Chest pain and Cardiology Flashcards
causes of long QT
antiarrhythmics: amiodarone, sotalol
TCA
antipsychotics
chloroquine
erythromycin
hypocalcaemia
hypokalaemia
hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage
acute management of torsades de pointes
IV magnesium sulphate
if VT occurs, defibrillation
management of long QT syndrome
avoid drugs
avoid strenuous exercise
beta blockers
implantable cardioverter defibrillators
definition of status epilepticus
a single seizure lasting >5 minutes, or
>= 2 seizures within a 5-minute period without the person returning to normal between them
management of status epilepticus
Secure the airway
Give high-concentration oxygen
Assess cardiac and respiratory function
Check blood glucose levels
Gain intravenous access (insert a cannula)
IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
If seizures persist: IV phenobarbital or phenytoin
acute management of SVT
valsalva
carotid sinus massage
adenosine or verapamil
direct current cardioversion
prevention of SVT episodes
beta blockers
radio-frequency ablation
hypoglycaemia management
If the patient is alert, a quick-acting carbohydrate may be given (as above)
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein
clinical features of HHS
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
HHS diagnosis
severe hyperglycaemia (>=30mmol/L)
hypotension
hyperosmolality (usually >320 mosmol/kg).
management of HHS
fluid resuscitation with saline and KCl
insulin at 0.05units/kg/hr if ketones>1 or glucose fails to fall
VTE prophylaxis
presentation of CO monoxide poisoning
Confusion
Nausea and vomiting
Cherry red skin
Tachycardia
100% oxygen saturations on pulse oximetry
CO poisoning investigation
VBG/ABG: A carboxyhaemoglobin concentration >20% is diagnostic
Chest x-ray - looking for evidence of Acute Respiratory Distress Syndrome
ECG - looking for ischaemic changes
Bloods including a Creatine Kinase (rhabdomyolysis)
management of CO poisoning
100% oxygen via face mask - helps unbind CO from the haemoglobin molecule
Hyperbaric oxygen - controversial but widely considered gold standard
causes of bradycardia
Can be normal in athletic individuals
Electrolyte disturbances
Hypothyrodism
Myocardial Infarction
Sepsis
Drugs e.g beta blockers
Increased intracranial pressure
Heart block
management of bradycardia
IV atropine
epinephrine
dopamine
temporary pacing if no response to medical therapy
causes of ventricular tachycardia
hypokalaemia
hypomagnesaemia
MI/HOCM
Brugada
common causes of AF (mrs SMITH)
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension
management of acute pulmonary oedema
Take an ABCDE approach
Sit the patient up
Administer oxygen
Ensure IV access
IV Furosemide
Consider non-invasive ventilation such as CPAP if failed medical therapy (usually in an intensive care setting)
Consider further therapies in the intensive care setting such as invasive ventilation and inotropic support if the above fails
pulmonary oedema management with heart failure and renal impairment
Therefore, by off-loading fluid with diuresis, the stroke volume improves, there is greater output from the heart, and so perfusion to the kidneys improve. Overall, when there is elevated central venous pressure, the renal function may recover with the aid of diuresis.
management of heart failure with hypotension
vasopressors
These measures are only temporary and aim to maintain perfusion to the end-organs until the acute trigger for the deterioration has been reversed, or a definitive therapy (e.g. coronary revascularisation, mechanical circulatory support, or heart transplantation) has been employed.
well’s PE
3 points:
Clinical signs and symptoms of a deep vein thrombosis (DVT)
If no alternative diagnosis is more likely than a PE
1.5 points:
Tachycardia (heart rate >100 beats/minute)
If the patient has been immobile for more than 3 days or has had major surgery within the last month
If the patient has had a previous PE or DVT
1 point:
If the patient presents with haemoptysis
If there is an active malignancy
acute management of PE
Airway: likely to be patent.
Breathing: the patient may be tachypnoeic and hypoxic. Oxygen should be administered.
Circulation: the patient may be tachycardic. Signs of right heart strain are suggestive of a sub-massive PE. Hypotension is suggestive of a massive PE. Consider intravenous fluids if the systolic blood pressure is <90 mmHg.
Disability: likely to be unremarkable.
Exposure: the patient may have a low grade pyrexia. It is important to check for signs of a deep vein thrombosis (DVT). Consider analgesia at this stage if required.
medical management of PE
dabigatran, edoxaban, warfarin
LMWH for 5 days and until 48 hours of therapeutic INR >2 has been achieved if using warfarin
if using dabigatran or edoxaban them LMWH should be used for d days prior
