efficiency → low LVEF
Hypertrophic Cardiomyopathy (HCM)
Characterised by LV wall thickening
Caused by genetic mutations in sarcomeric proteins
These mutations cause hypercontractility and inefficient energy use in cardiac myocytes
Restrictive Cardiomyopathy (RCM)
Defined by rigid, noncompliant ventricles with normal or near-normal systolic function
The ventricular myocardium becomes stiff and non-compliant due to infiltrative diseases
Dilated Cardiomyopathy (DCM) signs symptoms and complications
symptoms- Dyspnea, fatigue, orthopnea, PND, peripheral edema
signs- S3 gallop, displaced apex beat, mitral/tricuspid regurgitation
complication- Heart failure, arrhythmias, thromboembolism, sudden death
Hypertrophic Cardiomyopathy (HCM) signs, symptoms and complications
symptoms- Dyspnoea, chest pain, syncope, exertional symptoms, palpitations
signs- Systolic murmur, bisferiens pulse, forceful apex beat
complications- Sudden cardiac death (especially in young), AF, HF
Restrictive Cardiomyopathy (RCM) signs, symptoms, complications
symptoms- Dyspnoea, fatigue, oedema, exercise intolerance
signs- Elevated JVP, Kussmaul’s sign, S4, hepatomegaly
complication- Atrial arrhythmias, pulmonary hypertension, right HF
Shock definition
a state of cellular and tissue hypoxia resulting from Inadequate oxygen delivery, Increased oxygen demand or Impaired oxygen utilisation at the cellular level
Cardiogenic shock primary mechanisms and common causes
mechanisms: Impaired cardiac output
common causes= Acute MI, arrhythmias, myocarditis, severe valve disease
Hypovolemic shock primary mechanisms and common causes
mechanisms- Decreased preload
common causes- Haemorrhage, dehydration, burns
Obstructive shock primary mechanisms and common causes
mechanisms- Extracardiac obstruction to cardiac filling or output
common causes- Pulmonary embolism, cardiac tamponade, tension pneumothorax
Distributive shock primary mechanisms and common causes
mechanism- Severe peripheral vasodilation, low Systemic Vascular Resistance
common causes= Sepsis, anaphylaxis, neurogenic shock, adrenal crisis
Pathophysiology of Circulatory Shock
pathophysiological mechanism in all forms of shock is tissue hypoxia which leads to cellular hypoxia
Cellular hypoxia leads to:
Cellular Energy Failure → lactic acidosis
Cellular and Membrane Dysfunction: Dysfunction of ion pumps → cellular oedema
Systemic Inflammatory Response and Endothelial Dysfunction
Compensatory Mechanisms: Activation of sympathetic nervous system and RAAS → tachycardia, vasoconstriction, fluid retention
distributive shock
characterized by peripheral vasodilation
Clinical Manifestations of Shock
- Anxiety, restlessness, altered mental state
- Hypotension
- A rapid, weak, thready pulse
- Cool, clammy skin and mottled skin
- Rapid and shallow respirations
- Hypothermia
- Thirst and dry mouth
- Fatigue due to inadequate oxygenation
- Distracted look in the eyes or staring into space, often with pupils dilated
hypovolemic shock
due to reduced intravascular volume (ie reduced preload) which in turn reduces CO
obstructive shock
mostly due to extracardic causes of cardiac pump failure:assosiated with poor right ventricluar output
2 catogries= mechanical and plumonary vascular
cardiogenic shock
due to intracardiac causes of cardiac pump failure that results in reduced cardiac output
Septic shock/sepsis caused by
Infections
Systemic inflammatory response syndrome (SIRS)
response syndrome (SIRS): vigorous inflammatory response
caused by either infectious or noninfectious causes
Anaphylactic shock
severe hypersensitivity reaction mediated by immunoglobulin E
Neurogenic shock
interruption of autonomic pathways = decreased vascular resistance and
altered vagal tone in the setting of trauma to the spinal cord or the brain
