Clinical Scenarios part 2 Flashcards
Differentials for SOB and peripheral oedema?
Seconds to minutes – acute asthma attack, anaphylaxis, pneumothorax), inhaled foreign body, acute PE
Hours to days – Pneumonia, Heart Failure, Pleural Effusion, acute PE
Weeks to months – worsening COPD, chronic asthma, heart failure, pulmonary fibrosis, anaemia, pulmonary hypertensive, obesity.
Investigations for SOB and peripheral oedema?
I would send blood tests for FBC, U+Es, CRP as well as a troponin if it is indicated from the history. Acute coronary syndrome (ACS) may be the cause of the decompensated HF.
I will organise an urgent ECG to assess for any cardiac arrhythmia - especially as the patient has a history of AF - as well as any evidence of acute ischemic changes.
A CXR will be important to look for signs of pulmonary oedema. A CXR will also exclude pneumothorax and consolidation.
An ABG will be useful to assess the PaO₂ and PaCO₂.
I would continue to monitor the patient’s saturations. However, this may be inaccurate if the patient is peripherally shut down.
If there are signs of sepsis I would send off a septic screen – sputum, urine, blood cultures.
When the patient is more stable I will need to arrange an echocardiogram to assess the cardiac function.
CXR signs of pulmonary oedema ?
I would look for interstitial shadowing, enlarged hila, prominent upper lobe vessels, pleural effusion and Kerley B lines. Cardiomegaly may or may not be present.
Management of pulmonary oedema?
Sit up right and start high flow oxygen
Furosemide - the dose should be doubled at two-hour intervals as needed up to the maximum recommended doses. Urinary catheter - monitor urine out put
Vasodilator therapy - with urgent need for after load reduction (e.g. severe hypertension) It is recommended as an adjunct to diuretic therapy when there has been inadequate response. Therefore, based on the response to the above and if the SBP is >90 mmHg and the patient does not have aortic stenosis, then I could start an IV infusion of GTN and titrate the dose against the BP.
If BP < 90 - consider contacting ITU for inotropic support
Causes of decompensation of HF?
Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), acute coronary syndrome, cardiac arrhythmias (such as AF), uncontrolled hypertension, or the person’s failure to maintain an adequate fluid restriction, diet, or a lack of compliance with medication.
Classification of heart failure?
New York heart association function classification
I - Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. no shortness of breath when walking, climbing stairs, etc.
II - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III- Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m).
Comfortable only at rest.
IV - Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.
What medications improve morbidity and mortality in patients with heart failure?
Angiotensin converting enzyme (ACE) inhibitor and single-agent angiotensin receptor blockers (ARB), have both been shown to reduce morbidity and mortality in patients with heart failure with reduced ejection fraction. A well known study is the SAVE trial that demonstrated a 19% reduction in mortality with captopril compared to placebo.
In addition, beta-blockers and mineralocorticoid receptor antagonists (such as Spironolactone) have also been shown to reduce morbidity and mortality in these patients with heart failure with reduced ejection fraction.
It is important to initiate these treatments in these patients once they have been stabilised following their acute admission. They should be up titrated to the highest tolerated dose.
Recent evidence from the DELIVER trial suggests a role for SGLT2 inhibitors in reducing morbidity and mortality for patients with heart failure and a reduced ejection fraction, although these drugs are not yet part of the routine management as per the NICE guidelines (Reference).
Counselling on DOAC?
- importance of adherence
- no monitoring required
- Signs and symptoms of unusual bleeding and to seek urgent medical attention
- they may notice they are more at risk of bleeding from small innocuous events
- they need to inform doctor/dentist if having any planned procedures
- should carry a patent alert card
- provide written information
A-E assessment in epilepsy?
Open the airway by laying the patient on her side in a semiprone position.
If possible try to place an OP or NP airway.
B - high flow oxygen
E - look for head injury
causes of seizure?
If has diagnosis of epilepsy - usual presentation of seizure, new medication, reduced dose, poor compliance, withdrawal of medication
Alcohol
Overdose - e.g. tricyclic
Electrolyte disturbance
Infection - meningitis
head injury
hypoglycaemia
Space occupying lesion
Can be divided into
Metabolic and Electrolyte Disturbance - hypo/hyperglycaemia, hypo/hypernatraemia, hypocalcaemia, uremia, hepatic encephalopathy
Central Nervous System (CNS) pathologies - traumatic brain injury, stroke, tumours or lesions, CNS infections
Substance related causes - alcohol withdrawal, illicit drugs, carbon monoxide
Hypoxia
Eclampsia
Investigations for seizure?
