Cardio Flashcards
What is acute heart failure?
Acute heart failure (AHF) refers to the rapid onset or worsening of the signs and symptoms of heart failure.
This is a life-threatening condition in which the heart does not pump enough blood to meet the body’s needs.
AHF may present as new-onset heart failure or as acute decompensation of chronic heart failure (CHF).
Explain the 2 courses of pathology for AHF.
- Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia. These patients are ‘WET’.
- Hypoperfusion of vital organs as the cardiac output is reduced. These patients are ‘COLD’.
Name some causes of new-onset AHF
Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Acute valve dysfunction
Arrhythmias
Name some causes of acute decompensation of CHF
Infection
Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Uncontrolled hypertension
Arrhythmias
Worsening chronic valve disease
Non-adherence with drugs/diet
Change in drug regimen
Withdrawal/reduction of heart failure medications inappropriately
Initiation/increase of rate-control medications inappropriately
Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones
What are some typical symptoms of AHF ?
Dyspnoea
Reduced exercise tolerance (classify using the New York Heart Association classification)3
Ankle swelling (clarify how high and whether this is progressing)
Fatigue
Pink frothy sputum
Orthopnoea (ask about the number of pillows used)
Paroxysmal nocturnal dyspnoea
Signs of Pulmonary or Systemic Congestion seen in AHF.
Fine basal crackles (bilateral)
Peripheral oedema (bilateral)
Dull percussion at the lung bases
Raised jugular venous pressure (JVP)
Hepatomegaly
Gallop rhythm (S3 or S4 heart sounds)
Murmur
Signs of Hypoperfusion seen in AHF
Hypoxia
Tachypnoea and accessory muscle use
Tachycardia
Cyanosis
Cold, pale, and sweaty peripheries
Oliguria
Confusion/agitation
Syncope/pre-syncope
Narrow pulse pressure
Differential Dx for AHF
Asthma, chronic obstructive pulmonary disease (COPD), pneumonia, and pulmonary oedema due to AHF can be difficult to differentiate, especially where they may coexist in older patients.
Ix for AHF
Vital Signs
ECG
BNP
ABG
CXR
Echo
Lung USS
What may vital signs show in AHF?
may show hypoxia (often SpO2 < 90%), tachycardia, and tachypnoea. The systolic blood pressure may be normal, elevated, or reduced (hypotension is associated with cardiogenic shock and poor prognosis). The pulse pressure may be narrow (<25% of the sBP).
What may ECG show in AHF?
the ECG is rarely normal. Abnormalities (e.g. signs of ischaemia or arrhythmias) are very common in AHF and an alternative diagnosis should be considered if the ECG is completely normal.
What is BNP?
B‑type natriuretic peptide (BNP): BNP is a sensitive but non-specific marker of heart failure.
What may BNP show in AHF?
AHF is unlikely and can be ruled out if:
BNP is less than 100 ng/litre
NT‑proBNP is less than 300 ng/litre
What may an ABG show in AHF ?
often shows type 1 respiratory failure, or type 2 respiratory failure in those with pre-existing chronic lung conditions.
What Ix are used to R/O other causes/pathologies in suspected AHF?
Baseline Bloods : FBC, U&E, Coagulation, CRP –> anaemia?
Cardiac Troponin –> MI?
TSH –> abnormatlities can precipitatet AHF
D-dimer–> PE suspected
What may CXR show in AHF?
abnormalities are present in up to 80% of patients in AHF. If the chest X-ray is normal, consider alternative diagnoses such as a pulmonary embolism or exacerbation of asthma/COPD. It can help exclude other causes of dyspnoea such as pneumonia or pneumothorax.
What may an Echo show in AHF?
should be performed early in those with suspected AHF, especially if cardiogenic shock or life-threatening cardiac abnormalities are present. The echocardiogram assesses:
Biventricular systolic and diastolic function for ventricular dilation, reduced ejection fraction, ventricular hypertrophy and poor contractility
Valve disease
Ventricular wall rupture
Pericardial effusion
Intracardiac shunts: the presence of a dilated inferior vena cava with reduced respiratory variation is indicative of high venous pressure
What may a Lung USS show in AHF?
may reveal extracardiac pathology such as pulmonary embolism or B-lines (consistent with interstitial oedema in pulmonary oedema)
Chest X-ray findings in AHF
A mnemonic to remember chest x-ray findings in heart failure is ABCDE:
A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly (cardiothoracic ratio >50%) – may be difficult to assess on an AP film
D: dilated upper lobe vessels
E: effusions (i.e. pleural effusions – blunted costophrenic angles with meniscus sign)
Identify conditions early on which may have precipitated AHF and treat these urgently. Look out for CHAMP conditions:
Acute coronary syndrome (ACS)
Hypertensive crisis
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism
Acute Medical Management of AHF
Oxygen
Loop Diuretics
Nitrates
NIV
Tx for cardiogenic shock: inotopes + vasopressors
How do loop diuretics help in the acute management of AHF?
Diuretics increase sodium excretion causing diuresis and decrease afterload. All ‘WET’ patients will require diuretics as the cornerstone of their management.
Administer 40 milligrams furosemide intravenously initially to improve symptoms of congestion fluid overload.
Patients with chronic kidney disease and those already on oral diuretics will need a greater dose. Monitor renal function and urine output to titrate dose according to clinical response.
How do Nitrates help in the acute management of AHF?
Nitrates (sublingual glyceryl trinitrate or intravenous nitrates) are the second most used agents in AHF used for ‘WET’ patients. Do not use nitrates in those with SBP <90mmHg or aortic stenosis, who rely on sufficient preload to overcome their pressure gradient.
Nitrates cause venous and/or arterial dilation to reduce preload and/or afterload. They are given to patients with concomitant myocardial ischaemia or hypertension.
How do NIV help in the acute management of AHF?
