CV Diagnosis+Management Flashcards
General examination for PVDs
General inspection - appearance/colour of limb, skin colouring and check in-tact.
Temperature - Compare temp on both sides.
Capillary refill - Cap refill is sign of compromise ie in shock cap refill is longer, or if there is blockage (not specific to just vascular conditions more of a gross check) should be less than 3seconds normally
Pulse check
Auscultation - listen with stethoscope to (BRUIT look up)
Motor assessment
Sensation assessment
what is PVD (and causes)
peripheral vascular disease
refers to any disorder/disease of the circulatory system outside of the brain and heart
Most common cause is atherosclerosis
Can be asymptomatic; approx. 60% are symptomatic
Other causes can include:
blood clot
diabetes
inflammation (autoimmune diseases)
Infection (scarring causing weaker vessels)
structural defects (congenital)
Injury
PVD risk factors
Family history of heart disease, high BP. high cholesterol or stroke Older than 50 Overweight or obese Inactive (sedentary lifestyle) Smoking Diabetes High BP High cholesterol (LDL), high triglycerides and low HDL
Superficial vein thrombophlebitis and risk factors
Results from thrombus formation (commonly in saphenous vein)
may be idiopathic or multiple factors
varicose veins are most common risk factor
Other factors include IV cannulation, pregnancy, previous history of SVT
estimated incidence of 3-11%
superficial vein thrombophlebitis complications
DVT or pulmonary embolism main complications
others include infection, skin changes (hyperpigmentation), varicose veins
uncomplicated SVT generally considered benign and symptoms usually subside in 1-2 weeks; although vein hardness may persist for longer. If condition is associated with varicose vein, likely this will reoccur unless vein is excised.
when diagnosing - symptoms can overlap with cellulitis, however this would present with temperature and infection site smaller less widespread than SVT, due to being an infection not inflammation
SVT management
Refer if suspected underlying cause (eg cancer - 2 week referral rule)
Pain management with nonsteroidal antiinflammatory drugs/paracetamol; warm towel, avoid immobility, elevate affected leg
Consider referral for vascular service for duplex scanning to help further treatment
Compression stockings
Low molecular weight heparin and fondaparinux shown to reduce extension and recurrence.
DVT
Blood clot in deep vein (most commonly calf) partially or fully compromising blood flow
most common cause is immobility
estimated 1 in 1000 have a DVT each year
complication of DVT is pulmonary embolus and post-thrombotic syndrome (persistent symptoms after thrombus gone)
DVT risk factors
immobility surgery illness or injury (causing mobility) long journeys sitting/standing in same place damage to inside lining of vein Blood clotting conditions (APS) Contraceptive combined pill (7 day break pill containing oestrogen) Cancer or heart failure Over 60 years of age Pregnancy (usually improves 3-12 weeks post-partum) Obesity Dehydration (stickier blood)
DVT symptoms
Pain and tenderness around affected area; particularly on palpation
General limb swelling
Colour and temperature changes around the affected area. Blood that would normally go through the vein is diverted to outer veins making the skin warmer and more red
Sometimes patients are asymptomatic and a DVT is only diagnosed following a complication such as a pulmonary embolism.
DVT investigations
Ultrasound (GOLD STANDARD)
Wells score to measure symptoms and assist decision of further investigations:
Low wells score (0-2) - undertake DDIMER test to rule out DVT
High wells score (3+) - ultrasound, duplex doppler for blood flow
DVT treatment
NICE recommends: Apixaban or rivaroxaban for confirmed DVT or PE. If neither apixaban nor rivaroxaban is suitable, then either:
Low molecular weight heparin (LMWH) injections for at least 5 days followed by dabigatran or edoxaban, or
LMWH injections with Warfarin for at least 5 days, followed by Warfarin on its own.
Length of treatment varies depending on factors. Usually 3 months for a provoked below knee dvt. Unprovoked may be 6 months. Recurring - for life.
Compression stockings - act as skeletal muscle should to improve circulation in limb
Varicose veins
Twisted and enlarged veins
most commonly in legs (calf)
Similar to spider veins but spider veins are smaller and more superficial and often red\blue coloured and can appear in legs/face.
Difference in presentation of varicose veins and thrombophlebitis
Thrombo is hard, red and has no prominent veins, more of general swelling
Varicose are soft, very visible bulging and twisted veins
Signs and symptoms of varicose veins
May not cause pain
Dark purple veins appearing twisted or bulging; often cord-like
achy or heavy feeling
swelling, burning, throbbing, muscle cramping
worsened pain after sitting or standing for long periods
itching around veins
skin discolouration around vein
Varicose veins causes and risk factors
Weak or damaged valves from poor circulation/standing or sitting in same position for long time reducing skeletal muscle action. valves leak blood causing backflow and pooling in veins; resulting in bulging or twisting. Risk factors: Increases with age Women more likely (sex) Pregnancy Family history Obesity Standing/sitting for lengths
Varicose vein complications
very rare but include:
ulcers forming near veins particularly near ankles. usually start as discoloured spots
Blood clots causing pain - needs med attention as may indicate thrombophlebitis
Bleeding usually only minor but still needs med attention
Varicose vein management
aim to increase circulation and muscle tone
VV in pregnancy generally improves without treatment within 3-12weeks post partum
Exercise
Watching weight
High fibre, low salt diet
Elevating legs
Changing sitting/standing position regularly
Compression stockings
Cosmetic surgeries
Peripheral artery disease
PAD occurs with significant narrowing of arteries distal to arch of aorta, most commonly form atherosclerosis
Critical limb ischaemia is chronic condition and is most severe clinical presentation of PAD affecting limbs.
Acute limb ischaemia is the sudden decrease in arterial limb perfusion due to thrombotic or embolic causes.
Claudication causes and symptoms
Intermittent claudication caused by narrowing/blockage of main artery to lower limb. location of pain depends on site of stenosis:
buttock and thigh pain: aorta, iliac vessels.
Calf pain; femoral or popliteal vessels.
Ankle and foot pain; tibial or peroneal vessels.
