Cardiology Flashcards
Define acute coronary syndrome:
Acute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).
What is the pathophysiology of acute coronary syndrome?
Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI).
What are the modifiable and non modifiable risk factors for acute coronary syndrome:
Non-modifiable:
Age
Male sex
Family history
Ethnicity (particularly South Asians)
Modifiable:
Smoking
Hypertension
Hyperlipidaemia
Hypercholesterolaemia
Obesity
Diabetes
Stress
High fat diets
Physical inactivity
What three conditions is acute coronary syndrome split into to:
Unstable angina: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs.
Non-ST Elevation Myocardial Infarction: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation.
ST-Elevation Myocardial Infarction: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG.
Distinguish between Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin:
It is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.
What is the typical presentation of acute coronary syndromes:
Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:
Site - Central/left sided
Onset - Sudden
Character - Crushing (‘like someone is sitting on your chest’)
Radiation - Left arm, neck and jaw
Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope
Timing - Constant
Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN
Severity - Often extremely severe
What may an atypical presentation of acute coronary syndrome present as:
Epigastric pain
No pain (more common in elderly and patients with diabetes):
Acute breathlessness
Palpitations
Acute confusion
Diabetic hyperglycaemic crises
Syncope
How do you distinguish which acute coronary syndrome the patient may be presenting with:
Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + normal troponin.
NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + raised troponin
STEMI - cardiac chest pain at rest + persistent ST-elevation/new LBBB (note that there is no need for a troponin in this case).
How do you diagnose a STEMI on an ECG?
ST segment elevation >2mm in adjacent chest leads
ST segment elevation >1mm in adjacent limb leads
New left bundle branch block (LBBB) with chest pain or suspicion of MI
What bedside investigations do you do for acute coronary syndromes?
ECG
Looking for ST-elevation, LBBB or other ST abnormalities
This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.
If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.
What bloods do you do to investigate acute coronary syndrome:
Troponin: performed at least 3 hours after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise.
Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast.
HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease.
FBC and CRP - rule out infectious causes of chest pain
D-dimer - may be used in appropriate patients to rule out PE. Be very careful about who you do a D-dimer on!
What imaging do you do for acute coronary syndrome?
CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure).
What is the ECG interpretation for cardiac territories and affected vessels:
Describe troponin interpretation:
Troponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise 3 hours after myocardial infarction begins.
Different hospitals have differing guidelines (and assays) for interpretations of results.
In general there are three groups of troponin levels:
Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.
Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a 6-12 hour repeat test.
If repeat troponin is raised on the repeat they are having an MI.
If repeat troponin is stable or falling then they are unlikely to be having an MI.
Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)
Describe some non-ACS causes of raised troponin:
Myocardial infarction
Pericarditis
Myocarditis
Arrythmias
Defibrillation
Acute heart failure
Pulmonary embolus
Type A aortic dissection
Chronic kidney disease
Prolonged strenuous exercise
Sepsis
What is the management for a STEMI:
Targeted oxygen therapy (aiming for sats >90%)
Loading dose of PO aspirin 300mg
Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)
For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)
Sublingual GTN spray - for symptom relief
IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
Primary percutaneous coronary intervention (PPCI) for those who:
Present within 12 hours of onset of pain AND
Are <2 hours since first medical contact
Remember that (particularly in STEMI) time is heart therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.
What is the management for a NSTEMI/unstable angina:
Targeted oxygen therapy (aiming for sats >90%)
Loading dose of PO aspirin 300mg and fondaparinux
Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given prasugrel or ticagrelor unless they have a high risk of bleeding where PO clopidogrel 300mg is more appropriate.
Sublingual GTN spray - for symptom relief
IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
Start antithrombin therapy such as treatment dose low molecular weight heparin or fondaparinux if they are for an immediate angiogram
Patients with high 6 month risk of mortality should be offered an angiogram within 96 hours of symptom onset.
Note that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.
What is the post MI management:
ALL patients post-MI patients should be started on the following 5 drugs:
Aspirin 75mg OM + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)
Beta blocker (normally bisoprolol)
ACE-inhibitor (normally ramipril)
High dose statin (e.g. Atorvastatin 80mg ON)
All patients should have an ECHO performed to assess systolic function and any evidence of heart failure should be treated.
All patients should be referred to cardiac rehabilitation.
Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia.
What are the complications of acute coronary syndrome:
Ventricular arrhythmia
Recurrent ischaemia/infarction/angina
Acute mitral regurgitation
Congestive heart failure
2nd, 3rd degree heart block
Cardiogenic shock
Cardiac tamponade
Ventricular septal defects
Left ventricular thrombus/aneurysm
Left/right ventricular free wall rupture
Dressler’s Syndrome
Acute pericarditis
What is the prognosis of acute coronary syndrome:
Due to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not.
Bradycardia following a STEMI often indicates occlusion of the proximal right coronary artery, affecting AV node perfusion.
The key to answering this question is the realisation that the patient presents with bradycardia. The atrioventricular (AV) node is responsible for the conduction of electrical impulses from the atria to the ventricles, and it lies in the lower back section of the inter-atrial septum. In most (80-90%) individuals, there is a right-dominance of the coronary circulation - this means that the AV node is supplied by the right coronary artery. In the reminder, the AV node is supplied by the left circumflex artery. Thus, most individuals who present with a new onset bradycardia post-STEMI have suffered from a right coronary artery occlusion
Creatinine Kinase has three isoenzymes.CK-BB (brain), CK-MB (myocardium), and CK-MM (skeletal muscle). The one of clinical value in (re-)infarcts is CK-MB.
The one advantage of CK-MB over the troponins is the early clearance that helps in the detection of reinfarct. Troponin levels can be elevated for up to 2 weeks after the initial infarct episode, whilst CK-MB usually clear by 72 hours. A CK-MB level of more than 3 times the upper limit of normal is generally considered to be indicative of one.
Previously, before troponins existed as a blood test, CK-MB was the marker used to assist in the diagnosis of myocardial infarcts
In acute coronary syndromes, elevated levels of creatine kinase-MB (CK-MB) can indicate myocardial injury and help diagnose a reinfarct more quickly than troponins due to its earlier clearance from the blood.
PAILS - Post, Ant, Inf, Lat, Septal
ST elevation in one will cause reciprocal ST depression in the leads of the next letter in the mnemonic. So posterior STEMI - reciprocal ST depression in anterior leads
In a posterior myocardial infarction, ST depression is observed in leads V1-V4 instead of elevation, while upright T-waves and tall R-waves may also be present.
Define aortic aneurysm:
Abdominal aortic aneurysm (AAA) is a prevalent, potentially lethal condition characterised by an enlargement of the abdominal aorta exceeding a diameter of 3cm. This dilatation affects all three layers of the arterial wall. Many individuals with AAA are asymptomatic and do not cause any problems to the individual. In the absence of repair, a ruptured AAA is generally fatal.
What are the risk factors for aortic aneurysm:
The precise aetiology of AAA is complex and multifactorial, typically involving a combination of genetic, environmental, and lifestyle factors.
Risk factors include:
Being male
Age 65 or over
Smoking
Hypertension
Hypercholesterolaemia
Family history of AAA
Personal history of peripheral arterial disease or myocardial infarction
COPD
Connective tissue disorders (i.e. Marfan’s)
What are the signs and symptoms of aortic aneurysm:
Most AAAs remain asymptomatic for a long time and are often detected incidentally during radiological investigations for other abdominal or pelvic conditions.
When symptomatic, the clinical presentation can vary:
Pulsatile abdominal mass:
The most classical finding on physical examination is a pulsatile, expansile abdominal mass. This is typically non-tender unless rupture is imminent.
Approximately 3 in 5 AAA over 3 cm are palpable.
This may also be associated with abdominal bruit.
Abdominal or back pain:
Pain is usually a late manifestation, suggesting rapid expansion or impending rupture of the aneurysm.
It is typically severe, constant, and localised in the abdomen or lower back, often radiating to the flank or groin.
There can also be testicular pain if the blood supply to this area is compromised by rupture
90% of aortic aneurysms are infrarenal (originating below the renal arteries)
In advanced cases, a large aneurysm may cause symptoms due to compression or displacement of adjacent structures, resulting in early satiety, nausea, weight loss, altered bowel habits, or deep venous thrombosis (due to compression of the inferior vena cava).
What is the NHS AAA screening programme:
Offered to men at age 65
Consists of an abdominal ultrasound
Follow-up screening depends on the size of the aneurysm:
Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.
Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.
Large AAA (>5.5cm): Surgical intervention is generally recommended.
What other investigations do we do for AAA?
Once an abdominal aortic aneurysm has been detected, further investigations may be required, including:
Computed Tomography (CT) Angiography:
CT angiography is the imaging modality of choice for preoperative evaluation, determining the size, shape, and extent of the AAA, and planning the surgical approach.
It provides detailed information about the aneurysm’s relationship to branch arteries and the potential presence of thrombus or calcification within the aneurysm.
It is also the preferred imaging modality in suspected rupture cases due to its rapid acquisition time and high sensitivity and specificity.
Magnetic Resonance Angiography (MRA): MRA is an alternative to CT angiography for patients who cannot be exposed to ionizing radiation or iodinated contrast medium. MRA can provide high-resolution images of the AAA and surrounding structures but is less readily available and takes more time than CT.
Blood tests: While there is no specific blood test to diagnose AAA, complete blood count, coagulation profile, renal function tests, and electrolyte levels are typically evaluated prior to surgery.
Finally, regular surveillance of known AAAs is critical. The frequency of surveillance depends on the size of the aneurysm, with smaller aneurysms monitored less frequently and larger ones requiring closer observation.
What is the conservative management for AAA?
Management of abdominal aortic aneurysms may be through conservative measures such as:
Surveillance:
This is typically offered for smaller aneurysms with a lower risk of rupture. It is very rare for smaller AAA to rupture.
Small AAA (3-4.4cm): Yearly repeat ultrasound is offered.
Medium AAA (4.5-5.4cm): Repeat ultrasound every 3 months is offered.
Large AAA (>5.5cm) require referral to vascular surgery to be seen within 2 weeks of diagnosis.
Measures to reduce the risk of rupture:
Referral to a stop-smoking service
Management of hypertension
What is the surgical management for AAA:
Elective repair of AAA may be considered for individuals with AAA who meet the following criteria:
They are symptomatic
Their AAA has grown by more than 1 cm in 1 year and is larger than 4 cm
Their AAA is 5.5 cm or larger
Two primary surgical options are available for managing AAA:
Open surgical repair
Typically best for men under age 70.
However, it can be contraindicated by anaesthetic risks, medical comorbidities or anatomic difficulties (i.e. horseshoe kidney, stoma, numerous previous surgeries resulting in significant adhesions)
Endovascular Aneurysm Repair (EVAR)
A stent graft is inserted through the femoral arteries into the aorta, where it channels blood flow into the iliac arteries. The surrounding aneurysm then becomes thrombosed around the graft.
EVAR has reduced perioperative deaths and is associated with shorter hospital stays. However, it has an overall higher long-term morbidity and mortality than open repair.
What are the complications of an AAA?
Rupture
AAA rupture is a surgical emergency. Abdominal aortic aneurysms are more likely to rupture in women than men but are more common in men and such account for more presentations in men.
AAA tend to enlarge over time and with increasing size, the risk of rupture increases.
Embolization
Rarely distal embolisation from mural thrombus can lead to symptoms related to ischemia, most commonly affecting the distal extremities, such as blue toe syndrome.
Open Repair-Related Complications
Those undergoing open surgical repair of an AAA have risks including:
Spinal cord ischaemia
Anastomotic pseudoaneurysm
Graft infection
Death (mortality during elective repair is reported to be 5% of men and 7% of women)
EVAR-Related Complications
Patients who have undergone EVAR may require surveillance for EVAR-related complications.
Endoleak
Defined as the presence of blood flow within the aneurysm sac but outside the EVAR graft
Contrast-enhanced CT angiography, or contrast-enhanced ultrasound if CT is contraindicated, is used to assess for endoleak.
They can be repaired using open, endovascular or percutaneous intervention for endoleak
Post-implantation syndrome
Cytokine release due to EVAR can cause fever, back pain and feeling generally unwell following EVAR.
What is the prognosis of AAA?
Abdominal aortic aneurysms will continue to increase in diameter, with the ultimate outcome being rupture. However, many individuals with AAA do not rupture during their lifetimes. The rupture of AAA is fatal for many individuals.
For those who have had their AAA electively repaired before rupture, those who have had an open surgical repair tend to fare better with reduced complications and overall improved survival.
Which of the following is the most common location for an abdominal aortic aneurysm?
Abdominal aortic aneurysms most frequently occur below the level of the renal arteries (infrarenal region).
What is the management for a ruptured aortic aneurysm?
Take an A to E approach and put out a medical emergency call; patients may require intubation due to reduced levels of consciousness
Ensure patients where there is a strong suspicion of a ruptured AAA are urgently transferred to a specialist vascular centre
In some cases this may not be appropriate and a palliative approach to management may be taken in conversation with the patient and their family (e.g. patients over the age of 85 with significant comorbidities)
Ensure wide-bore IV access is obtained
Keep patients nil by mouth
Medical:
Resuscitation with IV fluids and blood, targeting a systolic blood pressure of 90-120mmHg
Inotropes may be required; these patients generally have a poor prognosis
Ensure adequate analgesia is given for pain
Surgical:
Emergency surgery is required to repair the rupture - this may be with endovascular aneurysm repair (EVAR) or open surgery
Define aortic dissection:
Dissection occurs when a tear in the tunica intima of the aorta creates a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta.
Name some risk factors for aortic dissection:
Hypertension
Connective tissue disease e.g. Marfan’s syndrome
Valvular heart disease
Cocaine/amphetamine use
What is the stamford classification for aortic dissection:
Stanford Type A: Involves the ascending aorta, arch of the aorta
Stanford Type B: Involves the descending aorta.
What are the clinical features of aortic dissections:
Usually presents in men over the age of 50
Sudden onset ‘tearing’ chest pain or interscapular pain radiating to the back.
It can also present with (depending on how far the dissection extends):
Bowel/limb ischaemia
Renal failure
Syncope
What are the clinical signs on an examination of aortic dissections:
Radio-radial delay
Radio-femoral delay
Blood pressure differential between arms of >20mmHg
What are the investigations for an aortic dissection:
CT angiogram is used to diagnose dissection but other investigations can suggest the diagnosis and/or its complications:
ECG - May show ischaemia in specific territories if dissection extends into coronary arteries.
Echocardiogram - May demonstrate pericardial effusion and aortic valve involvement.
Chest x-ray - May show a widened mediastinum
Bloods:
Troponin may be raised
D-dimer may be positive
What is the prognosis of aortic dissection:
Prompt diagnosis and treatment is required as rupture carries an 80% mortality rate.
What is the initial management for aortic dissection:
Resuscitation if necessary
Cardiac monitoring
Strict blood pressure control (e.g. IV metoprolol infusion)
What is the definitive management for aortic dissection:
Depends on the type of dissection
Type A: Usually requires surgical management (e.g. aortic graft)
Type B: Normally managed conservatively with blood pressure control. If there is evidence of end organ damage then endovascular/open repair may be performed.
In haemodynamically stable patients with confirmed Stanford type B aortic dissection initial management is with intravenous beta blockers (to prevent propagation of the dissection) and opioid analgesia
What are the complications of aortic dissection:
Death due to internal haemorrhage
Rupture
End organ damage (renal or cardiac failure)
Cardiac tamponade
Stroke
Limb ischaemia
Mesenteric ischaemia
Define a deep vein thrombosis:
A deep vein thrombosis (DVT) is a blood clot or thrombus that blocks a deep vein, commonly in the legs or pelvis.
Name some risk factors for a deep vein thrombosis:
Thrombophilia
Hormonal (COCP, pregnancy and the postpartum period, HRT)
Relatives (family history of VTE)
Older age (>60)
Malignancy
Bone fractures
Obesity
Smoking
Immobilisation (long-distance travel, recent surgery or trauma)
Sickness (e.g. acute infection, dehydration)
What are the signs and symptoms of deep vein thrombosis?
Unilateral erythema, warmth, swelling and pain in the affected area
Pain on palpation of deep veins
Distention of superficial veins
Difference in calf circumference if the leg is affected
This should be measured 10cm below the tibial tuberosity
3cm difference between the legs is significant
What is the criteria for investigation in deep vein thrombosis?