CPAP or BiPAP are used for those with cardiogenic pulmonary oedema, dyspnoea, and
NIV improves ventilation to reduce respiratory distress and drives fluid out of alveoli and into vasculature in those whose respiratory failure is not controlled with oxygen therapy given via a face mask.
How do you control cardiogenic shock in AHF?
Some ‘COLD’ patients whose AHF has led to a potentially reversible cardiogenic shock may present with haemodynamic instability (systolic blood pressure <90mmHg). These patients require early expert help. Specialists may consider inotropes (e.g. dobutamine) to increase cardiac output and peripheral perfusion, and vasopressors (e.g. adrenaline) to increase blood pressure and vital organ perfusion. The use of these drugs is associated with poorer outcomes.
Long term management of AHF aims to ____
Increase CO by optimising preload and contractility whilst decreasing afterload.
What is included in the long term management of AHF?
Before discharge, consider offering patients with reduced ejection fraction (LVEF <40%) heart failure a selection of treatments:
- Diuretics
- ACE inhibitors / ARBs
- Beta Blockers
- Aldosterone antagonist
What do ACEi do for the long term management of AHF?
ACEi/ARBs decrease activation of the renin-angiotensin-aldosterone system (RAAS).
Contraindications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
What do BBs do for the long term management of AHF?
Begin therapy once established on a diuretic and ACEi/ARB, and when BP and congestion are controlled.
Beta-blockers decrease heart rate, myocardium oxygen demand and RAAS activation.
Contraindications include asthma, 2nd or 3rd-degree atrioventricular block, sick sinus syndrome and sinus bradycardia.
‘Start low and go slow’
What do Aldosterone Antagonsits do for the long term management of AHF?
Antagonise aldosterone increasing sodium excretion causing diuresis and decreased afterload.
Which medication can be used for patients who cannot have a beta-blocker or who are on the maximum dose already, if they are in sinus rhythm with a heart rate >75? (AHF longterm management)
Ivabradine
Which medication can be used for patients who decompensate on an ACEi/ARB ? (AHF longterm management)
Sacubitril valsartan
Which medication can be used for patients who cannot tolerate an ACEi/ARB, or who are on the maximum dose ? (AHF longterm management)
Hydralazine and nitrate:
Which medication can be used for patients with atrial fibrillation and uncontrolled tachycardia despite a beta-blocker? (AHF longterm management)
Digoxin
Complications of AHF
About 40% of people admitted to hospital with heart failure die or are readmitted within 1 year.9
AHF may cause arrhythmias, particularly atrial fibrillation.
There is an increased risk of stroke and other thromboembolic diseases following an episode of AHF.
What is chronic heart failure (CHF) ?
Chronic heart failure (CHF) is a clinical syndrome involving reduced cardiac output because of impaired cardiac contraction. Typical clinical symptoms of CHF include shortness of breath, fatigue and ankle swelling
Causes of Heart failure
The most common causes of heart failure in the UK are coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension.
Other causes of heart failure include:
Endocrine disease: hypothyroidism, hyperthyroidism, diabetes, adrenal insufficiency, Cushing’s syndrome
Medications: calcium antagonists, anti-arrhythmics, cytotoxic medication, beta-blockers.
High-output cardiac failure occurs in states where demand exceeds normal cardiac output such as pregnancy, anaemia and sepsis.
Acronymn to rememeber causes of HF
The acronym HIGH-VIS is useful to remember some of the causes of CHF:
Hypertension (common cause)
Infection/immune: viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis)
Genetic: hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM)
Heart attack: ischaemic heart disease (common cause)
Volume overload: renal failure, nephrotic syndrome, hepatic failure
Infiltration: sarcoidosis, amyloidosis, haemochromatosis
Structural: valvular heart disease, septal defects
Typical symptoms of CHF
Dyspnoea on exertion
Fatigue limiting exercise tolerance
Orthopnoea: the patient may be using several pillows to reduce this symptom.
Paroxysmal nocturnal dyspnoea (PND): attacks of severe shortness of breath in the night that are relieved by sitting up (pathognomonic for CHF).
Nocturnal cough with or without the characteristic ‘pink frothy sputum’.
Pre-syncope/syncope
Reduced appetite
What is paroxysmal nocturnal dyspnoea?
Paroxysmal nocturnal dyspnoea (PND) describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
They may describe having to sit on the side of the bed or walk around the room, gasping for breath. They may feel suffocated and want to open a window to get fresh air. Symptoms improve over several minutes.
There are a few proposed mechanisms to explain paroxysmal nocturnal dyspnoea.
Firstly, fluid settles across a large surface area of the lungs as they lie flat to sleep, causing breathlessness. As they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively.
Secondly, during sleep, the respiratory centre in the brain becomes less responsive, so the respiratory rate and effort do not increase in response to reduced oxygen saturation like they would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before they wake up feeling very unwell.
Thirdly, there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed, reducing cardiac output.
Signs of CHF
Clinical findings on cardiovascular examination may include:
Tachycardia at rest
Hypotension
Narrow pulse pressure
Raised jugular venous pressure
Displaced apex beat (due to left ventricular dilatation)
Right ventricular heave
Gallop rhythm on auscultation (pathognomic for CHF)
Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis)
Pedal and ankle oedema
Clinical findings on respiratory examination may include:
Tachypnoea
Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields
Reduced air entry on auscultation with stony dullness on percussion (pleural effusion)
Clinical findings on abdominal examination may include:
Hepatomegaly
Ascites
Ix of CHF
ECG + urinalysis + Bloods + Echo + CXR + Cardiac MRI
What may ECG show in CHF?
should be performed on all patients with suspected heart failure. An ECG may identify evidence of previous myocardial infarction (e.g. ‘Q’ waves) or arrhythmias (AV block or atrial fibrillation). A normal ECG makes heart failure unlikely
What may urinalysis show in CHF?