Pain onset with exercise (cramps) and improves with rest
Symptoms can improve as collateral circulation increases (6-8 weeks)
usually occurs in age 50+, smokers, hypertenions, diabetes or high cholesterol
Claudication investigations
Blood pressure (doppler) compare both limbs Foot BP measured and compared with arm BP to measure ankle brachial pressure index ratio. provides objective measure of lower limb circulation. Arteriogram (artery x-ray injecting contrast dye into groin)
Claudication treatments
Not necessary with mild symptoms
often stable with no deterioration for long time
Blood tests rule out atherosclerosis, diabetes, thyroid and kidney function tests
Exercise brisk walk 3x a week improves function over 3-6 months
angioplasty - less effective long term usually under 10cm
surgery - bypass for above 10cm blocks and very bad symptoms, or if very short claudication, resting pain, ulceration or gangrene (when limb is threatened) due to limited success
Medication - statins lower cholesterol, asprin thin blood
Critical limb ischaemia
Condition with chronic ischaemia at rest, with ulcers, gangrene in one or both legs, attributable to objectively proven arterial occlusive disease.
Ischaemic rest pain - pain while at rest from lack of oxygen to limb
Chronic condition referring to longer than two weeks
Symptoms of critical limb ischaemia
Pain at rest with: paraesthesia (pins and needles) in foot/toes, ulceration, necrosis and gangrene.
Symptoms are exacerbated by leg elevation and relieved by dependency. Typically worse at night, relieved by hanging foot over the bed
Patients with diabetic neuropathy may have little/no pain despite severe ischaemia
Absent or decreased peripheral pulses
Bruits in aorta/groin (abnormal artery narrowing)
Hair loss
Smooth, shiny and cool skin
Muscle atrophy
Ulcers
Buergers test positive
elevation of leg with patient supine elicits ischaemia and leg goes pale (fails to overcome gravity). The more severe the PAD the lower the angle required to initiate response.
Rubor on dependency test positive
after elevation of leg, hanging legs off the bed causes change in colour from white to blue and eventually dark red (reactive hyperaemia).
Critical limb ischaemia treatment
Lifestyle advice: smoking, exercise, diet
Exercise rehabilitation: supervised exercise for 3 months. It enhances muscle metabolism, and promotes vasodilatation and vascular angiogenesis. It improves walking distances, and may also improve survival
Bp, cholesterol, diabetes, anti-platelet therapy: aspirin is first-line in order to reduce the risk of stroke, myocardial infarction and vascular death
Symptomatic relief of claudication using drugs
Endovascular treatment: angioplasty and stenting
Vascular surgery: most commonly bypass surgery
Amputation performed in CLI patients is usually due to significant necrosis or paresis
Acute limb iscaemia
Acute limb ischaemia is most often due to either acute thrombotic occlusion of a previously partially occluded, thrombosed arterial segment, or to embolus from a distant site.
Without surgical revascularisation, complete acute ischaemia leads to extensive tissue necrosis within six hours. The effects of sudden arterial occlusion depend on the state of collateral supply.
The collateral supply in the leg is usually inadequate unless there has been pre-existing occlusive disease.
The subclavian artery has many collateral vessels so that occlusion of a major artery does not necessarily make an upper limb non-viable.
Acute limb ischaemia symptoms
6 P's: Pain Pallor Pulselessness Paralysis Paraesthesia Perishing cold
Management of acute limb ischaemia
Urgent hospital admission - surgery or angioplasty
Immediate heparinisation (doubles salvage rate)
Provide analgesia (IV to corect hypotension, O2)
Doppler ultrasound,CT angiogram
Surgical embolectomy (for embolic occlusion)
bypass graft or intraoperative thrombolysis considered.
Anticoagulation post surgery (heparin) to prevent reoccurance
Amputation needed in 40$ people and 30 day mortality can be up to 30%
Acute vs critical limb ischaemia
Acute: sudden pain pale and motting no tissue loss no change in colour or dependency young and old patients history of claudication, heart disease or aneusym, atheroscleoric risk factor 6 Ps symptoms: marblewhite skin muscle tenderness proximity strong pulse
Critical
history of claudication, other non-joint related lower extremity symptoms
impaired walking function
ischaemic rest pain
exmaination:
abnormal lower extremity pulse, vascular bruit, nonhealing lower extremity wounds, gangrene,
Compartment syndome and risk factors
Limb threatening emergency build up of fluid within compartment risk factors: extremity fractures direct blows to extremity crush mechanism patients on anticoagulation reperfusion injuries tight bandages or dressings burns
compartment syndrome symptoms
significant swelling pain (increasing and out of proportion to injury) pain moving proximal digits numbness and tingling motor weakness cooler temperature of extremity
Compartment syndrome management
Immediate emergency surgery required for fasciectomy - call orthopaedic surgeon loosen dressings slight elevation hydration avoid hypotension supplemental oxygen
Aortic aneurysm and dissection
Aneurysms form when a weakened area in the aorta, leads blood to push against the vessel wall causing it to bulge like a balloon.
A dissection is a tear in the wall of the aorta that can cause life threatening bleeding or sudden death.
Large fast growing aneurysms also may rupture
Small slow growing aneurysms may never rupture (these may just be monitored until if required repaired)
Most common between ages of 50-70; rare under 40 years.
Thoracic aneurysm
Grow slowly often without symptoms
some never rupture, many start and stay small, some expand over time
as they expand may present with: Tenderness in chest, back pain, hoarseness, cough, shortness of breath
Less common than abdominal aneurysms
Abdominal aortic aneurysm (AAA) and symptoms
If a first degree relative has had an AAA, you are 12 times more likely to develop an AAA.
➤ Abdominal aortic aneurysms often grow slowly without symptoms, making them difficult to detect. Some aneurysms never rupture. Many start small and stay small; others expand over time, some quickly.
