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Paediatrics > Cardiovascular Learning Objectives > Flashcards

Cardiovascular Learning Objectives Flashcards

1
Q

Pulmonary Stenosis Pathophysiology

A

Narrowing of the circulature/valve/heart responsible for blood flow to the lungs.

Can be due to isolated valvular (90%), subvalvular or peripheral pbstruction.

Valvular - 2/3 have dysplastic pulmonary valve where valves are irregularly shaped with thickened leafelets, do not clsoe/seal well if at all and decrease mobility

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2
Q

Pulmonary Stenosis Epidemiology and Aetiology

A

Most common congenital heart disordr - 10% of cases

Slightly more common in females

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3
Q

Pulmonary Stenosis Clinical Signs

A

Most Asymptomatic

Exertional dyspnoea and fatigue

In rare cases -exertional angina, syncope or sudden death. Cyanosis present with significant right to left shunt via patent foramen ovale, ASD or VSD

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4
Q

Pulmonary Stenosis Management

A

Prehospital: Oxygen, Supportive cares, IV access.

Hospital: Surgery. Balloon Valve.

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5
Q

Aortic Stenosis Pathophysiology,

A

Narrowing of aortic valve.

Results in compensatory ventricular hypertrophy over time proportional to the obstruction.

Severe cases may lead to hypertrophy, valvular obstruction, MI, exercise induced syncope and death.

Severe obstruction in utero mmay cause variable heart hypoplasia, endomyocardial fibroelastosis, reduced ventricular function and significant mitral valve insufficiency

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6
Q

Aortic Stenosis Epidemiology and Aetiology

A

Approx 8 per 1,000 live births

3-5% of congenital heart defects

Male:female = 4:1

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7
Q

Aortic Stenosic Clinical signs

A

Symptoms of congestive heart failure - present when patient unable to adequately increase CO and or pulmonary or systemic fluid overload

  • Infants: tachypnoea, diaphoresis during feedings, easily fatigued, irritable, decreased volume of feeds, poor weight gain
  • Younger children: similar to common illness, GI symptoms (abdo pain, nausea, vomiting and poor appetite), failure to thrive, easily fatigued and recurrent or chronic cough with wheeze
  • Older children: exercise intolerance, anorexia, abdominal pain, dyspnoea, wheeze, oedema, palpitations, chest pain or syncope
  • Everyone: tachycardia, poor perfusion, pulmonary congestion, systemic congestion, high blood pressure, systolic murmur
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8
Q

Aortic Stenosis Management

A

Prehospital: Oxygen, IV access, supportive cares

Hospital: Surgery, balloon valve. Surgery to swap aortic and pulmonary valve and insert new valve as pulmonary valve.

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9
Q

Atrial Septal Defect Pathophysiology

A

Shunt between atria. Magnitude of shunt depends on defect size, relative compliance of ventricles and relative resistance in pulmonary and systemic circulation.

  • Small - L) atrial pressure may exceed R) by some mmHg. With large atrial pressures are nearly identical.
  • Shunting occurs in late ventricular systole and early diastole.
  • Increased pulmonary bloodflow and diastolic overload of R) ventricle
  • Altered ventrcular compliance may increase left to right shunting, exacerbating symptoms
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10
Q

Aortic Septal Defect Epidemiology and Aetiology

A

3 main types (ostium secundum, ostium primmum and sinus venousus) account for 10% of congenital heart diseases and 20-40% of congenital heart diseases presenting in adulthood

Female to male 2:1

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11
Q

Aortic Septal Defect Clinical signs

A

*May not present until adolescence or adulthood

  • Heart murmur
  • cyanosis
  • dyspnoea
  • easily fatigued
  • syncope

stroke and/or heart failure

  • sustained atrial arrhythmia
  • palpitations
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12
Q

Atrial Septal Defect Management

A

Prehospital: Supportive, Oxygen

Hospital: surgery to close valve

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13
Q

Coarctation of the Aorta Pathophysiology

A

Narrowing of the aorta

  • increases afterload on Left ventricle -> increased wall stress and compensatory ventricular hypertrophy
  • Occurs after ductus arteriosus occurs. increases left ventricular pressure which elevates left atrial pressure which can open the foramen ovale leading to left to right shunting and dilation of right atrium and right ventricle
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14
Q