Endocrine shock
aetiologies such as adrenal failure (Addisonian crisis) and myxedema
Haemorrhagic Hypovolemic shock:
Reduced intravascular volume from blood loss
* multiple causes of hemorrhagic shock
* blunt or penetrating trauma; upper or lower gastrointestinal bleeding
* intra/postop bleeding, ruptured aneurysm, tumors or abscess erosion into major
vessels
Nonhaemorrhagic Hypovolemic shock
Reduced intravascular volume from fluid loss other than blood
* Volume depletion from loss of sodium and water
* Gastrointestinal, skin losses, renal and third space losses into the extravascular space
or body cavities
Pulmonary vascular Obstructive shock
due to right ventricular failure from hemodynamically significant
pulmonary embolism (PE) or severe pulmonary hypertension
Mechanical Obstructive shock
Mechanical: decreased preload, rather than pump failure (eg, reduced venous return to
the right atrium or inadequate right ventricle filling)
Arrhythmic Cardiogenic shock
CO is severely compromised by significant rhythm disturbances
Cardiomyopathic Cardiogenic shock
MI involving > 40% left ventricular myocardium, MI of any size if
accompanied by severe extensive ischemia, severe right ventricular infarction, ect
Mechanical Cardiogenic shock
severe aortic or mitral valve insufficiency, and acute valvular defects due to
rupture of a papillary muscle or chordae tendineae
Treatment of shock
- Airway + breathing
- Treat underlying cause of shock
- Specific therapies refined
- Response to therapy monitored
Embryological lung development
during embryonic period
pseudoglandular period
cannicular phase
Saccular period
Alveolarisation period
Embyronic period (0-7 weeks) in re to lungs
- First stage of lung development
- Major organs beginning to form
- A lung bud develops from a tube of cells called the foregut (which will itself later go on to form the gut)
- This bud separates into two
- Two buds become a baby’s right and left lungs
- Pulmonary vasculature
Pseudoglandular period (5-17 weeks)
- Airway multiplication – bronchial branching and formation completed
- 3 buds right side – upper, middle and lower lobes of right lung
- 2 buds on left side - upper and lower lobes of left lung
- By 16 weeks lungs - bronchi and terminal
bronchioles ↑ in length and size - Formation of muscle fibres, elastic, early cartilage within the bronchi, and mucous glands
- Vascular system and diaphragm start to develop
Cannalicular period (13-27 weeks)
- Development of and vascularisation of
respiratory portion of the lung
-Differentiation of type I pneumocyte,
primary structural cell of alveolus
-Gas exchange occur across thin,
membrane-like cells
-Capillaries grow in close proximity to
distal surface of alveolar cells
-By 13 weeks cilia appear in trachea and
main bronchi
-Alveolar buds and sacculi form - Surfactant and lecithin production may
begin - May be able to survive in NICU towards the
end of this stage
Saccular period (24-40 weeks)
The primary phase of cilia, surfactant and alveoli development
* Terminal sacs appear as outpouchings of terminal bronchioles
* Over the next few weeks these multiply forming
* Pores of Kohn connect adjacent alveoli
* Recognizable differentiation of Type I and Type II cells
* Type 1 cells (95%): the surface epithelium thins as vascular proliferation increases.
* Type II (5%) – surfactant production
* Further development of pulmonary arterial system
what is surfactant
Surfactant decreases surface tension within alveoli and prevents collapse of alveoli during exhalation
Absence of surfactant, the alveolus would be unstable and collapse at the end of each breath
Development of the heart
Day 22: heart tube formed
Day 24: heart tube folds and loops
Day 28: heart tube folding completed →
primitive common ventricle and common
atrium.
