Cardiology

Mark A Rodrigues and Emily R McCall-Smith

Outline

Station 2.1: Acute pericarditis

Station 2.2: Acute left ventricular failure

Station 2.3: Acute coronary syndrome

Station 2.4: Bradycardia

Station 2.5: Tachycardia

Station 2.6: Warfarin prescribing

Station 2.1: Acute pericarditis

You are an emergency department junior doctor. Your next patient is Jason Anderson (DOB 22/03/85), a 29-year-old man who has come in with chest pain. He says he has felt generally unwell over the last few days with a fever, muscle ache and a sore throat. Today he developed sharp retrosternal chest pain radiating to his neck. The pain is worsened by movement and breathing. Please assess Mr Anderson and instigate appropriate management.

Patient Details

Name:	Jason Anderson
DOB:	22/03/85
Hospital Number:	4495039943
Weight:	60 kg
Height:	1.8 m
Consultant:	Dr Chang
Hospital/Ward:	RIE Ward 6
Current Medications:	None
Allergies:	None
Admission date:	19/10/14

Initial differential diagnosis of sharp chest pain

Cardiac: Acute pericarditis, acute coronary syndrome, angina

Respiratory: Pneumothorax, pneumonia, pulmonary embolism

Gastrointestinal: Oesophagitis, oesophageal spasm

Other: Musculoskeletal chest pain, shingles

Acute pericarditis management

NSAIDs (+gastric protection)

Colchicine

May require pericardiocentesis/drainage if a pericardial effusion is present

Initial Assessment

Airway

Assess the patency of the airway

‘The patient is maintaining a patent airway.’

No additional airway support required.

Breathing

Assess respiratory rate, oxygen saturations, and work of breathing. Palpate for chest wall tenderness. Percuss; hyper-resonance suggests a pneumothorax, dullness to percussion suggests pleural effusion or pneumonia. Auscultate for air entry, and additional sounds of wheeze and crepitations

‘Respiration rate (RR) 12/min, oxygen saturations are 97% on air. No chest wall tenderness. The chest is resonant throughout. Good air entry is heard bilaterally with no wheeze or crackles.’

No respiratory support required.

Circulation

Assess haemodynamic stability by measuring pulse, blood pressure, capillary refill time

Perform a cardiovascular exam. A pericardial friction rub points to pericarditis. Muffled heart sounds, a raised jugular venous pressure (JVP), and hypotension points to cardiac tamponade

‘Heart rate (HR) 78 bpm regular, blood pressure (BP) 128/64 mmHg, capillary refill time (CRT)<2 seconds. The JVP is not elevated. Cardiovascular (CV) exam shows normal heart sounds (HS), with a pericardial friction rub. No murmurs.’

Obtain intravenous (IV) access and send off bloods.

In patients with chest pain, ask a colleague to perform an ECG while you perform your clinical assessment.

Disability

Assess the patient’s conscious level, using AVPU (Is the patient Alert? If not, do they respond to Verbal or Painful stimuli? Or are they Unresponsive?). Check glucose levels

‘The patient is alert. Blood sugar 6.9 mmol/L.’

Exposure

Expose the patient, and perform a full examination (while maintaining the patient’s dignity). In particular, look at the throat for evidence of upper respiratory tract infection and the chest wall for signs of shingles. Measure the temperature

‘Temperature is 37.2°C. There is mild erythema in his throat, with some palpable cervical lymph nodes. The rest of the examination is normal.’

Causes of acute pericarditis

Viral

Acute myocardial infarction

Autoimmune disease, e.g. rheumatoid arthritis or SLE

Uraemia

Malignant disease

Bacterial or TB infection (rare in UK)

Rheumatic fever (rare in UK)

ECG changes in acute pericarditis

Initially concave anterior and inferior ST elevation

ST segments will return to baseline over the next couple of weeks with T wave inversion developing

PR depression

ECG returns completely to baseline usually after a few months

Initial Investigations

Bloods: FBC, U&Es, ESR, CRP. Look for evidence of inflammation. Troponin is used as a marker of myocardial damage (elevated in ≈50% with pericarditis) but may also help differentiate from acute coronary syndrome. U&Es will show elevated urea in uraemic pericarditis

ECG: Classical finding is widespread ‘saddle-shaped’ ST elevation with upwards concavity in I, II, aVF, aVL and V3–6. PR depression is virtually diagnostic of pericarditis. Helps distinguish from myocardial infarction

CXR: Can range from normal to the classic water-bottle-shaped heart seen with pericardial effusions. Helps exclude differential diagnoses such as pneumothorax and pneumonia