Coarctation of the Aorta Epidemiology and Aetiology

A

Common. 6-8% of congenital heart disease. Found most frequently in infants < 1 year

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15
Q

Coarctation of the Arota Clinical Signs

A

Poor feeding, tachypnoea, lethargy and progress to CHF and shock

Deterioratin coincides with closing of patent ductus arteriosus

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16
Q

Coarctation of the Aorta Management

A

Prehospital: Oxygen, IV access, supportive cares

Hospital: Surgery

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17
Q

Tetralogy of Fallot Pathophysiology

A

Combination of 4 defects

  1. Large Ventricular septal defect
  2. Pulmonary Stenosis - harder for blood to enter pulmonary circulation
  3. Right ventricular hypertrophy - harder for blood to enter pulmonary circulation
  4. Overriding aorta - located between left and right ventricles, directly over VSD. Blood flows into aorta instead of pulmonary artery
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18
Q

Tetralogy of Fallot Epidemiology and Aetiology

A

One of most common congenital disorder - 10%

Most common cause of cyanotic CHD

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19
Q

Tetralogy of Fallot Clinical Signs

A

Depend on severity of anatomical defects

  • Cyanosis if insufficient pulmonary bloodflow
  • Oxygen desaturation
  • Smaller than expected
  • Finger and toe clubbing
  • Systolic thrill
  • Haemoptysis
  • Retinal engorgement
  • Scoliosis
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20
Q

Tetralogy of Fallot Management

A

Prehospital: IV/IO access, Oxygen. Position knee to chest to increase systemic vascular resistance

Hospital: Palliative shunts and intracardiac repair

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21
Q

Hypoplastic Left Heart Syndrome

A

Small left ventricle and aorta. Blood flow to body suplied by ductus arteriosus. Mitral valve closed or atretic.

  • Oxygenated pulmonary venous blood returns to left atrium cannot pass through mitral valve then crosses atrial septum.
  • Bloodflow to systemic circulation is mixed
  • Systemic circulation decreased after birth when pulmonary resistance decreased
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22
Q

Hypoplastic left heart syndrome Epidemiology and Aetiology

A

1.2-1.5 congenital heart defects

55-70% male predominance

75% survivial rate

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23
Q

Hypoplastic Left Heart Syndrome Clinical signs

A

Presentation depends on the patency of the ductus arteriosus, level of pulmonary vascular resistance and size of interarterial communication

  • Cyanosis and after ductus arteriosus closes (24-48 hours) symptoms worsen and include tachypnoea, respiratory distress, pallor, lethargy, metabolic acidosis and oliguria
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24
Q

Hypoplastic Left heart Syndrome Management

A

Prehospital: Oxygen, IV access, supportive cares

Hospital: Surgery to repair defects

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25
Q

Patent Ductus Arteriosus Pathophysiology

A

Ductus arteriosus doesn’t close (Normally functional closing occurs after 15 hours)

Leads to mixing of systemic and pulmonary blood and pulmonary congestion as higher systemic pressure pushed blood into pulmonary circulation

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26
Q

Patent Ductus Arteriosus Clinical SIgns

A

Can present at any time

  • Decreased exercise tolerance
  • Pulmonary congestion with murmur
  • 3-6 week old: tachypnoea, diaphoresis, inability or difficulty with feeding, lack of weight gain or weight loss
  • Hoarse cry, cough, lower RTI, atelectasis (partial collapse or incomplete inflation of lung) or pneumonia
27
Q

Patent Ductus Arteriosus Epidemiology and Aetiology

A

Chromosomal abnormalities, premature birth

Female to male - 2:1

28
Q

Patent ductus arteriosus Management

A

Prehospital: Oxygen and supportive cares

Hospital:

29
Q

Total Anomalous Pulmonary Venous Drainage Pathophysiology

A

Pulmnary veins connect to vena cava

  • Mixture of pulmonary and systemic venous return leads to right atrial and right ventricular volume loading
  • If foramen ovale obstructed - pressure increases in right atria leading to pulmonary and systemic venous congestion
30
Q

Total Anomalous Pulmonary Venous Return Epidemiology and Aetiology

A

Female:male - 23:18

6.8 per 100,000 live births

31
Q

Total anomalous pulmonary venous return Clinical Signs

A

Depends on if there is Pulmonary Venous obstruction or not.