Bloods - U&E’s CBG, calcium, magnesiums, liver enzymes, and FBC
toxicology screen
***blood levels for anticonvulsants
ECG
monitoring observation
CT head
MRI head
EEG
management of seizure?
stabilise patient - most seizure terminate without any intervention - supportive management through oxygen< IV fluids and treat hypoglycaemia
> 5 minutes - benzes - Rectal diazepam or IV lorazepam.
if continues - ITU referral
IV infusion of phenytoin
why is lorazepam better than diazepam ?
Because lorazepam has strong cerebral binding, a long duration of action and does not accumulate in lipid stores, it has distinct advantages over diazepam in early status epilepticus.
what is status epileptics?
Status epilepticus is a single epileptic seizure lasting more than five minutes, or two or more seizures within a five minute period, without the person returning to normal in between them.
Status epilepticus can be divided into both convulsive and non-convulsive. Non-convulsive status can be difficult to diagnose.
what is refractory status and how is it managed?
Refractory status is where seizures continue beyond 60 minutes after initial therapy.
Refractory status should be treated by transferring the patient to ITU as they will require general anaesthesia (either propofol or thiopental). EEG monitoring should be commenced.
complications of status?
Hyperthermia
Acidosis (secondary to raised lactate)
Hypotension
Respiratory failure
Rhabdomyolysis
Aspiration
What is important to tell a patient presenting with seizures for the first time?
Driving - inform DVLA
not driving 6 months
LGV or passenger carrying vehicle should not drive for 5 years
Advice should be given about risks such as bathing – they should shower instead. A patient should be advised not to swim alone.
Describing SVT on ECG?
describe if regular or irregular
Are there p waves - no waves could be due to the rate nd may be buried in the preceding T wave. Not being able to see P waves indicates SVT rather than sinus tachy
look at QRS complex
ST depression or elevation
comment on the rate
causes of SVT?
Cardiac causes – MI, Heart Failure, Cardiomyopathy – anything which interferes with the conduction systems in the heart
Respiratory causes – the most common presentation of PE is tachycardia! Should be high on your initial differentials, however, normal sats point against this.
Infection – the most common cause of SVT presenting to hospital. You will want to look for other symptoms and signs. Lack of temperature reduces this possibility
Metabolic causes – Thyroid problems can cause arrhythmias
Volume loss – anaemia or volume loss secondary to increased GI loss
Electrolyte imbalance – Hypo/Hyperkalaemia (although there are no specific signs in this ECG, it should still be included), Hypomagnesaemia
Drugs and alcohol – caffeine, alcohol, beta-agonists (salbutamol), amphetamines
Pain and stress – A differential that should not be forgotten as it can be easily treated. May be linked with one above – e.g. MI
How do you manage SVT?
My management of tachycardia would then be determined by whether the patient is stable or unstable, the type of tachycardia, and the likely cause.
I would use an ABCDE approach to first establish this, and ensure the following key parts of the management are enacted.
Check airway, breathing, and circulation.
Give oxygen if the oxygen saturation is less than 94% or the patient is short of breath.
Perform a 12 lead ECG if the patient is stable.
Identify rhythm.
Check blood pressure.
Obtain IV access. A fluid challenge can be given to see if tachycardia is responsive to volume status.
Identify and treat reversible causes if the rhythm is sinus tachycardia.
If the ECG was SVT and patient stable - attempt to reverse the using vagal manoeuvres
if unsuccessful - follow ALS guidelines of management of SVT. Escalate to my senior
essential to continue assessing using the A-E approach.
Investigations for SVT?
Bedside: ECG; ABG/VBG (quickly alert you to electrolyte imbalance. An ABG would be more useful if underlying respiratory cause is suspected); Blood pressure.
Bloods: FBC (anaemia and infection markers); U+Es + Mg (electrolyte imbalances and kidney function – may have AKI if hypovolemic); TFTs; LFTs (if alcohol or medications are suspected); CRP (infection); Troponin (If MI is being considered)
CXR – underlying chest infection. Signs of cardiomegaly. Signs of heart failure
ECHO – to look for structural heart disease
24 hour tape – this is more of a long-term investigation if SVTs are thought to be secondary to cardiac arrhythmias or paroxysmal.
medications for SVT?
important for treating the underlying cause
IV fluids, Abx, ACS protocol etc
Adenosine 6mg, followed by a further 12mg in no initial effect
(if adenosine worked - the tachycardia can be considered nodal in origin (if it is atrial in origin, adenosine will only transiently block it. It can self terminate but often reverts back)
If tachycardia resumes - could consider beta blockers or CCB (diltiazem)
contraindications for adenosine?
what should you tell a patient before giving adenosine?
nd or 3rd degree heart block without a pacemaker; Long QT syndrome; decompensated heart failure; Asthma. B
Before giving you should explain to the patient that they may experience flushing, nausea, light-headedness associated with a ‘sense of impending doom’. This is secondary to TRANSIENT asystole following IV administration.