Echo: Will show pericardial effusions (present in 10% of cases of pericarditis) and tamponade if present–though tamponade should be diagnosed clinically. It will also demonstrate concomitant heart disease, such as left ventricular wall motion abnormalities seen post-myocardial infarction

Table 2.1

Mr Anderson’s blood test results

Parameter	Value	Normal range (units)
WCC	18×10⁹/L	3.2–11 (×10⁹/L)
Neutrophil	8×10⁹/L	1.9–7.7 (×10⁹/L)
Lymphocyte	9×10⁹/L	1.3–3.5 (×10⁹/L)
Platelet	350×10⁹/L	120–400 (×10⁹/L)
Haemoglobin	140 g/L	Men: 135–180 (g/L) Women: 115–160 (g/L)
ESR	48 mm/h	Men: (Age in years)/2 (mm/h) Women: (Age in years+10)/2 (mm/h)
CRP	63 mg/L	0–10 (mg/L)
Urea	6 mmol/L	2.5–6.7 (mmol/L)
Creatinine	80 μmol/L	70–130 (μmol/L)
eGFR	>60 mL/min	>60 (mL/min)
Sodium	140 mmol/L	135–145 (mmol/L)
Potassium	4 mmol/L	3.5–5.0 (mmol/L)
Troponin	0.01 μg/L	0–0.1 (μg/L)

‘Bloods show an elevated WCC (18×10⁹/L), ESR (48 mm/h) and CRP (63 mg/L). Troponin and U&Es are normal. ECG shows widespread concave ST elevation and PR depression. CXR shows mild cardiomegaly, with clear lungs and no pneumothorax. The ECHO shows a small pericardial effusion.’

Initial Management [1]

This patient has acute pericarditis, most likely secondary to a viral infection

Airway support: Airway patent in this case, with no intervention required

Supplementary oxygen: If saturations<94%

NSAID: Ibuprofen is preferred due to its side-effect profile and large dose range (300–800 mg 6–8 hourly depending on severity)

Colchicine: Can be used in combination with NSAIDs or as a monotherapy as a second line treatment. Dose is 0.5 mg oral twice daily

Additional analgesia: Use the World Health Organization pain ladder, starting at the most appropriate level

Gastric protection: Should be considered in all patients starting NSAIDs particularly those at increased risk of gastrotoxicity such as the elderly

Thromboembolic risk assessment: This should be considered but, in a potential pericardial effusion, avoid blood thinning agents due to risk of haemorrhagic transformation of the effusion.

Prescribe (see Figs 2.1 and 2.2)

Anti-inflammatory, e.g. IBUPROFEN 400 mg STAT then TDS ORAL

Gastric protection, e.g. OMEPRAZOLE 20 mg OD ORAL

Analgesia, e.g. CO-CODAMOL 30/500 2 tablets STAT then 2 tablets QDS ORAL

Mechanical thromboembolic prophylaxis, e.g. TED STOCKING TOP

Figure 2.1

Figure 2.2

Corticosteroids are not routinely used in acute pericarditis. They are reserved for patients with connective tissue disease, autoimmune or uraemic pericariditis. Corticosteroids may also be helpful in recurrent pericarditis, and in patients refractory to NSAIDs and colchicine.

Complications of acute pericarditis

Cardiac tamponade

Recurrence

Constrictive pericarditis

Pericardial effusion

Reassessment

After receiving some ibuprofen and co-codamol the patient is reassessed

‘Mr Anderson looks more comfortable. He still has chest pain but it is not as severe. His observations remain stable and his clinical examination is unchanged.’

Definitive Treatment

Tapered dose of NSAIDs as the patient recovers. The patient with viral pericarditis usually takes a few days to weeks to recover

Pericardiocentesis: Mandatory in patients with cardiac tamponade (hypotension, raised JVP, muffled heart sounds and pulsus paradoxus). It should be considered in patients with possible bacterial or neoplasic pericarditis. It is optional in patients with large or recurrent pericardial effusions or patients with small pericardial effusions in whom the other tests have been inconclusive (allows identification of underlying aetiology of the effusion).

Handing over the Patient

‘Mr Anderson is a 29-year-old man with acute viral pericarditis. He presented with sharp chest pain on a background of an upper respiratory tract infection. He is haemodynamically stable. Investigations are in keeping with viral pericarditis and a small pericardial effusion, confirmed on echo. He has commenced ibuprofen, co-codamol and gastric protection.