may show glycosuria (diabetes) or proteinuria (renal disease)
ECG associated with heart failure include:
Tachycardia
Atrial fibrillation (due to enlarged atria)
Left-axis deviation (due to left ventricular hypertrophy)
P wave abnormalities (e.g. P.mitrale/P.pulmonale due to atrial enlargement)
Prolonged PR interval (due to AV block)
Wide QRS complexes (due to ventricular dyssynchrony)
Bloods Ix for CHF
FBC: anaemia
U&Es: renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia)
LFTs: hepatic congestion
Troponin: if considering recent myocardial infarction
Lipids/HbA1c: ischaemic risk profile
TFTs: hyperthyroidism/hypothyroidism
Cardiomyopathy screen
N-terminal pro-B-type natriuretic peptide
What is a cardiomyopathy screen ?
Serum iron and copper studies (to rule out haemochromatosis and Wilson’s disease)
Rheumatoid factor, ANCA/ANA, ENA, dsDNA (to rule out autoimmune disease)
Serum ACE (to rule out sarcoidosis)
Serum-free light chains (to rule out amyloidosis)
NT-proBNP
N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured in all patients presenting with symptoms and clinical signs of heart failure to inform the type and urgency of further investigations such as echocardiography:
NT-proBNP level >2000 ng/L – refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks
NT-proBNP level 400-2000ng/L – refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks
NT-proBNP level <400 ng/L – heart failure unlikely
Other conditions in which NT-proBNP may be raised include:
Left ventricular hypertrophy
Tachycardia
Liver cirrhosis
Diabetes
Acute or chronic renal disease
What is the gold standard Ix for CHF?
Cardiac MRI is the gold standard investigation for assessing ventricular mass, volume and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views
Structural classification of CHF
Chronic heart failure can be classified structurally based on left ventricular ejection fraction (LVEF).
LVEF is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole.
LVEF is usually measured using transthoracic echocardiography, however, MRI, nuclear medicine scans and transoesophageal echocardiography can also be used
Symptomatic/ functional classification of CHF
The New York Heart Association’s (NYHA) classification system relies on patient symptoms and level of function:3
Class I: no symptoms during ordinary physical activity
Class II: slight limitation of physical activity by symptoms
Class III: less than ordinary activity leads to symptoms
Class IV: inability to carry out any activity without symptoms
Lifestyle Managment of CHF
Fluid and salt restriction
Regular exercise
Smoking cessation
Reduced alcohol intake
Medication review for CHF - which meds can damage more CHF?
Calcium channel blockers (e.g. verapamil, diltiazem)
Tricyclic antidepressants
Lithium
NSAIDs and COX-2 inhibitors
Corticosteroids
QT-prolonging medications
All patients with chronic heart failure require monitoring of:
Functional capacity, fluid status, cardiac rhythm, cognitive status and nutritional status
Renal function
The frequency of monitoring depends on the patient’s clinical condition.
The first-line medical treatment of chronic heart failure can be remembered with the “ABAL” mnemonic:
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)
Pharmalogical Management of CHF
Diuretics
ACEi
Beta Blockers
ARBs
Mineralocorticoid/aldosterone receptor antagonists (MRAs)
Sodium-glucose cotransporter-2 (SGLT2) inhibitors
What is the purpose of Diuretics in the management of CHF?
Diuretics should be prescribed to relieve symptoms of fluid overload (e.g. shortness of breath, peripheral oedema).
Diuretics (e.g. furosemide) work by increasing sodium excretion via diuresis, ultimately reducing cardiac afterload.
Doses should be titrated according to clinical response and renal function should be closely monitored.
What is the purpose of ACEi in the management of CHF?
All patients with CHF and a reduced ejection fraction (≤40%) should be commenced on an ACE inhibitor unless contraindicated.
ACE inhibitors have been shown to improve ventricular function and reduce mortality.
U&Es should be checked prior to starting treatment and then after 1-2 weeks of treatment.
Contraindications to ACEi
include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
What is the purpose of Beta Blockers in the management of CHF?
Beta-blockers (e.g. bisoprolol) should be prescribed for all patients with symptomatic heart failure and reduced LVEF (≤40%) unless contraindicated.
Beta-blockers decrease heart rate, myocardial oxygen demand and RAAS activation.
Blood pressure and heart rate need to be monitored carefully when adjusting doses.
Contraindications of BBs
include asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.
What is the purpose of ARBs in the management of CHF?
If a patient is unable to tolerate an ACE inhibitor (usually due to persistent cough) an ARB (e.g. candesartan) should be prescribed as an alternative.
Patients must have normal serum potassium and adequate renal function to commence an ARB.
What is the purpose of MRAs in the management of CHF?
A low-dose aldosterone antagonist (e.g. spironolactone or eplerenone) should also be prescribed if a patient continues to have symptoms of heart failure despite diuretics, ACE inhibitors and beta-blockers.
MRAs antagonise aldosterone, increasing sodium excretion via diuresis, ultimately decreasing cardiac afterload.
What is the purpose of SGLT2 inhibitors in the management of CHF?
SGLT2 inhibitors (e.g. dapagliflozin) can be used as add-on therapy in patients with a reduced LVEF (<40%). Dapagliflozin has been shown to reduce the risk of cardiovascular events and hospital admission. This benefit occurs regardless of the patient’s glycaemic control.
What is Ivabradine + what does it do?
Ivabradine inhibits the sinoatrial node, slowing the heart rate of patients in sinus rhythm, increasing stroke volume whilst preserving myocardial contractility.
It has been shown to reduce cardiovascular death or hospitalisation for heart failure by 18%.
Procedural and Surgical Interventions for CHF
Surgical procedures may be used to treat underlying valvular heart disease.