➤ If you have an enlarging abdominal aortic aneurysm, you might notice:
➤ Deep, constant pain in your abdomen or on the side of your abdomen
➤ Back pain
➤ Pulsating aorta
AAA causes and risk factors
Causes: Atherosclerosis high blood pressure blood vessel disease aortic infections trauma Risk factors: Tobacco use Age (65+) Males more at risk (sex) White people more at risk Family history of AAA Other aneurysm history
AAA screening
Ultrasound scan for men @ 65years in UK
Normal aorta size is < 3cm : no follow up scan required
If aneurysm present: size will determine how often monitoring will be
Large aneurysm more than 5.5cm will be referred to specialist and discuss treatment: surgery to repair
1 in 70 men who are screened have an aortic aneurysm
Men are 6 x more likely to have AAA than women
Aortic dissection/rupture
A dissection occurs when a tear of the intima (the inner lining) allows blood to leak into the media (middle layer). This creates two passages for blood: a true lumen, which is the normal passageway of blood, and a false lumen, the newly created passageway.
complications include pericardial tamponade (fatal)
80% mortality rate
Aortic dissection/rupture symptoms
Chest pain, aortic regurgitation, myocardial ischaemia, congestive heart failure, pleural effusions, syncope (loss of consciousness from decreased BP), neurological symptoms (eg, acute paraplegia, upper or lower limb ischaemic neuropathy), mesenteric ischaemia and acute kidney injury
THE PAIN: abrupt onset and maximal (very painful all at once), in contrast to MI which starts slowly and gains intensity gradually. Pain also MIGRATES as dissection progresses. In PROXIMAL dissections pain is usually RETROSTERNAL. In DISTAL dissections pain is between SCAPULAE
Aortic dissection/rupture investigations and treatment
Raised DDIMER
ECG changes (R-R delay)
Difference in blood pressure (20mmHg difference usually, but if not present doesn’t rule out dissection)
Analgesia, systolic aim 100-120: IV beta blockers to reduce BP.
Troponin - used to diagnose heart attacks will be raised levels.
GOLD STANDARD is CT ANGIOGRAM
**Treatment is stent or graft surgery
Hypertension
Persistently raised BP
arteries loose elasticity and heart overworks
ideal BP is 120/90. Under 140/90 is OK
Stage one - BP from 140/90-159/99 mmHg; subsequent ABPM/HBPM from 135/85 - 149/94
Stage 2 - 160/100 - 180/120 and average of 150/95
stage 3 - severe hypertension. 180/120 or more
White coat hypertension
White-coat’ hypertension is blood pressure that is unusually raised when measured during consultations with clinicians but is normal when measured in ‘non-threatening’ situations. Occurs in about 15–30% of the population, although this may be inflated due to inadequate evaluation of people.
causes roughly 10-20 mmHg descrepancy
Masked hypertension
clinic blood pressure measurements are normal (less than 140/90 mmHg) but blood pressure measurements are higher when taken outside the clinic using average daytime ABPM or average HBPM blood pressure measurements
Hypertension complications
Increases the risk of a number of conditions, including: •Heart failure. •Coronary artery disease. •Stroke. •Chronic kidney disease. •Peripheral arterial disease. •Vascular dementia with each 2 mmHg rise in systolic blood pressure associated with a 7% increased risk of mortality from ischaemic heart disease and a 10% increased risk of mortality from stroke.
Risk factors of hypertension
Increases with age
Up to 65 years; tends to be more common in men; form ages 65-74 seems to be higher in women
Ethnicities of black african and black carribean more at risk
Anxiety and emotional stress
Family history/genetics
Social deprivation
Lifestyle - smoking, alcohol, salt, obesity, sedentary lifestye
Hypertensive symptoms
Hypertension is typically asymptomatic however patients may present with:
Blurred vision
Nosebleeds (epistaxis)
Shortness of breath (dyspnoea)
Chest pain
Dizziness
Headaches
Subconjunctival haemorrhage - burst blood vessels in eye
Retinopathy – clinical finding w/ fundoscopy.
Hypertension diagnosis
Blood pressure in both arms. If difference greater than 15mmHg between arms then retake; if remains take higher reading arm.
Ambulatory BP monitoring: two measurements per hour taken during usual working hours. Average of at least 14 measurements (need several appointments) confirms diagnosis. ABPM average of 135/85 or more confirms
Home BP monitoring: Two consecutive measurements taken one min apart while seated. Recorded twice daily (morning and evening)
Hypertension investigations
Assess for target organ damage.
•U&E’s - assess kidney functions chronic kidney disease
•Urine albumin:creatinine ratio - proteinuria- rule out secondary hypertension from other cause
•HbA1C - Diabetes
•Urine dipstick - haematuria
NICE also recommends: •Fundoscopy - retinopathy •ECG - LVHAssess cardiovascular risk. •Lipid profile - Hyperlipidaemia •Q-risk score – 10 year risk of CVD
Hypertension lifestyle management
lifestyle
•Diet and exercise — a healthy diet and regular exercise can reduce blood pressure. If the person is overweight or obese, offer weight loss advice.
•Caffeine — discourage excessive consumption of coffee and other caffeine-rich products.
•Dietary sodium — encourage people to keep their dietary sodium intake low, by reducing or substituting sodium salt, as this can reduce blood pressure.
•Smoking — offer advice and help to smokers to stop smoking.
•Alcohol —a reduced intake because this can reduce blood pressure and has broader health benefits.
Hypertension medication management
ACEi/A2RB given if under age 55 and not of black afircan/carribean family origin.
escalated to ACEi/A2RB and CCB or Thiazide like diuretic if no improvements
escalated to all three if no improvement
Consider seeking expert advice or adding low dose spirolactone Or an alpha-blocker or beta-blocker if blood potassium is 4.5mmol/L or higher.
Iatrogenic hypertension and cause
translated as ‘caused by the doctor’:
Hypertension caused by drugs/medical intervention.
Causes include:
•Excessive alcohol consumption (more than 30 g per day)
•Glycerizine (active ingredient of the liquorice) – rare.
•Oral contraceptives – CHC
•Non steroidal anti-inflammatory drugs (NSAID – ibuprofen, naproxen)
•Immunosuppressants
•Sympathomimetics (nasal decongestants)
•Anabolic steroids
•Bromocriptine (inhibitor of lactation)
•Psychotropics (tricyclics antidepressants, monoamine oxydase inhibitors).