Patient with SVT - The patient starts becoming hypotensive, with a BP of 80/50 mmHg, HR 170 bpm, and sats 88%. What would you now do?
This patient is now UNSTABLE. At this point you should call a senior for help and put out a 2222 call. This shows to the examiners you have identified early that this patient could deteriorate further! Following this you should start IV fluid resuscitation and give oxygen.
As per ALS guidelines, since this patient has an SVT and is haemodynamically unstable, he should be considered for immediate DC cardioversion.
How to differentiate SVT?
SVTs can be broken down by site of origin and rhythm regularity. Is the SVT atrial in origin or atrioventricular? Is the rate regular or irregular?
Atiral tachycardias - AF, A flutter, focal atrial tachycardia.
AV node-dependent tachycardia - AVNRT (most common type of SVT), AVRT (involving an accessory pathway - Wolff-parkinson-white)
Can be classified based on mechanism (re-entry, focal or triggered) or site of origin (atrial, AV node dependent, or junctional)
what is DKA?
Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes mellitus, characterized by hyperglycemia, ketosis, and metabolic acidosis.
What leads to DKA?
DKA results from an absolute or relative deficiency of insulin, leading to increased hepatic glucose production, decreased peripheral glucose utilization, and enhanced lipolysis with subsequent ketone body formation.
Precipitants of DKA?
Infection - Acute infections can increase insulin requirements by inducing a state of physiological stress and elevating counter-regulatory hormones.
Non compliance with treatment
Newly diagnosed diabetes
Certain medications: Drugs such as glucocorticoids, thiazide diuretics, atypical antipsychotics and sodium-glucose co-transporter-2 (SGLT2) inhibitors can increase the risk of DKA by raising blood glucose levels or decreasing insulin sensitivity
myocardial infarction, stroke, pancreatitis, or medication non-compliance
Clinical features of DKA?
Hyperglycaemia - will lead to osmotic diuresis = polyuria and polydipsia, blurred vision, headache, and lethargy
Acidosis - thi will lead to deep rapid breathing (kussmaul) as a compensatory mechanism to expel carbon monoxide
Ketosis - due to insulin deficiency increased lipolysis leads to production of ketone - ketosis presents with characteristic sweet, fruity, or acetone odour on the breath
Dehydration and electrolyte imbalance - particularly hypokalaemia which can lead to cardiac arrhythmias
Neurological symptoms - altered mental status due to the effects of acidosis and hyperosmolarioty on cerebral function, seizures may be observed in severe cases
abdominal symptoms - abdo pain, nausea and vomiting are common due to ketones and delayed gastric emptying - the abdo pain can mimic an acute abdomen
Polyuria and polydipsia
Dehydration
weight loss
weakness
Hyperventilation or breathlessness
The acidosis can cause Kussmaul’s respiration (rapid deep breathing)
Abdominal pain - DKA may present as an acute abdomen
Vomiting
Confusion
blurred vision, headache, lethargy
DKA - key things to remember in A-E
A - as normal
B - as normal C - remember ECG, remember to start IV fluids, may need arterial line - easy access to get ABGs - contact ITU if these are required. Remember cap refill and urinary catheter
D- remember to check BM and ketones
Investigations for DKA?
ABG and blood glucose
Routine bloods
Serum osmolality
Blood cultures for underlying infection
urine sample and CXR as infection screen
DKA Diagnosis
British Diabetes Societies
CBG > 11
PH < 7.3
bicarb < 15
Ketones > 3 or urinary ketones +++
How is DKA managed?
I would follow the trust protocol
FLuid replacement - average fluid loss in DKA is 100mL/kg.
STAT bags as quickly as possible
Fixed rate insulin infusion should be started following fluid resuscitation - 0.1unit/kg/hour
Review response hourly
If blood glucose is not dropping by 5mmol/h and capillary ketones by 1mmol/L the infusion is increased by 1 unit/hour.
This is continued until capillary ketones <0.6, venous pH >7.3 and venous bicarbonate >18. At this point if the patient is eating and drinking regularly, you can change to a SC insulin regimen and stop the FRIII Insulin.
If the patient is on long-acting insulin this should be continued at their usual dose from the day of admission.
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
Closely monitor potassium.
Can fall quickly with insulin treatment
may need to be added to replacement fluids
what is resolution of DKA defined as?
pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L
Indicators for early referral to ITU in DKA?
pH < 7.1
Severe DKA by the following criteria: Ketones >6 mmol/L or Bicarbonate <5 mmol/L
Hypokalaemia on admission (<3.5)
GCS < 12
Systolic BP < 90
Significant co-orbidities
pregnant
