Block 2: Cardiomyopathy, Peripheral vascular disease Flashcards
1
Q
Acute heart failure: warm/cold, wet/dry
A
- Warm/cold: How peripherally perfused is the patient? Normal perfusion is warm. A low blood pressure, cool peripheries, prolonged capillary refill time, reduced urine output are signs of hypoperfusion - described as cold.
- Wet/dry: How congested is the patient? Normal/Not congested is dry. Pulmonary/peripheral oedema or a raised JVP are signs of fluid overload - described as wet.
2
Q
Acute heart failure: classification (informal)
A
- Warm and dry: best prognosis, perfused and not congested, compensated, optimise medication and treat triggers
- Warm and wet: most common type, perfused but congested, fluid overload, give diuretics +/- vasodilators
- Cold and dry: least common type, poorly perfused but not congested, hypovolaemic shock. Consider fluid bolus, may need ionotropes
- Cold and wet: worse prognosis, poorly perfused and congested, cardiogenic shock, consider diuretics if BP >90, may need vasopressors/inotropes
3
Q
Investigations for acute heart failure
A
- Bedside: observations, ECG
- Bloods: FBC, U&E, LFT, pro-BNP, troponin, d-dimer
- Imaging: chest x-ray, echocardiogram
4
Q
Management of acute heart failure
A
- Manage identified trigger
- Oxygen
- Position: sat upright
- Loop diuretics: IV furosemide
- Inotropes and vasopressors: in unstable/hypovolaemic patients, given in high dependency setting
5
Q
Cardiomyopathy: overview
A
- Disorders of the heart muscle that are not caused by another cardiac disease
- 4 types: Hypertrophic, Dilated, Restrictive and other (arrhythmogenic right ventricular, tako-tsubo, peripartum)
6
Q
Cardiomyopathy: types
A
- Hypertrophic: thickened walls, less ventricular filling
- Dilated: dilated and thin walls, less contractility
- Restrictive: stiff walls, less ventricular filling
- Primary:A primary disease of the heart muscle itself. These include genetic disease (e.g. hypertrophic) or those acquired during life (e.g. tako-tsubo, myocarditis).
- Secondary:Disease of the heart muscle that develops due to a systemic condition. These include infiltrative/inflammatory (e.g. amyloidosis, sarcoidosis), storage (e.g. haemochromatosis, Fabry’s disease), endocrine etc.
7
Q
Complications/red flags of cardiomyopathy
A
Complications: poor cardiac output, heart failure, arrhythmias and sudden cardiac death
Red flags for cardiomyopathy
- Exertional dyspnoea, angina, syncope
- Palpitation
- Family history of sudden cardiac death, unexplained heart transplants or devices, unexplained heart failure
8
Q
Cardiomyopathy: Investigations
A
- Bedside: ECG (likely abnormal but non-specific), blood pressure
- Bloods: FBC, U&E, LFT, TFT, HbA1c, Pro-BNP
- Imaging: Echocardiogram
9
Q
Cardiomyopathy: Specialist investigations
A
- Ambulatory ECG (worn over a prolonged period e.g. 48hours) - assessing for arrhythmias
- Exercise stress testing - physical or ECG changes on exertion
- Cardiac MRI - finer detailed imaging of the structure of the heart
- Genetic testing - if indicated or as part of familial screening
10
Q
Hypertrophic Cardiomyopathy
A
- Due to abnormal growth of the myocardium, particularly the left ventricle (>15mm) and the atrial septum. Not secondary to cardiovascular disease
- Mix of systolic and diastolic dysfunction so ejection fraction is preserved
- Can develop left ventricular outflow tract obstruction (LVOTO) due to septum growing asymmetrically and obstructing blood flow through the aortic valve. Heard as an ejection systolic murmur, can cause mitral valve regurgitation. This is Hypertrophic Obstructive Cardiomyopathy (HOCM)
11
Q
Hypertrophic cardiomyopathy- presentation
A
- Symptoms develop in late teens or twenties
- Exertional breathlessness, chest discomfort, palpitations or lightheadedness
- Can cause heart failure, arrhythmias and sudden cardiac death
12
Q
Hypertrophic cardiomegaly inheritance
A
- Caused by genetic mutation in sarcomere proteins
- Autosomal dominant inheritance
- Genetic testing confirms disorder. Used to identify responsible genes and screen high risk relatives
- If gene cant be identified then family should undergo regular cardiac screening with ECG’s and echocardiogram
- Patients with strong family history of HCM or sudden cardiac death are referred to genetic services
13
Q
Hypertrophic cardiomegaly: examination
A
- Systolic ejection murmur: made worse by valsalva manoeuvre
- S4 heart sound- atrial gallop
- Forceful apex beat +/- double impulse
14
Q
Hypertrophic cardiomegaly: investigations
A
- ECG - most will have an abnormal ECG, but with non-specific changes. There may be evidence of left ventricular hypertrophy and deep narrow Q waves.