The two-level DVT Wells score is used to risk-stratify patients into patients likely or unlikely to have a DVT as follows:
Add one point for each of:
Active cancer (treatment within the last 6 months or palliative)
Paralysis, paresis, or recent plaster immobilisation of the legs
Recently bedridden for 3 days or more, or major surgery within the last 12 weeks
Localised tenderness along the distribution of the deep venous system
Entire leg is swollen.
Calf swelling by more than 3 cm compared with the other leg
Pitting oedema confined to the symptomatic leg
Collateral superficial veins
Personal history of DVT
Minus 2 points if an alternative cause is considered at least as likely as a DVT.
If the score is 2 or more:
DVT is likely and an ultrasound doppler of the proximal leg veins should be done within 4 hours
If this isn’t possible within 4 hours, do a D-dimer test, start interim anticoagulation and arrange the doppler to happen within 24 hours
If the score is 1 or less:
DVT is unlikely and a D-dimer should be sent
If the results cannot be obtained within 4 hours, offer interim anticoagulation whilst awaiting results
If the D-dimer is positive, do an ultrasound doppler of the proximal leg veins
If it is negative, anticoagulation should be stopped if it was started and an alternative diagnosis considered
Baseline blood tests should be taken when anticoagulation is started, including a FBC, U&Es, LFTs and a coagulation screen.
What is the management for deep vein thrombosis?
First-line anticoagulant medications are DOACs (e.g. apixaban, rivaroxaban)
If these are not suitable, second-line options include low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban, or LMWH bridging with warfarin (with a target INR of 2.5)
Treatment duration should be at least 3 months for all patients, and 3-6 months for people with active cancer
At this point the risk of VTE recurrence should be weighed against the risks of continuing anticoagulation to make a decision about whether to continue
In cases of provoked DVTs (where a major transient risk factor is identifiable e.g. surgery), anticoagulation would usually be stopped at 3 months
In cases of unprovoked DVTs, consider testing for thrombophilia with antiphospholipid antibodies in patients who are stopping anticoagulation
Patients with unprovoked DVTs should be reviewed with baseline blood tests and an examination to investigate the possibility of an undiagnosed cancer - further investigations should be guided by the patient’s signs or symptoms
What are the complications for deep vein thrombosis:
Pulmonary embolism
Post-thrombotic syndrome (chronic venous hypertension post-DVT that may cause significant morbidity)
Complications of anticoagulation e.g. gastrointestinal bleeding
Patients undergoing elective surgery should receive both mechanical and pharmacological venous thrombosis prophylaxis, initiating mechanical methods immediately post-surgery and pharmacological methods 12 hours later to minimise the risk of bleeding.
Generally speaking surgical patients should receive both mechanical and pharmacological VTE prophylaxis after surgery. Mechanical prophylaxis can start immediately after surgery (assuming the surgery is not on the leg) and pharmacological prophylaxis should start 12 hours later to reduce the risk of bleeding. Please note that although this is what is suggested by guidance, many surgeons have personal preferences when it comes to VTE prophylaxis.
Define primary hypertension:
A ‘normal’ blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg.
What is the pathophysiology of hypertension?
Primary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.
Although the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.
How does one classify hypertension?
Hypertension can be classified according to how high a patient’s blood pressure is.
Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg
Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg
Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg
What are the signs and symptoms of hypertension?
Hypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension.
What are the investigations for hypertension?
Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of ‘white coat hypertension’, ABPM is now required for the diagnosis of hypertension.
Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg.
1st line: ABPM or home blood pressure monitoring if ABPM is not tolerated or declined.
Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores).
Urine dip and albumin:creatinine level
Blood glucose, lipids and renal function
Fundoscopy for evidence of hypertensive retinopathy
ECG: look for evidence of LV hypertrophy
N.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section).
N.B. Referral for same-day specialist assessment should be arranged for people with:
Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI).
What is the medical management of essential hypertension?
Step 1:
ACE-inhibitor (e.g. Ramipril) if <=55 years old
DHP-Calcium Channel Blocker (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity
If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan)
Step 2:
(If maximal dose of Step 1 has failed or not tolerated)
Combine CCB and ACE-I/ARB
Step 3:
(If maximal doses of Step 2 has failed or not tolerated)
Add thiazide-like diuretic (e.g. Indapamide)
Step 4: Resistant Hypertension
If blood potassium <4.5mmol/L then add spironolactone
If >4.5mmol/L increase thiazide-like diuretic dose
Other options at this point if the potassium is >4.5mmol/L include:
Alpha blocker (e.g. Doxazosin)
Beta blocker (e.g. Atenolol)
Referral to cardiology for further advice
What is the conservative management for essential hypertension?
Weight loss
Healthy diet (reduce salt and saturated fats)
Reduce alcohol and caffeine
Reduce stress
Stop smoking
What are the ABPM targets in hypertension?
Age <80 ABPM target <135/85
Age >80 ABPM target <145/85 (due to risk of postural drop and falls)
T1DM with end-organ damage <130/80
What are the complications of hypertension?
Increased risk of morbidity and mortality from all causes
Coronary artery disease
Heart failure
Renal failure
Stroke
Peripheral vascular disease
Angioedema can occur with ACE inhibitors like ramipril due to bradykinin accumulation, presenting as lip swelling and potential airway obstruction.
ACE inhibitors such as ramipril can sometimes cause angioedema as they lead to a build-up of bradykinin. This can present as swelling of the lips and the throat and, in severe cases, difficulty breathing.
Define secondary hypertension:
Secondary hypertension is the persistent elevation of blood pressure due to an identifiable cause.
Name some of the causes of secondary hypertension:
Primary intrinsic renal disease: most common cause of secondary hypertension.
Chronic kidney disease: complex pathophysiology as hypertension itself is a leading risk factor for CKD.
Glomerulonephritis
Diabetic nephropathy
Polycystic kidney disease
Chronic pyelonephritis
Vascular disease:
Renal artery stenosis: unilateral or bilateral stenosis of renal arteries. Older patients this can be attributed to atherosclerosis, younger female patients this may be due to fibromuscular hyperplasia.
Aortic coarctation: narrowing of the aortic arch near the remnants of the ligament arteriosum forces the left ventricle to pump harder leading to hypertension. More common in children or adolescents.
Vasculitides including Takaysau arteritis.
Endocrine disease:
Conn’s disease: primary hyperaldosteronism due to the overproduction of aldosterone by the adrenal glands. Blood tests reveal a hypokalaemia and hypernatraemia. Patients may present with tetany, muscle weakness, oliguria or nocturia.
Cushing’s syndrome: may be primary or secondary and is due to the excess of cortisol. Increase cortisol leads to increased absorption of sodium and increases vascular sensitivity to catecholamines and angiotensin II driving hypertension.
Phaeochromocytoma: rare, primary adrenal tumour producing catecholamines that drives hypertension. Presents with a classical triad of sweating, headaches and tachycardia. It is diagnosed with 24 hour urinary or plasma metanephrines.
Drugs: many drugs are indicated in secondary hypertension including NSAIDs, corticosteroids (Cushing’s syndrome), mineralocorticoids, immunosuppressants (e.g. ciclosporin), atypical antipsychotics (clozapine or olanzapine) or recreational drugs (cocaine, amphetamines etc.).
What are the symptoms and signs of hypertensive crisis/malignant hypertension::
Occipital pulsatile headache +/- visual disturbance
Bilateral retinal haemmorhages +/- exudates and papilloedema on fundoscopy
Chest pain +/- signs of heart failure
Acute-onset confusion
What are the symptoms and signs that may suggest the underlying cause of the secondary hypertension?
Intrinsic renal disease: ballotable kidneys, fingerpricks for glucose testing, signs and symptoms of renal failure.
Coarctation of the aorta: systolic murmur loudest over scapulae, radio-femoral delay or radio-radial delay (depends on site of coarctation).
Cushing’s syndrome: moon facies, abdominal striae, buffalow hump, thin skin etc.
Conn’s syndrome: weakness, tetany, cramps, or oliguria.
Phaechromocytoma: classical triad of episodic headaches, sweating and tachycardial.
When to suspect secondary hypertension:
A few clinical clues may suggest secondary hypertension including:
Younger patients (<40 years old) with few comorbidities
Severe hypertension or hypertension resistant to treatment
New hypertension in patients with previously stable or low readings
Hypertension with associated symptoms or electrolyte disturbances
It is important to refer patients who you think have secondary hypertension. Specialist centres often prefer that these patients are not started on antihypertensives as this may interfere with further investigation.
What are the investigations for secondary hypertension:
Bedside
24h ABPM: for the definitive diagnosis of hypertension.
Urine dipstick: evidence of glomerulonephritis, diabetic nephropathy or CKD.
Urinary metanephrines: diagnosis of phaeochromocytoma.
ECG: look for evidence of LVH.
Bloods
Dyselectrolytaemia: hypokalaemic and hypernatraemic suggests Conn’s.
Renal function: may suggest CKD or other primary renal pathology. Raised urea and creatinine if acute kidney injury.
Endocrinological:
Early morning cortisol, 24h urinary cortisole or dexamethasone suppression testing: Cushing’s syndrome.
Plasma or urinary metanephrines: phaeochromocytoma.
Aldosterone:renin ratio: Conn’s disease.
Imaging
Renal USS: shrunken kidneys (CKD), large, cystic kidneys (PCKD), or narrowing of renal arteries (renal artery stenosis).
Renal biopsy: intrinsic kidney disease.
Further imaging including CT CAP, MRI brain, or MR aortogram if looking for the weirder and wonderful causes of secondary hypertension.
What are the complications of secondary hypertension?
Complications of secondary hypertension include all the same complications of primary hypertension (including stroke, aneurysm formation, heart failure, renal failure) alongside complications of the underlying disease. Secondary hypertension often leads to resistant hypertension unless the underlying disease is treated.
Define gangrene:
Gangrene occurs when a tissue receives insufficient perfusion and dies. It can be considered to be wet or dry.
Define wet gangrene:
Wet gangrene is also referred to as infectious gangrene. It includes necrotising fasciitis (infection of the subcutaneous fascia and fat), gas gangrene (caused by Clostridium), and gangrenous cellulitis (typically found in immunocompromised individuals).
Define dry gangrene:
Dry gangrene is an ischaemic type of gangrene that occurs secondary to chronically reduced blood flow. It causes tissues to become cold, dry and die.
What is the epidemiology of wet gangrene?
The exact incidence is unknown, but wet gangrene is less common than dry gangrene. It is often seen in immunocompromised patients, those with diabetes mellitus, and individuals with peripheral vascular disease.
What is the epidemiology of dry gangrene?
The incidence is higher in the elderly, smokers, and individuals with peripheral arterial disease or diabetes mellitus. It’s estimated that about 10% of people with diabetes will have some form of gangrene during their lifetime.
What is the aetiology of wet gangrene?
This condition is commonly caused by an infectious agent.
Necrotising fasciitis is typically due to Streptococcus pyogenes or other bacteria.
Gas gangrene is most commonly caused by Clostridium perfringens.
These bacteria release exotoxins, which cause clotting of blood vessels, death of muscle and enable the proliferation of bacteria.
The gas produced causes the spreading of muscular fibres.
Necrotising fasciitis can be subdivided into:
Type I: Polymicrobial
Polymicrobial meaning it may involve gram-positive cocci, gram-negative rods and/or anaerobes
Most common form. Risk factors include peripheral vascular disease and diabetes mellitus.
Type II: Group A beta haemolytic streptococci
Type III: Marine Fibrio vulnificus
Type IV: Fungal
Name some risk factors for wet gangrene:
Immunocompromise
Diabetes mellitus
Older age
Trauma to the skin (which enables entry of the microbial into the tissue)
What causes dry gangrene?
This type of gangrene is often secondary to chronically reduced blood flow. Causes include:
Peripheral arterial disease (i.e. atherosclerosis)
Risk factors are the same as other cardiovascular risk factors (i.e. smoking, diabetes mellitus,
Thrombosis, often related to vasculitis and hypercoagulable states
Vasospasm, often linked to cocaine use or Raynaud’s phenomenon.
Extreme cold injury (frostbite)
Embolism (i.e. cardiogenic or septic)
Venous insufficiency
Prolonged venous insufficiency can result in high pressure and occlusion within the veins
What are the signs and symptoms of wet gangrene?
Patients typically present with symptoms of fever and sepsis.
Starts as swelling and erythema, but can progress to discharge and the area may darken/become black.
There may be bullae formation.
The necrotic area is poorly demarcated from the surrounding tissue.
There may be a foul-smelling odour.
In gas gangrene, there is subcutaneous crepitus and anaesthesia.
What are the signs and symptoms of dry gangrene?
Dry gangrene shows a well-demarcated necrotic area without signs of infection.
The area is often cold and pale.
Auto-amputation often occurs in these cases.
What are the investigations for wet gangrene?
Laboratory Investigations: Full blood count, inflammatory markers (CRP, ESR), blood cultures to identify the causative organism, and lactic acid levels to assess the severity.
Imaging: X-ray, ultrasound, or CT scan to assess the extent of the disease and look for gas within the tissue.
Tissue Biopsy: To confirm diagnosis and identify the causative organism.
What are the investigations for dry gangrene?
Doppler ultrasound: This can be used to determine ABI and degree of peripheral arterial disease.
Laboratory Investigations: Full blood count, inflammatory markers (CRP, ESR) to rule out wet gangrene, glucose level to evaluate for diabetes, and coagulation profile in case of suspected hypercoagulability.
Imaging: Doppler ultrasound or angiography to assess blood flow and locate the site of blockage.
Tissue Biopsy: Not typically needed but can confirm diagnosis if uncertain.
What is the management of wet gangrene?
Management requires:
Analgesia
Broad-spectrum intravenous antibiotics
Surgical debridement: Excision of removals of necrotic tissue.
Amputation may be done in severe cases
What is the primary management for dry gangrene?
Surgical debridement and restoration of blood supply to the affected area
Restoration of perfusion may be achieved through embolectomy, thrombectomy, thrombolysis or bypass surgery.
Amputation may be required depending on the severity and extent of the necrosis.
Hyperbaric oxygen is sometimes used
This delivers above-normal levels of oxygen to the patient. This oxygen is then delivered to the affected area and encourages more rapid healing.
What is the long term management for dry gangrene?
Antiplatelet agents for those with peripheral arterial disease
Lipid-lowering therapy (i.e. statins)
Smoking cessation
Diet and exercise advice
What are the complications of gangrene?
Gangrene can result in:
Conversion to wet gangrene
Dry gangrene can convert to wet gangrene if the tissue becomes infected.
Sepsis
Risk of sepsis is higher in wet gangrene due to the underlying infectious aetiology
Amputation
Define aortic stenosis:
Aortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body.
What is the pathophysiology of aortic stenosis:
Normally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.
Cause of aortic stenosis:
Senile calcification: most common cause in those >65y/o.
Congenital bicuspid valve: most common cause in those <65y/o.
Rheumatic heart disease
William’s syndrome: supravalvular stenosis
What are the symptoms of aortic stenosis:
The symptoms of severe AS can be remembered by the mnemonic ‘SAD’.
Syncope
Angina
Dyspnoea
Other symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death.
What are the signs of aortic stenosis:
Slow-rising carotid pulse
Narrow pulse pressure
Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy)
Ejection systolic murmur
Heard best at the second intercostal space on the right
Can be described as “harsh”
Radiates to the carotids
Soft S2 heart sound: absent S2 corresponds with severity
Ejection click may be heard in some cases (early systolic)
What are the investigations for aortic stenosis:
Bedside
ECG: LVH, left axis deviation, and poor R wave progreesion.
Imaging
CXR: cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible.
Echocardiogram: definitive diagnosis.
Definitive diagnosis of aortic stenosis.
Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters:
Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring)
Valve area < 1.0cm x2
Aortic jet velocity >4 m/s
Exercise testing: may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS.
Cardiac MRI: can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification.
Define aortic stenosis:
Aortic stenosis (AS) refers to the narrowing and tightening of the aortic valve leading to reduced blood flow from the left ventricle into the aorta and ultimately to the rest of the body.
What is the pathophysiology of aortic stenosis:
Normally, the aortic valve opens to allow blood to be pumped from the left ventricle into the aorta and to the rest of the body during systole. In aortic stenosis, there is a narrowing of the aortic valve which means that the left ventricle has to generate more pressure to enable sufficient blood to cross the aortic valve and pass into the aorta. Initially, this leads to left ventricular hypertrophy as the left side of the heart compensates for the narrowing. Over time, the left ventricle can no longer compensate and the left ventricle will start to enlarge, the ejection fraction will reduce, and this will ultimately leads to reduced cardiac output.
