Cardiology Flashcards

Day 3

1
Q

Define CHD ?

A

Anatomical malformation of the heart or great vessels occurring during fetal development
1/125 born with a congenital heart defect (1 in 100 in the UK)
Most common form of structural birth defect.

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2
Q

Define acquired disorders

A

Disease processes or abnormalities that occur after birth. They result from various causes such as infection, autoimmune diseases, environment factors.

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3
Q

Describe embryonic heart development

A

Cardio genesis begins at approximately 3 weeks of gestation. Most cardiovascular development occurs between weeks 4 and 8 when the formation of the atria and ventricles.
During prenatal development, the heart is already functioning and preparing to adapt to postnatal life.

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4
Q

Describe foetal circulation

A

Oxygenation of the blood is from the placenta rather than the lungs
Fetus has low levels of oxygen (60-70%)
To compensate the fetal cardiac output is high
Fetal cardiac shunts – Foramen ovale and ductus arteriosus

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5
Q

What are the 3 layers of an artery ?

A

Adventitia (protective outer layer)
Media (Smooth muscle layer)
Intima (non stick inner lining)

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6
Q

Examples of acyanotic CHD

A

Ventricular septal defect, atrio ventricular septal defect, patent ductus arteriosus, aortic valve stenosis, pulmonary valve stenosis, coarctation of aorta

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6
Q

How is CHD classified ?

A

Cyanotic - Not enough oxygen to the body.
Acyanotic - blood is shunted from the left to the right side of the heart often due to a hole.

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6
Q

Examples of cyanotic CHD

A

Tetralogy of Fallot, tricuspid atresia, hypoplastic left heart syndrome, transportation of great arteries, total anomalous pulmonary vein return, truncus arteriosus, severe pulmonary stenosis

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6
Q

Causes and factors associated with CHD

A

Environmental factors include:
Infection – intrauterine, systemic viral (rubella, herpesvirus)
Metabolic disorders – Diabetes, hypercalcemia, phenylketonuria (PKU)
Drugs – Alcohol, warfarin, phenytoin, thalidomide, lithium
Peripheral conditions – antenatal age, antepartum bleeding, prematurity, high altitude
A number of chromosomal anomalies and congenital lesions associated with increased risk of CHDs

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7
Q

What is VSD ?

A

A ventricular septal defect (hole) of the interventricular septum, the wall separating the right and left ventricles
The high pressure in left ventricle causes left-to-right shunt of blood into right ventricle
The increased blood flow to the lungs over time increases pulmonary vascular resistance
This causes the right ventricle to hypertrophy

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7
Q

How to diagnose CHD

A

Prenatal scans, structure of heart visualised at 20 weeks, if abnormal echocardiography undertaken before 24 weeks, murmur detected after birth

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7
Q

Symptoms of VSD in babies

A

Poor eating, failure to thrive
Fast breathing or breathlessness
Easy tiring

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7
Q

What is ASD ?

A

An atrial septal defect is a birth defect of the heart in which there is a hole in the wall (septum) that divides the upper chambers (atria) of the heart
The slightly higher pressure from left atrium causes oxygenated blood to flow from left atrium through the septal defect to right.
This additional blood flow to right side of heart can cause stretching and enlargement

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8
Q

What are the symptoms of ASD ?

A

Shortness of breath, especially when exercising
Fatigue
Swelling of legs, feet or abdomen
Heart palpitations or skipped beats
Stroke
Heart murmur

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9
Q

What is PDA ?

A

Patent ductus arteriosus (PDA) is a persistent opening between the aorta and the pulmonary artery
Higher pressure from aorta shunts blood into the pulmonary artery resulting in blood being pumped to lungs and back to left atrium
A small patent ductus arteriosus often doesn’t cause problems
A large patent ductus arteriosus allows poorly oxygenated blood to flow in the wrong direction, weakening the heart muscle and causing heart failure

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10
Q

What might a large PDA found during infancy cause ?

A

Poor eating, which leads to poor growth
Sweating with crying or eating
Persistent fast breathing or breathlessness
Easy tiring
Rapid heart rate

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11
Q

What is ACHD ?

A

Adult congenital heart disease, affects aged over 18 living with heart defect that occurred during foetal development.

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12
Q

What is acquired cardiac disease in CYP ?

A

Are those disease processes or abnormalities that occur after birth
Examples of acquired disorders are: Kawasaki disease, paediatric inflammatory multisystem syndrome, rheumatic heart disease, cardiomyopathy
Eating disorder and cardiovascular complications

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13
Q

What are the cardiovascular complications associated with ED ?

A

Most common are hypotension and bradycardia​
Sinus bradycardia- compensate for starved body to conserveenergy and is mediated by increased vagal tone​
Hypotension occurs secondary to increased vagal tone and may also result from poor fluidintake and dehydration, reduced elasticity in blood vessels, and dysregulation of circadianrhythm​

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14
Q

What is Kawasaki disease ?