Secondary hypertension
- High blood pressure due to a cause.
- About 10% of cases have an underlying cause, such as renal, endocrine, or vascular disorder, or the use certain drugs.
- Consider in patients under 40 years presenting with hypertension.
Secondary hypertension causes
Renal disorders are the most common cause of secondary hypertension. They include: •Chronic pyelonephritis •Diabetic nephropathy •Glomerulonephritis •Polycystic kidney disease •Obstructive uropathy •Renal cell carcinoma
Vascular disorders:
•Coarctation of the aorta
•Renal artery stenosis
Endocrine disorders: •Primary hyperaldosteronism •Phaeochromocytoma •Cushing's syndrome •Acromegaly •Hypothyroidism/Hyperthyroidism
Drugs and other substances:
•Alcohol//Cocaine//Combined Oral Contraceptive// Liquorice// NSAIDs//
Other conditions:
•Connective tissue disorders (scleroderma, systemic lupus erythematosus, polyarteritis nodosa).
•Retroperitoneal fibrosis.
•Obstructive sleep apnoea.
Malignant hypertension
•Accelerated (or malignant) hypertension is a severe increase in blood pressure to 180/120 mmHg or higher (and often over 220/120 mmHg) with signs of retinal haemorrhage and/or papilloedema (swelling of the optic nerve).
•It is usually associated with new or progressive target organ damage
medical emergency - send them to hospital
Malignant hypertension management
When to refer?
IMMEDIATELY – arrange same day admission.
•Medical emergency especially if systolic >200 mm Hg, diastolic >130 mm Hg
•A clinic blood pressure of 180/120 mmHg and higher with signs of retinal haemorrhage and/or papilloedema or
•Life-threatening symptoms, such as new onset confusion, chest pain, signs of heart failure, or acute kidney injury.
•A systolic >180 mm Hg, diastolic >120 mm Hg w/o end organ damage can be reduced over a few days w/ a repeat in 7 days.
Calcium channel blockers for hypertension
•Names/Classes: - PINE; Dihydropyridines (such as nifedipine and amlodipine) and non-dihydropyridines – rate limiting (diltiazem and verapamil).
•MOA: Reduce the amount of calcium entering cells of the heart and blood vessel muscle walls. CCB’s act as vasodilators. non-dihydropyridines also block calcium entering the conducting cells in the heart – slowing the rate.
•When to review: After 2 weeks.
•Monitoring: U&E’s and LFT’s prior to initiation, then annually.
•Side effects: Peripheral oedema (ankle swelling), flushing, palpitations, GI upset, bradycardia
•Avoid: Heart failure, AV block (conduction arrhythmia). Reduce dose in hepatic/renal impairment.
Reduce Ca entering to slow rate of conduction in cardiac tissue. review patient after two weeks especially to check for symptoms
ACEi/A2RB for hypertension
- Names: ACEi tend to end in -PRIL; enalapril, ramipril, lisinopril. A2RB tend to end in –SARTAN; candesartan, losartan
- MOA: Reduce the activity of angiotensin-converting enzyme – vasoconstrictor. Reduces conversion of angiotensin 1 to 2 via blocking the ACE enzyme or blocking the receptor stimulated by angiotensin 2 in order to promote vasodilation
- Criteria: <55 y/o & non-black – higher renin levels.
- When to review: 4 weeks after starting meds for repeat readings; check bp 6-12 months once stable.
- Monitoring: U&E’s after 1-2 weeks.
- Side effects: Dry cough, angioedema (especially in black people)
- Avoid: In pregnancy, 1st line for black people, renal artery stenosis.Angiotensin II receptor blockers (A2RBs) have a similar effect in lowering blood pressure and helping heart failure. They block the receptor that is stimulated by the hormone angiotensin II.
Thiazide-like diuretics
- Names: tend to end in -THIAZIDE; bendroflumethiazide, indapamide.
- MOA: Reduce fluid retention by the kidneys – cause volaemic depletion. Remove strain on kidneys.
- When to review: 4 weeks – repeat BP.
- Monitoring: U&E’s and LFT’s prior to initiation, then annually if stable. U&E’s should be repeated after 1 week to observe sodium/potassium levels.
- Side effects: Muscle cramps – due to electrolyte loss, postural hypotension, GI upset
- Avoid: Electrolyte disturbance (malnutrition or gland malfunction involving electrolyte imbalance), pregnancy, gout
Statins for hypertension
GPs should offer atorvastatin 20mg for the primary prevention of CVD to people who have a 10 per cent or greater risk of developing CVD within the next 10 years.
Patients with type 1 or type 2 diabetes should be offered 20mg atorvastatin for primary prevention of CVD
Patients with established CVD may need to be offered 80mg atorvastatin
GPs should discuss the benefits of changes to lifestyle with patients before initiating treatment with statins.
The risk of developing CVD should be estimated using the QRISK2 assessment tool.
Hypotension
a lower than usual blood pressure – ideal 120/80.
Low Blood Pressure:
•Systolic: lower than 90 mmHg
•Diastolic: lower than 60 mmHg
Hypotension causes
- Hypovolaemic shock: Significant bodily fluid loss.
- Orthostatic hypotension: Blood pressure drop asso w/ change of position.
- Cardiac tamponade: Fluid accumulation around the heart resulting in cardiac compression.
- Congestive heart failure
- Addisonian crisis (Addison’s disease/autoimmune adrenal failure): Sx of nausea, vomiting, fever, hypotension, hyperpigmentation, and electrolyte abnormalities.
- Pregnancy
- Diabetes
- Pernicious anaemia
- Phaeochromocytoma (RARE)
Orthostatic hypotension
Drop in systolic BP of at least 20 (30 in hypertensive patients) and drop in diastolic of at least 10mmHg within three minutes of sitting to standing
Orthostatic presentation and history
Presentation
Patients may be asymptomatic
Symptoms may include:
•Dizziness, light-headedness, blurred vision, weakness, fatigue, nausea, palpitations and headache.