He has been reviewed by the cardiology registrar and will be admitted to the cardiology ward overnight for observations with a view to discharge tomorrow and a repeat echocardiogram in a couple of days to ensure the pericardial effusion is not enlarging. He requires a pain review later this evening.’

Station 2.2: Acute left ventricular failure

You are the junior doctor on the hospital-at-night team. One of the nurses fast-bleeps you to see an 84-year-old lady, Mrs Margaret Jenkins (DOB 20/08/30), who has become acutely breathless and is coughing up pink frothy sputum. She was admitted last night, and has been given 4 litres of fluid in the last 12 hours following an episode of diarrhoea where she had become clinically dehydrated.

She was diagnosed with moderate left ventricular systolic dysfunction 2 weeks ago after an episode of collapse. At this point she was started on an ACE inhibitor, a beta-blocker, and furosemide: all of which have not been prescribed on this admission due to the dehydration.

Patient Details

Initial differential diagnosis of acute dyspnoea

Cardiac: MI, pulmonary oedema, cardiac tamponade

Respiratory: asthma, pneumothorax, PE, pneumonia

Anaphylaxis

Inhaled foreign body

Metabolic acidosis

Acute LVF initial management summary: ‘L, M, N, O, P’

Loop diuretic

Morphine (& metoclopramide)

Nitrates

Oxygen

Posture

Initial Assessment

Airway

Assess patency of the airway

‘There are a large amount of frothy pink secretions coming from the patient’s mouth, and you hear a strange choking noise.’

You clear the patient’s airway using suction, and the airway noises clear.

Breathing

Sit the patient up

Assess respiratory rate, oxygen saturations, and work of breathing

Perform a respiratory exam–particularly looking for use of accessory muscles and bibasal crackles on auscultation

‘RR is 34/min, oxygen saturations are 82% on room air. There is no history of COPD. Mrs Jenkins is using her accessory muscles. There are coarse bibasal crackles.’

Start the patient on 15 L oxygen via a non-rebreather mask. Perform an ABG and request an urgent portable CXR.

Circulation

Assess haemodynamic status by measuring pulse, blood pressure, capillary refill time and urine output

Perform a cardiovascular exam, looking at the JVP, listening to the heart for murmurs, e.g. VSD or mitral regurgitation, and additional heart sounds. Feel for hepatomegaly or ascites, and check for peripheral oedema in the ankles, or over the sacrum in bed-bound patients.

‘The patient is tachycardic at 150 bpm, with a BP of 152/90 mmHg and CRT of 3 seconds. She looks distressed and is sweating profusely. The JVP is raised–so much so that you see the earlobe ‘wiggling’. You hear a third heart sound on auscultation. Mrs Jenkins has pitting oedema of both legs to the knees.’

Stop IV fluids, and treat for pulmonary oedema (furosemide, glyceryl trinitrate, morphine (with metoclopramide)). Perform an ECG looking for any precipitating causes for the LVF, e.g. arrhythmias, LVH (secondary to hypertension) or ischaemia. Obtain IV access and take bloods. Insert a urinary catheter if not already in place, to allow accurate assessment of fluid balance.

Prescribe (see Figs 2.3–2.5)

High-flow oxygen, e.g. 15 L/min of OXYGEN (via a NON-REBREATHER MASK)

Loop diuretic, e.g. FUROSEMIDE 40 mg IV STAT

Nitrates, e.g. GLYCERYL TRINITRATE 800 micrograms (2 sprays) SL STAT

Analgesia/venodilator, e.g. MORPHINE SULFATE 1 to 10 mg (titrate to response) IV STAT

Antiemetic, e.g. METOCLOPRAMIDE 10 mg IV STAT

STOP

IV fluids

Figure 2.3

Figure 2.4

Figure 2.5

Disability

Assess the patient’s GCS or AVPU, and check the blood sugar.

‘The patient is GCS 14 (E4, M6, V4). Blood sugar is 4.0 mmol/L.’

Exposure

Expose the patient while ensuring you maintain her dignity

Examine the abdomen (although this can also be part of the CVS exam)

Check the temperature

‘Abdominal examination is unremarkable. Temperature is 35.9°C.’

LVF is most commonly caused by ischaemic heart disease, but it can also be due to hypertension, cardiomyopathy or aortic/mitral valve disease.

Cardiomegaly on CXR is defined as a cardiothoracic width ratio>50% (compare the transverse diameter of the heart with the transverse diameter of the lungs). This is only an accurate sign if seen on a PA (postero-anterior) CXR.