Day 28-37: Atrial septum forms with interatrial
shunt (foramen ovale) right to left (to bypass
the lungs)
Day 28-37: Intramembranous ventricular
septum forms creating left and right ventricles
Day 35-42: Truncus arteriosis and conus
cordis develop a spiraling septum →
pulmonary trunk and aorta
Foetal heart anatomy course of blood
Oxygenated blood from placenta enters
inferior vena cava via umbilical vein
Most blood is shunted from right atrium to left atrium via foramen ovale then passes through left ventrical into the aorta
* Blood which flows from the right atrium into the right ventrical and into the pulmonary arteries is redirected into the aorta via the ductus arterious
* These shunts bypass the pulmonary
circulation and close soon after birth
* Deoxygenated blood is sent to the placenta
via umbilical arteries
Congenital heart defects- Patent Foramen Ovale (PFO)
- Shunt (connection) between left and right atria
- Naturally occurs in about 25% of the
population – usually asymptomatic
Congenital heart defects- Patent Ductus Arteriosus (PDA)
- Shunt (connection) between pulmonary artery and aorta remains open after birth
- Increases pulmonary arterial volume and can damage vessels over time
- Small PDA may close on its own over months
- Large PDA can be closed via catheter or
surgery
Congenital heart defects- Coarctation of the aorta
- Narrowing of the aorta after the arch, where the ductus arteriosis closes
- Causes increased blood pressure to left side of the heart, arms and head
- Left ventricular hypertrophy can develop if left untreated
- Repaired via surgery or catheter
Congenital heart defects- Ventricular Septal Defect (VSD)
- Common cardiac defect with one or more
defects (holes/openings) in the intraventricular septum - Shunts from left ventricle into right ventricle and into the pulmonary system
- Can lead to increased pulmonary artery
pressure - Symptoms: ‘failure to thrive’, increased RR
- Small VSD may close on their own
- Large VSD may need a ‘staged’ repair
Congenital heart defects- Tetrology of Fallot (TOF)
- Severe cyanotic congenital cardiac condition combining four (4) defects
- Pulmonary valve stenosis
- Ventricular septal defect (VSD)
- Right ventricular hypertrophy
- “Overriding Aorta”: An inferior and
centrally located Aorta that emerges from
both ventricles (above the VSD) - Usually corrected over 2 procedures – a
temporary repair soon after birth, and a
complete repair around 6 months of age - Does not return cardiac function to ‘normal’
Airway diameter and length effect on airways
A small change in airway diameter will
increase resistance significantly; this will
lead to airway collapse and marked increase
in work of breathing
compare adult and infant Airway diameter and length
- Smaller in diameter (infant 1/3 diameter of
adult trachea) - Nasal passages 30-50% of total airway
resistance (infants) - Infants - high resistance to flow
- Increase in airway diameter as children grow
- Trachea and main bronchi increase over 1st few years, then terminal bronchioles increase after 5 years
Comparative heart size between adult and infant
- Adult 1/3 of rib cage
- Infant 1/2 of rib cage
- Less space for lungs
Chest Wall Thorax in infants compared to adults
- Cross-sectional shape in infant is
cylindrical - Cross-sectional shape in adolescent
and adult is elliptical
Chest wall - Ribs of newborn infant: soft; more
cartilaginous; horizontal - Older children and adults’ chest wall
is more rigid
Bucket handle movement not possible
in infants and children < 3 years old
Respiratory muscles: Diaphragm in adults compared to infants
- Horizontal angle of insertion in infants compared to older children and adults
- Combined with compliant ribs results in
- Less efficient ventilation
- Distortion of chest wall shape on inspiration
- Pattern is piston, not bucket handle.
- Infant diaphragm has lower relative muscle mass & lower content of high-endurance muscle fibres
- Susceptibility to respiratory compromise e.g. feeds; abdominal distension
Respiratory muscles: Intercostals in infants compared to adults
Infants: weak, poorly developed intercostal muscles
* Contraction of intercostal muscles is inefficient at improving thoracic volumes
* Increased ventilatory requirements by increasing respiratory rate rather than depth
Chest wall compliance decreases rapidly for first 2 years of life - becomes approximately equal to lung compliance as in the adult
* Intercostal muscles develop
* Bucket and pump handle movement of chest wall achieved by 2 yo
breathing w infants
Infants are preferential nasal breathers
Prone to obstruction:
* Airway due to shape and orientation of head and neck
* Small nasal passages
Issues with feeding:
* Nutritive suck-swallow-breathe control
* Minute ventilation decreased, exhalation is
prolonged, and inhalation is shortened during feeding
Upper airway structures in infants
- Infants’ trachea is short, narrow, more compliant than older children and adults
- Due to presence of immature/thinner cartilages
- Airways prone to collapse with neck
hyperflexion, hyperextension or rotation - Higher resistance to airflow due to small
diameters
bronchial walls and mucociliary transport mechanism in infants
- Less smooth muscle
- More compliant
Mucous glands - High proportion and larger number
compared to adult airway.