•Less common symptoms include syncope, dyspnoea, chest pain and neck and shoulder pain. Symptoms typically do not occur while supine, should get worse on standing, and should be relieved by sitting or lying down.
History Patient may report symptoms occur: •Early in the morning •In hot environments •After meals •After standing motionless •After exercise
Orthostatic hypotension investigations
Full blood count FBC
U&E’s to check kidney functioning/investigate primary cause
Glucose (fasting)
Haematinics - B12, folate, ferritin/iron
ECG
Tilt-table testing - Compare lying and standing bp
Orthostatic hypotension diagnosis
- Measure blood pressure whilst the patient is lying down. NB sitting is also sufficient in a GP setting.
- Then measure standing blood pressure (after standing for 3 minutes).
- A fall in systolic blood pressure of at least 20 mmHg (at least 30 mmHg in people with hypertension) and/or a fall in diastolic blood pressure of at least 10 mmHg within 3 minutes of standing confirms the diagnosis.
Orthostatic hypotension management lifestyle
- Review medications – particularly hypovolaemic/hypotensive causing meds/polypharmacy.
- E.G. alpha-blockers, diuretics, tricyclic antidepressants, and levodopa or dopaminergic agonists.
- Review hydration and deconditioning (prolonged bed rest).
- Trigger avoidance.
- Positioning - stand slowly, dorsiflex feet first and cross the legs whilst upright. Go from lying to sitting to standing.
- Raising the head of the bed, which helps prevent diuresis and supine hypertension caused by fluid shifts.
- Compression hosiery, or body suits.
- Caffeine (coffee or tablet form) may be effective.
- Constipation avoidance – straining.
Orthostatic hypotension management medication
- Increase salt intake – may be given in tablet form
- 1st line: Fludrocortisone
- Requires a high dietary salt and adequate fluid intake. Head-up tilt sleeping (20-30 cm).
- Side effects: Supine hypertension is a common - last dose should be administered > 4 hours before going to sleep and BP should be monitored.
- 2nd line : Alpha-receptor agonists•Midodrine is recommended for monotherapy or combined therapy (with fludrocortisone).
- Side effect: Supine hypertension.
- Contra-indicated in heart disease, renal failure, phaeochromocytoma and thyrotoxicosis.
- 3rd line: Other options
- Dihydroxyphenylserine (DOPS)
- A prodrug which is converted to noradrenaline (norepinephrine). It is the only effective treatment of dopamine beta-hydroxylase deficiency.
- The somatostatin analogue octreotide:
- Inhibits release of gastrointestinal peptides, some of which may cause vasodilatation.
- Subcutaneous injection > 30 minutes before a meal.
- Side effects: Nausea and abdominal cramps.
- Pyridostigmine - a cholinesterase inhibitor
- Modest effect on orthostatic hypotension but does not aggravate supine hypertension.
Hypovolaemic shock
When the volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body (hypoperfused).
•Risk of mortality depends on the amount of blood loss and time taken to correct. Increased age intensifies this risk.
Stages of blood loss
- Class 1: 10-15% blood loss; physiological compensation and no clinical changes appear.
- Class 2: 15-30% blood loss; postural hypotension, generalised vasoconstriction and reduction in urine output to 20-30 ml/hour.
- Class 3: 30-40% blood loss; hypotension, tachycardia over 120, tachypnoea, urine output under 20 ml/hour and the patient is confused.
- Class 4: 40% blood loss; marked hypotension, tachycardia and tachypnoea. No urine output and the patient is comatose.A healthy adult can bear the loss of half a litre from a circulation of about five litres(average for an adult) with minimal effect.
Hypovolaemic shock presentation
- SYMPTOMS: Patients may report feeling cold, malaise, anxiety, feeling faint/lightheaded and dyspnoea.
- SIGNS: may include tachypnoea, sweating/clamminess, reduced capillary refill, hypotension, tachycardia and in some cases coma.
Hypovolaemic shock causes
•Blood loss - may be revealed or occult. E.G. Stab wound or internal bleeding - clear or covered up
•Trauma
•Burns – may result in leakage of plasma and/or blood. Depends on degree and percentage spread of burn.
•Severe loss of water and salt – following vigorous exercise in a hot environment, poor fluid intake, fluid loss from diarrhoea and vomiting, and inappropriate diuresis.
hydration - pregnant women may suffer from morning sickness so not as hydrated as usual causing BP drop
Investigations to confirm hypovolaemic shock
- FBC – Hb
- U&E
- LFT - liver functioning
- Group and cross-match (Group&save) - in haemorrhage and burns.
- Coagulation screen.
- Blood gases (arterial or venous) – hypoperfusion (lactate).
- Monitor urine output - catheter.
- Ultrasound (cardiac) - can show any pump failure.
- Central venous pressure
- Vital obs
Categories of shock
Stage 1: Compensated shock:
•Baroreceptor reflexes result in increase in myocardial contractility, tachycardia and vasoconstriction. They maintain cardiac output and BP and lead to the release of vasopressin, aldosterone and renin.
Stage 2: Progressive or uncompensated shock:
•Myocardial depression, failure of vasomotor reflexes and failure of the microcirculation, with increase in capillary permeability, sludging and thrombosis, resulting in cellular dysfunction and lactic acidosis.
Stage 3: Irreversible shock:
•Failure of vital organs with inability to recover.