Causes of aortic stenosis:
Senile calcification: most common cause in those >65y/o.
Congenital bicuspid valve: most common cause in those <65y/o.
Rheumatic heart disease
William’s syndrome: supravalvular stenosis
What are the symptoms of aortic stenosis?
The symptoms of severe AS can be remembered by the mnemonic ‘SAD’.
Syncope
Angina
Dyspnoea
Other symptoms include: pre-syncope, palpitations, left ventricular heart failure symptoms (exertional dyspnoea, orthopnoea, PND) or can present in cardiac arrest/sudden cardiac death.
What are the signs of aortic stenosis?
Slow-rising carotid pulse
Narrow pulse pressure
Heaving, non-displaced apex beat (can be displaced if there is left ventricular hypertrophy)
crescendo-decrescendo Ejection systolic murmur
Heard best at the second intercostal space on the right
Can be described as “harsh”
Radiates to the carotids
Soft S2 heart sound: absent S2 corresponds with severity
Ejection click may be heard in some cases (early systolic)
What are the investigations for aortic stenosis?
Bedside
ECG: LVH, left axis deviation, and poor R wave progreesion.
Imaging
CXR: cardiomegaly and evidence of pulmonary oedema. Occasionally, a calcified aortic valve is visible.
Echocardiogram: definitive diagnosis.
Definitive diagnosis of aortic stenosis.
Severity of AS can be quantified with doppler echocardiography. AS is classified as severe if it meets the following parameters:
Peak gradient > 40 mmHg (note, in severe left ventricular dysfunction, a low peak gradient can be falsely reassuring)
Valve area < 1.0cm x2
Aortic jet velocity >4 m/s
Exercise testing: may be used in physically active patients to assess the true severity of asymptomatic patients with echocardiography confirmed AS.
Cardiac MRI: can be used to provide additional, more details information regarding valve morphology, dimensions of the aortic root and the extent of valve calcification.
What is the conservative management of aortic stenosis?
Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all.
Patients who do not meet the criteria for intervention should have regular echocardiography follow-up, with severe AS being monitored every 6 months, mild-to-moderate AS monitored yearly, and younger patients can be monitored every two to three years.
What is the medical management of aortic stenosis?
Medical management of AS involves symptom management of left ventricular failure with diuretics and optimising heart failure medications with beta-blockers and ACE-I etc. Isolated medical therapy should only be used in those who are not suitable for intervention.
What is the surgical management of aortic stenosis?
Intervention in AS is indicated in the following patients:
All patients with symptomatic aortic stenosis
Asymptomatic patients with a left ventricular ejection fraction (LVEF) < 55%
Asymptomatic patients with an LVEF > 50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing
Asymptomatic patients with an LVEF > 50% who have the following risk factors
Aortic valve peak velocity > 5m/s x2
Severe calcification and peak velocity progression >= 0.3m/s x2
Markedly elevated BNP levels (more than twice upper limit) without other explanation
Severe pulmonary hypertension (pulmonary artery systolic pressure > 60mmHg)
Aortic valve area less than 0.6 cm2
Choices of intervention are transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR).
TAVI is favoured with patients with severe comorbidities, previous heart surgery, frailty, restricted mobility, and those older than 80 years of age.
SAVR is favoured for patients who are low risk and younger.
What are the complications of aortic stenosis?
Aortic stenosis if left untreated can lead to LV failure. It is also implicated in sudden cardiac death.
What is aortic sclerosis?
It can be defined as an irregular aortic leaflet thickening and focal increased echogenicity, but is distinguished from aortic stenosis because there is no impairment of valve leaflet excursion, and peak doppler velocities are normal or only minimally elevated (markedly elevated in stenosis)
Aortic sclerosis is an asymptomatic condition that can be incidentally revealed through physical examination or via echocardiogram. It is caused by age-related senile degeneration of the valve.
What are the clinical findings of aortic stenosis?
Classic findings are an ejection systolic murmur that does not radiate to the carotids, there is normal S2, pulse character and volume.
what does the loud fourth heart sound indicate?
A loud fourth heart sound is due to a rigid ventricle. In the above case, stenosis of the aortic valve has resulted in left ventricular hypertrophy and likely failure. This is secondary to increased afterload.
Define aortic regurgitation?
Aortic regurgitation (AR), or aortic insufficiency (AI), occurs when the aortic valve fails to prevent blood from leaking back across the valve during diastole.
What are the risk factors for aortic regurgitation:
Older populations
M>F
congenital aortic valve/root defects (bicuspid aortic valve, Marfan’s syndrome)
What is the pathophysiology of aortic regurgitation:
Normally, the aortic valve closes tightly at the end of systole (S2) and prevents blood from flowing back into the left ventricle. In aortic regurgitation, the valve leaflets fail to close tightly due to valve disease or the aorta around the valve has dilated which allows the backflow of blood across the valve and into the left ventricle.
Name some causes of acute aortic regurgitation:
Infective endocarditis: infective process leads to valve destruction and leaflet perforation. Most common acute cause of acute AR.
Aortic dissection: primarily causes regurgitation due to dilatation of aortic root (functional AR).
Traumatic rupture of valve leaflets: blunt chest trauma or deceleration injury can disrupt valve leaflets leading to valve incompetence.
Iatrogenic causes: balloon valvotomy or TAVI.
Non-native aortic valve regurgitation: valve replacements can be complicated by acute AR. Tissue prosthetic valves may degenerated and mechanical valves may thrombose causing incomplete closure of the valve or paravalvular leak.
Name some causes of chronic aortic regurgitation:
Rheumatic heart disease - most common in developing countries.
Age-related calcification
Congenital bicuspid aortic valve
Connective tissue disorders: Marfan’s syndrome, Ehler’s Danlos
Infective endocarditits
Rheumatological conditions: rheumatoid arthritis, ankylosing spondylitis, APLS, giant cell arteritis,
Name some symptoms of acute aortic regurgitation:
Sudden cardiovascular collapse
Acute pulmonary oedema - shortness of breath, sweating, pallor, peripherally vasoconstricted
Name some symptoms of chronic aortic regurgitation:
More insidious, slower onset
Exertional dyspnoea, orthopnoea, PND
Stable angina even in absence of coronary artery disease (due to reduction in diastolic coronary perfusion)
What are the signs of aortic regurgitation:
De Quincke’s sign - nail bed pulsation
Waterhammer pulse
De Musset’s sign - head hobbing
Corrigan’s sign - dancing carotids
Muller’s sign - pulsation of the uvula
Traube’s sign - pistol shot (bruit heard on auscultation of femoral pulse)
Auscultation:
*Early diastolic murmur - heard best at the aortic region, leaning forward and on expiration. Soft S1 and occasional ejection flow murmur.
What are the investigations for aortic regurgitation:
Observations: widened pulse pressure.
Throat swab for group A strep.
ECG: LVH and p mitrale in chronic AR.
Bloods
Inflammatory markers and blood cultures - infective endocarditis.
Auto-antibody screen - rheumatological causes.
Imaging:
Transthoracic echocardiogram - definitive diagnosis.
Cardiac MRI - indicated in those with moderate-to-severe AR with suboptimal TTE findings.
Invasive cardiac catheterisation - detailed information on AR severity, LV function and size, pressures and valve gradient, and dimensions of aortic root.
What is the medical management of aortic stenosis?
Used to slow the rate of aortic root dilatation in high risk patients (e.g. Marfan’s or bicuspid aortic valve).
Beta blockers +/- losartan are used to lower systolic blood pressure.
Patients with severe asymptomatic AR should be seen and monitored annually. If LV diameters or systolic function change significantly, follow-up should be 3-6 monthly.
What is the surgical management of aortic stenosis?
Surgical intervention is indicated in:
Symptomatic AR.
Asymptomatic AR with: poor LVEF (<=50%), LV and diastolic diameter >70mm or LV end-systolic diameter >50mm.
Infective endocarditits refractory to medical therapy.
Significant enlargement of ascending aorta.
What are the complications of aortic regurgitation?
Acute AR can lead to cardiovascular collapse and de novo acute heart failure. Chronic AR that is not treated will lead to chronic heart failure with predominantly left ventricular symptoms (pulmonary oedema).
In asymptomatic patients with small aortic root dilation (<4.5 cm), regular yearly surveillance is crucial for early detection of progression.
:)
Why do you get a soft s1 in aortic regurgitation?
In aortic regurgitation, blood flows back into the left ventricle (LV) during diastole, leading to volume overload.
This results in an elevated LVEDP, which causes the mitral valve to close earlier and less forcefully during the start of systole.
The early closure of the mitral valve diminishes the intensity of the S1 sound.
Define an arterial thrombosis:
Arterial thrombosis refers to the formation of a blood clot (thrombus) in an artery, which can lead to serious health complications.
What are the two types of arterial thrombosis:
It is primarily categorised into two types: coronary thrombosis, affecting the arteries that supply the heart, and cerebral thrombosis, impacting those supplying the brain.
What is the pathogenesis of arterial thrombosis:
Pathogenesis involves endothelial injury, stasis or turbulence of blood flow, and hypercoagulability - collectively known as Virchow’s triad.
What is the clinical presentation of arterial thrombosis?
The clinical presentation varies depending on the affected site. Coronary thrombosis may manifest as myocardial infarction, while cerebral thrombosis can lead to stroke symptoms.
What are the investigations for arterial thrombosis?
Diagnosis typically involves imaging techniques such as angiography or ultrasound alongside laboratory tests for coagulation parameters.
What is the management of arterial thrombosis?
Management strategies encompass anticoagulant and antiplatelet therapy to prevent further clot formation and propagation. In some cases, surgical interventions like thrombectomy or angioplasty may be necessary. Secondary prevention includes addressing modifiable risk factors such as hypertension, hyperlipidaemia, smoking cessation and diabetes control.
- Thrombolysis- what’s this?dissolve blood clot
- Embolectomy- what’s this?operation to remove clot
- Angioplasty- what’s this?operation to widen the affected artery
- CABG- what’s this?surgery to divert blood around the blocked artery
What causes arterial thrombosis?
Atherosclerosis
- Atrial fibrillation
- Antiphospholipid syndrome
Define an arterial ulcer?
Any break in the skin that is located beneath the knee and has lasted longer than 2 weeks without healing is defined as an ulcer by NICE.
Arterial ulcers, also known as ischaemic ulcers, are open sores that develop due to insufficient blood supply, commonly associated with peripheral arterial disease.
What is the epidemiology of arterial ulcer?
Arterial ulcers are believed to account for 10% of ulcers in the UK, whilst venous ulcers account for 80%. The majority of the remaining 10% are mixed (i.e. both arterial and venous in aetiology) and other more rare causes of ulcers.
These ulcers are particularly common among elderly populations and are more common in men.
What is the pathophysiology of an arterial ulcer?
Arterial ulcers are primarily caused by peripheral arterial disease, typically due to atherosclerosis, leading to inadequate blood supply to the distal extremities. When a minor injury occurs to the limb, there is poor perfusion, and the injury is unable to heal, resulting in the formation of an ulcer. For individuals with more advanced arterial disease, the perfusion may be sufficiently poor to cause cellular death and ulcer formation without a preceding trauma to the leg. This may also occur as a result of rupture of an atherosclerotic plaque, which produces an embolism and occlusion of a downstream artery, ischaemia to the portion of tissue and the formation of an ulcer.
Name some risk factors for an arterial ulcer?
Smoking
Hypertension
Coronary artery disease
Personal history of stroke or TIA
Diabetes mellitus
Peripheral arterial disease
Obesity
Being male
Signs and symptoms of arterial ulcers:
Occur distally (e.g. at the heel or toe tips)
Are small and deep
Have a well-defined, ‘punched out’ margin
Limited exudate
Granulated base, which does not bleed much on debridement
They are typically painful with pain at rest
The pain is often worse at night and relieved by dangling legs out of the bed
Associated with other features of peripheral arterial disease:
Weak distal pulses and cool temperature of extremities
The surrounding skin may be shiny and pale, with prolonged capillary refill time.
Hair atrophy
Nail dystrophy
Claudication pain: Pain in buttocks and calves occurring on exertion, and resolving with rest. This progresses to rest pain with increasing severity of peripheral arterial disease.
What are the primary investigations for arterial ulcers?
Physical examination
Capillary refill time will be prolonged
Buerger test:
With the patient lying supine, their leg is raised 45 degrees for 1 minute and then lowered.
The test is considered to be positive if the leg appears white on elevation and then hyperaemic when lowered.
Ankle-brachial pressure index (ABPI)
Calculated by measuring ankle blood pressure using a hand-held Doppler and dividing this by the brachial blood pressure
< 0.8: indicates peripheral arterial disease
0.5-0.8: indicates significant peripheral vascular disease
<0.5: indicates severe arterial disease
1.3: may indicate stiff arteries due to calcification. ABPI may be falsely high in diabetics.
Doppler ultrasound: To assess the patency of the arteries and veins.
In some cases, angiography might be needed to evaluate the extent of arterial blockage.
Skin swabs are done when there are associated skins of infection, and should not be done routinely.
What is the management for arterial ulcers?
Lifestyle modification
Smoking cessation advice should be provided.
Wound care: The ulcer should be cleaned and properly dressed regularly.
Management of comorbidities (i.e. diabetes and blood pressure management)
Medications
Antiplatelet drugs (such as aspirin or clopidogrel)
Statins to reduce cholesterol levels
Surgical interventions:
Skin grafting to repair the damaged skin
Angioplasty: Re-opening of the stenosed vessels to reperfuse the tissue to enable the ulcer to heal.
Bypass grafting: The stenosed vessel is bypassed using a graft to enable re-perfusion of the ischaemic tissue.
What are the complications of arterial ulcers?
Non-healing
Recurrence
Amputation
Severe, non-healing ulcers may require amputation.
Compare arterial and venous ulcers:
Name a hallmark feature of peripheral arterial disease:
Intermittent claudication - cramping pain, discomfort, or fatigue in the muscles of the legs (most commonly the calves), that occurs during exercise or walking and is relieved by rest
Name some signs of peripheral artery disease:
hair loss and shiny appearance of the skin
Define cardiac arrest:
Cardiac arrest is a severe medical emergency characterised by the cessation of functional circulation due to failure in the heart’s pumping action
How can cardiac arrest be categorised:
The condition can be categorised as asystole, pulseless electrical activity (PEA), ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT).
How does one recognise cardiac arrest:
Recognition of cardiac arrest often relies on the absence of pulse, consciousness, and normal breathing. Resuscitation efforts should commence immediately with cardiopulmonary resuscitation (CPR) and early defibrillation if VF or pVT is identified.
Name the reversible causes of cardiac arrest starting with an H
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Name the reversible causes of cardiac arrest starting with T
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins
How do the 2021 Resus Council guidelines divide patients who have had a cardiac arrest?
into those with:
‘shockable’ rhythms: ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT)
‘non-shockable’ rhythms: asystole/pulseless-electrical activity (asystole/PEA)
What is the management for cardiac arrest?
Major points include:
chest compressions
the ratio of chest compressions to ventilation is 30:2
chest compressions are now continued while a defibrillator is charged
defibrillation
a single shock for VF/pulseless VT followed by 2 minutes of CPR
if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend ‘up to three quick successive (stacked) shocks’, rather than 1 shock followed by
CPR
drug delivery
IV access should be attempted and is first-line
if IV access cannot be achieved then drugs should be given via the intraosseous route (IO)
delivery of drugs via a tracheal tube is no longer recommended
adrenaline
adrenaline 1 mg as soon as possible for non-shockable rhythms
during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
amiodarone
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead
thrombolytic drugs
should be considered if a pulmonary embolus is suspected
if given, CPR should be continued for an extended period of 60-90 minutes
What are the four specific cardiac arrhythmias causing cardiac arrest?
- Ventricular fibrillation (VF) → shockable rhythm
- Pulseless ventricular tachycardia (VT) → shockable rhythm - what is this?Absence of carotid pulse in the presence of sinus tachycardia
- Pulseless electrical activity (PEA)- non-shockable rhythm - what is this?Absence of carotid pulse in the presence of sinus rhythm
- Asystole- non shockable rhythm
- What are the most common causes of VT and VF? (2)IHD and acute MI
Define cardiac failure:
Heart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.