WITHOUT pulmonary venous obstruction - signs of cardic failure. Will usually present within 24-36 hours. Decreased blood flow and increaseing cyanosis, respiratory distress, abnormal heart sounds.

WITH pulmonary venous obstruction - similar to ASD, cyanosis is infrequent and Right ventricular volume loading

32
Q

Total Anomalous Venous Return Management

A

Prehospital: Oxygen, supportive cares, IV/IO

Hospital:

33
Q

Transposition of Great Arteries Pathophysiology

A

Oxygenated pulmonary blood is returned to the L) atria where it is recirculated to pulmonary system via abnormal pulmonary arterial connection.

  • Systemic venous blood returns to the R) atria then pumped back into the body from right ventricle
  • Oxygenated and deoxygenated blood will commonly mix at: ASD, VSD and patent ductus arteriosus
34
Q

Transposition of Great Arteries Epidemiology and Aetiology

A

Most common aetiology for cyanotic congenital heart disease in newboens

5-7% of congenital heart disease

60-70% male predominance

35
Q

Transposition of Great Arteries Clinical Management

A
  • Cyanosis, apparent within hours of birth
  • Presentation depends on extent of intracirculatory mixing
  • Intact ventricular septum - prominent and progressive cyanosis within 24 hours
  • Large VSD - may not initially manifest symptoms of heart disease, mild cyanosis. Signs of congestive heart failure present in 3-6 weeks
  • VSD and left ventricular outflow obstruction -> extreme cyanosis at birth, proportional to degree of obstruction
36
Q

Transposition of Great Arteries Management

A

Prehospital: Oxygen, transport, IV access, supportive cares

Hospital: IV prostaglandin E1, Cardiac catheter, surgery to transpose arteries

37
Q

Tricuspid Atresia Pathophysiology

A

Tricuspid valve abnormally closed.

Forces blood from both vena cavae through foramen ovale into left atrium

Blood doesn’t circulate through pulmonary system/isn’t oxygenated. Decreased Partial pressure O2 in heat and brian

if VSD is present pulmonary system also perfused (Vital for survival)

38
Q

Tricuspid Atresia Epidemiology and Aetiology

A

53% male

Approx 1 in 10,000 live births

Onset within first few days of life

39
Q

Tricuspid Atresia Clinical Signs

A

Cyanosis is minimal

Hyperpnoea and acidosis

Recurrent RTI

Failure to thrive

40
Q

Tricuspid Atresia Management

A

Hospital: Surgery

41
Q

Ventricular Septal Defect Pathophysiology

A

Defect in intraventricular septum allows communication between systemic and pulmonary circulations - From high pressure to low pressure.

  • Increase LV volume load -> excessive pulmonary bloodflow

Reduces systemic cardiac output

42
Q

Ventricular septal defect Epidemiology and Aetiology

A

Aetiological factors - maternal diabetes and genetics

2-7% of live births

More common in females

43
Q

Ventricular Septal Defects Clinical Signs

A

Depends on size of defect

  • Small – mild or no symptoms
  • Moderate – excessive sweating (due to increased sympathetic tone), fatigue during feeding
  • Tachypnea
  • Inadequate growth
  • Pulmonary vascular resistance
  • Large – same as moderate but more severe
44
Q

Ebstein’s Anomal Pathophysiology

A

Tricuspid valve displaced and part of right ventricle becomes atrialized.

Abnormal tricuspid valve -> tricuspid regurgitation

Atrialized part of right ventricle still contracts with ventricle not atria

45
Q

Ebstein’s Anomaly Clinical Signs

A
  • Cyanosis
    • Common and usually due to right to left shunting at atrial level or severe heart failure
    • Once apparent becomes progressively worse
  • Fatigue and dyspnoea
  • Palpitations and sudden cardiac death
  • Symptoms of right heart failure – ankle oedema, ascites
  • Other less common
    • Brain abscess
    • Bacterial endocarditis
    • Paradoxical embolism, stroke and TIA
46
Q