Hypovolaemic shock management
Hospital management:
•O2
•Venous access/central venous pressure (CVP) line
•IV fluids
•Blood transfusion – in cases of haemorrhage
Hypertension treatment pathway for diabetic patients
Patients with type 2 diabetes are treated same as patients without
Patients with type one diabetes are put immediately on ACEi regardless of age of ethnicity; if calcium channel blockers are added then only use modified release formulations
Whole separate guideline for type one diabetic patients
Hyperlipidaemia management overview
Primary prevention: 20mg atorvastatin daily is prescribed to prevent those who have a 10% or more 10-year risk of developing cardiovascular disease (e.g. suffer a cardiac event). Please look at the QRISK and Q2RISK tools (freely available online)
Secondary prevention: 80mg atorvastatin daily is prescribed to those who are diagnosed with cardiovascular disease (e.g. suffered a cardiac event)
For both groups, we aim for a 40% reduction in non-HDL at 3 months after initiation
Diet and lifestyle are key – it is just not just about drugs
Pulmonary embolism and causes
Clot blocking the blood supply to the lungs
causes: DVT, recent surgery, pregnancy, but in 40% of cases is idiopathic and so called ‘unprovoked’
PE symptoms
Chest pain Shortness of breath Coughing, coughing up blood Feeling dizzy or fainting Blood clot from DVT can break off and travel to the lungs; so other signs can be painful, red or swollen leg/calf usually
PE risk factors
operation or a serious limb injury
after long periods of bed rest
during a long-haul flight or a long train or car journey lasting more than 6 hours
Around half of all people with a pulmonary embolism get it while they’re in hospital.
Cancer, or cancer treatments such as chemotherapy and radiotherapy - increases blood clot risk
being overweight
pregnancy – your risk is increased for up to 6 weeks after giving birth
smoking
taking some forms of hormone-based contraception or hormone replacement therapy (HRT). Your chances of developing a blood clot are very small if you’re taking the contraceptive pill or HRT, and your health care professional will consider your individual risk before they prescribe them.
PE diagnosis
Chest X-ray
DDIMER to look for clotting agents
Leg ultrasound to confirm DVT
V/Q perfusion test to see airflow to lungs
CTPA - see blood vessels in the lungs by injecting dye
PE treatment
Immediate anticoagulant treatment; followed by average 3 months taking these if prescribed (if warfarin will need regular blood tests). Review and assess need for further investigations as to why the clot occured
Angina history overview
Heavy retrosternal pain which may radiate into the neck or left arm
Brought on by effort or emotion and relieved by rest and nitrates
Constricting heavy pain
Associated features of breathlessness
timing: 2-10mins
Risk factors for ischaemic heart disease are likely
A family history of ischaemic heart disease, aortic stenosis, hypertrophic cardiomyopathy
MI history overview
Retrosternal, constricting and heavy Pain typically comes on over a few minutes
Pain is similar to that of angina but is typically severe, long lasting (>20 mins) and unresponsive to nitrates
Often associated with sweating, nausea and breathlessness
Risk factors for ischaemic heart diseases are likely
A family history of ischaemic heart disease is likely
Pleuritic pain history overview
Sharp stabbing ‘catching pain’
May radiate to the back of the shoulder
Typically aggrevated by deep breathing and coughing
Can be caused by pleurisy which can occur with pneumonia, PE and pneumothorax, or by pericarditis which can occur post MI, in viral infections and in autoimmune diseases
Plural pain in localised to one side of the chest and it no position dependent
Pericardial pain is central and positional, aggravated by laying down and alleviated by sitting up or leaning forward
Dressiers syndrome
(post MI syndrome) is characterised by pleuritic chest pain from pericarditis accompanies by a low-grade fever, can occur up to three months follows MI
PE history overview
Sharp, stabbing pain that is of sudden onset
May be associated with shortness of breath, haemoptysis and/or pleurisy
Typically aggravated by deep breathing and coughing
May be a history of recent surgery, prolonged bed rest or long-haul travel
Gastro-oesophageal reflux history overview
Retrosternal burning
clear relationship with food, alcohol, no relation to effort
may be associated with odynophagia and nocturnal asthma
aggrevated by lying down
alleviated by sitting up and antacids like gaviscon or milk
Musculoskeletal complaints history overview
May be associated with history of physcial injury or unusual exertion
pain aggrevated by movement but not reliably alleviated with rest
site of pain tender to touch
Panic attack history overview
Rapid onset severe anxiety lasting 20-30minutes
Associated with chest tightness and hyperventilation
Aortic dissection history overview
sudden onset, sharp, tearing pain maximal at onset
Interscapular and retrosternal pain
Radiates to the back between shoulders
Prolonged timing
No manouvers to relieve pain, spontaneous onsets
If you cannot differentiate between gastro-oesophaheal reflux and angina what investigations can you perform
If no signs of ischaemia on ECG, advise an exercise ECG stress test (can show if blood flow to the heart is reduced - angina) If this is negative consider a theraputic trial of antacid or nitrate
Pleural and pericardial pain are located (symptomatically)
Plural pain in localised to one side of the chest and it no position dependent
Pericardial pain is central and positional, aggravated by laying down and alleviated by sitting up or leaning forward
Pericardial pain SOCRATES
Retrosternal of left sided
gradual onset
postural change may aggravate
Character is sharp stabbing
radiates to left shoulder or back
Associated features flu-like, breathlessness and fever
Timing: gradual onset of varying duration
Exacerbated by sitting/lying down, NSAIDS may help
Oesophageal pain SOCRATES
Retrosternal or epigastric pain
Onset within 1-2 mins or sudden spasm
Gripping, tight or burning pain
Often radiates to back and sometimes arms
Associated features include heartburn and acid reflux
Often at nighttime variable durations
Exacerbated by lying flat, some foods, not relieved by rest.
sometimes nitrates will ease
Dyspnoea overview
symptoms:
Breathlessness
tight in chest
short breaths - air hungry
Most common in CV, pulomary or neuomuscular diseases
can be acute (heart failure, PE), subacute (worsening asthma, COPD exacerbation), or chronic (stable COPD, stable interstitial lung disease)
Common differentials: COPD, congestive heart failure, asth,a, pneumonia
Palpitation overview
Awareness of ones heartbeat
Mostly due to non-arrhythmia aetiologies
Palpitations associated with syncope are particularly worrying as more likely associated with malignant arrhythmias such as VT
needs full history and physical exam and 12 lead ECG
Further ECG and physiological testing needed
Common differentials: sinus tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation
Syncope overview
transient loss of conciousness due to global cerebral hypoperfusion
rapid onset, short duration, spontaneous recovery
Risk factor identification most important as can be associated with fatal diseases (CAD, structural heart disease etc.)