Poorly developed cilia at birth - Not clear what age ciliated epithelium is
active and functional - Risk of secretion retention
Alveoli - Neonates and children
Decreased SA for gas exchange
* Full term infant has no alveoli but 150 million saccules (terminal respiratory unit)
* Alveoli develop @ 2 months old
* Full compliment (3-400 million) by 8 years
old
Collateral ventilation in infants and children
- Poorly developed until 2yo – fully developed at 8yo
- Pores of Kohn: intra-alveolar (1-2 years)
- Canals of Lambert: bronchiole-alveolar (6 years)
- Channels of Martin: interbronchiolar
- Late development
- high incidence of lower obstructive airways disease in young children
- atelectasis
- VQ mismatch
Respiratory compliance
Measure of pressure required to increase volume of air in lungs and reflects combinations of lung and chest wall compliance
* Child-adult: Lung compliance is comparable BUT infant lung compliance is decreased due to amount of cartilage in
airways
* Chest wall compliance is high (as cartilaginous –calcifies with age)
* Intercostals unable to stabilise rib cage during diaphragm contraction
* Respiratory compromise → ↑ respiratory rate, rather than depth of diaphragmatic excursion
- Diaphragm is primarily type 1 (ST) muscle fibres in pre-term, newborn, adults, 8months, 3 monsths
- adults 55%
- 8/12 50%
- 3/12 30%
- newborn 25%
- preterm 10%
- Respiratory rate much higher in infants pre-term, newborn, adults, 8months, 3 monsths
- preterm infant 50-70 bpm
- infant 40 bpm
- children 18-30 bpm
- adult 12-15 bpm
Lung volumes adaption
infants will get closing capacity in normal breathing. can cause gas trapping in alveloi
Ventilation and perfusion
- Pattern of ventilation is not uniform
- Some children better ventilate the nondependent lung others may not
- Variability may also be due to differences in
development - Size of chest wall; or changes in respiratory
muscle strength and function and chest wall
compliance aged 2 yo
Metabolic rate in children in re to o2 consumption
Infants and children have higher metabolic
rate and higher oxygen consumption than
adults
* Growth and to maintain body temperature e.g. newborn 2x O2 consumption
compared to adult
Haemoglobin
- Higher mean haemoglobin (Hb) in foetal
blood - 70% of the haemoglobin is Foetal
haemoglobin (HbF) and a higher affinity for
O2 - Metabolic acidosis and a high CO2 resulting
from a high metabolic rate help to improve
oxygen delivery to the tissues by shifting
the curve to the right. - HbF replaced by adult haemoglobin (HbA)
by 6 to 12 months of age
Nitrates actions, side effects and egs
Action: Potent vasodilators used in angina and coronary artery disease (CAD). They decrease myocardial oxygen demand and increase coronary blood flow
Side Effects: Headaches, light-headedness
Examples: Glyceryl trinitrate (GTN)
Cholesterol-Lowering Medications actions, side effects and egs
Action: Block enzyme activity leading to greater clearance of LDL cholesterol
Side Effects: Nausea, constipation, diarrhea, myopathy
Examples: HMG CoA reductase inhibitors
Antiplatelet Agents actions, side effects and egs
Action: Prevent blood clots and reduce the risk of cardiac events
Side Effects: Bleeding propensity, peptic ulcer
Examples: Glycoprotein IIb/IIIa inhibitors
Beta-Blockers actions, side effects and egs
Action: Reduce blood pressure by blocking epinephrine effects, leading to slower heart rates and decreased myocardial oxygen demand
Side Effects: Bradycardia, fatigue, bronchospasm
Examples: Atenolol,
