cardio

Question 1

wtf is stable angina? + symptoms

Answer 1

narrowing of the coronary arteries reduces blood flow to the myocardium
= insufficient blood supply during exercise etc
= symptoms of angina
stable when symptoms are always relieved by rest or GTN spray

• constricting chest pain with or without radiation to jaw or arms

Question 2

investigate stable angina?

Answer 2

CT Coronary Angiography is the Gold Standard diagnostic - injecting contrast and taking CT images, highlighting any narrowing

also have the following baseline investigations:
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)

Question 3

manage stable angina?

Answer 3

R – Refer to cardiology (urgently if unstable)
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions

immediate relief =
glyceryl trinitrate spray (causes vasodilation, repeated after 5 mins, if in next 5 mins symptoms persist then 999)

long term relief =
beta blocker (eg. bisoprolol)
calcium channel blocker (eg. amlodipine)
long acting nitrates, ivabradine, nicorandil, ranolazine

secondary prevention =
aspirin, atorvastatin, ace inhib, already on beta blocker

Question 4

surgery for stable angina?

Answer 4

Percutaneous Coronary Intervention (PCI) with coronary angioplasty - dilating the blood vessel with a balloon/stent
catheter into the patient’s brachial or femoral artery, injecting contrast so that the coronary arteries and any areas of stenosis are highlighted

Coronary Artery Bypass Graft (CABG) - severe stenosis, opening the chest along the sternum (causing a midline sternotomy scar), graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis
slower recovery, higher complication rate

Question 5

wtf is unstable angina? + diag & treatment

Answer 5

heart doesn’t get enough blood flow
angina is “unstable” when the symptoms come on randomly whilst at rest - considered as Acute Coronary Syndrome (usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery)

diag:
ECG - ST segment depression, T-wave inversions
unstable angina vs nstemi not distinguishable initially
elevated troponin = myocardial infarction
treat:
clopidogrel (anti-platelet)
low molecular weight heparin (anti-clot forming)
enoxaparin

Question 6

wtf is prinzmetal’s angina?

Answer 6

vasospastic/variant angina

coronary artery vasospasms occurring spontaneously even at rest - constriction of smooth muscle around artery
likely due to vasoconstrictors eg. platelet thromboxane A2

• constricting chest pain (pressure, squeezing, burning, tightness) with or without radiation to jaw or arms, less than 20 mins - may occur at rest

Question 7

diagnose and treat prinzmetal’s angina?

Answer 7

imaging = transient ST segment elevation, transmural ischaemia

meds = calcium channel blockers, vasodilators

Question 8

wtf is myocardial infarction? + causes

Answer 8

medical emergency in which the supply of blood to the heart is suddenly blocked, usually by a blood clot

causes:
death of heart muscle cells due to lack of oxygen-rich blood flow, plaque build-up, blood platelets adhere to plaque creating blockage, necrosis of myocardial cells

Question 9

wtf is STEMI? + treat

Answer 9

ST segment elevation myocardial infarction - coronary artery completely blocked, full thickness of myocardial wall involved, ECG shows ST elevation, possible Q waves

treat = emergency reperfusion via percutaneous coronary intervention eg. catherterisation, thrombolysis, very time sensitive

Question 10

complications of MI? (mnemonic)

Answer 10

Death
Arrhythmia
Rupture (ventricular wall/septum/papillary muscles)
Tamponade (fluid buildup in the sac around the heart)
Heart failure
Valve disease
Aneurysm of ventricles
Dressler's syndrome
thromboEmbolism
Recurrence/mitral Regurgitation

Question 11

risk factors of MI?

Answer 11

modifiable - old age, smoking, HTN, diabetes mellitus, high cholesterol, low physical activity, obese, excessive alcohol, drug use, chronic stress

non mod - fam history, male

Question 12

wtf is NSTEMI? + treat

Answer 12

non-ST segment elevation MI
coronary artery not completely blocked, sub endocardium may be especially vulnerable to ischaemia
ECG shows ST depression

treat = reperfusion via percutaneous coronary intervention, no thrombolysis, less time sensitive

Question 13

signs/symptoms of MI & diagnosis?