Implantable cardioverter defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus rhythm if they identify a shockable arrhythmia. These are used in patients who previously had ventricular tachycardia or ventricular fibrillation.
Cardiac resynchronisation therapy (CRT) may be used in severe heart failure, with an ejection fraction of less than 35%. CRT involves biventricular (triple chamber) pacemakers, with leads in the right atrium, right ventricle and left ventricle. The objective is to synchronise the contractions in these chambers to optimise heart function.
A heart transplant may be considered in suitable patients with severe disease.
Complications of CHF include:
Arrhythmias: atrial fibrillation and ventricular arrhythmias
Depression and impaired quality of life
Loss of muscle mass
Sudden cardiac death
Prognosis is poor overall, with approximately 50% of people with heart failure dying within five years of diagnosis.7
Left sided heart failure
HF-rEF and HF-pEF typically develop left-sided heart failure. This may be due to increased left ventricular afterload (e.g. arterial hypertension or aortic stenosis) or increased left ventricular preload (e.g. aortic regurgitation resulting in backflow to the left ventricle).
Right sided heart failure
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).
Left ventricular failure typically results in:
pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles
Right ventricular failure typically results in:
peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)
Causes of Increased BNP levels
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis
Causes of Decreased BNP levels
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
What are arrthymias ?
Arrhythmias are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle.
Shockable rhythms:
Ventricular tachycardia
Ventricular fibrillation
Non-shockable rhythms:
Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)
Narrow complex tachycardia
refers to a fast heart rate with a QRS complex duration < 0.12 seconds (3 small squares)
There are four main differentials of a narrow complex tachycardia:
Sinus tachycardia (treatment focuses on the underlying cause)
Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
Atrial fibrillation (treated with rate control or rhythm control)
Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)
Sinus tachycardia
Sinus tachycardia will take the normal P wave, QRS complex and T wave pattern. Sinus tachycardia is not an arrhythmia and is usually a response to an underlying cause, such as sepsis or pain.
Supraventricular tachycardia (SVT)
looks like a QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, and so on. There are P waves, but they are often buried in the T waves, so you cannot see them. It can be distinguished from atrial fibrillation by the regular rhythm and atrial flutter by the absence of a saw-tooth pattern.
How do you distinguish SVT from sinus tachycardia ?
It can be tricky to distinguish SVT from sinus tachycardia. SVT has an abrupt onset and a very regular pattern without variability. Sinus tachycardia has a more gradual onset and more variability in the rate. The history is also important, where sinus tachycardia usually has an explanation (e.g., pain or fever), while SVT can appear at rest with no apparent cause.
Atrial fibrillation
absent P waves and an irregularly irregular ventricular rhythm.
Atrial Flutter
the atrial rate is usually around 300 beats per minute and gives a saw-tooth pattern on the ECG. A QRS complex occurs at regular intervals depending on how often there is conduction from the atria. This often results in two atrial contractions for every one ventricular contraction, giving a ventricular rate of 150 beats per minute. Atrial flutter gives a sawtooth appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia. There may be 3:1, 4:1 or variable conduction ratios.
What are the life-threatening features of arrythmias?
loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure
Treatment of life-threatening arrythmia
synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.
Broad complex tachycardia
refers to a fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.
The resuscitation guidelines break down broad complex tachycardia into:
Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)
Pathophysiology of atrial flutter
Normally the electrical signal passes through the atria once, stimulating a contraction, then disappears through the atrioventricular node into the ventricles. Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. The atrial rate is usually around 300 beats per minute. The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute.
Treatment of atrial flutter
Treatment is similar to atrial fibrillation, including anticoagulation based on the CHA2DS2-VASc score. Radiofrequency ablation of the re-entrant rhythm can be a permanent solution.
QT interval
from the start of the QRS complex to the end of the T wave.
Parametes of Prolonged QT Interval
More than 440 milliseconds in men
More than 460 milliseconds in women
Pathophysiology of Prolonged QT interval
A prolonged QT interval represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraction. Depolarisation is the electrical process that leads to heart contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.
Torsades de pointes
Torsades de pointes is a type of polymorphic ventricular tachycardia. It translates from French as “twisting of the spikes”, describing the ECG characteristics. On an ECG, it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes gets progressively smaller, then larger, then smaller, and so on. Torsades de pointes will terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac arrest.
Causes of prolonged QT include:
Long QT syndrome (an inherited condition)
Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
Management of a prolonged QT interval involves:
Stopping and avoiding medications that prolong the QT interval
Correcting electrolyte disturbances
Beta blockers (not sotalol)
Pacemakers or implantable cardioverter defibrillators
Acute management of torsades de pointes involves:
Correcting the underlying cause (e.g., electrolyte disturbances or medications)
Magnesium infusion (even if they have normal serum magnesium)
Defibrillation if ventricular tachycardia occurs
Ventricular ectopics
premature ventricular beats caused by random electrical discharges outside the atria. Patients often present complaining of random extra or missed beats. They are relatively common at all ages and in healthy patients. However, they are more common in patients with pre-existing heart conditions (e.g., ischaemic heart disease or heart failure).
Appearance of Ventricular Ectopics
appear as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.
Bigeminy
Bigeminy refers to when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on.
Management of Ventricular Ectopics
Reassurance and no treatment in otherwise healthy people with infrequent ectopics
Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
Beta blockers are sometimes used to manage symptoms
First Degree Heart Block
First-degree heart block occurs where there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex. On an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square).
Second Degree Heart Block
Second-degree heart block is where some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block:
Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2
There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block).
A 2:1 block is where there are two P waves for each QRS complex. Every other P wave does not stimulate a QRS complex. It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.
Mobitz Type 1
Mobitz type 1 (Wenckebach phenomenon) is where the conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.