Common differentials: acute coronary syndrome, ventricular arrhythmias, AV block, acute atrial fibrillation
Uncommon: cardiac tamponade, aortic dissection, PE
Cyanosis and associated differentials
bluish discolouration of the skin due to poor circulation (e.g. peripheral vasoconstriction secondary to hypovolaemia) or inadequate oxygenation of the blood (e.g. right-to-left cardiac shunting).
Shortness of breath associated differentials
may indicate underlying cardiovascular (e.g. congestive heart failure, pericarditis) or respiratory disease (e.g. pneumonia, pulmonary embolism).
Pallor associated differentials
pale colour of the skin that can suggest underlying anaemia (e.g. haemorrhage, chronic disease) or poor perfusion (e.g. congestive cardiac failure). It should be noted that a healthy individual may have a pale complexion that mimics pallor, however, pathological causes should be ruled out
Malar flush and associated differentials
plum-red discolouration of the cheeks associated with mitral stenosis.
Oedema associated differentials
Congestive heart disease Kidney disease Liver cirrhosis Pregnancy Result of medications
Hands colouring and associated differentials
pallor suggests poor peripheral perfusion (e.g. congestive heart failure) and cyanosis may indicate underlying hypoxaemia.
Xanthomata and associated differentials
raised yellow cholesterol-rich deposits that are often noted on the palm, tendons of the wrist and elbow. Xanthomata are associated with hyperlipidaemia (typically familial hypercholesterolaemia), another important risk factor for cardiovascular disease (e.g. coronary artery disease, hypertension).
Arachnodactyly (spiders fingers) and associated differentials
condition in which the fingers and toes are abnormally long and slender, in comparison to the palm of the hand and arch of the foot. Also, the individual’s thumbs tend to be pulled inwards towards the palm.
can also be associated with certain medical conditions. Examples include Marfan syndrome,Ehlers-Danlos syndromes,Loeys–Dietz syndrome
Finger clubbing, how to assess and differentials
Finger clubbing involves uniform soft tissue swelling of the terminal phalanx of a digit with subsequent loss of the normal angle between the nail and the nail bed. Finger clubbing is associated with several underlying disease processes, but those most likely to appear in a cardiovascular OSCE station include congenital cyanotic heart disease, infective endocarditis and atrial myxoma (very rare).
To assess for finger clubbing:
Ask the patient to place the nails of their index fingers back to back.
In a healthy individual, you should be able to observe a small diamond-shaped window (known as Schamroth’s window)
When finger clubbing develops, this window is lost.
Signs in the hand associated with endocarditis
Splinter haemorrhages: longitudinal red-brown haemorrhage under nails look like spliters. causes include trauma, infective endocarditis, sepsis, vasculitis and psoriatic nail disease
Janeway lesions: non-tender, haemorrhagic lesions that occur on the thenar and hypothenar eminences of the palms (and soles). Janeway lesions are typically associated with infective endocarditis.
Osler’s nodes: red-purple, slightly raised, tender lumps, often with a pale centre, typically found on the fingers or toes. They are typically associated with infective endocarditis
heart rate stats
60-100bpm normal
below 60 is bradycardia - associated with athletes, AV block, medication side effects, sick sinus syndrome
Above 100bpm is tachycardia - anxiety, supraventricular tachycardia, hypovolaemia, hyperthyroidism
Irregular rhythms mostly caused by atrial fibrillation
Radio-radial delay causes
Subclavian artery stenosis
aoritc dissection
Aortic coarctation
Collapsing pulse differentials
normal physiological states (pregnancy, fever)
Cardiac lesions (aortic reguritation, patent ductus arteriosus)
High output states (anaemia, arteriovenous fistula, thyrotoxicosis)
Brachial pulse characters and differentials
Normal
Slow rising - aortic stenosis
Bounding - aortic reguritation, CO2 retention
Thready - intravascular hypovolaemia in conditions like sepsis
Narrow pulse pressure and differentials
less than 25 mmHg of difference between the systolic and diastolic blood pressure. Causes include aortic stenosis, congestive heart failure and cardiac tamponade.
Wide pulse pressure and differentials
more than 100 mmHg of difference between systolic and diastolic blood pressure. Causes include aortic regurgitation and aortic dissection.
Difference in BP between arms may suggest ..
More than 20mmHg difference may suggest aortic dissection
Carotid artery Bruit differentials
carotid stenosis
radiating cardiac murmur
Raised JVP differentials
Indicates venous hypertension. causes include:
Right sided heart failure; commonly from left sided HF or pulmonary hypertension often from COPD or interstitial lung disease
Tricuspid regurgitation from infective endocarditis and rheumatic heart disease
Constrictive pericarditis: often idiopathic but possibly rheumatoid arthritis and tuberculosis causes.
Conditions associated with positive hepatojugular reflux result
Constrictive pericarditis
Right ventricular failure
Left ventricular failure
Restrictive cardiomyopathy
Eyes and CV associated problems
Conjunctival pallor: suggestive of underlying anaemia. Ask the patient to gently pull down their lower eyelid to allow you to inspect the conjunctiva.
Corneal arcus: a hazy white, grey or blue opaque ring located in the peripheral cornea, typically occurring in patients over the age of 60. In older patients, the condition is considered benign, however, its presence in patients under the age of 50 suggests underlying hypercholesterolaemia.
Xanthelasma: yellow, raised cholesterol-rich deposits around the eyes associated with hypercholesterolaemia.
Kayser-Fleischer rings: dark rings that encircle the iris associated with Wilson’s disease. The disease involves abnormal copper processing by the liver, resulting in accumulation and deposition in various tissues (including the heart where it can cause cardiomyopathy).
Mouth and associated CV problems
Central cyanosis: bluish discolouration of the lips and/or the tongue associated with hypoxaemia (e.g. a right to left cardiac shunt)
Angular stomatitis: a common inflammatory condition affecting the corners of the mouth. It has a wide range of causes including iron deficiency.
High arched palate: a feature of Marfan syndrome which is associated with mitral/aortic valve prolapse and aortic dissection.