Answer 13

acute chest pain over 20 mins radiating to arm/jaw
uncomfortable chest/back/neck/jaw/stomach
dyspnoea, fatigue, diaphoresis (sweating), nausea
feeling full/indigestion

diagnose:
detecting sensitive markers = troponin I, troponin T, rise apparent within 2-4 hrs, peak 24 hrs
CK-MB test (form of enzyme in heart muscle): levels increase 4hrs after infarction, peak @ 24hrs
ECG - can confirm diagnosis but time sensitive/not accurate after 6 hrs
30 mins = st elevation in stemi, st depression in nstemi
<24hrs = T wave inversion
>24hrs = Q waves appear

Question 14

wtf is a DVT?

Answer 14

blood clots developing in circulation due to secondary stagnation of blood and hypercoagulable states

can travel (embolise) from the deep veins, through the right side of the heart and into the lungs = lodged in pulmonary arteries = pulmonary embolism
if atrial septal defect, clot can pass to other side of heart and travel to brain = stroke

Question 15

risk factors of DVT?

Answer 15

Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
Malignancy
Polycythaemia (increase in RBC)
Systemic lupus erythematosus
Thrombophilia (clots form too easily) - Antiphospholipid syndrome, common association is recurrent miscarriage, antiphospholipid antibody test to diagnose

Question 16

wtf is VTE prophylaxis?

Answer 16

If patient at increased risk of VTE, they should receive prophylaxis unless contraindicated
Prophylaxis is usually with low molecular weight heparin, such as enoxaparin. Contraindications include active bleeding or existing anticoagulation with warfarin or a DOAC
Anti-embolic compression stockings, main contraindication for compression stockings is significant peripheral arterial disease

Question 17

DVT presentation?

Answer 17

almost always unilateral. Bilateral DVT is rare and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure

DVT:
Calf or leg swelling
Dilated superficial veins
Tenderness to the calf (particularly over the site of the deep veins)
Oedema
Colour changes to the leg

measure the circumference of the calf 10cm below the tibial tuberosity. More than 3cm difference between calves is significant
wells score = predicts risk for patient

Question 18

diagnose DVT?

Answer 18

D-dimer is a sensitive (95%), but not specific, blood test for VTE. This makes it helpful in excluding VTE where there is a low suspicion. It is almost always raised if there is a DVT; however other conditions can also cause a raised d-dimer:

Pneumonia
Malignancy
Heart failure
Surgery
Pregnancy

doppler ultrasound (may need to be repeated to rule out false negative)

Pulmonary embolism can be diagnosed with a CT pulmonary angiogram (CTPA) or ventilation-perfusion (VQ) scan - latter if contrast allergy or kidney impairment

Question 19

manage DVT?

Answer 19

initial = anticoagulation, apixaban or rivaroxaban started immediately
catheter-directed thrombolysis in patients with a symptomatic iliofemoral DVT w/ symptoms lasting less than 14 days

long term anticoagulation in VTE are a DOAC “direct-acting oral anticoagulants” (suitable for most patients, including patients with cancer), warfarin - first-line in patients with antiphospholipid syndrome (vitamin K antagonist), or LMWH (first-line anticoagulant in pregnancy)

• 3 months if there is a reversible cause
• Beyond 3 months if the cause is unclear, recurrent VTE, irreversible thrombophilia
• 3-6 months in active cancer

Inferior vena cava filters = sieve inserted into the inferior vena cava, designed to filter the blood and catch any blood clots travelling from the venous system, towards the heart and lungs - unusual cases or patients who can’t take anticoagulants

Question 20

wtf is budd-chiari syndrome?

Answer 20

Budd-Chiari syndrome is where a blood clot (thrombosis) develops in the hepatic vein, blocking the outflow of blood. It is associated with hyper-coagulable states. It causes acute hepatitis.