Ebstein’s Anomaly Epidemiology and Aetiology

A

0.5% of congenital heart diseases

Poor prognosis if presens in infancy

Most commonly presents in middle teen years

47
Q

Truncal Ateriosis Pathophysiology

A
  • Blood flows from both ventricles into a common arterial trunk
  • Ventricular septal abnormality
  • Mixing of left and right ventricular output during systole is incomplete leads to subnormal systemic arterial oxygen saturation
  • Pulmonary blood flow increase -> increased myocardial work -> increased O2 demand and decreased metabolic reserve
48
Q

Truncal Arteriosis Epidemiology and Aetiology

A
  • 1-2% of congenital heart defects
  • Without surgery median age at death is 2 weeks – 3 months
    • Almost 100% mortality by 1 year
49
Q

Truncal Arteriosis Clincial signs

A
  • Poor feeding
  • Diaphoresis
  • Tachypnoea
  • Cyanosis (may not be evident)
  • Signs of congestive heart failure as pulmonary over circulation increases
50
Q

Pulmonary Atresia Pathophysiology

A

Narrow or absent pulmonary valve due to malformation

Type A: Pulmonary blood flow is provided by native pulmonary arteries. Patency of the ductus maintains pulmonary circulation.

Type B: Pulmonary blood flow is supplied by native pulmonary arteries and by major aortopulmonary collateral arteries. The native pulmonary arteries may be supplied by either a ductus and/or major aortopulmonary collateral arteries (MAPCAs)

Type C: Pulmonary blood flow is provided by major aortopulmonary collateral arteries. Native pulmonary arteries are absent.

51
Q

Pulmonary Atresia Epidemiology and Aetiology

A

2,5-3.4% of all congenital heart defects

0.07 per 1000 live births

52
Q

Pulmonary Atresia Clinical Signs

A

Presentation depends on amount of pulmonary bloodflow and patent ductus arteriosus and ventricular septal defect

  • cyanotic and hypoxic\
  • Apnoic
  • Clubbing
  • cerebral embolism
  • cerebral absccess
53
Q

Kawasaki Disease

A

Generalised vasculitis involving small to medium sized arteries

  • Vascular inflammation most pronounced in coronary vessels, can also occur though in veins, capillaries, small arterioles and larger arteries
  • Early stages – endothelial cells and vascular media form oedema, internal elastic lamina remains intact
  • 7-9 days after onset of fever, influx of neutrophils occurs, quickly followed by proliferation of cytotoxic lymphocytes and immunoglobulin A producing plasma cells
  • Cytokines and matrix metalloproteinases target endothelial cells which leads to fragmentation of internal elastic lamina and vascular damage
  • In affected vessels the media develops inflammation with necrosis of smooth mscle cells
    • Internal and external elastic laminae can split, leading to aneurysms
  • Over weeks to months active inflammatory cells are replaced by fibroblasts and monocytes leads to intima proliferation and thickening
  • Vessel wall then narrows, leading to stenosis or thrombi
    • Death is most likely to occur at the point when progressive increase in serum platelet count occurs
54
Q

Kawasaki Disease Clinical Signs

A
  • Prolonged fever often first sign (at least 5 days)
  • 3 phases – acutefebrile stage, subacute and convalescent stages (if continues post this then becomes chronic)
  • Acute Febrile Stage – 7-14 days, high fever unresponsive to antibiotics or antipyretics. Also:
    • Nonexudative bilateral conjunctivitis
    • Anterior uveitis
    • Perianal erythema
    • Erythema and oedema of hands and feet
    • Hepatic, renal and GI dysfunction
  • Subacute Stage
  • Begins when fever abated and continues till week 4-6
  • Hallmarks – desquamation of digits, thrombocytosis and development of coronary aneurysms. Risk for sudden death highest at this stage
  • Convalescent phase
  • Complete resolution of clinical signs
  • Deep transverse grooves in nails
55
Q

Kawasaki Disease Management

A

Management

  • Symptomatic
  • Paracetamol for fever
  • Manage dehydration if present and hypotension