What is the epidemiology of cardiac failure:
HF is common: the prevalence in the UK is estimated at 1-2%.
HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.
In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease.
Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.
How is heart failure categorised?
HF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features).
Distinguish between low output HF and high output HF:
Low-output HF vs. High-output HF
Low-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body’s needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet.
What are the common causes of high-output HF?
The common causes of low-output HF will be further discussed below. Common causes of high-output HF include:
Anaemia
Arteriovenous malformation
Paget’s disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)
These can be remembered with the AAPPTT mnemonic.
Distinguish between systolic and diastolic HF:
Systolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis).
In comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis.
Distinguish between acute and chronic HF:
HF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop.
How does New York Heart Association (NYHA) Classify HF?
The NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest).
Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.
Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.
Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
What are the signs and symptoms of left heart failure?
Clinical features of left heart failure (LHF)
LHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion.
Symptoms
Shortness of breath on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Nocturnal cough (± pink frothy sputum)
Fatigue
Signs
Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Cyanosis
Prolonged capillary refill time
Hypotension
Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation.
What are the signs and symptoms of right heart failure:
Clinical features of right heart failure
Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).
Symptoms
Ankle swelling
Weight gain
Abdominal swelling and discomfort
Anorexia and nausea
Signs
Raised JVP
Pitting peripheral oedema (ankle to thighs to sacrum)
Tender smooth hepatomegaly
Ascites
Transudative pleural effusions (typically bilaterally)
What is first line in chronic heart failure:
NT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value.
Interpret NT-pro-BNP results as follows:
2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks.
400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks.
If <400ng/L: diagnosis of heart failure is less likely.
Name other investigations you would do in heart failure?
Arrange a 12-lead ECG in all patients
ECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias).
Transthoracic echocardiogram (TTE)
An echocardiogram will confirm the presence and degree of ventricular dysfunction.
Bloods: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors)
Chest Xray
How does EF and BNP signify heart failure:
EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction).
EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction).
EF 50-70% with normal BNP = normal.
What chest x-ray findings would you see in heart failure:
CXR: CXR findings in heart HF can be remembered by the ABCDEF mnemonic:
A: Alveolar oedema (with ‘batwing’ perihilar shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio >0.5)
D: upper lobe blood diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure
What is the conservative management for heart failure:
Weight loss if BMI >30.
Smoking cessation
Salt and fluid restriction - improves mortality
Supervised exercise-based group rehabilitation programme for people with heart failure.
Offer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure.
What is the medical management for heart failure:
Medical management
Symptom management:
For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure.
Management which improves mortality:
1st line = ACE-I and beta-blocker
Consider ARB if intolerant to ACE-I.
Consider hydralazine if intolerant to ACE-I/ARB.
If symptoms persist and NYHA Class 3 or 4 consider adding:
Aldosterone antagonists = spironolactone or eplerenone.
Hydralazine and a nitrate for Afro-Caribbean patients.
Ivabradine if in sinus rhythm and impaired EF.
Digoxin = useful in those with AF. This worsens mortality but improves morbidity.
NICE also advices seeking specialist guidance for prescribing SGLT2 inhibitors (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.
Which drugs demonstrate a mortality benefit in patients with HFrEF?
Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine.
What is the Surgical/Interventional management for heart failure?
Cardiac resynchronisation therapy
Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled:
QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
QRS interval 120-149ms without LBBB, NYHA class I-III
QRS interval 120-149ms with LBBB, NYHA class I
Name some adverse effects of beta blockers:
Bradycardia, hypotension, fatigue, dizziness
ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema
tiredness, peripheral coldness and bronchospasm.
Name some adverse effects of Spironolactone?
Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido
Name some adverse effects of Furosemide
Hypotension, hyponatraemia/kalaemia,
The BNF reports high doses or rapid intravenous administration of loop diuretics can cause tinnitus and deafness.
Name some adverse effects of Hydralazine/nitrates
Headache, palpitations, flushing
Name some adverse effects of Digoxin
Dizziness, blurred vision, GI disturbances
Name some adverse effects of SGLT-2 inhibitors
Thrush, UTIs, DKA in patients with pre-existing diabetes
What is pulses alternans?
Pulsus alternans is an arterial pulse which alternates between strong and weak beats due to variations in systolic pressures. The variation of systolic pressure is secondary to poor ejection fraction, resulting in raised end-systolic volume. This raised end-systolic volume causes raised diastolic volume, resulting in stretching of the myocardial muscle and a stronger subsequent contraction of the heart. It is an indicator of dysfunction of the left ventricle and is a poor prognostic indicator of heart failure.
In patients with heart failure and atrial fibrillation, digoxin may be considered over newer treatments for symptomatic relief and improvement of cardiac function despite being second-line therapy.
Digoxin is no longer considered first-line management in atrial fibrillation, however, it is useful in patients with co-existent heart failure with a reduced ejection fraction and those who do very little exercise and is therefore the correct answer.
Tender hepatomegaly is a common sign in cor pulmonale, which is characterised by right heart failure due to chronic lung disease.
The patient presents with features consistent with cor pulmonale (right heart failure caused by chronic lung disease). Signs of right heart failure include ankle/sacral pitting oedema, ascites, tender smooth hepatomegaly, and a raised JVP
COPD or any chronic lung disease can result in cor pulmonale, defined as a deterioration in the function and/or structure of the right ventricle caused by respiratory pathology
Chronic lung diseases, including COPD, can cause cor pulmonale, leading to right ventricular dysfunction and manifesting as signs such as raised JVP, hepatomegaly, pitting oedema, and a cough with white sputum.
Define infective endocarditis:
Infective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves.
Name some risk factors for infective endocarditis:
Age >60 years
Male sex
IVDU: predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis.
Poor dentition and dental infections
Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology.
Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.
Prosthetic valves
Previous history of infective endocarditis
Intravascular devices: central catheters and shunts.
Haemodialysis
HIV infection
What is the pathophysiology for infective endocarditis:
A damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis.
How is Infective endocarditis classified by duration of symptoms?
IE can be considered according to duration of symptoms.
Acute IE: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to S.aureus infection.
Subacute IE: patients has signs or symptoms for 6 weeks up to 3 months.
Chronic IE: patients has signs or symptoms that persist for longer than 3 months.
How is infective endocarditis classified by valve involvement:
Native-valve endocarditis: patient without prosthetic valve implant.
Prosthetic-valve endocarditis:
Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination.
Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections.
List the valves in the order of likeliness of being affected from most to least
MATP
- Mitral valve
- Aortic valve
- Tricuspid valve
- Pulmonary valve
- Which valve is most likely affected in IV drug use?Tricuspid
What is commonly the causative agent of Infective endocarditis if <2 months post valve surgery?
Staphylococcus epidermidis
Name the common organisms causing infective endocarditis:
Staph. aureus: now the most common cause of IE. Coagulase positive.
Strep. viridans: used to be the most common cause of IE. Implicated in patients with poor dental hygiene.
Enterococci
Coagulase negative staphylococci e.g. staph. epidermidis: common culprit of prosthetic valve endocarditis.
Strep. bovis: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.
Fungal
HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE.
Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE).
What are the symptoms of infective endocarditis?
Common presenting symptoms:
Fever: most common symptom.
Night sweats
Anorexia
Weight loss
Myalgia
Others:
Headache
Arthalgia
Abdominal Pain
Cough
Pleuritic pain
What are the systemic signs of infective endocarditis?
Febrile
Cachectic
Clubbing
Splenomegaly
What are the cardiac, vascular phenomena, and immunological phenomena of infective endocarditis:
Cardiac:
Murmur: fever + new murmur is infective endocarditis until proven otherwise.
Bradycardia: aortic root abscess tracks down to the AVN causing heart block.
Vascular phenomena:
Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers.
Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles.
Immunological phenomena: due to immune-complex deposition.
Splinter haemorrhages
Osler’s nodes: painful pulp infarcts on end of fingers.
Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy.
Glomerulonephritis: identified on urine dip.
For the diagnosis of infective endocarditis what criteria needs to be followed:
Duke Criteria
Explain the duke criteria for infective endocarditis:
useful mnemonic to remember the criteria is ‘BE FIVE PM’:
Major Criteria:
Blood Cultures
Evidence of Endocardial Involvement: Echo
Minor Criteria:
Fever
Immunological phenomena
Vascular phenomena
Echocardiogram minor criteria
Predisposing features
Microbiological evidence that does not meet major criteria.
For a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present.
Explain what a blood test positive for infective endocarditis is:
2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus).
Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis).
Single positive blood culture for Coxiella burnetti or positive antibody titre
Explain what Evidence of endocardial involvement with imaging positive for IE is:
Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation.
Abnormal activity around site of prosthetic valve implantation on PET-CT
Paravalvular lesions on cardiac CT
Explain the minor criteria for the duke’s classification for infective endocarditis:
Fever: >38.0 degrees celsius.
Immunological phenomena: Roth spots, splinter haemorrhages or Olser’s nodes.
Vascular phenomena: evidence of septic embolis (splenic infarct/abscess), Janeway lesions.
Echocardiogram minor criteria: not meeting above criteria.
Predisposing features: known valvular disease, IVDU, prosthetic valves etc.
Microbiological evidence that does not meet major criteria: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE
What might you see in an ECG of someone with IE:
increasing prolongation of PR interval suggests development and worsening of aortic root abscess.
What might you see in a urine dip of someone with IE?
look for haematuria which may suggest development of glomerulonephritis.
What is the treatment for infective endocarditis:
Mainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term.
What is the specific treatment for Infective endocarditis if the organism and sensitives are not known yet:
Native valve: amoxicillin (+/- gentamicin)
Pen-allergy/MRSA: vancomycin (+/- gentamicin)
Prosthetic valve: vancomycin + rifampicin + gentamicin
What is the specific treatment for Infective endocarditis if its a Native Valve with a S. aureus IE
1st line: flucloxacillin
2nd line: vancomycin + rifampicin
What is the specific treatment for Infective endocarditis if its a Prosthetic Valve S. aureus IE
1st line: flucloxacillin + rifampicin + gentamicin
What is the specific treatment for infective endocarditis if its Strep viridans IE
1st line: benzylpenicillin
2nd line: vancomycin + gentamicin
What is the specific treatment for HACEK IE?
1st line: ceftriaxone
When is surgery indicated as treatment for IE?
Despite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention:
Haemodynamic instability
Severe heart failure
Severe sepsis despite antibiotics/failed medical therapy
Valvular obstruction
Infected prosthetic valve
Persistent bacteraemia
Repeated emboli
Aortic root abscess
Common exam question: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess
What are the complications of IE?
Acute valvular insufficiency causing heart failure
Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)
Embolic complications causing infarction of kidneys, spleen or lung
Infection e.g. osteomyelitis, septic arthritis
What are the general thoughts of prevention in IE?
Antibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis.
Evidence has shown that there is no consistent association between having an interventional procedure and the development of infective endocarditis. In fact, regular brushing of teeth causes much greater, repetitive bacteraemia compared to a single interventional procedure.
Further to this, the clinical effectiveness of antibiotic prophylaxis has never been proven.
NICE (CG94), on balance of the evidence, suggests that antibiotic prophylaxis against infective endocarditis results in a greater risk of anaphylaxis than any potential benefit, and is also not cost effective.
Prophylaxis is therefore not recommended.
Organisims belonging to the HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) group should be considered in patients who present with culture negative endocarditis.
Staphylococcus aureus is considered the most common cause of infective endocarditis, particularly in acute presentations. It is a coagulase-positive organism frequently associated with intravenous drug use or healthcare-associated infections. However, this patient’s subacute presentation and negative blood cultures should raise suspicion of HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) infective endocarditis.
In infective endocarditis, partial haemolysis on blood agar is commonly observed with alpha-haemolytic Streptococci such as S. viridans.
This typically causes a subacute presentation of infective endocarditis in patients with existing cardiac disease. It is one of the alpha haemolytic Streptococci and causes partial haemolysis on agar
In patients with a history of valve replacement, severe abdominal pain is suggestive of acute mesenteric ischaemia as a complication of septal emboli from a subacute infective endocarditis; CT angiography is crucial for diagnostic confirmation.
This patient has subacute infective endocarditis, with acute mesenteric ischaemia due to septic emboli as a complication. CT angiography is the definitive diagnostic method for acute mesenteric ischaemia
Define acute mesenteric ischaemia?
Acute mesenteric ischemia (AMI) is a life-threatening surgical emergency characterized by the abrupt onset of blood flow restriction (hypoperfusion) to a portion of the small intestine. This disruption may be either occlusive or non-occlusive, affecting primarily the superior mesenteric artery.
What are the causes of acute mesenteric ischaemia?
Arterial Embolism: The most common cause, often resulting from atrial fibrillation or other embolic sources such as infective endocarditis or aortic aneurysm.
Arterial Thrombosis: Usually associated with atherosclerosis, especially in patients with a history of ischemic heart disease or peripheral vascular disease.
Venous Thrombosis: Occurs less commonly and is often linked to hypercoagulable states.
Non-Occlusive Mesenteric Ischemia: Typically associated with low-flow states such as heart failure, shock, or during major surgery.
What are the signs and symptoms of acute mesenteric ischaemia?
Sudden severe abdominal pain and guarding, often out of proportion to the physical examination
Nausea and vomiting
Signs of shock, such as hypotension, tachycardia, altered mental status
Metabolic acidosis on arterial blood gas (ABG) analysis
Rectal bleeding can occasionally be seen in advanced ischemia
The embolic nature of a mesenteric infarction causes a sudden evacuation of the bowels that may contain blood, as the infarction leads to bleeding into the gut wall, lumen and peritoneal cavity
new onset atrial fibrillation
What are the investigations for acute mesenteric ischaemia?
Blood tests: Full blood count, liver function tests, renal function, coagulation profile, and lactate levels
Arterial blood gas (ABG): To identify metabolic acidosis
Imaging: CT angiography is the diagnostic modality of choice due to its ability to visualize the occlusion and surrounding bowel.
What is the management for acute mesenteric ischaemia?
The primary objectives in managing AMI are rapid diagnosis, stabilization of the patient, and restoration of bowel perfusion. This can be achieved through:
Resuscitation: Including fluid management and correction of metabolic abnormalities
Anticoagulation: Typically with intravenous heparin to limit progression of thrombosis or embolism
Surgical intervention: Including embolectomy, arterial bypass, or bowel resection if necrosis is present
Non-surgical intervention: Such as intra-arterial vasodilators or thrombolytic therapy
Supportive care: Including analgesia, antibiotics if needed, and nutritional support.
Define chronic mesenteric ischaemia:
Chronic mesenteric ischaemia is a pathological condition typically presenting in elderly patients, characterized by insufficient blood supply to the intestines, usually due to gradual blockage or narrowing of the mesenteric arteries.
What is the epidemiology of chronic mesenteric ischaemia?
Chronic mesenteric ischaemia (CMI) is a relatively uncommon condition primarily affecting the elderly population. The overall incidence and prevalence are difficult to establish due to underdiagnosis and the coexistence of other diseases with similar presentations.
Typically, CMI is most frequently observed in patients aged 60 years and above. It is estimated that significant stenosis or occlusion of the celiac and mesenteric arteries, which leads to CMI, may be present in up to 7% of individuals over the age of 65. The condition appears to be slightly more prevalent in women compared to men, with a ratio of approximately 3:2.
The underlying risk factors for CMI, including smoking, hypertension, hyperlipidemia, diabetes, and a history of cardiovascular disease, align with those of the general atherosclerotic disease. Consequently, the prevalence of CMI is expected to rise alongside the increasing prevalence of these risk factors in the aging population.
CMI is a serious condition, with untreated symptomatic disease associated with high mortality rates, often due to the development of acute mesenteric ischaemia. However, with prompt diagnosis and appropriate management, the prognosis can be significantly improved.
What is the aetiology of chronic mesenteric ischaemia?
Patients often have risk factors for arterial disease, such as smoking, diabetes, hypercholesterolemia, and a history of myocardial infarction. They may also have risk factors for embolic disease, notably atrial fibrillation.
What are the signs and symptoms of chronic mesenteric ischaemia?
Diffuse, colicky abdominal pain, which worsens after eating
Significant weight loss, as patients avoid eating due to the pain
Diarrhoea
Gastrointestinal bleeding, presenting as melaena or haematochezia (secondary to mucosal sloughing)
Physical examination often reveals abdominal tenderness. An epigastric bruit may be present, indicative of turbulent flow in the narrowed vessels.