Initial Investigations

CXR: Look for the typical features of LVF, although the radiographic changes can lag behind the clinical picture. Features of pulmonary oedema on chest X-ray are bat’s wing shadowing, pleural effusions, Kerley-B lines, cardiomegaly and upper lobe diversion. Look for other causes of acute dyspnoea, such as consolidation or pneumothorax

ECG: Look for ischaemic changes indicating an MI which may have caused the LVF, or arrhythmias, such as fast AF, which can cause or be a consequence of LVF

ABG: This will likely show hypoxia. Initially the PaCO₂ might be low due to hyperventilation, but may rise later due to reduced gas exchange. Look to see if the patient is acidotic, as this is important in determining whether CPAP (type 1 respiratory failure) or BiPAP (type 2 respiratory failure) is required. Remember patients with renal failure may already have a metabolic acidosis, and therefore could be acidotic with a normal PaCO₂ as well as with type 2 respiratory failure. Indeed a metabolic and respiratory acidosis might exist together

Echo: An important investigation to be performed early. This may demonstrate the cause of heart failure, e.g. left ventricular systolic dysfunction or aortic stenosis, which guides decision about treatment later on, e.g. ACE inhibitor/beta-blocker for LVSD, surgery for AS

Bloods: FBC, U&Es, LFTs, TFTs, CRP. Look for evidence of infection by doing an FBC and CRP. Look for anaemia as this may exacerbate heart failure. Check U&Es as you will be treating the patient with diuretics and an ACE inhibitor, and look at the LFTs–which may be deranged if there is hepatic congestion in right heart failure. Check blood glucose for diabetes. Troponin may be high if an MI has precipitated the LVF; however, it may be difficult to interpret as it can be raised by LVF itself. Thyroid function tests should be done, as thyroid disease can aggravate or mimic heart failure

Table 2.2

Mrs Jenkins blood test and arterial blood gas results

Parameter	Value	Normal range (units)
WCC	10×10⁹/L	3.2–11 (×10⁹/L)
Neutrophil	6×10⁹/L	1.9–7.7 (×10⁹/L)
Lymphocyte	3×10⁹/L	1.3–3.5 (×10⁹/L)
Platelet	200×10⁹/L	120–400 (×10⁹/L)
Haemoglobin	150 g/L	Men: 135–180 (g/L) Women: 115–160 (g/L)
CRP	4 mg/L	0–10 (mg/L)
Urea	6.8 mmol/L	2.5–6.7 (mmol/L)
Creatinine	156 μmol/L	70–130 (μmol/L)
eGFR	58 mL/min	>60 (mL/min)
Sodium	140 mmol/L	135–145 (mmol/L)
Potassium	4.2 mmol/L	3.5–5.0 (mmol/L)
Bilirubin	5 μmol/L	3–17 (μmol/L)
ALT	20 IU/L	5–35 (IU/L)
ALP	57 IU/L	30–300 (IU/L)
pH	7.35	7.35–7.45
PaO₂	8 kPa on air	>10 (kPa) on air
PaCO₂	4.9 kPa	4.7–6.0 (kPa)
HCO₃	24 mmol/L	22–26 (mmol/L)

‘CXR shows cardiomegaly, upper lobe venous diversion, pleural effusions, with fluid in the horizontal fissure, and Kerley-B lines. ECG shows sinus tachycardia. Bloods show a normal FBC, urea 6.8 mmol/L, creatinine 156 µmol/L, eGFR 58 mL/min, Na 140 mmol/L, K 4.2 mmol/L. TFTs are in progress. LFTs are normal. ABG on air shows type 1 respiratory failure, with a PaO₂8 kPa, PaCO₂4.9 kPa, pH 7.35, HCO₃24 mmol/L.’

Initial Management [2]

The acronym ‘L, M, N, O, P’ is a helpful way to remember the most important treatments:

Loop diuretic: Treat with furosemide. If the patient is diuretic naïve and has normal renal function, then 40 mg IV is adequate. If the patient is already on diuretics or has renal failure, then higher doses may be needed, e.g. 50–100 mg IV. Doses above 50mg must be given by IV infusion, and at a rate no faster than 4 mg/min. Elderly people, especially if they have a low body weight, will also require a dose reduction. Diuretics will cause immediate vasodilation as well as the delayed diuresis

Morphine Sulfate: Titrate 1–10 mg in 1 mg increments according to response. It will reduce anxiety and pain, as well as causing vasodilation which will reduce preload on the heart. Reduce the dose if the patient is elderly, frail or has a history of respiratory disease. Don’t forget to prescribe a prophylactic antiemetic with it, for example, metoclopramide 10 mg IV. Monitor respiratory rate while giving morphine