In-Hospital Management

  • Aspirin
    • IV Immunoglobulin
56
Q

Congestive Heart Failure Causes

A
  • Three causes – Ventricular pump dysfunction, volume overload with preserved ventricular contractility and pressure overload with preserved ventricular contractility
  • Ventricular Pump Dysfunction
  • Results in reduced ventricular contractility that leads to decreased ejection of blood from ventricle. Commonly a secondary presentation (though children with congenital heart defects may present at birth)
  • Volume overload with preserved ventricular contractility
  • Increased preload due to congenital heart lesions with left to right shunting or valvular insufficiency
  • Pressure overload with preserved ventricular contractility
    • Pressure overload due to congenital heart disease with severe ventricular outflow obstruction that impedes ejection of blood from the heart, resulting in inadequate cardiac output
57
Q

Congestive Heart Failure Clinical Signs

A
  • Present when patient is unable to adequately increase cardiac output and/or pulmonary or systemic fluid overload
  • Infants – tachypnoea, diaphoresis during feedings, easily fatigued, irritable, decreased volume of feeds, poor weigh gain
  • Young children – similar to common childhood illness, GI symptoms (abdo pain, nausea, vomiting and poor appetite), failure to thrive, easily fatigued and recurrent or chronic cough with wheeze
  • Older children – exercise intolerance, anorexia, abdo pain, dyspnoea, wheeze, oedema, palpitations, chest pain or syncope
  • Physical findings depend on reduction of cardiac output
    • Tachycardia
    • Poor perfusion
    • Pulmonary congestion (Tachypnoea, respiratory distress, grunting)
    • Systemic congestion (hepatomegaly, JVD)
    • High blood pressure
    • Systolic murmur
58
Q

Bacterial Endocarditis Pathophysiology

A
  • Combination of bacteraemia, local cardiac invasion by organism, peripheral embolization and formation of immune complex
  • Begins with blood flow through stenotic or incompetent valve causing turbulence at valve, within communication or downstream. Turbulence damages or denudes endothelium
    • Platelets and fibrin adhere to form small sterile, nonbacterial thromnus
    • Transient bacteraemia leads to adherence of pathogen to injured endocardium and thrombus
    • Fibrin and platelet deposition over the infection then forms a protective sheath that isolates the organisms from host defences and permits rapid proliferation of the infectious agent.

Can then progress to vasculitis, acute and chronic heart failure.

59
Q

Bacterial Endocarditis Clincial Signs

A
  • Toxic appearance
  • Febrile
  • Symptoms for less than 2 weeks
  • Fatigue, chills, sweats, anorexia, malaise, cough, headache, myalgia and/or arthralgia and confusion
  • Hx of congenital heart disease
60
Q

Acute Rheumatic Fever Epidemiology and Aetiology

A
  • Caused by streptococcal infection
  • Peak age 6-20
  • Rheumatic heart disease accounts for 25-50% of cardiac admissions worldwide (Higher incidence in areas where access to antibiotics is limited)
61
Q

Acute Rheumatic Fever Clinical Sings

A
  • Key presentation
    • Polyarthritis (5 or more joints)
    • Carditis
    • Erythema marginatum
    • Chorea
    • Subacute nodules
    • Hx of streptococcal pharyngitis
62
Q

Pericarditis Epidemiology and Aetiology

A
  • Viral or bacterial
  • Usually secondary to other infection such as adjacent pneumonia
  • Most cases of urulent pericarditis occur in < 4 years old
  • More common in developing countries
63
Q

Pericarditis Pathophysiolosy

A
  • Inflammation of pericardium secondary to an infection.
  • Increase in permeability to proteins and inflammatory cells leading to fluid accumulation between visceral and parietal layers (pericardial effusion) à can limit filling of chambers
64
Q

Pericarditis Presentation

A
  • Depends on if viral or bacterial
  • Viral
  • Fever, chest pain
  • Cough, diarrhoea, rash and runny nose
  • Pain relieved by sitting
  • Bacterial
  • Symptoms of sepsis
  • Nonspecific symptoms à fever, respiratory distress, tachycardia out of proportion to fever
  • Abdominal discormort
  • Chest pain worsened by positioning
  • Hx of infection (e.g. pneumonia, meningitis etc.)
  • Both
  • Cardiac friction rub
  • Ecg changes
  • Venous congestion
  • Cardiac tamponade
  • Pulsus paradoxus

Paediatrics (5 decks)

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