What are the investigations for chronic mesenteric ischaemia?
Bedside investigations - VBG to check for raised lactate
Duplex ultrasound: A non-invasive method to detect blood flow and identify blockages in the mesenteric arteries.
Gold standard: Computed Tomography (CT) angiography: Helps to visualize the anatomy of the mesenteric arteries and the presence of any blockages.
Mesenteric angiography: An invasive procedure that provides detailed images of the blood vessels supplying the intestines, typically used when other investigations are inconclusive or prior to intervention.
What is the management for chronic mesenteric ischaemia?
Risk factor modification: Smoking cessation, control of diabetes and hypercholesterolemia.
Symptom relief: Medications like vasodilators may be used to increase blood flow to the intestines.
Revascularization: Percutaneous transluminal angioplasty (PTA) with or without stenting or surgical revascularization procedures are typically used for patients with severe symptoms or when conservative management fails.
Define ischaemic colitis:
Hypoperfusion of the large bowel
Which artery is usually compromised in ischaemic colitis:
Inferior mesenteric artery
Which areas are at a high risk of colonic ischaemia?
- Area near splenic flexure
- 2/3 transverse colon is at high risk due to being watershed areas
List risk factors associated with ischaemic colitis?
- Age
- AF
- Smoking
- Hypertension
- Diabetes
Define ischaemic heart disease:
Ischaemic heart disease (IHD), also known as coronary artery disease, is a condition characterised by reduced blood supply to the myocardium due to stenosis or occlusion of the coronary arteries.
What is the primary cause of ischaemic heart disease:
The primary aetiological factor is atherosclerosis, which leads to progressive narrowing and hardening of the arteries.
What is the clinical presentation of ischaemic heart disease:
Clinical presentations can vary from asymptomatic disease to angina pectoris, myocardial infarction or sudden cardiac death.
What is the diagnosis of ischaemic heart disease:
Diagnosis usually involves clinical assessment, electrocardiogram (ECG), exercise stress testing, and imaging techniques like echocardiography or coronary angiography. Biomarkers such as troponins can also be used to identify acute ischaemia.
What is the 1st line management for ischaemic heart disease?
- Beta blocker- Bisoprolol/atenolol
OR
- Rate limiting CCB- Verapamil/diltiazem
- When would you need to prescribe both?If only 1 isn’t working
- Overall medical management? (4)BAGS
- Beta blocker (or CCB)
- Aspirin (75mg)
- GTN
- Statin (20mg)
- What can you do if symptoms are not controlled medically?May have PCI or CABG
What do we do in ischaemic heart disease if we prescribe both beta blockers and CCB ?
- What do we use if we prescribe both?
- Nifedipine/amlodipine (non-cardioselective CCB) as CCB can’t be used alongside beta blocker
- Causes severe bradycardia and heart block
- In what condition are BB’s contraindicated?Asthma
Define mitral stenosis?
Mitral stenosis refers to the narrowing of the mitral valve which reduces blood flow to the left ventricle.
What is the pathophysiology of mitral stenosis?
Normally, the mitral valve opens during diastole to allow left ventricular filling. In mitral stenosis, the thickened and calcified mitral valve reduces the amount of blood that can flow through the valve into the left ventricle during diastole. This leads to a reduction in the end-diastolic volume in the left ventricle and increases the volume of blood in the left atrium. The increased volume of blood in the left atrium leads to atrial dilatation (predisposes to atrial fibrillation), pulmonary congestion and ultimately right heart failure.
What is the most common cause of mitral stenosis:
The commonest cause of mitral stenosis is rheumatic heart disease.
Pathophysiology: the body produces antibodies to target the streptococcal antigens that occur in rheumatic fever. These antibodies also attack valvular tissue (autoimmune molecular mimicry) leading to valvular disease.
Name some other causes of mitral stenosis?
Mitral annular calcification (age-related)
Congenital mitral stenosis (rare)
Mucopolysaccharidosis (metabolic disorder affecting connective tissue)
Carcinoid syndrome, causing valve disease
Systemic disease, including systemic lupus erythematosus (SLE) and rheumatoid arthritis.
Atrial outflow obstruction due to other conditions, such as atrial myxoma, may cause symptoms similar to MS.
What are the symptoms of mitral stenosis:
Mitral stenosis typically remains asymptomatic until the degree of stenosis is advanced. Symptoms tend to begin when the valve area falls <1.5cm^2.
Common symptoms include:
Gradual exertional dyspnoea and reduced exercise tolerance.
Dyspnoea secondary to pulmonary venous congestion.
Haemoptysis: increased pulmonary pressures and vascular congestion, which can manifest as pink/blood stained sputum, or frank haemoptysis.
Palpitations: atrial fibrillation (AF) is common in patients with MS due to elevated left atrial pressures and subsequent left atrial enlargement
Chest pain: can occur as a result of pulmonary hypertension and right ventricular hypertrophy, or due to AF with fast ventricular response.
Thromboembolism (cerebral or systemic): secondary to AF.
Hoarseness: enlarged L atrium can compress the recurrent laryngeal nerve (Ortner’s syndrome).
Peripheral oedema / abdominal discomfort (hepatomegaly) - due to right heart failure.
What are the peripheral signs of mitral stenosis:
Mitral facies (malar flush): cutaneous vasodilation due to carbon dioxide retention.
Low volume pulse
Irregularly irregular pulse: AF.
Elevated JVP (prominent ‘a’ wave due to raised right atrial pressure, or absent ‘a’ wave in AF).
Tapping, non-displaced apex beat (palpable S1).
Right ventricular heave (suggestive of pulmonary hypertension).
Inspiratory crepitations (pulmonary oedema) and other signs of right heart failure.
What are the findings on auscultation of mitral stenosis?
Loud S1 (becomes softer with increasing calcification)
Loud P2 with pulmonary hypertension (later stages S2 splits)
Opening snap heard at apex (only with pliable valves)
Mid-to-late diastolic murmur
Low pitched rumble, most prominent at apex
Loudest in expiration
Heard best with patient lying on left side
Heard best using stethoscope bell (low frequency)
Graham-Steell murmur (early diastolic murmur - only if pulmonary regurgitation present secondary to pulmonary hypertension)
What are the investigations in mitral stenosis?
ECG may show:
P-mitrale (a broad notched P wave due to left atrial enlargement)
Right ventricular hypertrophy
Right axis deviation
Atrial fibrillation: caused by left atrial enlargement
CXR may show evidence of pulmonary oedema and left atrial enlargement
Echocardiogram: will show degree of stenosis and impairment of ventricular filling.
Cardiac MRI may show valvular vegatations.
What is the conservative management of mitral stenosis:
Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all.
If a patient has asymptomatic MS they should undergo regular follow-up echocardiography to assess degree of stenosis and its progression.
What is the medical management of mitral stenosis:
Treatment of complications including atrial fibrillation with rate control and anticoagulation.
Diuretics can provide symptomatic relief for pulmonary congestion and peripheral oedema.
Medical management is not an alternative to definitive interventional treatment.
What is the interventional and surgical management of mitral stenosis:
For symptomatic patients there are three treatment options:
Balloon valvuloplasty: only appropriate if valve is pliable and non-calcified.
Percutaneous mitral valvotomy: for patients with moderate disease.
Open valve repair/replacement: for patients with severe disease who are not too high risk for surgery but are not candidates for percutaneous intervention. Valves are more likely to be metal than bioprosthetic.
Treatment is difficult in patients who have severe disease or who have inadequate valve morphology and are high risk for open surgery.
What are the complications of mitral stenosis?
t first, progression is slow but once the onset of symptoms occurs the progression happens more rapidly.
Initial symptoms are related to the following complications:
Atrial fibrillation (AF) and thromboembolism - palpitations, poor exercise tolerance and symptoms of cardioembolic stroke.
Pulmonary hypertension - dyspnoea and haemoptysis.
Dilated left atrium - can impinge on local structures, leading to hoarseness, dysphagia and bronchial obstruction.
Patients may also present with symptoms of decompensated heart failure, either due to the valvular disease itself (along with a precipitant like infection) or can be secondary to non rate-controlled AF.
define mitral regurgitation:
Mitral regurgitation (MR) is the backflow of blood into the left atrium during systole due to the incompetence of the mitral valve.
What is the pathophysiology of mitral regurgitation:
Normally, the mitral valve closes at the beginning of systole to prevent backflow of blood into the left atrium. In mitral regurgitation, the mitral valve fails to close sufficiently meaning there is a backflow of blood across the mitral valve into the left atrium. Over time, this leads to the enlargement of the left atrium and leads to volume overload in the left side of the heart ultimately leading to LV failure.
Causes of acute mitral regurgitation?
Acute MR is a cardiac emergency and may present with sudden-onset pulmonary oedema, hypotension and cardiogenic shock. See section on management of acute pulmonary oedema.
Causes of Acute MR
Ischaemic MR: primarily due to papillary muscle rupture secondary to a postero-inferior myocardial infarction.
Non-ischaemic MR: ruptured chordae tendineae due to any of a number of causes.
Myxomatous disease (mitral prolapse)
Infective endocarditis
Rheumatic heart disease - acute or chronic
Trauma
Spontaneous rupture
Prosthetic valve MR:
Tissue valvelet rupture due to endocarditis, degeneration or calcification.
Paravalvular regurgitation due to infection or suture rupture.
Valve thrombus or infection causing impaired closure.
Causes of chronic mitral regurgitation:
Leaflet causes:
Mitral valve prolapse (MVP) is a common cause of chronic MR (accounting for approximately 5% of cases). Please see separate section on MVP.
Degenerative disease (causing prolapse)
Rheumatic fever (presents typically in the younger patients <20, whereas MS is more common in older patients)
Infective endocarditis
Systemic inflammatory disorders e.g. SLE, scleroderma
Connective tissue disorders e.g. Marfan’s, Ehlers-Danlos syndromes
Congenital causes e.g. mitral valve clefts
Hypertrophic cardiomyopathy causing abnormal valve movements
Drug related damage, e.g. ergotamine, bromocriptine, ‘fen-phen’ (fenfluramine - anorectic drug, now banned)
Chordae related causes:
Myxomatous valve disease (causing prolapse)
Trauma
Papillary muscle related causes::
Myocardial ischemia or infarction (regional wall motion abnormalities - RWMA - can cause inadequate systolic function and poor closure)
Dilated cardiomyopathy
Annular related causes:
Calcification, either due to rheumatic fever or age-related
Dilation due to dilated cardiomyopathy or connective tissue disorders
Prosthesis related causes:
Paravalvular leak
Ring or strut fracture
Leaflet deterioration in tissue valves
Infective endocarditis
Thrombus or pannus formation which can obstruct valve closure
Symptoms of acute Mitral regurgitation:
Shortness of breath
Exertional dyspnoea
Fatigue
Weakness
and signs of overt pulmonary oedema, hypotension and cardiogenic shock.
Symptoms of chronic mitral regurgitation:
Mild-to-moderate MR: asymptomatic until significant systolic dysfunction, pulmonary hypertension or symptomatic atrial fibrillation (AF).
Fatigue and exertional dyspnoea are most common, a result of decreased cardiac output as well as increased pulmonary pressures due to increased left atrial pressures.
What are the signs of chronic mitral regurgitation:
‘Blowing’ pansystolic murmur
Loudest at the apex
Radiates to the axilla
Louder on expiration
Louder on rolling to the left
S1 may be quiet or absent
If patients are in decompensated heart failure
Bilateral lung crepitations
Raised JVP
S3/S4
Peripheral/sacral oedema oedema
Acute MR can present with signs of acute pulmonary oedema, hypotension and cardiogenic shock.
Investigations for mitral regurgitation:
Bedside
ECG: p-mitrale (broad notched p wave due to left atrial enlargement), LVH and left axis deviation.
Bloods
NT pro-BNP: raised in heart failure reflects increased ventricular stress.
Imaging
CXR: evidence of pulmonary oedema and left atrial enlargement.
Definitive diagnosis is made using echocardiogram which allows assessment of:
Size and pressure of regurgitant jet
Size of valve lesions
Structural complications such as left atrial enlargement or systolic dysfunction
What is the conservative management for mitral regurgitation:
Timing of intervention is crucial as many cases remain asymptomatic and stable and may not require treatment at all.
If a patient has asymptomatic MR they should undergo regular follow-up echocardiography.
What is the medical management for mitral regurgitation:
Treatment of concurrent complications:
AF with rate control and anticoagulation
Heart failure with diuretics, ACE-Inhibitors, and beta-blockers.
Acute MR is a medical emergency and should be treated according to acute pulmonary oedema guidelines (please see section).
What is the surgical management for mitral regurgitation:
The definitive management for symptomatic MR is surgery - there are two main options:
Mitral valve repair (mitral valvuloplasty) - this is preferable as is preserves all components of the native valve and avoids use of prostheses.
Mitral valve replacement - offers the choice between a mechanical valve (lifelong anticoagulation but long-lasting), and a bioprosthetic valve (limited durability but no need for anticoagulation)
Define myocarditis:
Myocarditis, also known as an inflammatory cardiomyopathy, refers to inflammation of the myocardium (heart muscle). It often occurs alongside inflammation of the pericardium (sac that surrounds the heart) and it is then described as myopericarditis.
What are the complications of mitral regurgitation:
Heart failure
Thromboembolism secondary to AF
Haemoptysis secondary to pulmonary hypertension and symptoms of right heart failure are possible but less common than in mitral stenosis (MS).
Infective endocarditis and associated symptoms can also complicate MR.
What is the pathophysiology of myocarditis:
Myocarditis occurs due to the infiltration of inflammatory cells into heart tissue.
How is myocarditis classified:
Classification of myocarditis can be considered according to cause. The most common cause in Europe and the UK are viruses, with Cocksackie B being the most common culprit. Worldwide, Chagas disease is the most common cause following infection from Trypanosoma cruzi.
What viral infections cause myocarditis:
Cocksackie B virus: most common cause of myocarditis in Europe and the UK.
COVID-19
Adenovirus
Epstein Barr Virus
What bacterial infections cause myocarditis:
Diphtheria
Clostridia
Neiseria gonorrhoea
What Protozoan cause myocarditis:
Trypanosoma cruzi
What Auto-Immune diseases cause myocarditis:
Kawasaki disease
Scleroderma, SLE, sarcoid and systemic vasculitides
What drug reactions cause myocarditis:
Antipsychotics incl. clozapine
Immune-checkpoint inhibitors
Mesalazine
What are the symptoms of myocarditis:
Chest pain: often described as sharp, stabbing. If pericardial involvement, chest pain may be worse on lying down.
Shortness of breath
Palpitations
Lightheadedness
Syncope
Fever and viral prodrome
Severe cases can present with sudden unexplained cardiac death.
What are the signs of myocarditis:
Asymptomatic or non-specific signs may be present.
Dull heart sounds
If myopericarditis a pericardial rub may be heard.
In fulminant myocarditis the patient may have signs of heart failure.
What are the investigations for myocarditis:
Bedside
ECG: non-specific ST segment and T wave changes (may suggest location of myocardial involvement); arrhythmias; tachycardia; and ectopic beats.
Bloods
Raised Troponin and CK-MB: can be markedly elevated.
Inflammatory markers: may also be elevated and may indicate cause.
Consider viral serology to determine aetiology of the myocarditis.
Imaging
Echocardiogram: reveal ventricular dysfunction or regional wall motion abnormalities.
Cardiac MRI: help confirm diagnosis of myocarditis and indicate extent of inflammation.
Endomyocardial biopsy: gold-standard diagnostic tool. Histopathology shows infiltration of inflammatory cells into the myocardium and myocardial necrosis.
What is the management of myocarditis:
Hallmark of treatment is supportive and addressing the underlying cause.
Patients with severe myocarditis may require ITU support and vasopressors.
Patients with viral acute myocarditis may benefit from a course of corticosteroids.
After recovery, patients should be advised to limit activity for a few months.
What are the complications of myocarditis:
Complications of myocarditis may include heart failure, arrhythmias, or dilated cardiomyopathy.
ECG changes that may be seen in myocarditis include sinus tachycardia, ST changes and T wave inversion.
A young adult presenting with acute chest pain, breathlessness, and a recent history of viral illness, alongside sinus tachycardia and T wave inversion on ECG, should raise suspicion for myocarditis.