Mobitz Type 1
Mobitz type 2 is where there is intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves. The PR interval remains normal. There is a risk of asystole with Mobitz type 2.
3rd Degree Heart Block
Third-degree heart block is also called complete heart block. There is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.
What is bradycardia
Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. A heart rate under 60 can be normal in healthy fit patients without causing any symptoms.
Causes of Bradycardia
Medications (e.g., beta blockers)
Heart block
Sick sinus syndrome
Sick sinus syndrome
Sick sinus syndrome encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.
Asystole
refers to the absence of electrical activity in the heart (resulting in cardiac arrest).
There is a risk of asystole in:
Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds
Management of unstable patients and those at risk of asystole involves:
Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available
Options for temporary cardiac pacing are:
Transcutaneous pacing, using pads on the patient’s chest
Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly
Atropine
antimuscarinic medication and works by inhibiting the parasympathetic nervous system.
SE of atropine
Inhibiting the parasympathetic nervous system leads to side effects of pupil dilation, dry mouth, urinary retention and constipation.
NICE definition of Hypertension
The NICE guidelines on hypertension (updated 2022) suggest a diagnosis of hypertension with a blood pressure above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.
Essential hypertension accounts for __% of hypertension
90
What is essential HTN?
also known as primary hypertension. It means a high blood pressure has developed on its own and does not have a secondary cause.
Secondary causes of HTN
can be remembered with the “ROPED” mnemonic:
R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
What is the most common cause of secondary HTN?
Renal disease ; When the blood pressure is very high or does not respond to treatment, consider renal artery stenosis. Renal artery stenosis can be diagnosed with duplex ultrasound or an MR or CT angiogram.
Which endocrine conditions can cause HTN?
Most endocrine conditions can cause hypertension. Hyperaldosteronism (Conn’s syndrome) is an important cause and may be present in 5-10% of patients with hypertension.
Examples of Kidney diseases that cause HTN
Glomerulonephritis
Chronic pyelonephritis
Diabetic nephropathy
Renal cell carcinoma
Polycystic kidney disease
Obstructive uropathy
Examples of Vascular diseases that cause HTN
Renal artery stenosis
Coarctation of the aorta
Examples of Endocrine diseases that cause HTN
Primary hyperaldosteronism
Phaeochromocytoma
Cushing’s syndrome
Acromegaly
Hypothyroidism
Hyperthyroidism
Examples of Drugs that cause HTN
Combined oral contraceptive pill
Corticosteroids
Non-steroidal anti-inflammatories (NSAIDs)
Venlafaxine
Alcohol
Illicit drugs (e.g. cocaine)
Risk Factors for developing HTN
Sex: up to 65 years women tend to have lower blood pressures than men, however, between the ages of 65-74 years women tend to have higher blood pressures.
Ethnicity: people of Black African and Black Caribbean origin are at a higher risk of developing HTN.
Age: blood pressure rises with increasing age.
Lifestyle factors: cigarette smoking, excess alcohol consumption, excess dietary salt intake, obesity and lack of physical activity.
Red Flag Symptoms of accelerated or malignant HTN
Headache
Visual disturbances
Seizures
Nausea and vomiting
Chest pain
Symptoms suggestive of kidney disease as a secondary cause of HTN include:
Haematuria
‘Frothy’ urine suggestive of proteinuria
Dyspnoea (pulmonary oedema)
Lower limb swelling (peripheral oedema)
Flank tenderness and pain
Weight loss is suggestive of renal cell carcinoma
Symptoms suggestive of coarctation of the aorta as a secondary cause of HTN include:
Headache
Epistaxis
Intermittent claudication
Lower limb weakness
Cold legs and feet
Symptoms suggestive of endocrine disease as a secondary cause of HTN include:
Muscle weakness, muscle spasms and paraesthesia are suggestive of hyperaldosteronism.
Severe headache, palpitations and sweating are suggestive of phaeochromocytoma.
Weight gain particularly abdominal, facial and on the back of the neck and shoulders is suggestive of Cushing’s syndrome.
Tall statures, swelling of the hands and feet and deepening of the voice are suggestive of acromegaly.
Weight gain, cold intolerance and low mood are suggestive of hypothyroidism.
Weight loss, heat intolerance and palpitations are suggestive of hyperthyroidism.
Typical clinical findings in secondary causes of HTN include:
Autosomal dominant polycystic kidney disease: enlarged palpable kidneys when balloting the kidneys.
Renal artery stenosis: renal bruits heard when auscultating over the area of the renal arteries.
Coarctation of the aorta: systolic murmur in the left infraclavicular region under the left scapula and radio-femoral delay.
Cushing’s syndrome: moon facies, abdominal purple striae and bruising.
Hypothyroidism: brittle nails, dry skin and thin hair.
Hyperthyroidism: fine tremor, palmar erythema and a neck goitre.
Complications of HTN
Ischaemic heart disease (angina and acute coronary syndrome)
Cerebrovascular accident (stroke or intracranial haemorrhage)
Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
Hypertensive retinopathy
Hypertensive nephropathy
Vascular dementia
Left ventricular hypertrophy
Heart failure
NICE recommend measuring blood pressure every _ years to screen for hypertension. It should be measured more often in borderline cases and every year in patients with type 2 diabetes.
5
What should you use to confirm dx of HTN?
Patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24-hour ambulatory blood pressure or home readings to confirm the diagnosis. Having blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect involves more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.
Which arm do you take BP readings from?
NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.
Clinic Reading and Confirmed Ambulatory/Home Reading for Stage 1 HTN
Clinic Reading : > 140/90
Ambulatory/Home Reading : > 135/85
Clinic Reading and Confirmed Ambulatory/Home Reading for Stage 2 HTN
Clinic Reading : > 160/100
Ambulatory/Home Reading : > 150/95
Clinic Reading for Stage 3 HTN
Clinic Reading : > 180/120
NICE recommend all patients with a new diagnosis of HTN should have:
Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities, including left ventricular hypertrophy
With patients, who have a new HTN dx, what should you calculate for them (in relation to their hearts in the next 10 years), and what should you do about that?
