Non-Ischemic Cardiac Conditions

Question 1

Layers of the heart

Answer 1

Pericardium:

• Fibrous sack with visceral and parietal layer
• Anchors the heart to adjacent structures
• non compliant and unable to adapt to rapid increase in pericardial fluid
• provides barrier to infection
• *Cardiac tamponade** - blood collection in the sac
• *Pericardial effusion** - collection of serum in the sack

Epicardium:

• Fatty, beneath visceral pericardium
• adheres to the heart, contains coronary blood vessels

Myocardium:
- Thick muscular layer, nevessary for contraction

Endocardium:

• Innermost layer of connective tissue
• Damage from surgery, trauma or abnormalities pre-dispose it to infection

Question 2

Valvular regurgitation vs valvular stenosis

Answer 2

Valvular stenosis:
Narrowing/stiffening of the valve, keeping it from opening fully and restricting blood flow
- problem with opening

Valvular regurgitation/insufficient:
Valve does not close effectively, causing a backflow of blood in the heart
- problem with closing

*both can cause fatigue, SOB and oedema*

Question 3

Aortic valve stenosis and aortic valve regurgitation

Answer 3

Stenosis - causes increased afterload, L ventricular hypertrophy, heart failure
*cause - usually mechanical stress over time, RHD

Treatment - valve replacement after onset of symptoms, ?cardioversion

Regurgitation - causes blood flow back to L ventricle during diastole - increases L blood volume, increases SV, ventricular hypertrophy
*cause - aortic rool dialation (pulling leaflets apart) - idiopathic, syphilis, infective endocarditis, rheumatic fever causing fibrosis which disrupts seal

Treatment - replacement of valve after symptomsm vasodilators for HTN

Clinical presentation
- APO
- Hypoxia
- HTN - regurgitation, hypotension - stenosis
- Tachycardia
Chest pain

Question 4

Mitral valve stenosis and regurgitation

Answer 4

Stenosis:
Increased pressure in L atrium –> increased pulmonary congestion –> pulmonary hypertension

Treatment - consistent with APO

Regurgitation:
Increased L atrial volume –> APO –> increased systemic vascular resistance

Treatment - surgical repair, treatment of APO and improved contractility

Question 5

Tricuspid valve stenosis and tricuspid valve regurgitation

Answer 5

Experience R atrial enlargement –> hepatic enlargement, peripheral oedema, decreased blood supply to the pulmonary vasculature

Question 6

Endocarditis definition and management

Answer 6

Inflammation of the endocardium - tends to primarily affect valves.

Acute

• develops over days to weeks
• clinical manifestations more severe

Subacute:

• Develops over weeks to months
• vague and nonspecific clinical manifestations

Cause:
Bcteria, virus, fungi, ricketts, parasites

Assessment:
Fever, malaise with other non-specific symptoms

Management:

• Blood cultures, UA, echo
• ABx, managing other systemic complications

Question 7

Pericarditis definition and management

Answer 7

Inflammation of the pericardium, commony caused by a viral ilness.

Assessment:
Chest pain improved with leaning forward
Tachycardic, palpitations
Febrile
Pericardial rub on auscultation

Management:
Path - FBE, UEC, CRP, trop
Echocardiogram
Pulsus paradoxus - suspect cardiac tamponade
ECG - wide speread ST elevation and PR depression, tachy

Treatment:
NSAIDS
Observe for pericardial effusion
Treat arrhythmia’s

Question 8

Myocarditis definition and management

Answer 8

Inflammation of the heart muscle
* caused by infection, drugs and toxins, immune mediated response

Clinical manifestations:
non-specific
- SOB, tachycardia, chest pain
severe - cardiogenic shock

Management:
CXR
ECG
Path - extensive to rule out other possible diagnosis’
Echocardiogram

Treatment:

• O2
• Treatment of cardiac failure
• Analgesia
• ?Inotropes or vent assistance
• ACE inhibitors