Define acute pericarditis:
Acute pericarditis is inflammation of the pericardium, the fibroelastic sac that surrounds the heart. Inflammation can also extend to the myocardium (heart muscle), in which case the condition is referred to as perimyocarditis or myopericarditis depending on which is predominant.
What are the causes of acute pericarditis:
Idiopathic
Infective causes
Viruses - viruses which cause pericarditis are coxsackie B viruses, echovirus, CMV, herpesvirus, HIV among other rarer causes.
Bacteria - staphylococcus, pneumococcus, streptococcus (rheumatic carditis), haemophilus and M. tuberculosis.
Fungi and parasites (rare)
Malignant causes
Lung cancer
Breast cancer
Hodgkin’s lymphoma
Cardiac causes
Heart failure may cause pericarditis
Post-cardiac injury syndrome (Dressler’s syndrome) including post-traumatic
Radiation - often secondary to therapy for other malignancies
Drugs and toxin causes
Anthracycline chemotherapy (Doxorubicin)
Hydralazine
Isoniazid
Methyldopa
Phenytoin
Penicillins (hypersensitivity)
Rheumatological disease
Systemic lupus erythematous (SLE)
Rheumatoid arthritis
Sarcoidosis
Vasculitides (Takayasu’s, Behcet’s)
Other causes
Renal failure (uraemia) - indication for emergency dialysis.
Hypothyroidism
Inflammatory bowel disease
Ovarian hyperstimulation
What are the symptoms of acute pericarditis?
Pleuritic chest pain: central, worse on inspiration.
Postural chest pain: worse on lying flat and relieved on leaning forward.
Fever
What are the signs of pericarditis:
Pericardial friction rub - high-pitched scratching noise, best heard over the left sternal border during expiration. Pathogonomonic of pericarditis.
Pericarditis can lead to the development of a pericardial effusion and cardiac tamponade in which case signs such as hypotension, raised JVP and muffled heart sounds (Beck’s Triad) may be present.
What are the first line investigations in pericardial disease and what do we look for?
Bedside
1st line = ECG
ECG features include:
Widespread saddle ST elevation (not following vascular territories) and PR depression.
ECG changes can sometimes evolve over weeks:
1-3 weeks: normalisation of ST changes, T wave flattening
3-8 weeks: flattened T waves become inverted
8+ weeks: ECG returns to normal
What are the bloods and imaging used in pericardial disease?
Bloods
Serial troponins: tend not to peak as in an MI, but tend to stay consistently elevated in the acute phase.
Inflammatory markers: raised inflammatory markers (WCC, CRP and ESR) are in keeping with an acute pericarditis.
Viral serology: may help to identify cause of the acute pericarditis.
Imaging
Echocardiogram - used to assess for pericardial effusion and distinguish between pericarditis and MI (e.g. looking for the absence of regional wall motion abnormalities).
Angiogram - shows normal coronary arteries (which excludes MI).
Cardiac MRI - in atypical cases, cardiac MRI can be used to visualise inflammation of the pericardium.
What is the management for Idiopathic or Viral Pericarditis?
1st line: exercise restriction and NSAIDS (+ PPI) for 1-2 weeks.
2nd line: colchicine (SE: diarrhoea, use in caution in those with renal or hepatic impairment).
3rd line: corticosteroids (for those who cannot tolerate or refractory to NSAIDS).
What is the management for bacterial pericarditis
1st line: IV antibiotics +/- pericardiocentesis if purulent exudate present.
Rare cases - pericardectomy may be performed if adhesions or recurrent tamponade occurs.
What is the management for non-infective pericarditis:
1st line: corticosteroids (due to the risk of reactivation and if infection has been ruled out).
What are the complications of pericarditis:
Complications are rare but include cardiac tamponade and pericardial effusion requiring pericardiocentesis. In the long term patients occasionally develop constrictive pericarditis.
What is Dressler’s syndrome?
Dressler’s syndrome is acute pericarditis occuring several weeks after a myocardial infarction, where an ECG shows widespread ST elevation, PR depression, and a downward sloping T-P segment (Spodick’s sign
The most specific ECG finding in Dressler’s syndrome is PR depression which may be seen in addition to concave ST-segment elevation.
what is kussmaul’s sign?
A raised jugular venous pulse that increases with inspiration is indicative of increased right atrial pressure, suggesting restricted heart chamber filling in conditions such as constrictive pericarditis.
Define constrictive pericarditis:
Constrictive pericarditis is the result of scarring and loss of elasticity of the pericardial sac. The scarred pericardium prevents normal cardiac filling which leads to the restriction of ventricular volume, stroke volume, and ultimately cardiac output.
Symptoms of constrictive pericarditis:
Patients present with symptoms of heart failure:
Fatigue
Reduced exercise tolerance
Exertional dyspnoea
Peripheral oedema
What are the signs of constrictive pericarditis:
Raised JVP
Kussmaul’s sign: paradoxical rise in JVP with inspiration.
Pulsus paradoxus: more commonly seen in cardiac tamponade. It results due to the drop in cardiac output on inspiration.
Heart sounds may be quiet (if pericardial effusion also present)
Pericardial knock: high-pitched, early diastolic sound that occurs when stiff pericardium results in sudden arrest of ventricular filling.
What are the investigations for constrictive pericarditis ?
CXR: small heart +/- pericardial calcification
Echocardiogram: demonstrates ventricular filling defect and heart failure with preserved ejection fraction (HFpEF).
Cardiac MRI: helps differentiate from restrictive cardiomyopathy.
What is the management of constrictive pericarditis:
Hallmark of management of constrictive pericarditis is surgical excision of the fibrosed pericardium (pericardiectomy).
How do you distinguish between constrictive pericarditis and restrictive cardiopathy?
Constrictive pericarditis is the result of a fibrosed and scarred pericardium. Restrictive cardiomyopathy is when there is increased myocardial stiffness. Causes of restrictive cardiomyopathy include amyloidosis and post-radiotherapy. These two conditions are very difficult to distinguish clinically.
Clues that suggest constrictive pericarditis over restrictive cardiomyopathy:
Paradoxical pulse
CXR shows pericardial calcification
Cardiac MRI shows a thickened pericardium
Endomyocardial biopsy shows an absence of amyloid or other infiltrative diseases.
Define a pulmonary embolism?
A pulmonary embolism (PE) is when one or more blood clots lodge in and obstruct the pulmonary arterial vasculature. Typically these emboli arise from a thrombus in the deep veins of the lower limb (a DVT).
How does one classify pulmonary embolism?
Once a PE is diagnosed, severity can be determined using the PE Severity Index (PESI) score - This looks at 11 factors (e.g. presence of tachycardia, hypotension, confusion) to give an overall score which can be used to classify patients as very low risk/low risk/intermediate risk/high risk/very high risk - These correspond to estimated 30 day mortality rates which range from 0.7% in very low risk patients to 25% in very high risk patients - This can be used to stratify appropriateness for outpatient care versus admission
Patients who are clearly haemodynamically unstable are high-risk and all require admission
Another important marker of high-risk patients is right ventricular strain - All patients should have a troponin; if this is elevated or there are features of right heart strain on the CTPA then an echocardiogram should be done
What are the symptoms of pulmonary embolism?
The ““typical triad”” of symptoms is as follows, although all three features are rarely present simultaneously:
Sudden-onset shortness of breath (the commonest symptom, present in around half of patients)
Pleuritic chest pain
Haemoptysis
Cough may also be present without haemoptysis
Syncope or pre-syncope are concerning symptoms indicating massive PE
Right ventricular ischemia can lead to retrosternal chest pain
Symptoms of a DVT such as leg pain or swelling may be present
Small PEs may be asymptomatic and detected incidentally on imaging
What signs to look for in pulmonary embolism?
Tachypnoea
Crackles on auscultation
Tachycardia
Hypoxia
Low-grade pyrexia in some
In massive PE: - Hypotension - Cyanosis - Signs of right heart strain (e.g. a raised JVP, parasternal heave and loud P2)
What score do we use to risk stratify patients with pulmonary embolism?
Well’s score:
How does the Well’s score work in pulmonary embolism?
3 points
clinical signs and symptoms of a DVT
PE is the most likely diagnosis
1.5 points
tachycardia (heart rate >100 beats/minute)
immobility > 3 days or major surgery within 1 month
previous PE or DVT
1 point
haemoptysis
current malignancy
Wells score 4 or less - PE unlikely, do a D-dimer
a low D-dimer excludes a PE
a raised D-dimer should be further investigated (e.g. with a CTPA)
Wells score more than 4 - PE likely - Further investigate with a CTPA or V/Q scan
What other investigations do we use in pulmonary embolism?
Bedside tests
ECG may be normal or show sinus tachycardia
In a massive PE, there may be evidence of right-heart strain (P pulmonale, right axis deviation, right bundle branch block, nonspecific ST/T wave changes)
The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III and inverted T waves in lead III) is seen in less than 20% of patients
ABG may be normal or show type 1 respiratory failure and/or a respiratory alkalosis due to hyperventilation
Bloods
D-dimer - not a specific test but has a 95% negative predictive value (i.e. it is useful to help rule out a PE if negative)
FBC may show anaemia or thrombocytosis in underlying malignancy
CRP may be raised in malignancy or intercurrent infection
U&Es are needed to assess renal function prior to a CTPA
LFTs as a baseline e.g. to assess suitability for anticoagulation
Coagulation screen as a baseline before starting anticoagulation
Troponin to assess for myocardial damage
Imaging
Chest X-ray - typically normal in PE but helpful in ruling out differentials (e.g. pneumonia, pneumothorax), may show:
Fleischner sign - an enlarged pulmonary artery
Hampton’s hump - a peripheral wedge shaped opacity
Westermark sign - regional oligaemia
CT pulmonary angiogram (CTPA) - the diagnostic test of choice for a PE, will show filling defect(s) in the pulmonary vasculature
V/Q scan - preferred in severe renal impairment or contrast allergy
Ultrasound doppler of the lower limbs - to investigate for an underlying DVT
Transthoracic echocardiogram - to investigate for right heart strain
What is the conservative management for pulmonary embolism:
Oxygen if hypoxic
Fluid resuscitation if hypotensive
Analgesia for chest pain
Patient education - if starting anticoagulation ensure patient has an alert card
Low-risk patients may be suitable for discharge with anticoagulation and outpatient follow up - The simplified PESI (Pulmonary Embolism Severity Index) may be used to help risk stratify - Patients get 1 point for each of age > 80, history of cancer, chronic cardiopulmonary disease, heart rate > 110, systolic blood pressure < 100, oxygen saturations < 90%) - Outpatient management can be considered in patients scoring zero
What is the medical management for pulmonary embolism?
Anticoagulation with low molecular weight heparin (LMWH) or a direct oral anticoagulant (DOAC such as rivaroxaban) should be administered immediately if there is high clinical suspicion of a PE
This can be stopped if a PE is ruled out
Once a PE is confirmed, most patients will continue on a DOAC as these tend to be more convenient for patients
If a DOAC is unsuitable, warfarin or LMWH may be considered
In cases of massive PE (hypotension for over 15 minutes), patients should be treated with thrombolysis (an IV bolus of Alteplase)
There is an associated risk of haemorrhage but this is lower than the risk of death from a massive PE
High risk PEs should also be considered for thrombolysis on a case-by-case basis
How long is the duration of anticoagulants in pulmonary embolism?
The duration of anticoagulation treatment depends on the aetiology of the PE
A provoked PE should be treated for 3 months (3-6 months if active cancer)
Consider continuing treatment for unprovoked PEs beyond 3-6 months
In some cases (e.g. certain thrombophilias), patients should be anticoagulated for life - however this needs to be balanced with bleeding risk
What is the interventional treatment in pulmonary embolism?
Interventional:
Embolectomy may be considered in patients with a massive PE when thrombolysis is contraindicated
Catheter-directed thrombolysis can be used in specialist centres for patients with a high bleeding risk (ie. postoperative patients)
In patients with Antiphospholipid syndrome, PE should be initially treated with LMWH for rapid anticoagulation, along with warfarin for long-term anticoagulation. LMWH should be continued for 5 days or until the INR reaches a therapeutic range (typically 2-3) with warfarin.
:))
Patients with recurrent venous thromboembolism and antiphospholipid syndrome require long-term anticoagulation with a higher target INR (3-4) compared to those without thrombophilia.
:,)
A haemodynamically unstable patient with suspected pulmonary embolism and risk factors such as recent surgery or cancer should receive thrombolytic therapy, specifically IV Alteplase.
:(
Define peripheral vascular disease:
Disease characterised by narrowing and occlusion of the peripheral arteries due to atherosclerotic plaques
What are the risk factors for peripheral vascular disease:
- Smoking- main one
- Diabetes
- Hypertension
- Hyperlipidaemia
What is claudication?
Pain on exertion due to inadequate blood flow during exercise, causing fatigue, discomfort, or pain
What is critical limb ischaemia?
Compromise of blood flow to an extremity, causing chronic limb pain at rest (worse at night) for at least 2 weeks
- What can patients develop? (2)
- Arterial ulcers
- Gangrene
What is acute limb ischaemia?
Sudden decrease in limb perfusion that threatens limb viability
What are the symptoms of acute limb ischaemia?
- Pain
- Paralysis
- Paraesthesia
- Pulseless
- Pallor
- Perishingly cold
What is a major risk factor for acute limb ischaemia?
Atrial fibrillation
What is Buerger’s disease (thromboangiitis obliterans)?
Happens in young male smokers with symptoms similar to limb ischaemia
- List symptoms of Buerger’s disease (2)
- Paraesthesia/cold sensation in fingers or limbs
- Raynaud’s phenomenon
What is leriche’s syndrome?
- Buttock claudication
- Impotence
- Absent/weak distal pulses
What are the clinical features of peripheral vascular disease?
- Most patients are asymptomatic
- Intermittent claudication- Cramping pain of leg which is worse upon exertion, relieved by rest
- Diminished or absent pulse
- ED (impotence)
- Thigh or buttock pain when walking
- What artery is affected in calf pain?Femoral artery
- What artery is affected in buttock pain?Iliac artery
- What are red flags? (2)
- Resting pain
- Skin changes- Ulcers or Gangrene
- What is this indicative of?Critical limb ischaemia
What is first line investigations for peripheral vascular disease?
- What is 1st line?Ankle-brachial pressure index
- What is ABPI?Ratio of systolic ankle BP to systolic brachial BP
- What ABPI indicates PAD?<0.8
- What ABPI indicates critical limb ischaemia?<0.5
- What is 1st line for intermittent claudication?Duplex ultrasound scan
- What do we determine?Can determine site, severity and length of stenosis
- What is 1st line for acute limb ischaemia?Bedside handheld arterial doppler scan
- What do you do after & why?Lower limb CT angiography to quantify extent of occlusion
What is buerger’s test in peripheral vascular disease?
- Lie patient flat on bed and lift leg to 45°
- Limb developing pallor indicates arterial insufficiency
- What does <20° Buerger’s angle indicate?Severe limb ischaemia
- What happens when patient swings leg over bed?Reactive hyperaemia is seen
What is the management for intermittent claudication?
- What is lifestyle management for intermittent claudication? (2)
- Smoking cessation
- Exercise training
- What is medical therapy for intermittent claudication? (3)
- Antiplatelet therapy (Clopidogrel or Aspirin)
- Statins
- Anti-hypertensives
- What’s the overall prescription then for intermittent claudication? (3)
- Lifestyle measures (exercise)
- Clopidogrel 75mg once daily
- Atorvastatin 80mg once daily (as secondary prevention)
- What can you prescribe if exercise is ineffective and patient doesn’t want to be referred for angioplasty or bypass surgery?Naftidrofuryl oxalate- vasodilator that can alleviate pain in PVD
- What do we do if risk factor modification and exercise hasn’t improved symptoms?Refer for surgical revascularisation
What is the management for acute limb ischaemia?
- IV heparin initially
- Analgesia + fluids + oxygen
- Then refer to vascular surgery- what different options are there? (3)
- Embolectomy
- Bypass
- Amputation
What is pulmonary hypertension?
Normal mean pulmonary arterial pressure is 11-20mmHg. Pulmonary hypertension is characterised by an increase in this to above 25mmHg at rest. There are a variety of causes, all of which involve an increase in pulmonary vascular resistance which ultimately leads to right heart failure due to increased backpressure on the right ventricle.
What causes pulmonary hypertension?