NICE recommend calculating the QRISK score, which estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. When the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.
Lifestyle advice for HTN management
healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.
Medications used in the management of HTN
A – ACE inhibitor (e.g., ramipril)
B – Beta blocker (e.g., bisoprolol)
C – Calcium channel blocker (e.g., amlodipine)
D – Thiazide-like diuretic (e.g., indapamide)
ARB – Angiotensin II receptor blocker (e.g., candesartan)
When are ARBs used in HTN Management?
Angiotensin receptor blockers (ARBs) are recommended by NICE instead of ACE inhibitors in patients of Black African or African-Caribbean family origin. (Can replace ACEi) ARBs are an alternative if the person does not tolerate ACE inhibitors (commonly due to a dry cough). ACE inhibitors and ARBs are not used together.
When are Thiazide-like diuretics used in HTN Management?
Thiazide-like diuretics are used as an alternative if the patient does not tolerate calcium channel blockers (commonly due to ankle oedema).
Step 1 HTN Management : patient is <55y/o or T2DM of any age or family origin
ACEi e.g. Ramipril or ARB e.g. Losartan
Step 1 HTN Management : patient is >55y/o or Black African
Calcium Channel Blocker e.g. amlodipine
Step 2 HTN Managament : patient is <55y/o or T2DM of any age or family origin
ACEi/ARB + CCB
Step 2 HTN Managament :patient is <55y/o or T2DM of any age or family origin + patient does not tolerate CCBs
ACEi/ARBs + thiazide-like Diuretics e.g Indapamide
Step 2 HTN Managament : patient is >55y/o or Black African
CCBs + thiazide-like Diuretics or ACEi/ARBs
Step 3 HTN Management
ACEi/ ARBs + CCBs + thiazide-like Diuretics
Step 4 HTN Management : patients [K+] ≤ 4.5 mmol/L
ACEi/ ARBs + CCBs + thiazide-like Diuretics + Spironolactone
Step 4 HTN Management : patients [K+] > 4.5 mmol/L
ACEi/ ARBs + CCBs + thiazide-like Diuretics + Doxazocin/ Atenolol
What does Step 4 HTN management depend on?
Step 4 depends on the serum potassium level:
Less than or equal to 4.5 mmol/L consider a potassium-sparing diuretic, such as spironolactone
More than 4.5 mmol/L consider an alpha blocker (e.g., doxazosin) or a beta blocker (e.g., atenolol)
How does Spironolactone work?
Spironolactone is a potassium-sparing diuretic. It works by blocking the action of aldosterone in the kidneys, resulting in sodium excretion and potassium reabsorption. It can be helpful when thiazide diuretics are causing hypokalaemia.
Using Spironolactone increases the risk of ___kalaemia
hyper
ACEi can cause ___kalemia
hyper
Treatment targets for patient w/ HTN <80 y/o
Systolic : <140
Diastolic : < 90
Treatment targets for patient w/ HTN >80 y/o
Systolic : < 150
Diastolic : > 90
What is accelated HTN / Malignant HTN?
refers to extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema.
Management of patients with Malignant HTN?
The NICE guidelines recommend a same-day referral for patients with accelerated hypertension. Therefore, patients with a blood pressure above 180/120 require a fundoscopy examination to look for these key findings. Additional complications also warrant same-day assessment, such as confusion, heart failure, suspected acute coronary syndrome or acute kidney injury.
Patients admitted with a hypertensive emergency are assessed for secondary causes and end-organ damage. Their blood pressure is closely monitored while medications bring it under control.
IV options for Hypertensive emergency
Sodium nitroprusside
Labetalol
Glyceryl trinitrate
Nicardipine
MoA of ACEi
Inhibit the conversion angiotensin I to angiotensin II
SE of ACEi
Cough
Angioedema
Hyperkalaemia
MoA of CCB
Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction
SE of CCB
Flushing
Ankle swelling
Headache
MoA of Thiazide-like Diuretics
Inhibit sodium absorption at the beginning of the distal convoluted tubule
SE of Thiazide-like Diuretics
Hyponatraemia
Hypokalaemia
Dehydration
MoA of ARBs
Block effects of angiotensin II at the AT1 receptor
SE of ARBs
Hyperkalaemia
What is Peripheral Arterial Disease (PAD)?
Peripheral arterial disease (PAD) refers to the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas. It usually refers to the lower limbs, resulting in symptoms of claudication.
What is Intermittent Claudication?
Intermittent claudication is a symptom of ischaemia in a limb, occurring during exertion and relieved by rest. It is typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.
What is Chronic Limb-threatening Ischaemia?
Chronic limb-threatening ischaemia (previously critical limb ischaemia) is the end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest. There is a significant risk of losing the limb.. The features are pain at rest, non-healing ulcers and gangrene. Critical limb ischaemia typically causes burning pain that is worse at night when the leg is raised, as gravity no longer helps pull blood into the foot.
What is acute limb ischaemia?
Acute limb ischaemia refers to a rapid onset of ischaemia in a limb. Typically, this is due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.
What is Ischaemia?
Ischaemia refers to an inadequate oxygen supply to the tissues due to reduced blood supply.
What is Necrosis?
Necrosis refers to the death of tissue.
What is Gangrene?
Gangrene refers to the death of the tissue, specifically due to an inadequate blood supply.
What is Atherosclerosis?
Athero- refers to soft or porridge-like and -sclerosis refers to hardening. Atherosclerosis is a combination of atheromas (fatty deposits in the artery walls) and sclerosis (the process of hardening or stiffening of the blood vessel walls). Atherosclerosis affects the medium and large arteries. It is caused by chronic inflammation and activation of the immune system in the artery wall. Lipids are deposited in the artery wall, followed by the development of fibrous atheromatous plaques.
