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).
Compare arterial and venous ulcers:
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 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.
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 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.