- Echocardiogram
- Stress test ECG
- Cardiac MRI
- Genetic testing
15
Q
Complications of HCM
A
- Cardiac failure: patients with symptomatic LVOTO should be managed with beta blockers
- Atrial fibrillation: consider anticoagulation
- Arrhythmias: non-sustained ventricular tachycardia and ventricular fibrillation. Implantable cardiac defibrillators can reduce this week. Manage with beta blockers and CCB (verapamil)
- Sudden cardiac death: usually occurs during exertion, are advised against competitive athletic sport
16
Q
Medications in HOCM
A
- Beta-blockers: First-line agents
- Calcium channel blockers: Verapamil is an alternative or addition to beta blockers
- Disopyramide: This antiarrhythmic agent may be used as a second-line agent in combination with beta-blockers for refractory symptoms.
- Diuretics: Caution due to the potential for hypovolemia and exacerbation of LVOT obstruction.
- Anticoagulation: Indicated in patients with atrial fibrillation or a history of thromboembolic events.
- Surgery in symptomatic LVOT obstruction: septal myectomy, alcohol septal ablation
17
Q
Dilated cardiomyopathy
A
- Dilation of ventricle wall: heart looks bigger but muscles are thinner and weaker so reduced pumping power
- Causes heart failure: dyspnoea and oedema
- Can cause arrhythmias, clots, angina and a smaller risk of sudden cardiac death
- Risks: mostly idiopathic, genetic (some genes via autosomal dominant inheritance), alcohol, chemotherapy, viral myocarditis, autoimmune disease, pregnancy
- Examination may show signs of heart failure or alcohol excess
- Investigations: ECG, 48 hour ECG, Echocardiogram and cardiac MRI are used in diagnosis
- Treatment: ACEi, beta blockers, spironolactone, pacemaker or ICD
18
Q
Restrictive cardiomyopathy
A
- Stiff ventricle walls that do not stretch and fill properly
- Atria becomes enlarged due to extra pressure
- Can cause heart failure, angina and arrhythmias
- Maybe be idiopathic or secondary to Amyloidosis, Sarcoidosis, Haemochromatosis
- Diagnosis: ECG, Cardiac MRI and rarely ventricular biopsy
- Management depends on cause. For symptoms use normal heart failure medication and pacemakers/ICD
- Usually due to protein infiltration or scarring of the ventricle walls
19
Q
Arrthymogenic right ventricular cardiomyopathy (ARVC)
A
- The replacement of normal myocardium with fibro-fatty tissue. Causes poor conduction of electrical signal and life threatening ventricular arrhythmias
- Causes palpitation and syncope
- Can cause sudden cardiac death or heart failure later on
- Genetic: can run in families or be due to a spontaneous mutation
- Investigations: ECG, Echo, cardiac MRI
- Treatment= Beta blockers are used and an ICD may be implanted. Radio-ablation can reduce the number of VTs.
20
Q
Peripheral vascular disease
A
A branching term that refers to any disease of the vasculature and circulation, including veins and arteries.
21
Q
PAD and chronic venous insufficiency
A
Peripheral arterial disease (PAD) is disease specifically of the arterial supply, usually a narrowing or blockage of the arteries. The lack of blood supply to the tissues can cause claudication or ischaemia. Features may include reduced pulses, coolness, paleness.
Chronic venous insufficiency is used to describe peripheral venous disease. Failure to return blood adequately to the heart can lead to congestion. This is also associated with varicose veins. Features may include oedema and skin changes.