What do atherosclerotic plaques cause?
Stiffening of the artery walls, leading to hypertension (raised blood pressure) and strain on the heart (whilst trying to pump blood against increased resistance)
Stenosis, leading to reduced blood flow (e.g., in angina)
Plaque rupture, resulting in a thrombus that can block a distal vessel and cause ischaemia (e.g., in acute coronary syndrome)
Non-modifiable risk factors for atherosclerosis?
Older age
Family history
Male
Modifiable risk factors for atherosclerosis?
Smoking
Alcohol consumption
Poor diet (high in sugar and trans-fat and low in fruit, vegetables and omega 3s)
Low exercise / sedentary lifestyle
Obesity
Poor sleep
Stress
Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:
Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions such as rheumatoid arthritis
Atypical antipsychotic medications
Complications of atherosclerosis
Angina
Myocardial infarction
Transient ischaemic attack
Stroke
Peripheral arterial disease
Chronic mesenteric ischaemia
The features of acute limb ischaemia can be remembered with the “6 P’s” mnemonic
Pain
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold
Leriche Syndrome
Leriche syndrome occurs with occlusion in the distal aorta or proximal common iliac artery. There is a clinical triad of:
Thigh/buttock claudication
Absent femoral pulses
Male impotence
Signs of arterial disease on inspection are:
Skin pallor
Cyanosis
Dependent rubor (a deep red colour when the limb is lower than the rest of the body)
Muscle wasting
Hair loss
Ulcers
Poor wound healing
Gangrene (breakdown of skin and a dark red/black change in colouration)
Examination signs of PAD
Reduced skin temperature
Reduce sensation
Prolonged capillary refill time (more than 2 seconds)
Changes during Buerger’s test
Explain Buerger’s Test
Buerger’s test is used to assess for peripheral arterial disease in the leg. There are two parts to the test.
The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.
The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:
Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration
The dark red colour is referred to as rubor.
Causes of arterial ulcers
Arterial ulcers are caused by ischaemia secondary to an inadequate blood supply
Typical features of arterial ulcers
Are smaller than venous ulcers
Are deeper than venous ulcers
Have well defined borders
Have a “punched-out” appearance
Occur peripherally (e.g., on the toes)
Have reduced bleeding
Are painful
Causes of venous ulcers
Venous ulcers are caused by impaired drainage and pooling of blood in the legs.
Typical features of venous ulcers
Occur after a minor injury to the leg
Are larger than arterial ulcers
Are more superficial than arterial ulcers
Have irregular, gently sloping borders
Affect the gaiter area of the leg (from the mid-calf down to the ankle)
Are less painful than arterial ulcers
Occur with other signs of chronic venous insufficiency (e.g., haemosiderin staining and venous eczema)
Ix for PAD
Ankle-brachial pressure index (ABPI)
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation
What is ABPI ?
Ankle-brachial pressure index (ABPI) is the ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm. These readings are taken manually using a Doppler probe. For example, an ankle SBP of 80 and an arm SBP of 100 gives a ratio of 0.8 (80/100).
Interpretation (as per NICE CKS 2024):
1.0 – 1.4: normal
0.9 – 0.99: possible peripheral arterial disease
Less than 0.9: suggests peripheral arterial disease
Less than 0.5: suggests severe and limb-threatening ischaemic
An ABPI above ___ can indicate calcification of the arteries, making them difficult to compress. This is more common in diabetic patients.
1.3
Lifestyle management of PAD
Lifestyle changes are required to manage modifiable risk factors (e.g., stop smoking). Optimise medical treatment of co-morbidities (such as hypertension and diabetes).
Exercise training, involving a structured and supervised program of regularly walking to the point of near-maximal claudication and pain, then resting and repeating.
Medical management of PAD
Atorvastatin 80mg
Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
Surgical management of PAD
Endovascular angioplasty and stenting
Endarterectomy – cutting the vessel open and removing the atheromatous plaque
Bypass surgery – using a graft to bypass the blockage
Endovascular angioplasty and stenting involve inserting a catheter through the arterial system under x-ray guidance. At the site of the stenosis, a balloon is inflated to create space in the lumen. A stent is inserted to keep the artery open. Endovascular treatments have lower risks but might not be suitable for more extensive disease.
Management of Critcal Limb Ischaemia
Patients with critical limb ischaemia require urgent referral to the vascular team. They require analgesia to manage the pain.
Urgent revascularisation can be achieved by:
Endovascular angioplasty and stenting
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply
Management of Acute Limb Ischaemia
Patients with acute limb ischaemia need an urgent referral to the on-call vascular team for assessment.
Management options include:
Endovascular thrombolysis – inserting a catheter through the arterial system to apply thrombolysis directly into the clot
Endovascular thrombectomy – inserting a catheter through the arterial system and removing the thrombus by aspiration or mechanical devices
Surgical thrombectomy – cutting open the vessel and removing the thrombus
Endarterectomy
Bypass surgery
Amputation of the limb if it is not possible to restore the blood supply
What are varicose veins ?
Varicose veins are distended superficial veins measuring more than 3mm in diameter, usually affecting the legs.
What are Reticular veins?
Reticular veins are dilated blood vessels in the skin measuring less than 1-3mm in diameter.
What is Telangiectasia?
Telangiectasia refers to dilated blood vessels in the skin measuring less than 1mm in diameter. They are also known as spider veins or thread veins.
How do varicose veins develop?
Veins contain valves that only allow blood to flow in one direction, towards the heart. In the legs, as the muscles contract, they squeeze blood upwards against gravity. The valves prevent gravity from pulling the blood back into the feet. When the valves become incompetent, the blood is drawn downwards by gravity and pools in the veins and feet.
