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What is definition of HOCM and it's prevalence?

LVH in absence of other loading conditions
Prevalence 0.2% or 1 in 500!


Epidemiology of HOCM?

AD with variable penetrance
Offspring of affected = 50%
Can be benign
Commonest cause of sudden cardiac death <35 years
Can have angina, signs of pulm congestion (PND, orthopnoea), syncope, and palpitations


What are the clinical examination features of HOCM?

Jerky rapidly rising pulse
Prominent LV impulse
Apical systolic murmur that increases with valsalva (related to dynamic obstruction)
Fourth heart sound


What are the ECG findings in HOCM?

Q waves


What are the causative genes of HOCM?

Primarily encode sarcomere or sarcomere related proteins

Cardiac β-myosin heavy chain (β MHC) (45%)
Myosin binding protein C (MyBPC) (35%)

Cardiac troponin T, tropomyosin, cardiac
troponin I, essential and regulatory myosin light c
hain, and more recently, titin and actinin-2 genes


What is the role of genetic testing in HOCM?

Identifies at-risk earlier
Avoids unecessary screening of non-carriers
Can distinguish between other causes of LVH
Pick up rate of 50-50%


When does sudden death in HOCM most frequently occur?

Sudden death occurs most commonly in HCM either during or immediately after exercise, although death can also occur at rest


Who should be screened for HOCM and how often?

All first-degree relatives of an affected individual be clinically screened for HCM. As a minimum, this involves a physical examination by a cardiologist, an ECG and a transthoracic echocardiogram.

>31 - every 3-5 years

21-30 - every 2-3 years

11-20 - every 1-1.5 years


When should the physician report someone to the RTA?

The health professional should consider
reporting directly to the driver licensing authority in situations where the patient is either:
unable to appreciate the impact of their condition, or
unable to take notice of the health professional’s recommendations due to cognitive impairment, or
continues driving despite appropriate advice and is likely to endanger the public


What are the driving rules for:

Elective PCI

Elective PCI - 2 days
MI - 2 weeks
CABG - 4 weeks
Arrest - 6 months


What are the driving rules for:

Cardiogenic syncope

DVT - 2 weeks
Cardiogenic syncope - 4 weeks
PE - 6 weeks


What is the driving license rule with regard to heart failure?

Sx on moderate exertion = no licence


What are the driving rules for seizures?

First seizure - six months

First treatment - on treatment for six months and compliant, even if they had a seizure within those six months.

Otherwise - 12 months


How long after a stroke can you drive?

4 weeks - 2 if TIA
SAH - 3 months


How do you differentiate between chronic hypertension and pre-eclampsia?

Chronic hypertension
 - hypertension before 20 weeks gestation, often diastolic
 - no or stable proteinuria

(if after 20 weeks gestation and no proteinuria --> gestational hypertension)


What does the a-wave of JVP mean?

'a' wave = atrial contraction
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation

coincides with first heart sound


What is a cannon a-wave?

Cannon 'a' waves
caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing


What is the v wave of the JVP?

'v' wave
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation - very reliable sign


What does the S1 of the heart sound refer to?  Pathology?

closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis


What does the S2 of the heart sound refer to? Pathology?

closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal


What is the significance of an ASD?

- most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years. 

DVTs can cross the circulation and embolise to the brain.


What are the features of an ASD?

ejection systolic murmur

fixed splitting of S2

embolism may pass from venous system to left side of heart causing a stroke


How do you calculate stroke volume?

Stroke Volume = End Diastolic Volume– End Systolic Volume


How do you calculate cardiac output?

Cardiac Output = Heart Rate x Stroke Volume


What is VO2 max?

VO2 max (also maximal oxygen consumption, maximal oxygen uptake, peak oxygen uptake or maximal aerobic capacity) is the maximum rate of oxygen consumption as measured during incremental exercise


Why is it useful to measure the mixed venous oxygen concentration?

It can be used as a marker of how well O2 is being delivered to the peripheral tissues by extrapolation (if SvO2 low and patient in multiorgan failure then we can add a inotrope to help increase cardiac output ie. in severe sepsis)

    increased O2 delivery (increased FiO2, hyperoxia, hyperbaric oxygen)
    decreased O2 demand (hypothermia, anaesthesia, neuromuscular blockade)
    high flow states: sepsis, hyperthyroidism, severe liver disease

    decreased O2 delivery:

1. decreased Hb (anaemia, haemorrhage, dilution)
2. decreased SaO2 (hypoxaemia)
3. decreased Q (any form of shock, arrhythmia)

    increased O2 demand (hyperthermia, shivering, pain, seizures)


How do you calculate venous oxygen content?

Venous Oxygen content = Arterial Oxygen content - Oxygen consumption / Cardiac output.

Therefore, mixed venous O2 content is directly related to arterial oxygen content (therefore related to hemoglobin concentration and partial pressure of Oxygen) and cardiac output (therefore it will increase in cases of low cardiac output) and oxygen consumption which means tissue perfusion (therefore you have increased mixed venous O2 content in shock and in any case of impaired tissue perfusion).


What is Fick's principle?

CO = VO2 (oxygen consumption) / arteriovenous oxygen difference (Ca-Cv)


How do you measure VO2?

VO2, oxygen consumption in ml of pure gaseous oxygen per minute. This may be measured using a spirometer within a closed rebreathing circuit incorporating a CO2 absorber


What happens to the heart in old people?

Heart rate decreases (really affects max CO)
Stroke volume declines (major factor for the decline lower cardiac output in submax exercise)
LV contractility declines
Decreased vascular capacity and local blood flow autoregulation
Poor O2 delivery
Poor muscle oxidative capacity
Increased TPR