cardio Flashcards
(36 cards)
wtf is stable angina? + symptoms
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
investigate stable angina?
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)
manage stable angina?
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
surgery for stable angina?
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
wtf is unstable angina? + diag & treatment
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
wtf is prinzmetal’s angina?
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
diagnose and treat prinzmetal’s angina?
imaging = transient ST segment elevation, transmural ischaemia
meds = calcium channel blockers, vasodilators
wtf is myocardial infarction? + causes
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
wtf is STEMI? + treat
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
complications of MI? (mnemonic)
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
risk factors of MI?
modifiable - old age, smoking, HTN, diabetes mellitus, high cholesterol, low physical activity, obese, excessive alcohol, drug use, chronic stress
non mod - fam history, male
wtf is NSTEMI? + treat
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
signs/symptoms of MI & diagnosis?
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
wtf is a DVT?
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
risk factors of DVT?
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
wtf is VTE prophylaxis?
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
DVT presentation?
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
diagnose DVT?
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
manage DVT?
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
wtf is budd-chiari syndrome?
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
wtf is a pulmonary embolism? + RF & prophylaxis
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
presentation of PE? + diagnosis
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)
what would an ABG show in a patient with a PE?
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)
manage a PE?
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)