The deep and superficial veins are connected by vessels called the perforating veins (or perforators), which allow blood to flow from the superficial veins to the deep veins. When the valves are incompetent in these perforators, blood flows from the deep veins back into the superficial veins and overloads them. This leads to dilatation and engorgement of the superficial veins, forming varicose veins.
How does venous eczema happen?
When blood pools in the distal veins, the pressure causes the veins to leak small amounts of blood into the nearby tissues. The haemoglobin in this leaked blood breaks down to haemosiderin, which is deposited around the shins in the legs. This gives a brown discolouration to the lower legs.
Pooling of blood in the distal tissues results in inflammation. The skin becomes dry and inflamed, referred to as venous eczema.
What is lipodermatosclerosis?
The skin and soft tissues become fibrotic and tight, causing the lower legs to become narrow and hard, referred to as lipodermatosclerosis.
Risk factors for varicose veins
Increasing age
Family history
Female
Pregnancy
Obesity
Prolonged standing (e.g., occupations involving standing for long periods)
Deep vein thrombosis (causing damage to the valves)
Presentation for varicose veins
Varicose veins present with engorged and dilated superficial leg veins. They may be asymptomatic or have symptoms of:
Heavy or dragging sensation in the legs
Aching
Itching
Burning
Oedema
Muscle cramps
Restless legs
Patients may also have signs and symptoms of chronic venous insufficiency (e.g., skin changes and ulcers).
What is the tap test for varicose veins?
apply pressure to the saphenofemoral junction (SFJ) and tap the distal varicose vein, feeling for a thrill at the SFJ. A thrill suggests incompetent valves between the varicose vein and the SFJ.
What is the cough test for varicose veins?
apply pressure to the SFJ and ask the patient to cough, feeling for thrills at the SFJ. A thrill suggests a dilated vein at the SFJ (called saphenous varix).
What is the Trendelenburg’s test for varicose veins?
with the patient lying down, lift the affected leg to drain the veins completely. Then apply a tourniquet to the thigh and stand the patient up. The tourniquet should prevent the varicose veins from reappearing if it is placed distally to the incompetent valve. If the varicose veins appear, the incompetent valve is below the level of the tourniquet. Repeat the test with the tourniquet at different levels to assess the location of the incompetent valves.
What is the Perthes Test for varicose veins?
apply a tourniquet to the thigh and ask the patient to pump their calf muscles by performing heel raises whilst standing. If the superficial veins disappear, the deep veins are functioning. Increased dilation of the superficial veins indicates a problem in the deep veins, such as deep vein thrombosis.
How is duplex US used for varicose veins?
Duplex ultrasound can be used to assess the extent of varicose veins. It is an ultrasound that shows the speed and volume of blood flow.
Simple managment of varicose veins?
Varicose veins in pregnancy often improve after delivery.
Simple treatment measures include:
Weight loss if appropriate
Staying physically active
Keeping the leg elevated when possible to help drainage
Compression stockings (exclude arterial disease first with an ankle-brachial pressure index)
Surgical options for varicose veins
Endothermal ablation – inserting a catheter into the vein to apply radiofrequency ablation
Sclerotherapy – injecting the vein with an irritant foam that causes closure of the vein
Stripping – the veins are ligated and pulled out of the leg
Complications of varicose veins
Prolonged and heavy bleeding after trauma
Superficial thrombophlebitis (thrombosis and inflammation in the superficial veins)
Deep vein thrombosis
All the issues of chronic venous insufficiency (e.g., skin changes and ulcers)
What is Syncope?
Syncope is the term used to describe the event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall. Syncopal episodes are also known as vasovagal episodes, or simply fainting.
What is a Vasovagal Episode?
A vasovagal episode (or attack) is caused by a problem with the autonomic nervous system regulating blood flow to the brain. When the vagus nerve receives a strong stimulus, such as an emotional event, painful sensation or change in temperature it can stimulate the parasympathetic nervous system. Parasympathetic activation counteracts the sympathetic nervous system, which keeps the smooth muscles in blood vessels constricted. As the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”.
What is “prodrome”?
Patients often remember the event and can recall how they felt prior to fainting. This is called the prodrome, and involves feeling:
Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache
Collateral Hx for a vasovagal episode may sound like…
A collateral history from someone that witnessed the event is essential to get an accurate impression of what happened. During a vasovagal episode they may describe the person:
Suddenly losing consciousness and falling to the ground
Unconscious on the ground for a few seconds to a minute as blood returns to their brain
There may be some twitching, shaking or convulsion activity, which can be confused with a seizure
The patient may be a bit groggy following a faint, however this is different from the postictal period that follows a seizure. Postictal patients have a prolonged period of confusion, drowsiness, irritability and disorientation.
There may be incontinence with both seizures and syncopal episodes.
Primary syncope (simple fainting) causes
Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood
Secondary causes for syncope
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
Key features that may be seen with syncope
Prolonged upright position before the event
Lightheaded before the event
Sweating before the event
Blurring or clouding of vision before the event
Reduced tone during the episode
Return of consciousness shortly after falling
No prolonged post-ictal period
Key features that may be seen with seizures
Epilepsy aura (smells. tastes or deja vu) before the event
Head turning or abnormal limb positions
Tonic clonic activity
Tongue biting
Cyanosis
Lasts more than 5 minutes
Prolonged post-ictal period
Ix for syncope
ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome
24 hour ECG if paroxysmal arrhythmias are suspected
Echocardiogram if structural heart disease is suspected
Bloods, including a full blood count (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)
Advice for simple vasovagal episode
Avoid dehydration
Avoid missing meals
Avoid standing still for long periods
When experiencing prodromal symptoms such as sweating and dizziness, sit or lie down, have some water or something to eat and wait until feeling better