A

Acute vasculitis (inflammation of blood vessels)
Leading cause of acquired heart disease in children
Aetiology and pathogenesis – unknown (may be immune response)

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15
Q

What are the symptoms and treatment of Kawasaki disease ?

A

fever >39 for 5 days or longer, bilateral conjunctivitis, red cracked lips, strawberry tongue, oedematous hands and feet and peeling
Treatment: IV gamma globulin, Aspirin +/- Anticoagulation, corticosteroids

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16
Q

What is PIMS ?

A

Paediatric inflammatory multisystem syndrome, temporally associated with COVID. Similar coronary artery changes as Kawasaki disease.

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17
Q

What are the symptoms of PIMS ?

A

persistent fever, inflammation (neutrophilia, elevated CRP and lymphopaenia) and evidence of single or multi-organ dysfunction ( shock, cardiac, respiratory, renal, gastrointestinal or neurological disorder)

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18
Q

What is rheumatic fever ?

A

Immune-mediated multi-system inflammatory disease (heart, skin connective tissue)
Rheumatic heart disease is the cardiac aspect of RF (inflammation of pericardium, myocardium, endocardium, can cause cardiac dilation and heart failure)

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19
Q

What is the treatment for RF ?

A

Prompt treatment of GAS
Suppression of the inflammatory response
(salicylates and corticosteroids)
+/- Surgery to repair valves

20
Q

What are cardiomyopathies ?

A

Disorder of heart muscle with abnormal enlarging or thickening. Can be caused by genetics, myocarditis, or infections.
Usually begins in ventricles and progresses to atria

21
Q

What is hypertrophic cardiomyopathy ?

A

Genetic: autosomal dominant disorder (mutation in genes encoding cardiac muscle fibres)

22
Q

What are the symptoms of hypertrophic cardiomyopathy ?

A

dyspnoea, tiredness, palpitations and chest pain
Abnormal growth of fibres leads to thickening of ventricular septum
Impaired ventricular filling and LV outflow obstruction
Cardiac arrhythmias
Most common cause of sudden cardiac death in young people

23
Q

Treatment for hypertrophic cardiomyopathy

A

needs to reduce left ventricular outflow obstruction and increase ventricular compliance – Beta-blockers.

24
Q

What is ARVD ?

A

Arrhythmogenic right ventricular dysplasia (cardiomyopathy), genetic, autosomal disorder

25
Q

What are the symptoms of ARVD ?

A

Dizziness, fatigue, palpitations, abdominal pain, decreased exercise tolerance
Progressive replacement of the right ventricular myocardium by fibrofatty tissue (dysplasia)

26
Q

What causes arrhythmias in ARVD ?

A

The presence of arrhythmias are due to the progressing tissue dysplasia and impact on the electrical conducting myocytes.

27
Q

Treatment for ARVD ?

A

Prevent cardiac arrest. Control via lifestyle modifications.

28
Q

What are the functions of the intima ?

A

Vasoregulation
Vessel growth
Resists adhesion of WBC
Prevents clot formation

29
Q

What is the endothelium ?

A

Single layer of cells that line the internal surface of CVS. Selective barrier to most components of blood and plasma.
Metabolically active - generate vasoactive substances, non thrombogenic, produce growth factors

30
Q

What is endothelial dysfunction ?

A

Reduced vasodilatation (reduced generation of nitric oxide)
Leads to a prothrombotic state through the activation of prothrombotic mechanisms.
Increased oxidative stress leads to reduced bioavailability of NO, decreased ACE which exacerbates oxidative stress.

31
Q

What is atherosclerosis ?

A

Development of fatty lesions within the artery wall
A chronic inflammatory disease mediated by the immune system
Normal endothelial function is disrupted – artery is less able to dilate
Triggered by damage to the endothelium covering the intima

32
Q

What are the stages of development of atherosclerosis ?

A

Damaged endothelium permeable to low-density cholesterol -LDL
Collect in the inner wall
Activates the inflammatory response
Macrophages containing LDL = foam cells
Fatty streaks
Advanced fibrous plague

33
Q

What causes atherosclerosis ?

A

The process can begin in childhood
Hypercholesterolaemia increases the incidence and progression of disease – low-density lipoprotein (LDL) cholesterol – development of arterial plaque
Smoking increases levels of plasma fibrinogen, damages blood vessels and accelerates plaque formation
Hypertension increases arterial wall stress and workload of the heart and accelerates atherosclerosis
Diabetes is associated with hypertension and dyslipidaemia

34
Q

How do you manage atherosclerosis ?