There are a variety of causes of pulmonary hypertension (with the main ones given below). An important differentiation should be made between pulmonary hypertension (the umbrella term for multiple causes) and pulmonary arterial hypertension which is one specific subtype.
Pulmonary arterial hypertension - may be idiopathic, familial, associated with other diseases (e.g. HIV, connective tissue disorders or portal hypertension) or secondary to drugs or toxins (e.g. amphetamines, fenfluramine)
Chronic pulmonary disease e.g. COPD, interstitial lung disease, bronchiectasis and obstructive sleep apnoea
Chronic thromboembolic disease e.g. persistent or recurrent pulmonary emboli
Chronic hypoventilation e.g. kyphosis or scoliosis, neuromuscular disorders
Left heart disease e.g. chronic left heart failure or mitral stenosis
Unclear or multifactorial mechanisms e.g. sarcoidosis, myelofibrosis, glycogen storage diseases
How does the world health organisation classify pulmonary hypertension?
Group 1: pulmonary arterial hypertension
Group 2: secondary to left heart diseases
Group 3: secondary to chronic pulmonary diseases and/or hypoxia
Group 4: due to chronic thrombotic or embolic disease
Group 5: other causes including metabolic disorders, systemic disorders and haematological disease
What are the signs and symptoms of pulmonary hypertension?
Progressive shortness of breath
Fatigue
Syncope
Fluid overload with ascites and peripheral oedema (late sign)
Raised JVP
Parasternal heave
Loud P2
Presence of an S3 sound
Pansystolic murmur indicative of tricuspid regurgitation (occurs due to the right ventricle becoming pressure and volume overloaded)
End-diastolic murmur indicative of pulmonary regurgitation (due to high pulmonary pressures)
What are the investigations for pulmonary hypertension?
Bedside:
ECG: may be normal or show signs of right heart strain such as P pulmonale, right ventricular hypertrophy and right axis deviation
Bloods:
LFTs: to investigate for liver disease (as portal hypertension may contribute to pulmonary hypertension)
TFTs: as hyperthyroidism (or more rarely hypothyroidism) may cause pulmonary hypertension
Autoimmune screen: e.g. ANA, ENA, scl-70 if an underlying connective tissue disorder is suspected
Imaging:
Chest X-ray: not diagnostic of pulmonary hypertension but abnormalities include an enlarged right atrium and ventricle, enlarged pulmonary arteries
High resolution CT chest: to further investigate for underlying causes e.g. if interstitial lung disease is suspected
CT or MR pulmonary angiography: to investigate for chronic thromboembolic disease
Transthoracic echocardiogram: to assess right ventricular function, can be used to estimate pulmonary arterial pressures; may also show signs of left heart disease
Special tests:
Right heart catheterisation: the gold standard for diagnosing pulmonary hypertension as it allows direct measurement of pulmonary arterial pressure
What is the conservative management for pulmonary hypertension?
As with any chronic disease, patient counselling and education
Early involvement of palliative care especially in deteriorating patients or those with troubling symptoms
In women of childbearing age with pulmonary arterial hypertension, counselling regarding the risks of pregnancy and provide contraceptive advice
What is the medical and surgical management for pulmonary hypertension?
Medical:
Supportive treatment with supplementary oxygen for hypoxia
Diuretics for fluid overload secondary to right heart failure
Medical optimisation of the underlying condition (e.g. anticoagulation for chronic pulmonary emboli)
Medications that reduce pulmonary vascular resistance:
Calcium channel blockers e.g. nifedipine
PDE-5 inhibitors e.g. sildenafil
Prostacyclin analogues e.g. iloprost
Endothelin receptor antagonists e.g. bosentan, ambrisentan
Soluble guanylate cyclase stimulators e.g. riociguat
Surgical:
Thrombo-arterectomy or pulmonary balloon angioplasty may be considered for chronic thromboembolic disease
Atrial septostomy is a palliative treatment where a hole is made between the atria to reduce right sided pressures
A heart-lung transplant may be considered in severe cases
What are the complications of pulmonary hypertension?
Right heart failure leading to peripheral oedema and congestive hepatopathy
Exertional syncope which may lead to injuries
Alveolar haemorrhage
Pulmonary artery dissection (can be spontaneous or due to iatrogenic injury during cardiac catheterisation)
Pericardial effusions
High risk of death during pregnancy (25-50%) due to increased right ventricular stress
Define cor pulmonale?
Cor pulmonale refers to right ventricular failure as a result of lung disease. Longstanding lung disease leads to pulmonary hypertension which puts increased stress on the right ventricle.
What is the pathophysiology of cor pulmonale?
In a patient with a chronic lung condition, like severe COPD, chronic pulmonary arterial vasoconstriction occurs due to hypoxia. In order to overcome the increased pressures in the pulmonary circulation, the right side of the heart has to work harder. Initially, this leads to right ventricular hypertrophy but at a certain point the right ventricular can no longer compensate and this leads to right heart failure.
What are the symptoms of cor pulmonale?
Symptoms:
Fatigue
Peripheral oedema
Ascites
Significant symptoms associated with the chronic lung conditions e.g. dyspnoea
What are the signs of cor pulmonale?
Cyanotic
Raised JVP with prominent a and v waves
RV heave
Loud P2
Pansystolic murmur with tricuspid regurgitation
Graham-Steel murmur: functional pulmonary regurgitation as the valve itself is not diseases but chronic pulmonary arterial hypertension stretches the valvular attachments.
Peripheral oedema
Render, pulsatile hepatomegaly.
What are the investigations for cor pulmonale?
Bedside
ECG: p pulmonale, RVH and R axis deviation.
Bloods
Routine bloods: chronic hypoxia in severe COPD may lead to a secondary polycythaemia.
Imaging
CXR: enlarged R atrium and ventricle with prominent pulmonary arteries.
Echocardiogram: diagnostic to view impaired right ventricular function.
What is the management for cor pulmonale?
There are no specific cardiac treatments for right ventricular failure apart from diuretics to aid symptom relief (bumetanide and furosemide).
The mainstay of treatment is to optimise the underlying respiratory pathology. Giving long-term oxygen therapy can help reduce pulmonary hypertension which can reduce the stress on the right ventricle.
Rarely, heart-lung transplantation can be considered in young people.
What is a cause of tricuspid stenosis?
Rheumatic fever, which almost always occurs with mitral or aortic valve disease
List clinical features of tricuspid stenosis (4)
- Fatigue
- Ascites
- Oedema
- Early diastolic murmur
What is the management for tricuspid stenosis?
- Diuretics
- Surgical repair
Define tricuspid regurgitation:
Tricuspid regurgitation (TR) occurs when the tricuspid valve fails to prevent blood from leaking back into the right atrium during systole.
What is the pathophysiology of tricuspid regurgitation?
Normally, the tricuspid valve closes tightly at the beginning of systole (S1) and prevents blood from leaking back into the right atrium.
In tricuspid regurgitation, the valve fails to seal tightly and blood leaks back into the right atrium thus increasing pressures in the right atrium and forcing the right ventricle to pump harder. Severe TR causes right-sided HF.
Name some causes of tricuspid regurgitation:
Infective endocarditis: consider in IVDU who present with fevers and a new murmur.
Rheumatic heart disease
Chronic lung disease
Pulmonary embolism
Secondary to pulmonary stenosis
Name the symptoms of tricuspid regurgitation:
Asymptomatic
Fatigue
Ankle swelling
Abdominal swelling
Name the signs of tricuspid regurgitation:
Signs of right-sided heart failure:
Raised JVP: prominent systolic ‘V’ waves.
Ascites
Peripheral oedema
Pulsatile hepatomegaly
Heart sounds
Pansystolic murmur: loudest in the left parasternal region and on inspiration.
Name the investigations for tricuspid regurgitation:
Bedside
ECG: non-specific or p pulmonale (peaked p waves) or incomplete right bundle branch block.
Bloods
Inflammatory markers and blood cultures if infective endocarditits suspected.
Imaging
Transthoracic echocardiogram (TTE): to detect and quantify TR alongside assessing ventricular function.
Cardiac MR: to further evaluate right ventricular size and function.
Cardiac catheterisation (angiography): may be required prior to surgery to assess for coronary artery disease.
Name the management for tricuspid regurgitation?
Conservative
If asymptomatic and non-severe, tricuspid regurgitation may be monitored with sequential TTEs.
Medical
Treat underlying causes: e.g. IV antibiotics for infective endocarditits.
Treat the right-sided heart failure and treat for fluid overload (loop diuretics).
Surgical
Consider surgery if severe, symptomatic and refractory to medical management.
Surgical options include:
Ring annuloplasty
Valve replacement
What are the complications of tricuspid regurgitation?
If left untreated, severe TR will cause right-sided heart failure.
- What is RILE? (2)
- Right sided murmurs louder on inspiration
- Left sided murmurs louder on expiration
Define pulmonary stenosis?
Pulmonary stenosis (PS) obstructs the blood flow from the right ventricle (RV) into the pulmonary bed, resulting in a pressure gradient greater than 10 mmHg across the pulmonary valve during systole.
What are the causes of pulmonary stenosis?
Pulmonary stenosis is usually congenital is associated with the following syndromes:
Tetralogy of Fallot (valvular)
Noonan syndrome (valvular)
Williams syndrome (supravalvular)
It can also be as a result of congenital rubella infection.
Very rarely, pulmonary stenosis can be acquired due to carcinoid syndrome.
What are the symptoms of pulmonary stenosis?
Pulmonary stenosis typically causes right heart failure and may present with the following symptoms:
Dyspnoea
Fatigue
Peripheral oedema
Ascites
What are the signs of pulmonary stenosis?
Dysmorphic facies if it occurs with a congenital syndrome such as Noonan syndrome or Williams syndrome.
Raised JVP
Right ventricular heave
Ejection systolic murmur that radiates to the left shoulder and is best heard on expiration.
Widely split S2 with a delayed P2.
What are the investigations for pulmonary stenosis?
ECG: p pulmonale, right axis deviation, and right ventricular hypertrophy.
CXR: prominent pulmonary arteries and post-stenotic dilatation.
Echocardiogram: degree of stenosis and ventricular function.
What is the management for pulmonary stenosis?
Like with all valve disease, mild asymptomatic valve disease rarely requires intervention. Surgical options for severe pulmonary stenosis include valvotomy (for valvular lesions) and balloon angioplasty (for supravalvular lesions). Treatment is considered in those with transvalvular pressure gradients >50mmHg.
What are the complications of pulmonary stenosis?
The main complication of pulmonary stenosis is right heart failure. These patients are also at increased risk of infective endocarditis.
What causes pulmonary regurgitation?
Any cause of pulmonary hypertension
What type of murmur do you hear in pulmonary regurgitation?
Decrescendo murmur in early diastole
Define a vasovagal syncope:
Loss of consciousness due to transient drop in blood flow to the brain caused by excessive vagal discharge
What is vasovagal syncope the most common cause of?
Most common cause of fainting in young people
List precipitating factors of vasovagal syncope (2)
- Emotions- such as? (3)
- Fear
- Severe pain
- Blood phobia
- Orthostatic stress- caused by? (2)
- Prolonged standing
- Hot weather
What are the clinical features of vasovagal syncope?
- What are they? (4)
- Loss of consciousness lasting a short time
- Patients may experience vagal symptoms before passing out
- Dizziness
- Sweating
- Light-headedness
- Twitching of limbs during blackout
- Short post-ictal phase
What investigations would we do for vasovagal syncope?
- ECG- why?Check for arrhythmia
- When would you do a 24hr ECG?Should be requested in those with multiple episodes of loss of consciousness with quick recovery times
- Echocardiogram- why?Check for outflow obstruction
- Lying/standing BP- why?Check for orthostatic hypotension
- Fasting blood glucose- why?Check for DM/hypoglycaemia
What’s the management plan for vasovagal syncope?
- Patient education & avoiding triggers
- Volume expansion- how? (2)
- Increased dietary salts
- Electrolyte rich sports drinks
- Fludrocortisone
What is the prognosis for vasovagal syncope?
- Recurrences are common but often occur in clusters
- In the long term, the mortality risk is very low, but injury is a concern due to recurrent falls, especially in older people
- List complication of falls (2)
- Injuries and fractures
- Extradural or cerebral haemorrhages
Define venous ulcers:
Any break in the skin that is located beneath the knee and has lasted longer than 2 weeks without healing is defined as an ulcer by NICE.
Venous ulcers, or stasis ulcers, on the other hand, arise due to inefficient blood return from the lower limbs, often associated with chronic venous insufficiency.
What is the epidemiology of venous ulcers?
Venous ulcers are more common than arterial, accounting for up to 80% of leg ulcers, with the remaining 20% being mainly arterial or mixed venous/arterial. Approximately 1% of individuals will develop a venous ulcer during their lifetime. Venous ulcers are more frequent in middle-aged women.
What is the pathophysiology of venous ulcers?
Venous return in the lower limb relies on the action of the calf muscle pump to return blood up the leg. When the leg muscles relax, valves throughout the venous system prevent the blood from flowing backwards down the venous system. Venous ulcers result when this system fails, in what is referred to as chronic venous insufficiency. Through malfunction of venous valves and reduced calf muscle pump, venous return is impaired and results in venous hypertension in the lower limbs.
Venous hypertension then causes dilation of the veins and oedema and venous skin change as fluid and pigment pass through the walls of the vein to deposit within the tissues.
What are the risk factors for venous ulcers?
Older age
High BMI
Reduced calf muscle pump action (i.e. immobility, sedentary lifestyle, limited range of motion of the ankle, prolonged standing)
Being female
History of deep vein thrombosis, leg fracture, or varicose veins
Family history of leg ulcers
Pregnancy
Signs and symptoms of venous ulcers:
Occur in the gaiter area (the distal half of the leg)
They are more often on the medial side of the leg
Have sloping edges
Bleed or ooze
Associated with features of chronic venous insufficiency
Haemosiderin deposition: brown-red discolouration of the skin
Lipodermatosclerosis: an “inverted champagne bottle” appearance of the leg is produced due to hardening and tightening of the skin
Atrophy blanche: Depressed white atrophic scars which form slight indentations on the surrounding pigmented skin. They are the result of venous hypertension causing dilatation of capillaries which then atrophy.
Venous eczema: flaky, itchy and erythematous skin changes
Venous oedema: Pitting oedema which improves on elevation of the lower limbs.
What are the investigations for venous ulcers?
Physical examination
An ankle brachial pressure index is calculated to assess for peripheral arterial insufficiency prior to application of compression bandaging.
Bloods:
FBC, Albumin, U+Es, and HbA1c to investigate for anaemia, poor nutrition, dehydration and diabetes, which all may slow healing
ESR/CRP may be done to assess for inflammation and infection of the ulcers
Doppler ultrasound: To assess the patency of the arteries and veins.
This can be used to assess for deep venous incompetency.
Skin swabs are done when there are associated skins of infection, and should not be done routinely.
What is the management of venous ulcers?
Wound care:
Ideally done by a district nurse or tissue viability nurse
They should be debrided as appropriate and then cleaned with tap water. This is followed by appropriate dressing before the application of compression bandaging
Patients may require simple analgesia prior to cleaning to reduce pain.
Compression therapy to reduce venous hypertension
Ankle-brachial pressure index (ABPI) must be done prior to the start of compression therapy.
Individuals should be offered the strongest compression they can tolerate.
Pentoxifylline
This medication is sometimes used to enhance wound healing
Individuals should be referred to secondary care if there is diagnostic uncertainty or if the ulcer has features of alternative diagnosis (i.e. rapidly developing)
If an ulcer is rapidly developing, a referral to dermatology may be required for a biopsy to rule out malignancy.
Surgical intervention for severe or refractory cases, where a skin graft may be used.
Hyperbaric oxygen therapy has previously been used, but there is limited evidence to support its use.
Measure to prevent venous ulcer recurrence include:
Encourage patients to mobilise
Elevation of legs
Use of emollients and well-fitting footwear
Compression hosiery
Weight loss if BMI > 30
What are the complications of venous ulcers?
Infection
Cellulitis
Suggested by erythema, pain, warmth and swelling surrounding the ulcer, and may be associated with increased exudate
Typically treated with oral antibiotics (i.e. flucloxacillin)
Compression bandaging should continue during infection if possible.
Osteomyelitis of underlying bone
Sepsis
Pain
Typically managed with elevation of the affected limb and simple analgesia.