Dental hygiene: poor dental hygiene is a risk factor for infective endocarditis.
Secondary hypertension causes mnemonic
ROPE Renal disease - most common cause Obesity Pregnancy induced and per-eclampsia Endocrine diseases such as Conns disease
Hypertension stages BP measurements
stage 1 - greater than 140/90 clinic reading and average A/HBPM above 135/85
Stage 2 - between 160/100-180/120 clinic and average A/HBPM above 150/95
Stage 3 - above 180/120
Drugs for hypertension mnemonic
ABCD Acei/A2RB e.g. ramipril or candestartan Beta blockers - bisoprolol Calcium channel blockers - amlodipine Diuretics (thiazide like) - indapamine
ECG leads and areas they show
4 limb leads: 3 of electrical significance and 1 ground lead
6 chest (V) leads:
V1 - 4th ICS to the right of the sternum
V2 - 4th ICS to left of sternum
V3 - Diagonally between V2 and 4
V4 - between ribs 5+6 in midclavicular line
V5 - Same level as V4 but in anterior axillary line
V5 - placed on same level as V4+5 but in midaxillary line
function:
V1-2: Septal leads; primarily observes ventricular septum but may display right ventricle (in 12 lead ECG)
V3-4: Anterior leads; observes anterior wall of left ventricle
V5-6: anterolateral leads; observes lateral wall of left ventricle
first degree block ECG characteristics
Normal waves but longer PR interval greater than 0.2 seconds delay between the SAN and AVN firing; usualy benign
third degree block ECG characteristics
bradycardia often dangerously slow; p wave show no relationship to QRS complex (sometimes there, sometimes not etc.) and absolute characteristic is presence of stacked P and T wave (this is how to differentiate between third degree block and second degree type 1 block!)
QRS may be normal or wide
second degree block ECG characteristics
mobitz type 1 - sometimes AVN conducts, conducts badly or not at all; this will often progress to third degree block. serious bradycardia
shows gradual prolongation of PR interval
type 2 - serious bradycardia with slow R-S complex and very exaggerated repolarisation following S-J point
may skip QRS complex entirely when purkinje fibres fail to conduct at all
Sinus tachycardia types ECG characteristics
Increased SAN firing shows good ECG but just much higher frequency
Narrow ST/supraventricular tachycardia shows only shortened QRS complex with no P waves present and exaggerated T waves
Atrial fibrillation ECG characteristics
Irregular discharge from multiple atria sites shows irregular QRS complexes; has no defined patterns and patient will have an irregular ‘tapping’ pulse also
no defined T or P waves
Ventricular tachycardia ECG characteristics
broad complex tachycardia due to discharges generated elsewhere in ventricles than the conducting system
Impulse is slow spreading, broader depolarisations; electricity travels BACKWARD in the heart and so is shown as UPSIDEDOWN on the ECG
Ventricular fibrillation ECG characteristics
uncoordinated discharges from multiple ventricular sites; no recognisable ECG trace; simple ocscillations; no identifiable P, QRS or T waves
Asystole ECG
only background baseline picked up; no traceable electrical activity (flatline)
Shockable arrhythmias
Ventricular fibrillation (helps reset cardiomyocyte activity) and PULSELESS ventricular tachycardia only!
how to diagnose acute coronary syndrome
MI and unstable angina should be suspected on basis of chest pain (and other areas of radiation) is associated with: nausea, sweating, vomiting, breathlessness or combo
haemodynamic instability (systolic BP less than 90mmHg)
of new onset or is result of abrupt deterioration of stable angina - pain occurring frequently with little/no exertion often lasting longer than 15 mins
DIAGNOSIS: need 12 lead ECG, look for pathological Q waves, left bundle branch block, ST segment and T wave abnormalities
high sensitivity troponin blood test indicates myocardial damage
ACS can be subcategorised to
ST elevation ACS:STEMI
Non-ST elevated ACS: NSTEMI and unstable angine
ACS pathology
Plaque rupture in coronary artery
Thrombosis
Inflammation
All causing decreased O2 delivery eventually causing myocardial death/infarction
ACS presentation SOCRATES
Site: Chest pain Onset: sudden new onset or deterioration of stable angina Character: usually tight/heavy Radiating: arms/neck/jaw Associated symptoms: nausea and vomiting, sweating, breathlessness, S4 present, cold pallor, 3rd heart sound and pansystolic murmur (HF). haemodynamic instability Timing: lasting longer than 15 minutes Exacerbating/alleviating factors: none Severity: bad
ACS immediate management
MONCAC
Morphine: 10mg in 10ml slow IV: titrate to pain (+metoclopramide IV)
Oxygen: if sats are below 94% (or between 88-92% in COPD)
Nitrates: sublingual GTN (2 sprays) if not hypotensive
Aspirin: 300mg loading dose and 75mg for life
Clopidogrel: 300-600mg loading dose then 75mg for year
managing hyperglycemia in ACS patients within 48 hours
Keep blood glucose levels below 11mmol/L while avoiding hypoglycemia
Consider dose adjusted insulin infusion with regular blood glucose monitoring
Do not offer this unless clinically indicated
always offer hyperglycemia patients HbA1c level tests before discharge and fasting BG levels 4 days post ACS onset (don’t delay discharge though)
inform GPs of annual HbA1c monitoring if needed and FBC levels
Unstable angina test results
Coronary lumen not fully occluded. No necrosis No troponin Normal ECG at rest Stenosis seen in angiogram
STEMI and NSTEMI test results
NSTEMI: Even if lumen is closed, limited necrosis Increased troponin No ST elevation STEMI: Coronary lumen fully occluded Deep and extensive necrosis Increased troponin ST elevation New onset LBBB (left bundle branch block) Needs urgent coronary revascularization
MI definition
detection and/or rise in cardiac biomarker (preferrably troponin) with at least one of the following:
symptoms of ischaemia
new or significant ST segment or T wave changes or new LBBB
pathological Q waves
imaging evidence of new loss of viable myocardium
identification of intracoronary thrombus by angiography