A

Hyperlipidaemia – statins (pharmacology module) – cholesterol-lowering effects and stabilization of existing atherosclerotic plaques, making them less prone to rupture – regular follow ups to monitor both efficacy and safety – lipid profile monitoring
Hypertension – use of antihypertensive medications to control blood pressure and reduce stress on arterial walls; regular blood pressure monitoring and life-style modifications alongside medication for comprehensive management

Prevent - low sat and trans fat diet, exercise, stress management techniques

35
Q

What are the implications of atherosclerosis ?

A

Coronary arteries - IHD, stable angina, acute coronary syndromes, cardiac arrest, HF
Carotid artery - stenosis, cerebral infarction (stroke)
Aorta - aneurysm
Femoral / iliac - peripheral vascular disease
Renal - chronic kidney disease

36
Q

Explain coronary blood flow

A

Heart has highest oxygen consumption per tissue mass of any organ
Oxygen extraction from blood flowing through the heart is 70-80%, compared to 25% in other tissues.

37
Q

What are the determinants of coronary blood flow ?

A

Coronary perfusion pressure
Perfusion time
Vasomotor tone – vessel dilates to increase flow

38
Q

What is IHD ?

A

Sometimes referred to as (CHD) (CAD)
Chronic condition that develops over many years
Interruption or temporary blockage of a coronary artery
Patient may be asymptomatic until the artery becomes significantly blocked.

39
Q

Signs and symptoms of IHD ?

A

Fatigue
Dyspnoea
Chest pain on exercise (resolves with rest or GTN -glyceryl trinitrate )- stable angina
ECG changes only present during exercise or with pain

40
Q

Describe the pathophysiology of IHD

A

An imbalance between myocardial oxygen supply and demand
Atherosclerosis narrows coronary arteries, leading to reduced blood flow to the heart muscle during increased demand – myocardial ischaemia and characteristic chest pain
However, the degree of pain maybe related to adenosine – molecule released during myocardial ischaemia which directly stimulates pain fibre in the heart (Alaeddini and Shirani, 2015)

41
Q

What is the management and treatments of IHD ?

A

Control hypertension (ACE inhibitors, beta blockers), thrombosis development control (aspirin), hypercholesterolaemia (statins)

42
Q

What is ACS ?

A

Spectrum of conditions including myocardial infarction, unstable angina.
Result from formation of thrombus on an atheromatous plaque in coronary artery.

43
Q

How is ACS managed ?

A

Pain relief, aspirin, oxygen (maximise myocardial perfusion), blood test for troponin T level to confirm myocardial infarction.

44
Q

What is plaque rupture ?

A

Tear in artery wall, fissure exposes the lipid core to lumen of artery. Common in most occlusive coronary events. Arterial stress is caused by changes in arterial BP

45
Q

What is thrombus formation ?

A

Intraluminal thrombi extend from lipid core to lumen. Precipitates occlusive coronary events. Thrombus can propagate along artery.

46
Q

What are the differences between stemi and nstemi myocardial infarction ?

A

Stemi - ECG changes present on ST elevation on 12 lead. Total occlusion of coronary artery proximal. Full thickness of myocardial wall is damaged. Troponin T levels elevated.
Nstemi - ECG changes present - T wave inverted but ST not elevated. Total occlusion of coronary artery - distal. Partial thickness of myocardial wall is damaged. Troponin T levels elevated.

47
Q

Describe the characteristics of an unstable angina

A

Atheromatous plaque rupture. ECG changes present - T wave may be flat or inverted, ST may be depressed. Partial occlusion of coronary artery. No myocardial wall damage. Troponin T levels normal

48
Q

What is AF ?

A

Irregular HR. No obvious P waves, narrow (normal) QRS complexes, chaotic activity on baseline. Maybe intermittent or continuous, fast or slow, increased risk of stroke

49
Q

What causes AF ?

A

Age, hypertension, heart valve dysfunction, CHD, cardiomyopathy, pericarditis, electrolyte imbalance

50
Q

AF treatment options

A

Rate and rhythm control - Digoxin, diltiazem, beta, flecainide.
Anticoagulation - warfarin, vit K antagonists
DC electrical cardioversion
Left atrial ablation

51
Q

Describe the components of the ECG complex

A

P wave - spread of impulse from SA node across atria.
PR interval - time taken for impulse to spread from SA node to purkinjie fibres in from ventricles
QRS complex - spread of impulse through ventricular myocardium (depolarisation)
T wave - ventricular recovery (repolarisation)

52
Q

What is sinus rythem ?

A

Normal

53
Q

What is atrial flutter ?

A

Regular HR, sawtooth pattern on baseline, rhythm originated in one area of atria (not SA node)

54
Q

What is ventricular tachycardia ?

A

reg but rapid HR, broach QRS complexes, no P wave, associated with loss of consciousness, cardioversion or defib required

55
Q

What is VF ?

A

Emergency, no cardiac output, no waves or QRS activity

56
Q

What rhythm are shockable / non shockable ?

A

Shock - VF and pulseless VT
No shock - Pulseless electrical activity and asystole (wavy line)