Marjolin’s ulcer
A rare complication in which a malignancy develops in the base of the ulcer
Reduced quality of life (i.e. pain limiting mobility, loss of independence)
Eczematous skin changes
Topical emollients can be used
Recurrence
It is common for venous ulcers to recur. It is advised that individuals use compression stockings to prevent recurrence.
What is the prognosis of venous ulcers?
It is estimated that approximately 50% of venous ulcers will heal within 6 months, but recurrence rates are reported to be as high as 70%. It is common for individuals to develop multiple venous ulcers which can then recur.
Ulcers are less likely to heal and more likely to recur in individuals with:
Wounds that are large or have been present for more than 12 months
Impaired calf muscle pump
Lower socioeconomic status
Poor compliance with treatment
Low ankle brachial pressure index (ABPI<0.8)
In patients with venous ulcers and an ABPI over 1.3, avoid compression therapy and refer to vascular surgery for further evaluation.
:))
Define atrial fibrillation:
Atrial fibrillation (AF) is characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute. Delay at the AVN means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.
What is the pathophysiology of atrial fibrillation?
The exact pathophysiology of AF is unclear, but factors that cause atrial dilatation through inflammation and fibrosis leads to disorganised electrical impulses (which originate near the pulmonary veins) that overwhelm the SAN. These disorganised electrical impulses are usually at a rate of 300-600 beats per minute and are intermittently conducted through the AVN leading to irregular activation of the ventricles.
What is the classification of atrial fibrillation?
Acute: lasts <48 hours
Paroxysmal: lasts <7 days and is intermittent
Persistent: lasts >7 days but is amenable to cardioversion
Permanent: lasts >7 days and is not amenable to cardioversion
Atrial fibrillation can also be classified as to whether it is ‘fast’ or ‘slow’. Fast AF refers to AF that is at a rate of =>100bpm. Slow AF refers to AF that is at a rate of <=60bpm.
What are the cardiac causes of atrial fibrillation?
Ischaemic heart disease: most common cause in the UK.
Hypertension
Rheumatic heart disease (typically affecting the mitral valve): most common cause in less developed countries.
Peri-/myocarditis
What are the non-cardiac causes of atrial fibrillation?
Dehydration
Endocrine causes e.g. hyperthyroidism
Infective causes e.g. sepsis
Pulmonary causes e.g. pneumonia or pulmonary embolism
Environmental toxins e.g. alcohol abuse
Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia
What are the symptoms of atrial fibrillation?
Palpitations
Chest pain
Shortness of breath
Lightheadedness
Syncope
Signs of atrial fibrillation?
Irregularly irregular pulse rate with a variable volume pulse.
A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).
An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).
On auscultation there may be a variable intensity first heart sound.
Features suggestive of the underlying cause e.g. hyperthyroidism, alcohol excess, sepsis
Features suggestive of complications resulting from the AF e.g. heart failure.
What are the investigations for atrial fibrillation?
Definitive diagnosis: 12-lead ECG shows absence of p waves with an irregularly irregular rhythmn.
If a person has a suspected diagnosis of paroxysmal AF which is not detected on standard ECG, arrange ambulatory electrocardiography or cardiology referral, depending on the frequency and duration of symptoms and local referral pathways
Bloods
Routine bloods: to look for reversible causes including infection (raised WCC or CRP), hyperthyroidism (raised T3/T4) or alcohol use (raised MCV and GGT).
Imaging
Echocardiogram: can be used to see if there is a cardiac cause of the AF e.g. left atrial dilatation secondary to mitral valve disease.
When should a patient with AF be considered for emergency admission or cardiology referral?
New-onset AF within 48 hours and haemodynamic instability
Severe symptoms with ventricular rate >150 bpm or <40 bpm
Acute decompensated heart failure
AF complications (e.g., TIA/stroke)
Acute reversible triggers (e.g., pneumonia, sepsis, thyrotoxicosis)
What is the acute management for AF with adverse signs like shock or syncope?
Synchronised DC cardioversion +/- amiodarone
What are the steps for managing stable AF with onset <48 hours?
Rate or rhythm control
Rhythm control: DC cardioversion or anti-arrhythmics (e.g., flecainide, amiodarone)
Anticoagulation with heparin if cardioversion is delayed
How is stable AF with onset >48 hours managed?
Rate control (beta-blockers, diltiazem, or digoxin)
Anticoagulate for 3 weeks before attempting cardioversion, or perform TOE to exclude mural thrombus
What are the first-line medications for rate control in chronic AF?
Beta-blocker (e.g., bisoprolol)
Rate-limiting calcium channel blocker (e.g., diltiazem)
When is rhythm control preferred in AF management?
AF due to a reversible cause
Heart failure caused by AF
New-onset AF
When clinical judgment favors rhythm control
What options exist for rhythm control in AF?
Electrical cardioversion
Pharmacological cardioversion (e.g., flecainide, amiodarone, or sotalol)
What is the purpose of the CHADS2VASc score in AF?
To assess stroke risk for determining the need for anticoagulation.
What CHADS2VASc scores warrant anticoagulation?
Males: ≥1
Females: ≥2
What is the ORBIT score used for in AF management?
To evaluate bleeding risk when considering anticoagulation.
What are key considerations for warfarin use in AF?
Requires LMWH cover for 5 days when initiating
INR monitoring is necessary
Only oral anticoagulant licensed for valvular AF
What are the first-line anticoagulants for AF?
Direct Oral Anticoagulants (DOACs): edoxaban, apixaban, rivaroxaban, dabigatran
What is catheter ablation in AF management?
Ablation of arrhythmogenic focus between pulmonary veins and left atrium
High recurrence rate (50%); anticoagulation still required
What are the complications of atrial fibrillation?
Heart failure
Systemic emboli:
Ischaemic Stroke
Mesenteric ischaemia
Acute limb ischaemia
Bleeding:
GI
Intracranial
What is in the orbit score?
Older age (>74) = 1 point
R: Reduced hemoglobin (<13 mg/dL males, <12 mg/dL females) = 2 points
B: Bleeding history = 2 points
I: Insufficient renal function (eGFR <60) = 1 point
T: Treatment with antiplatelets = 1 point
In patients with atrial fibrillation and severe asthma, rate control is best achieved using calcium channel blockers such as verapamil.
:)
In patients with atrial fibrillation and severe chronic kidney disease, warfarin is preferred for anticoagulation due to contraindications of direct oral anticoagulants.
:(
Define supraventricular tachycardia?
Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.
What is the management of supra ventricular tachycardia?
Acute management
vagal manoeuvres:
Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
carotid sinus massage
intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option
electrical cardioversion
Prevention of episodes
beta-blockers
radio-frequency ablation
- What is atrioventricular nodal re-entry tachycardia (AVNRT)?
- What is atrioventricular re-entry tachycardia? (AVRT)?
Local re-entry circuit within the AV node
Re-entry circuit forms between atria and ventricles due to presence of accessory pathways (Bundle of Kent)
What is the pathophysiology of supraventricular tachycardia?
Normally, there is a co-ordinated electrical conduction system through the heart, starting at the sinoatrial node (SA node), the original pacemaker of the heart. This signal then travels down the surrounding atrial tissue to the atrioventricular node (AV node), which delays the signal to allow for atrial contraction first. After approximately 100 milliseconds of delay, the signal travels through the His-Purkinje system to send the signal to the left and right bundle branches, distributing the electrical signs to the ventricles and allowing for ventricular contraction.
In general, SVT is caused by 1 of 3 mechanisms, either re-entry of signals, increased automaticity, or triggered activity.
Re-entry
This mechanism occurs most notably in AVRT, AVNRT and some forms of atrial tachycardia
In this mechanism, there is normal electrical conduction from the atria to the ventricles in the normal pathway
However, after this, retrograde conduction occurs via an accessory pathway from the ventricles back up to the atria
This leads to repetitive impulse propagation and subsequent tachycardia
Increased automaticity
This mechanism is responsible for greater than 70% of cases of focal atrial tachycardia
Normally, the SA node is responsible for generating the spontaneous action potentials to trigger myocardial contraction
However, due to increased automaticity, a group of cardiac cells gain the ability to generate a spontaneous action potential which takes over from the normal SA node functioning
The occurs due to pathological changes in the normal membrane resting potential of these cells
This leads to rapid and spontaneous depolarisation of cells, which become the dominant rhythm and therefore result in episodes of tachycardia
Alternatively, the SA node itself may exhibit enhanced automaticity and therefore trigger action potentials more frequently, leading to tachyarrhythmias
Triggered activity
This mechanism is largely responsible for atrial fibrillation and atrial flutter, as well as approximately 30% of focal atrial tachycardias
SVT as a result of triggered activity occurs due to extra depolarisations which occur immediately after cell re-polarisation, termed ‘after-depolarisations’
If the after-depolarisations reach a sufficient amplitude to bring the membrane to the electrical threshold for depolarisation, a spontaneous action potential occurs
These spontaneous action potentials, called a triggered response, lead to extra-systoles, which have the potential to trigger subsequent tachyarrhythmias
What are the classifications of supraventricular tachycardia?
Atrio-ventricular nodal re-entrant tachycardia (AVNRT)
Most common form of paroxysmal SVT
Originates from a re-entrant retrograde electrical circuit involving the AV node, resulting in initiation and propagation of a cardiac tachyarrhythmia
Atrio-ventricular re-entrant tachycardia (AVRT)
The second most common form of paroxysmal SVT
Similar to AVNRT, it originates via a re-entrant retrograde electrical circuit, however it involves an accessory pathway between the atria and the ventricles, rather than the AV node
Some forms of AVRT may exhibit a Wolff-Parkinson-White pattern, whereby an accessory pathway capable of anterograde conduction leads to pre-excitation of the ventricles
This accessory pathway is a bypass tract, therefore avoiding the AV node and therefore the normal delay which occurs at this point
Leads to the characteristic ‘delta wave’ on ECG, whereby there is up-sloping at the start of the QRS complex due to the early ventricular excitation
Atrial tachycardia
May be either focal or multi-focal
Focal: due to a single focus of atrial tissue generating more rapid action potentials, leading to a rapid tachyarrhythmia
Multi-focal: this is synonymous with atrial flutter, whereby there is a re-entrant electrical circuit in the atria (usually around the tri-cuspid annulus and cavo-tricuspid isthmus) leading to rapid and recurrent de-polarisation without normal SA node functioning and conduction
Atrial fibrillation
The most common cardiac arrhythmia in general, which can sometimes be paroxysmal, however is more frequently persistent (lasting greater than seven days)
Often present in older populations
Usually due to long-term remodelling of the atrial tissue, leading to abnormalities in the normal SA node de-polarisation and conduction
Instead, rapid and irregular firing from focuses in the atria other than the SA node lead to fibrillatory conduction throughout the atria, and this arrhythmia tends to be sustained due to the atrial tissue structural abnormalities
What are the clinical features of supra ventricular tachycardia?
Clinical features
Common symptoms for SVT include:
Recurrent episodes of palpitations (95%)
Dizziness or light-headedness (75%)
Dyspnoea (45%)
Chest pain or tightness
Progressive fatigue
Pounding in the head and/or neck
SVT tends to present in discrete episodes which become more frequent and severe with time:
Recurrent and paroxysmal
Abrupt onset and offset
Average duration of episode 10-15 minutes, but can last any period of time from seconds to hours
Syncope
Very uncommon
When present, is a warning sign due to significant increase in risk of sudden cardiac death
In adults, SVT episodes tend to present with a heart rate greater than 100 beats per minute
Define ventricular tachycardia?
Ventricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.
Factors that increase the risk of ventricular tachycardia?
Factors that increase the risk of VT include:
Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia
Structural heart disease including previous myocardial infarction and cardiomyopathies
Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes)
Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)
What is the management of pulseless VT?
Pulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines:
CPR will be in progress
120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes
IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
Adrenaline should be administered every 3-5 minutes thereafter
A further dose of amiodarone 150 mg IV should be given after 5 shocks
What is the management of Pulsed VT with adverse features?
If a patient has a pulse, management is determined by whether they have any of the following adverse features:
Heart failure
Myocardial ischaemia (chest pain)
Shock
Syncope
If one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia.
If this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).
What is the management of Pulsed VT with no adverse features:
First line treatment is amiodarone 300mg IV over 10-60 minutes.
If this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.
What is the management of torsades de pointes?
This is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest).
IV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).
Define ventricular fibrillation?
An irregular broad complex tachycardia. This is always a pulseless rhythm.
ECG features include:
Tachycardia >100bpm
QRS complexes are polymorphic and irregular (>120ms)
What is the management of ventricular fibrillation?
The patient should be managed according to the Advanced Life Support algorithm.
VF is a shockable rhythm so a 200J bi-phasice unsynchronised shock should be administered.
IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock.
Adrenaline should be administered every 3-5 minutes thereafter.
What do survivors of ventricular fibrillation require?
Implantable cardioverter defibrillator (ICD)
Define heart block:
Heart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves.
Sinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail.
Patients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death.
Define first degree heart block:
This is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.
What are the causes of first degree heart block?
High vagal tone: e.g. athletes
Acute inferior MI
Electrolyte abnormalities: e.g. hyperkalaemia
Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors
What is the management of first degree heart block:
First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.
Define Mobitz type 1 heart block:
Wenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.
What are the causes of mobitz type 1 heart block:
MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery
What is the management of mobitz type 1 heart block?
It is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.
Define mobitz type 2
Mobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The PR interval is constant (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.
In most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.
What are causes of Mobitz type 2:
Infarction: particularly anterior MI which damages the bundle branches
Surgery: mitral valve repair or septal ablation
Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis
Fibrosis: Lenegre’s disease
Infiltration: sarcoidosis, haemochromatosis, amyloidosis
Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone
Managment of mobitz type 2:
Definitive management is with a permanent pacemaker as these patients are at risk of complete heart block and at risk of becoming haemodynamically unstable.
Define complete heart block (third degree):
Complete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.
ECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest.
What are the causes of complete heart block (third degree):
Myocardial infarction: especially inferior
Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine
Idiopathic fibrosis
What is the management of third degree heart block:
Management of complete (third degree) heart block is via the acute bradycardia guideline (see section). Permanent pacemaker requires insertion due to the risk of sudden death.
A complete heart block warrants urgent referral to hospital for potential external pacing. Anticholinesterase inhibitors may worsen or cause this condition.
:))
Define bundle branch block:
A bundle branch block (BBB) refers to when electrical impulses to the ventricles are slower than normal, leading to a widened QRS complex >120ms. It can be definied as a left bundle branch block (LBBB) or a right bundle branch block (RBBB). An incomplete BBB refers to when there is a partial delay in electrical conduction in the ventricles and the QRS complex is between 110 to 120ms.
How do you distinguish between left bundle branch block and right bundle branch block:
The pneumonic WILLAM MARROW can be used to distinguish between LBBB and RBBB on ECG.
In both, the QRS complex has a duration of >120ms.
In V1 if the QRS complex has the appearance of a W (the rS’ pattern) and in V6 the QRS has the appearance of M (due to a notched R wave) this is a left bundle branch block. WiLLaM.
In V1 if there is an appearance of an M (due to the rSr’pattern) and in V6 the QRS complex usually looks normal (N). This is a right bundle branch block. MaRRoW.
Name some causes of left bundle branch block:
Aortic stenosis
Ischaemic heart disease
Hyperkalaemia
Digoxin toxicity
Myocardial infarction - new LBBB can indicate STEMI.
Name some causes of right bundle branch block:
Right ventricular hypertrophy
Pulmonary embolism
Ischaemic heart disease
Congenital heart disease (ASD)
Normal variant
Define dehydration:
Dehydration refers to a state of negative fluid balance, typically resulting from inadequate intake or excessive loss of body fluids. Clinically, it presents with symptoms such as dry mucous membranes, tachycardia, hypotension and reduced skin turgor. It can be categorised into isotonic, hypertonic or hypotonic dehydration based on alterations in serum osmolarity.
What are the common causes of dehydration:
The most common etiologies include diarrhoea, vomiting, polyuria and fever. In certain patient groups such as the elderly or those with impaired cognition, inadequate fluid intake may also contribute significantly.
What are the investigations for dehydration?
Investigation involves assessment of renal function and electrolytes. Elevated urea and creatinine levels suggest prerenal acute kidney injury due to volume depletion whereas disproportionate elevation of urea over creatinine is indicative of gastrointestinal losses.
What is the GCS score:
