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
Silent ACS
common in elderly or diabetic patients Signs include: Pulmonary oedema Epigastric pain and vomiting Post-operative hypotension or oliguria Syncope, acute confusion Stroke Diabetic hyperglycaemic states
Classifications of MI
type 1 - spontaneous: plaque rupture type 2 - secondary to ischaemia: common in hospitals or stable CAD patients with or without history or PCI or CABG type 3 - post mortem dianosis type 4 - A: related to PCI B: related to stent thrombosis type 5 - related to CABG
MI complications
Cardiac arrest brady/tachyarrhythmias LVHF RVF Pericarditis Systemic embolism Cardiac tamponade Mitral regurgitation (papillary muscle dysfunction) Ventricular septal defects Late malignant ventricular arrhythmias (1-3 weeks after MI) Dressler’s syndrome (1-3 weeks post MI; inflammatory condition) Left ventricular aneurysm
Post MI lifestyle changes
Mediterranean style diet (fruit, bread, vegetables and fish; less meat) and replace butter/cheese with plant oil based foods
Physical activity for 20-30 minutes every day to slight breathlessness. Start gradually and build up if needed
Stop smoking advice is needed
Post MI drug therapy
ACEi: titrate dose upwards at short intervals (every 12-24 hours) before leaving hospital until max tolerance/target dose is reached. Or complete within 4-6 weeks discharge
Dual antiplatelet therapy (aspirin plus second antiplatelet)
Beta blocker: communicate plans of titrating beta blockers up to max tolerance/target dose
Statin
Offer left ventricular function assessment
STEMI management
initial ACS emergency management (O2, vitals check, loading dose, ECG, troponin, FBC, BP)
Gold standard is PCI within 90 minutes. PCI is still beneficial up to 12 hours post pain onset
Clopidogrel 75mg post 1 year
Aspirin 75mg for life
Thrombolysis is not favoured treatment - risk of bleeding too high
NSTEMI and unstable angina management
Initial management of ACS (vitals; BP, O2 sats, ECG etc)
Further management: Confirm NSTEMI with serial troponin measurement first:
Beta blockade (or alternative rate-limiting agent if contraindicated – aim HR of 50-60 bpm)
ACE inhibitor (unless contraindicated – aim for a systolic blood pressure of 120 mmHg or less)
Atorvastatin 80mg OD
Clopidogrel 75mg 1 year post MI
Aspirin 75mg for life
Use GRACE scoring to assess benefits of invasive angiography (+/- PCI) when predictive 6 month mortality score is 3.0% or more; or is less than this but patient experiences subsequent ischaemia
take into account; renal function; bleeding risk and co-morbidities
Assess left ventricular function
Manage CV risk factors
Cardiogenic shock
Circulatory failure resulting in inadequate organ perfusion OR
Hypotension (systolic BP below 90mmHg) with evidence of hypoperfusion (mottled skin, reduced urine output above 0.5mL/kg/h, elevated serum lactate above 2mmol/L)
signs of cardiogenic shock
GCS increased Cold pallor Cold peripheries Tachycardia Slow capillary refill longer than 2seconds Tachypnoea - abnormally rapid breathing Oliguria - urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults May occur suddenly or gradual onset
Cardiogenic shock causes
MI Arrhythmias Myocarditis, myocardial depression (drugs, hypoxia, acidosis, sepsis) Valve destruction (endocarditis) PE Tension pneumothorax Cardiac tamponade Aortic dissection
types of shock
Low CO2:
Hypovolaemia: haemorrhagic shock from trauma; fluid loss/dehydration; vomiting, burns etc.
Pump failure: cardiogenic shock; obstructive/secondary causes eg PE, tension pneumothorax, cardiac tamponade
Low SVR, distributive shock:
Sepsis: infection, inflammatory cytokines leads to vasodilation
Anaphylaxis
Neurogenic: spinal cord injury, epidural or spinal anaesthesia
Endocrine failure: addison’s disease, hypothyroidism
Drugs: anaesthetics, antihypertensives, cyanide poisoning
Stages of shock from blood loss
Initial stage - cardiac output (CO) is decreased, and tissue perfusion is threatened.
Compensatory - Almost immediately, the compensatory stage begins as the body’s homeostatic mechanisms attempt to maintain CO, blood pressure, and tissue perfusion.
Progressive - The compensatory mechanisms begin failing to meet tissue metabolic needs, and the shock cycle is perpetuated.
Refractory - at around 50% blood loss Shock becomes unresponsive to therapy and is considered irreversible.
Cardiogenic shock investigations
FBC Serum creatinine and electrolytes Blood glucose Liver biochem Coagulation Blood gasses ECG
Cardiogenic shock management
Oxygenation and ventilation: maintain airway; give oxygen; monitor RR, blood gasses and CXR
Diamorphine 1.25-5mg for pain and anxiety
Restore CO and BP: lay patient flat/head down; give fluids via IV; vasodilators; monitor skin pallor, pulse, BP, urine output, ECG
Treat underlying cause: haemorrhage, sepsis, anaphylaxis
Treat complications: coagulopathy, acute kidney injury etc.
ACS investigations
ECG FBC troponin CXR Angiography U+E's Left ventricular function assessment
IHD pathology
Atherosclerosis makes the arteries narrow and the organs ischaemic, demanding heart to work harder due to imbalance of oxygen supply to cardiac demand
SUPPLY decrease;
DEMAND increase
IHD treatent
Heart transplant
Artificial heart? Don’t work as well
PREVENTION better than treatment; including controlling diabetes and hypertension (if present)
IHD diagnosis
Coronary angiography to visualise the artery occlusions
Retrograde route easy access to inject dye into arteries
IHD causes
Supply (O2) decrease:
Atherosclerosis
Coronary artery thrombosis
Coronary spasm
Severe anaemia
Tachyarrhythmias
Rarely; arteritis eg polyarteritis - inflammation of arteries causing occlusion
Demand increase (myocardium):
Myocardial hypertrophy (from hypertension, aortic stenosis etc.)
Thyrotoxicosis - excess of thyroid hormones in the bloodstream increases resting HR increasing work
Exercise, anxiousness temporarily increase demand
Angina pectoris and symptoms
Angina pectoris - chest pain arising from heart as result of myocardial ischaemia
atheroma/plaque on coronary lumen causing stenosis and fixed reduced blood flow through the vessel. Despite this, at rest, patient has no symptoms
Classic exertional angina symptoms:
Central, crushing, retrosternal chest pain
Onset following exertion
Relieved by rest or GTN (Nitroglycerin) within few minutes
Exacerbated by cold weather, anger, excitement or heavy meals
Radiates to arm and neck
Angina pectoris variations
Decubitus angina - occurs lying down
Nocturnal angina - at night; may cause to wake up
Varitant (Prinzmetals) angina - caused by CA spasm pain occurs without provocation usually at rest
Unstable angina - increases rapidly in severity, occurs at rest, recent onset (less than 1 month pain history)
Cardiac syndrome X, microvascular angina - angina symptoms, positive exercise test (Stress test) and normal coronary arteries on angiogram. Thought to result from functional abnormalities of coronary microcirculation
Complications of stable angina
ACS: MI
Diagnosis of stable angina
Clinical history - typical angina features
Physical examination - can be normal as will be at rest
ECG may show ST depression, T wave flattening/inversion at rest
Stress ECG test; usually positive but does not exclude diagnosis
Blood tests; FBC; U&E; TFTs (thyroid functioning tests); lipids; HbA1c (serum glucose marker over last 2-3 months)
Echocardiography; CXR (chest X ray)
to determine severity:
CT-angiography
functional imaging of the heart: myocardial perfusion scan; stress echo; cardiac MRI (CMR)
transcatheter angiography (+/- PCI) can pair with stenting or balloon if inconclusive
Stable angina management
Symptom relief; GTN (glyceryl trinitrate) in spray or sublingual tablets; PRN (means as necessary)
Prevention of deterioration; control exacerbating factors; anaemia, tachycardia, thyrotoxicosis. Control risk factors; smoking, exercise, diet, hypertension, diabetes etc.
Aspirin or if contraindicated; clopidogrel to prevent clotting
Medication; beta blockers (atenolol) or calcium antagonists (amlodipine)
Invasive treatment; when symptoms persist or worsen; PCI or coronary artery bypass grafting (CABG)
Patients with stable angina should be advised:
Stop what they are doing and rest.
Use GTN spray or tablets as instructed.
Take a 2nd dose of GTN after 5 min if the pain has not eased.
Take a 3rd dose of GTN after a further 5 min if the pain has still not eased.
Call 999/112/911 for an ambulance
if the pain has not eased after another 5 min (i.e. 15 min after onset of pain),
or earlier if the pain is intensifying
or earlier if the person is unwell ie vomiting, pale, sweaty
Prinzmetals variant angina and risk factors
Pathology:
Angina from coronary artery spasm can occur in normal (angio) arteries
Risk factors:
Smoking
Triggers; drugs (cocaine, amphetamine, marijuana); low magnesium and instrumentation (eg during angiography
Prinzmetals variant angina presentation and investigations/diagnosis
Presentation: Pain at rest Resolves rapidly with short acting nitrates eg GTN diagnosis: ECG: During pain; ST elevation Normal at rest *ST elevation like in STEMI, but this is NOT and ACS!* CT-angiography Functional imaging Transcatheter angiography *similar to stable angina; but no stenosis in coronaries*
Prinzmetals variant angina mx
Avoiding triggers
Symptomatic drug relief as needed (PRN); GTN; CCB; long acting nitrates (isosorbide)
Heart sounds
S1 - louder and longer sound: closing of the AV valves at the start of ventricular systole
S2 - shorter and sharper sound: closing of semilunar valves at the start of ventricular diastole
S3 - roughly 0.1 seconds post S2; very subtle; sounds like a faint woooooshy sound. Caused by rapid ventricular filling, causing chordae tendinae to pull to full length and ‘twang’. Common in young patients 14-40 but may be pathological in elderly patients due to their chordae tendinae being weaker and stiffer; causing a LUB - DE DUB sound.
S4 - always pathological and very rare; heard directly before S1; indicates hypertrophic ventricle; caused by turbulent flow in the atria of blood flowing into a non-compliant ventricle; sounds like LE LUB - DUB
SCRIPT - diagnosing murmurs
Site - where is the murmur loudest
Character - soft? Blowing? Crescendo? decrescendo?
Radiation - into the carotids (aortic stenosis)? Axilla (mitral regurgitation)?
Intensity - grade of murmur: probably grade 2 or 3.
Pitch - high? Low? Grumbling? : indicates velocity
Timing - systolic (between S1-2: AS or MR) /diastolic (between S2-1: MS or AR)
Grade of murmus
Grade 1: difficult to hear
Grade 2: quiet
Grade 3: easy to hear
Grade 4: easy to hear with palpable thrill
Grade 5: hear with stethoscope barely touching chest
Grade 6: hear with stethoscope off of chest
Murmur investigations
severity is assessed by Doppler echocardiography, which measures the direction and velocity of blood flow and allows a calculation to be made of the pressure across a stenotic valve.
Doppler shows more physiological changes
TEE (transesophageal echocardiogram) transducer (a unit that directs the sound waves) is placed in the esophagus closer to the heart with no bony elements in the way giving better picture of the heart, MRI or invasive cardiac catheterisation (taking X-rays of the heart’s arteries (coronary arteries) using a technique called coronary angiography or arteriography) usually used to assess complex situations
Phonocardiogram - shows placement of sounds giving clear indication of where murmur lies
Murmur treatments
Surgery: valve replacement valve repair valvotomy (fused cusps of stenotic valve Surgical timing cannot be delayed as this increases irreversible damage to myocardial tissue
Mitral stenosis causes and complications
Cause:
Infective endocarditis
Acute rheumatic fever in childhood (most common)
Primarily affects women
Complications:
Chronic heart failure
Secondary pulmonary hypertension
Majority will suffer atrial fibrillation arrhythmia also. Mostly affects left atira, leads to irreversible changes in myocardium when heart can no longer compensate (lungs increase tenacity resulting in stiffer vessels over time etc.)
Mitral stenosis
Thickening and immobility of the Mitral leaflets leads to obstruction of blood flow resulting in an increase in LA pressure and dilation.
LA dilation/Enlargement can lead to Atrial fibrillation.
Chronically-elevated LA pressure leads to an increase in pulmonary capillary pressure and chronic pulmonary oedema.
Signs and symptoms of mitral stenosis
Exertional dyspnoea; progressively more severe
Cough with blood-tinged sputum
Atrial fibrillation and precipitate pulmonary oedema
pulmonary hypertension - fatigue and lower limb oedema
Cardiac failure
Malar flush
irregular pulse (AF)
Tapping apex beat (palpable S1 and LV backward
displacement from enlarging RV)
Mitral stenosis investigations and diagnosis
Auscultation at apex: loud tapping S1; opening snap and rumbling mid-diastolic murmur. Loud LUB - DUB Duuuuur sound.
can palpate
CXR shows enlarged LA, pulmonary venous hypertension and calcified mitral valve, pulmonary oedema (severe)
ECG shows AF; P mitrale
right ventricular hypertrophy pattern
Echo confirms diagnosis and assesses severity
Mitral stenosis management
General treatment is often not required for mild mitral stenosis.
Complications are treated medically: (e.g.)
β-blockers/Digoxin for atrial fibrillation
Anticoagulation for atrial fibrillation (to prevent clot formation and embolization)
Diuretics for heart failure
Surgery and Specific Mechanical relief of the mitral stenosis is indicated if symptoms are severe or if pulmonary hypertension develops
Mitral regurgitation and causes
During systole valve doesnt fully close leading to backflow of blood
Causes:
Valve leaflet malfunction
Most commonly via idiopathic deterioration with age
Dilation of ring (LV dilation)
Rupture of chordae tendineae or papillary muscle (occurs in bacterial endocarditis, MI when myocardial death occurs)
Rheumatic heart disease
Mitral valve prolapse
Infective endocarditis
Ruptured chordae tendineae
Ruptured papillary muscle
Dilating left ventricle disease casuing functional MR
Hypertrophic cardiomyopathy
Rarely - systemic lupus erythematsus, marfans syndrome
Mitral regurgitation signs and symptoms
symptoms:
Acute MR - pulmonary oedema
Chronic regurgitation - exertional dyspnoea, fatigure and lethargy from reduced CO
Right heart failure; congestive heart failure
signs:
displaced apex beat; S1 is soft
pansystolic murmur palpated as thrill
radiates to axilla
S3 often present
high pitched whistling murmur BUUUUURRRRRRR sound
mitral regurgitation investigations
Echocardiography can establish the aetiology and haemodynamic consequences of MR.
Doppler and colour flow Doppler is used to measure the severity of mitral regurgitation (Chest X-ray and ECG changes are NOT sensitive or specific for the diagnosis of mitral regurgitation.)
Mitral regurgitation management
Mild MR, in the absence of symptoms following the patient with serial echocardiograms every 1–5 years (depending on the severity)
Diurectics or ACEi
Surgery (mitral valve replacement or repair) if severe symptoms such as left ventricular dysfunction (ventricular dilatation or reduced ejection fraction)
Mitral valve prolapse
Aka: Click-murmur syndrome - Barlow’s syndrome - Floppy valve syndrome
During systole, under pressure of LV contraction, mitral valves bulge (prolapse) upward into the LA. [but blood regurgitation into the LA is zero or minimal]. Not well understood and aetiology differs for individuals.
Many times the mitral valve is abnormally thickened (degenerated). Valves are floppier than usual.
For unknown reasons MVP patients tend to have lower BMI and are typically leaner
Most common valvular abnormality (5%)
Usually occurs alone or with other pathologies such as: atrial septal defect; patient ductus arteriosus; cardiomyopathies; turners syndrome; marfans syndrome
Mitral valve prolapse signs and symptoms
Symptoms
Usually Asymptomatic [diagnosed on an incidental finding during echo]
May have atypical chest pain, palpitations, autonomic dysfunction symptoms (dizziness)
Signs
Mid-systolic click
and/or Late systolic murmur [due to regurgitation]. Some have one or the other.
SOUNDS: LUB DU DUUUUURR - DUB
Mitral valve prolapse complications
Mitral Regurgitation, cerebral emboli, arrhythmias, Endocarditis sudden death
Mitral valve prolapse investigations and treatment
Best heard in apex beat using diaphragm of stethoscope
echocardiogram
treatment:
beta blockers for symptomatic patients to help palpitations and reduce heart work
Severe may need surgery
Aortic stenosis and causes
Obstruction to left ventricular emptying results in left ventricular hypertrophy (LVH).
In turn, this results in increased myocardial oxygen demand, relative ischaemia of the myocardium and consequent Angina, Arrhythmias and eventually Left Ventricular Failure and CHF.
causes
Calcification of the aortic valve, usually after age 65 (idiopathic)
Congenital Bicuspid Aortic Valve»_space; AS in adulthood, from age 40; only two valves present in tricuspid valve leading to too smaller lumen and stenosis
Rheumatic fever
Aortic stenosis signs and symptoms
Exertional Dyspnoea • Exertional chest pain • Exertional dizziness or syncope • rarely >> Sudden Cardiac Death Signs Slow rising pulse Narrow pulse pressure* pulse pressure is the difference between sys and diastole (represents the force the heart generates each contraction) Left Ventricular heave Ejection systolic murmur - high pitched Murmur will Radiates to carotid Crescendo-decrescendo murmur Systolic murmur best heard in right 2nd ICS radiating to the neck Left ventricular hypertrophy LVH Low CO; exertional dyspnoea BUUUUR - DUB sound
Aortic stenosis investigations and treatment
Investigations: ECG may show LVH Echocardiogram to show LV function, valve structure, severity of stenosis Coronary angiogram to assess for CAD MANAGEMENT: If mild; follow up; medications Aortic valve surgery: Indicted if severe stenosis: valve area above 0.6cm Symptomatic Left ventricular dysfunction Episodes of ventricular tachycardia Undergoing other cardiac surgery
Aortic regurgitation, causes and compilcations
Aetiology
Aortic regurgitation results from /either disease of the valve cusps /or dilatation of the aortic root and valve ring.
Causes:
Rheumatic fever
Infective endocarditis complicating an already- damaged valve.
Complications:
Heart failure
Austin flint murmur (low pitched rumbling) heard in apex
Aortic regurgitation signs and symptoms
A ‘collapsing’ (water-hammer) pulse with wide pulse pressure is pathognomonic.
A blowing early diastolic murmur is heard at the left sternal edge/border in the fourth intercostal space.
LUB - TAAAAR sound: normal S1 with dragging S2 ‘taaar’ sound
Highly associated with CORRIGAN’S PULSE/ aka COLLAPSING PULSE
Aortic regurgitation investigations and management
CXR: larger heart dilation of ascending aorta
ECG: left ventricular hypertrophy
Echocardiography with doppler exam of aortic valve estimates severity
Early diastolic murmur best heard in held expiration at lower sternal edge
management:
Mild symptoms may respond to the reduction of afterload with Vasodilators and Diuretics.
Surgery: AV replacement
Right sided heart valve failure and causes
TR; TS; PR; PS these are uncommon diseases
Causes:
80% Functional cause ie RV dilatation; eg due to chronic pulmonary hypertension
PE causes chronic pulmonary hypertension, severe RV failure, dilation of RV, dilation of Tricuspid Ring resulting in TR
Much less common causes:
Rheumatic Heart Disease
Infective endocarditis (IV-drug abusers)
Carcinoid syndrome
Congenital eg ASD (Atrial Septal Defect), (Atrio-ventricular) AV canal, Ebstein’s anomaly (downward displacement of the tricuspid valve, highly dilated RA and TR; atrial septum defect causing R to L blood shunt)
Drugs eg ergot-derived dopamine agonists [Bromocriptine, Cabergoline for Parkinson’s disease]
Right sided valve failure signs and symptoms
Symptoms
Fatigue
Hepatic pain on exertion (due to hepatic congestion)
Ascites, Oedema
Signs
High JVP (Jugular vein engorgement)
Giant v waves in JVP (produced by the regurgitant jet, through the tricuspid valve, in systole)
RV heave
Pansystolic murmur»_space; heard best at lower sternal edge, in inspiration
Pulsatile Hepatomegaly, in systole
Jaundice, Ascites, severe peripheral Oedema
Right sided valve failure management
Diuretics for systemic congestion to improve the signs
Drugs to treat underlying cause
Valve repair or replacement »_space; 10% mortality in 1 month! Very risky but very necessary for severe cases.
TR resulting from myocardial dysfunction or dilatation»_space; has a mortality of up to 50% at 5 yrs.
[10% from surgery vs 50% from no surgery!]
Tricuspid stenosis causes
Main cause is Rheumatic Fever, almost always; MS + AR + TS
Congenital valve problem
Infective Endocarditis
tricuspid stenosis signs and symptoms
Symptoms: Fatigue Ascites Oedema Signs Giant a wave and slow y descent in JVP Opening Snap Early diastolic murmur, heard at the left sternal edge in inspiration
Tricuspid stenosis diagnosis and management
Diagnosis: Echocardiogram Treatment Diuretics Surgical repair
Pulmonary stenosis causes
congenital (turners syndrome; presents in specific patterns)
Acquired: Rheumatic fever, carcinoid syndrome
Pulmonary stenosis signs and symptoms
Symptoms: Dyspnoea Fatigue Oedema Ascites Syncope Signs Dysmorphic facies (congenital syndromes) prominent a wave in JVP RV heave Ejection Click, Ejection Systolic Murmur (which radiates to the left shoulder); widely split S2
Pulmonary stenosis investigations and management
Tests
ECG: RAD (Right Axis Deviation), P- pulmonale, RVH, RBBB
Echocardiogram (TTE)/TOE
CXR: prominent pulmonary arteries, caused by post-stenotic dilatation.
Cardiac catheterization is diagnostic.
Treatment: Pulmonary Valvuloplasty or Valvotomy
Pulmonary regurgitation causes
Any cause of pulmonary hypertension causes dilatation of the valve ring. Sometimes, Endocarditis usually in IV-drug abusers
Pulmonary regurgitation signs and management
Signs: Decrescendo Early Diastolic Murmur, at the left sternal edge (Graham–Steell murmur), similar to that of aortic regurgitation Treatment Usually there are no symptoms Treatment is rarely required;
ACS investigations
12 lead ECG and continuous cardiac monitoring
Bloods: U+E’s; FBC; LFTs; CRP; glucose and cardiac enzymes (troponin). Take troponin immediately; then again 10-12 hours post pain onset.
CXR
causes of arrhythmias
CHD Heart valve diseases Hypertension Ageing Cardiomyopathy Congenital abnormalities Medications Hyperthyroidism
Symptoms of arrhythmias
are often asymptomatic: Palpitations Dizziness and syncope Dyspnoea (shortness of breath) Chest pains
Arrhythmia investigations
Clinical history and physical assessment of patients
12 lead ECG
Ambulatory ECG - walking about for a day in normal activities
Exercise/stress ECG
Management of arrhythmia’s
Medication depending on type Catheter destruction (ablation) Cardioversion Artificial pacemakers Implantable cardioverter defibrillators ICDs
Tachycardia broad types
Increased automaticity:
Stimulation of sympathetic pathways can increase.
Found in exercise
Anxiety
Ectopic firing in some conditions like atrial fibrillation
Triggered activity:
Abnormal action potentials triggered by normal APs
Affects any part of system
Following normal depolarisation is several arrhythmic events: early after-depolarisation
Can occur also once normal AP is nearly re-polarised; called delayed afterdepolarization
Caused by mismatched AP firing throughout conduction tissues (some AP travel too slow and end up ‘re-exciting’ myocardium after the ‘fast’ conduction has already depolarised). For example these ‘reentry circuits’ can form and cause atrial fibrillation or flutter.
Bradycardia broad types
Reduced automaticity (reduced firing of SAN)
Increase in vagal tone decreases HR.
Found in athletes
While sleeping
Some medications reduce SAN firing
Some diseases also cause this
Conduction block
Block of conduction anywhere along the conduction system
In cases of specific left or right bundle branch blockages; doesn’t always result in bradycardia as contractions still delivered to rest of the heart in time via alternate branch
Atrial fibrillation
Most common arrhythmia.
Irregular, chaotic
Caused by ectopic foci or single localised reentry circuit
Most often occurs in LA which is where there is such high risk of stroke
Arises from atrium at rate of 300-600bpm
AVN conducts small proportion of these atrial impulses leading to irregular ventricular rhythm and HR
AF causes and risk factors
Causes: remember it affects Mrs SMITH Sepsis Mitral valve pathologies (stenosis/regurgitation) Ischaemic heart disease Thyrotoxicosis Hypertension
also caused by:
Coronary heart disease
Hyperthyroidism
Risk factors: Complication of CHD Valve problems Hyperthyroidism Pneumonia PE Obesity Alcohol Lung cancer Caffeine
AF presentation
Dyspnoea Palpitations Syncope and dizziness Chest discomfort Stroke/transient ischaemic attack (TIA): due to blood stasis in atria increasing likelihood of clot formation
Types of AF
Paroxysmal:
Lasting less than 7 days then restores to sinus rhythm
Each episode onset is sudden and will stop suddenly also (usually around 2 days)
Period between episodes varies
Persistent:
Lasting longer than 7 days but can still restore to sinus rhythm
Can be reverted back to normal rhythm with treatment
Likely to come back intermittently
Permanent:
Cannot be restored to sinus rhythm; HR is slowed but rhythm remains irregular
Due to progressive damage and change to morphology in atria creating atrial circuits and multiple ectopic sites increasing risk of AF occuring
AF investigations
Clinical examination: pulse irregularity ECG; absent P waves; variable R-R intervals; f-waves (fibulatory) instead of baseline; narrow QRS complex May require ambulatory ECG if arrhythmia is paroxysmal FBC Thyroid function tests (TFT) Renal function Electrolytes CXR Echocardiogram
AF management
Hospital admission if signs of HF or deteriorating condition
Routine referral for stable but uncertain how to treat patients under 50
Acute: IV metaprolol (beta blocker), cardioversion, IV amioderone
Rate control: beta blockers, CCBs or digoxin to slow HR
Rhythm control: preferred in recent AF onset or irreversible cause identified. Cardioversion. Amiodarone therapy.
Ablation: remove ectopic sites
Thromboprophylaxis: asses stroke, bleeding risk and monitor and modify as needed. Anticoagulation drugs to those with CHA2DS2VASc score of 2 or more
AF complications
Stroke
Thromboembolism
Heart failure
Tachycardia-induced cardiomyopathy and ischaemia
Assessing stroke risk
CHA2DS2-VASc to assess a patients risk for having a stroke
Factors are each worth one point; added and evaluated for risk potential
Then using HAS-BLED assess the pts risk of bleeding and weigh these two scores up to decide if the pt would benefit from anticoagulants (high stroke low bleed risk) or would be more at risk (less stroke vs bleed risk) from anticoagulant treatment
Atrial flutter and management
Similar to and often associated with AF with atrial contractions around 300bpm but ventricles unable to keep up so AVN conducts ever second beat around 75-150bpm
ECG shows a sawtooth pattern
Narrow complex tachycardia at 150 bpm (range 130-170)? Yes -> Suspect flutter!
Turn the ECG upside down and scrutinise the inferior leads (II, III + aVF) for flutter waves.
management:
similar management to AF
First degree block
PR interval greater than 0.2seconds
Each atrial activation leads to ventricular activation (1:1 ratio); P wave always conducted
Caused by conduction system impairment
Usually asymptomatic; found incidentally on ECG
Investigations/treatment not required if patient is asymptomatic
When due to AV nodal disease; usually benign and good long term prognosis
When due to His-Purkinje abnormalities are likely to progress to 3rd degree block
Second degree block type one
Prolonged PR interval
intermittent conduction failure of atria to ventricles
Causes dropped beats (2:1 or 3:1)
Usually associated with cardiac pathology
Type I Mobitz type: progressive prolongation of PR following atrial impulse; atrial impulse fails to conduct to ventricles and ventricular impulse is dropped; QRS complex is normal width
second degree block type two
Type II: intermittent conduction failure to ventricles; PR interval is constant; often due to bundle of His or bundle branches failure; QRS complex may be wider than normal; often progresses to 3rd degree block; also associated with stokes-adams attacks (syncope caused by slow ventricular rate); needs 24 hour ECG monitoring; pacemaker may be needed
Third degree block
Complete heart block/failure to transmit from atria to ventricles
P waves occur from atrial contraction (75bpm) but have no relation to QRS complex
Ventricular rhythm is ‘slow escape rhythm’ originating below block site at rate of 30-50bpm
Can occur at AVN or His-Purkinje system and this determines rate of QRS complex
May occur as result of MI or second degree block
P/T wave stacking is solid indicator of third degree block
Management:
Cardiology referral
Tropine and temporary pacing wire
Permanent pacemaker - CHB is most common indicator for pacemaker
Bundle branch blocks
Wide QRS complex (more than 0.12s) with unusual shape
Shape depends on which bundle is blocked
can be either left or right BB
RBBB
Sometimes occurs in healthy individuals (physiological not pathological)
Can be caused by PE, ischaemic heart disease or right ventricular hypertrophy
Activation of right ventricle is delayed slowing conduction from the left to right
Results in prolonged QRS complex
Secondary R wave in V1+2 (M shape)
T wave inversion (leads I and V6)
Deep, slurred S wave in leads I and V6
WilliaM MarroW there’s a W in V1 and M in V6 of LBBB
And there’s an M in V1 and W in V6 in RBBB
RBBB causes
ischaemic heart disease rheumatic heart disease right ventricular hypertrophy PE cardiomyopathy myocarditis congential heat disease degenerative conduction system disease
LBBB causes
ischaemic heart disease anterior myocardial infarction hypertension aortic stenosis dilated cardiomyopathy primary fibrosis of conducting system hyperkalaemia digoxin toxicity
LBBB
Indicated underlying cardiac pathology; aortic stenosis; hypertension and severe CAD
Interventricular septum conduction is slowed (activated by left branch) causing activation to start form the right bundle branch
Causes prolonged QRS
Q waves
Secondary R waves in left ventricular leads I; V4,5+6 (M shape)
Left axis deviation may be seen
WilliaM MarroW there’s a W in V1 and M in V6 of LBBB
And there’s an M in V1 and W in V6 in RBBB
Ventricular tachycardia
is an uncommon arrhythmia. The ventricles beat faster than normal (between 120 and 200 bpm). The rate in the atria is normal. There is a trigger of electrical impulses somewhere in the ventricles which overrides the normal impulses coming down from the atria.
Paroxysmal supraventricular tachycardias
Also known as AV junctional tachycardias
Often in young patients with no structural heart disease
Present between ages of 12-30 years
In both types the AVN is essential component of re-entry circuit
AV nodal reentrant tachycardias
Most common type of SVT - HT 100-250bpm
Twice as common in women
Sudden onset palpitations
Anxiety
Shortness of breath
Sometimes precipitated by caffeine, alcohol and exercise but often idiopathic
Commonly benign needing no treatment
Caused by presence of two functionally and anatomically distinct pathways of conduction within the AVN
One is fast conducting and the other is slow
One acts as an antegrade (forward from atria to ventricles) limb of reentrant circuit while other acts as retrograde (ventricles to atria) limb.
ECG findings: tachycardia, regular rhythm, narrow QRS, P waves may be hidden within QRS complex
AV reentrant tachycardia
type of SVT Caused by an accessory circuit not involving the AVN. Pathway is outside of the AVN
Circuit is comprised of the AVN; His bundle; ventricles and then back to the AVN via abnormal accessory pathway (retrograde)
Usually congenital; wolff-parkinson-white syndrome is the most well known form
Presents in young patients
ECG findings: tachycardia, regular rhythm; P waves visible between QRS complexes and T waves
Paroxysmal supraventricular tachycardias investigations
ECG; presence of pre-excitation (WPW pattern) defined as short PR interval (less than 0.12s) and presence of delta wave
Ambulatory ECG
Exercise ECG
Cardiac enzymes: if chest pain in patients with risk of MI
Electrolytes - underlying cause
FBC - anaemia contributing?
TFTs
Digoxin can cause PSVT - check medical history
CXR - rule out PE, pneumonia; associated with PSVT
echocardiogram
Paroxysmal supraventricular tachycardia management
Many cases stop on their own and need no treatment
Non pharmacological first line for stable patients: vagal stimulation required; valsalva manoeuvre - patient blows against resistance (closed glottis) into syringe for 15 seconds. Carotid sinus massage - massage carotid artery at thyroid cartilage level. Putting their face into cold water may also stop this (diving reflex causing bradycardia).