Nitrates: Give 800 micrograms (2 sprays) of sublingual glyceryl trinitrate immediately providing the systolic BP is>100 mmHg. Common side effects are headache and hypotension. For patients with severe LVF, or patients who haven’t responded to SL glyceryl trinatrate+morphine, consider a nitrate infusion (if BP still>100 mmHg). The starting dose depends on baseline BP, usual dose is 0.3 mg/h–1 mg/h. This will reduce the cardiac preload

Oxygen: Should be given to treat hypoxaemia when oxygen saturation is<90%, which is associated with an increased short-term mortality. Oxygen shouldn’t be given routinely, as it can cause vasoconstriction and reduced cardiac output. Consider CPAP for early refractory hypoxia

Posture: Simple but important–sit the patient up

Monitor urine output: Insert a catheter. This will demonstrate whether a good diuresis has occurred. Start a fluid balance chart

If the patient has evidence of bronchospasm, treat with salbutamol nebulizer, e.g. 5 mg, which will improve work of breathing and improve oxygen saturation

DVT prophylaxis: As per local protocol, to be given in patients not already on anticoagulation with no risk factors

Consider early HDU/ITU referral: The patient may need CVP monitoring, or ventilation support (CPAP for type 1 respiratory failure, or BiPAP for type 2 respiratory failure).

Prescribe (see Figs 2.3–2.5)

Loop diuretic, e.g. FUROSEMIDE 40 mg OD and 60 mg OD IV (total 100 mg in 24 h)

Ensure on appropriate thromboprophylaxis

Reassessment

Repeat the ABCDE process

‘Mrs Jenkins does not appear to be much better. She is still producing secretions and is now requiring airway support with an NP tube. RR is now 36/min. Oxygen saturations are 93% on 15 L oxygen. There are still loud bibasal crackles. HR is 125 bpm and BP is 98/66 mmHg. Peripheries are clammy with a CRT of 3 seconds. Cardiac examination is unchanged. Mrs Jenkins has passed approximately 10 mL of urine over the last 45 minutes. The nurse is worried about managing her on the ward as they have other patients who require their attention.’

You need to speak with ITU urgently. The patient has had a poor response to the initial treatment. In severe or resistant cases, patients may require support with an intra-aortic balloon pump. Invasive monitoring and inotropes may be required, particularly as she is now hypotensive. Obviously this is something that a junior doctor will not be required to deal with, but it is useful to know what further treatment may be available.

When you’re working night shifts you will often be given a pile of fluid charts for patients who are on IV fluids. While it can be time consuming to assess every individual patient, this scenario highlights the importance of regular fluid reviews.

When doing a fluid review:

Look at the fluid chart to calculate the fluid balance

Check the observations and recent U&E results

Examine the patient–look at the capillary refill, look for dry mucous membranes, check the JVP, listen to the heart and lungs, and look for peripheral oedema

If you’ve done a fluid review, by all means write up a couple of bags of IV fluid at one time if the patient is stable, but why not write on the chart ‘assess fluid status after bag 3’ as a reminder for the next doctor who comes along to prevent situations like this happening.

Handing over the Patient to ITU

‘My name is Emma Smith and I’m the FY1 covering the wards tonight. I’d like to discuss a patient with you, whom I’d like you to review please.

The patient is Mrs Jenkins, an 84-year-old lady, who has developed acute pulmonary oedema this evening, after treatment with IV fluids for the last 2 days. She is known to have a history of moderate LVSD, but has no other significant medical history.

She has failed to improve significantly despite high-flow oxygen, morphine, furosemide and glyceryl trinitrate spray. Her current observations are oxygen sats 93% on 15 L oxygen, RR is 36/min, HR 125 bpm, BP 98/66 mmHg. She has a markedly elevated JVP, coarse bibasal crackles and bilateral pitting oedema. She has only passed 10 mL of urine in the last 45 minutes.

She was previously independent and had a good quality of life, and we feel that she would be a candidate for escalation of her care. I’m just about to repeat her ABG, but please could you review her urgently.’

When referring a patient to ITU you should be able to give a bit of background about their co-morbidities and pre-morbid functioning. Was Mrs Jenkins living independently prior to admission or was she in a nursing home? Did she get out to socialize or do her shopping or was she housebound with a package of care? Does she have any other chronic illnesses for example chronic respiratory disease or end-stage cancer? These are all important factors in considering whether a patient is an appropriate candidate for intensive care treatment.