It presents with a classic triad of:

Abdominal pain
Hepatomegaly
Ascites

Question 21

wtf is a pulmonary embolism? + RF & prophylaxis

Answer 21

blood clot (thrombus) forms in the pulmonary arteries (usually due to DVT that developed in the legs, travelled (embolised) through the venous system, via right side of hear to pulmonary arteries.
blocks blood flow to lung tissue = strain on right side of heart
DVT & PE = venous thromboembolism

RF:
Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia

(prophylactic treatment for patients at risk =
low molecular weight heparin - Contraindications are active bleeding or existing anticoagulation with warfarin or NOAC)
compression stockings - contraindications is peripheral arterial disease

Question 22

presentation of PE? + diagnosis

Answer 22

Shortness of breath
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension
May be signs of DVT

wells score predicts risk:
likely = perform CT pulmonary angiogram
unlikely = perform d-dimer and if posi perform a CTPA

History
Examination
Chest xray

definitive diagnosis using:
CT pulmonary angiogram =
- chest CT scan with intravenous contrast which highlights pulmonary arteries
- could give alternative diagnoses eg. pneumonia, malignancy
ventilation–perfusion (VQ) scan =
- radioactive isotopes & gamma camera to compare ventilation with perfusion of lungs
- used in patients with renal impairment/contrast allergy/risk of radiation
- isotopes are inhaled to fill lungs, picture is taken to demonstrate ventilation, contrast containing isotopes is injected, picture is taken to demonstrate perfusion = comparison (in PE there is deficit in perfusion as thrombus blocks blood flow to lung tissue - this area of lung tissue will be ventilated but not perfused)

Question 23

what would an ABG show in a patient with a PE?

Answer 23

respiratory alkalosis when an ABG is performed
because the high respiratory rate causes them to “blow off” extra CO2
the low CO2 causes blood to become alkalotic
= respiratory alkalosis
(other main cause is hyperventilation syndrome but Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2)

Question 24

manage a PE?

Answer 24

supportive:
Admission to hospital
Oxygen as required
Analgesia if required
Adequate monitoring for any deterioration

initial management:
DOAC eg. apixaban or rivaroxaban
alternatively LMWH (in antiphospholipid syndrome) eg. enoxaparin, dalteparin

long term:
warfarin, a DOAC (oral anticoag, no monitoring) or LMWH (first line in pregnancy or cancer)

• 3 months if there is a reversible cause
• Beyond 3 months if the cause is unclear, recurrent VTE, irreversible thrombophilia
• 3-6 months in active cancer

thrombolysis
- signif risk of bleeding
- only used in cases of massive PE with haemodynamic compromise (unstable blood flow) as benefits here outweigh risk
- inject fibrinolytic med which breaks down fibrin (when tissue damage results in bleeding, fibrinogen is converted at the wound into fibrin by the action of thrombin, a clotting enzyme) which rapidly dissolves clots
- eg.
streptokinase, alteplase, tenecteplase
- can be IV or directly into pulmonary arteries using central catheter (catheter-directed thrombolysis, inserted into the venous system, through the right side of the heart)

Question 25

functions of mitral and aortic valves?

Answer 25

• Mitral valve = lets blood flow from left atrium to the left ventricle
• Aortic valve = opens when the left ventricle squeezes to pump out blood, and closes in between heart beats to keep blood from going backward into the heart

Question 26

wtf is aortic stenosis? + signs eg. details of murmur

Answer 26

most common valvular disease
aortic orifice (aortic opening) is restricted eg. by calcific deposits and so the LV can't eject blood properly in systole = pressure overload
LV function is initially maintained due to compensatory hypertrophy
Overtime this becomes exhausted = LV failure

causes an ejection-systolic, high-pitched murmur (high velocity of systole) - has a crescendo-decrescendo character due to the speed of blood flow across the valve
slow rising carotid pulse and decreased pulse amplitude

murmur radiates to the carotids as the turbulence continues up into the neck
Slow rising pulse and narrow pulse pressure
Patients may complain of exertional syncope (light-headedness and fainting when exercising) due to difficulty maintaining a good flow of blood to the brain

Question 27

causes & symptoms of aortic stenosis? + investigation

Answer 27

Congenital bicuspid aortic valve
Rheumatic heart disease
Senile calcification of the valve

exertional Syncope
Angina
exertional Dyspnoea

(onset of symptoms = poor prognosis)

investigate:

• Echocardiography - reduced aortic outflow, LVH
• Two measurements obtained: left ventricular size and function + Doppler derived gradient and valve area
• CXR
• ECG

Question 28

manage aortic stenosis? + who offered valve replacement

Answer 28

Ensure good dental hygiene - poor dental health increases the risk of a bacterial infection in the blood stream, which can affect the heart valves
Consider Infective Endocarditis prophylaxis - antibiotics to high-risk patients when they undergo procedures that can induce bacteremia
Aortic valve replacement or TAVI (Transcatheter Aortic Valve Implantation)

valve replacement offered to:

• Symptomatic patients with aortic stenosis
• Any patient with decreasing ejection fraction
• Any patient undergoing CABG (coronary artery bypass graft) with moderate/severe aortic stenosis

(problem is mechanical and so medical therapy does not prevent progression)

Question 29

wtf is mitral regurgitation? + causes & signs

Answer 29

second most common
Backflow of blood from the LV to the LA during systole (contraction of LV) - LV volume overload
s1-s2
leaking valve causes a reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart = congestive cardiac failure

causes:
Idiopathic weakening of the valve with age
Ischaemic heart disease
Papillary muscle rupture
Mitral valve prolapse
Rheumatic heart disease
Infective Endocarditis
Connective tissue disorders eg. Ehlers Danlos syndrome or Marfan's syndrome

signs:
LA enlargement and LVH = to maintain BP
progressive LV vol overload = dilation and progressive heart failure
atrial fibrillation
displaced, thrusting apex

Question 30

symptoms and heart murmur details for mitral regurgitation?

Answer 30

symp:
palpitations
exertional dyspnoea
fatigue

Mitral regurgitation causes a pan-systolic, high pitched “whistling” murmur due to high-velocity blood flow through the leaky valve. The murmur radiates to the left axilla
soft 1st heart sound & third heart sound

In chronic MR, the intensity of the murmur correlates with disease severity

Question 31

investigate and manage mitral regurgitation?

Answer 31

investigate:
ECG - may show LA enlargement, atrial fibrillation and LV hypertrophy
CXR - LA enlargement
Echocardiogram: estimates LA/LV size and function

manage:

• Rate control for AF, e.g. beta blockers
• Vasodilators, e.g. ACEI
• Anticoagulation for AF
• Diuretics for fluid overload
• IE prophylaxis
• If symptomatic = surgery

Question 32

wtf is aortic regurgitation? + causes & symptoms

Answer 32

blood leaks back into the LV during diastole due to ineffective aortic cusps
Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation leads to HF

Bicuspid aortic valve (should be tricuspid), Rheumatic heart disease, IE, Marfan’s syndrome

Palpitation
Angina
Dyspnoea

Question 33

aortic regurgitation: signs, investigation, manage?

Answer 33

Wide pulse pressure
Water hammer pulse
Diastolic blowing murmur
Austin flint murmur (low pitched rumbling)

CXR and echocardiogram

manage:
IE prophylaxis
Vasodilators e.g. ACEI
Regular echocardiograms to monitor progression
Surgery if symptomatic

Question 34

wtf is mitral stenosis? + causes/RF & murmur

Answer 34

narrowing of mitral valve/obstruction to LV inflow that prevents proper filling during diastole

causes:
Rheumatic heart disease (most common)
Congenital bicuspid aortic valve
Calcification
drug use (increases likelihood of infective endocarditis)
diabetes, HTN, smoking

Murmur = rumbling mid-diastolic murmur with opening snap

Question 35

signs/symptoms of mitral stenosis?

Answer 35

Dyspnoea
Haemoptysis - coughing blood (due to pulmonary oedema)
Palpitations (AF)

‘a’ wave in jugular venous pulsations (due to pulmonary hypertension and right ventricular hypertrophy)
Malar flush - pink patches on cheeks due to vasoconstriction
Low pitched diastolic murmur
Loud S1
Tapping apex beat

Question 36

investigate and manage mitral stenosis?

Answer 36

ECG - atrial fibrillation and LA enlargement
CXR - LA enlargement and pulmonary congestion
Echocardiogram - GOLD STANDARD. Assess mitral valve mobility, gradient and mitral valve area

manage:
If in AF rate control, e.g. beta blockers/CCBs
Anticoagulation if AF
Balloon valvuloplasty or valve replacement
IE prophylaxis

(problem is mechanical and so medical therapy does not prevent progression)