If unsuccessful: IV adenosine 6mg then 12mg (if unsuccessful) or an alternative such as verapamil
Electric shock treatment may be used
All patients should be referred to cardiologists for further investigations or treatments (such as ablation of accessory pathways, beta blockers, verapamil, diltiazem therapy etc.)
Ectopic beats overview
Extra heartbeats occurring out of sinus rhythm. Also called extrasystoles
Usually benign
Occur due to electrical activity not conducting through normal channels.
Can be either atrial or ventricular origin
Often asymptomatic; but may complain of ‘missing’ beats, experiencing ‘extra’ beats or ‘heavy’ beats
Can occur in healthy individuals or in cardiac disease such as CAD or MIs
Treated with beta blockers
Treatment of underlying condition
ECG shows variation of waves
For example non-sinus P waves followed by normal QRS
Or a wide QRS (above 0.12s) and absent P waves
atrial ectopic: narrow QRS ± preceding ectopic P wave (resets the P wave cycle)
ventricular ectopic: abnormal broad QRS at abnormal time (doesn’t affect the SA node so next P wave occurs at predicted time)
Ventricular tachycardia
Usually occurs in patients with CAD or cardiomyopathies
Most common cause of broad complex tachycardia - if in doubt as to weather its VT or SVT; treat as VT to be safe
May cause haemodynamic compromise
Frequently degenerates into ventricular fibrillation
ECG: rate usually 120bpm; broad QRS
May be monomorphic: regular rhythm originating from single focus. Each QRS will be identical or similar in morphology
May be polymorphic: variation in QRS complexes and irregular rhythm.
Non-sustained VT is a run of tachycardia of less than 30 seconds; longer duration is needed to be described as sustained VT
VT management
If BP is less than 90; DC cardioversion is needed
If VT is tolerated then IV amiodarone can be administered
Electrolytes abnormalities eg hypokalaemia must be corrected
Implantable cardiac defibrillator may be considered
Torsades de pointes
Specific type of polymorphic VT associated with long QT syndrome; inherited condition where heart muscle takes longer to recharger between beats
ECG shows rapid broad complexes appearing to twist around baseline; when it does should sinus rhythm there is typically a prolonged QT interval
Typically non-sustained but may degenerate into VF and cardiac arrest.
Management:
IV magnesium to all patients
Treatment is directed at underlying cause; long QT syndrome may need implantable cardiac defibrillator
Ventricular fibrillation
Most serious rhythm disturbance
Electrical activity is disordered and rapid
No mechanical effect - reduced CO and SV
No obvious atrial activity: broad and irregular QRS complex
VF causes
Associated with CAD, MI or ischaemia, tension pneumothorax, PE, aspiration, seizure, stroke, electric shock, drowning, sepsis some drugs
VF management
Medical emergency
CPR
Only effective treatment is electrical defibrillation and any treatment of other reversible causes
In the absence of identifiable reversible cause patients are at high risk of sudden death and implantable cardioverter-defibrillators are first line of therapy
Sick sinus syndrome
SAN becomes damaged. The heart then tends to beat slowly or miss a few beats. But, in some cases, the heart alternates between beating slowly for a while and then fast for a while.
infective endocarditis
infection affecting endocardium; usually involving heart valves
in UK occurs in 20 million per year
most common valve is mitral valve; in IV drug users it the tricuspid valve
bacterial endocarditis
Endocarditis occurs when there is presence of organisms, in this case bacteria, in the bloodstream and the presence of abnormal cardiac endothelium facilitates their adherence and growth. The vegetation is formed from fibrin, platelets and bacteria. The bacteria then destroy the valve. Additionally, the heart valves have a limited blood supply and consequently white blood cells cannot reach the valves easily, making them vulnerable to infection. This process results in valvular regurgitation and worsening heart failure.
Strep. Viridans are the most common causative organism; often results in sub-acute disease.
In IV drug users staph. Aureus (gram +ve commensal bacterium known to asymptomatically colonized skin) is most common causative. This is due to bacteria going straight into the bloodstream from the skin coming into contact with the tricuspid valve first. This is also most common skin colonising bacteria
Endocarditis acute symptoms
severe febrile illness prominent/changing heart murmur Fever Cardiac damage Extracardiac sites involved by hematogenous spread: subconjunctival haemorrhages, cerebral emboli, Roth’s spots of fundi, petechial haemorrhages on mucous membranes and fundi, poor dentition, systemic emboli, nail-fold infarct, digital clubbing and splinter haemorrhages (long term only) loss of pulses, haematuria, osler's nodes, petechial rash
can be remembered by FROM JANE Fever Roth spots Osler nodes (OUCH osler nodes are painful) Murmur Janeway lesions (JUST janeway lesions they don’t hurt) Anaemia Nail-bed/splinter haemorrhages Emboli
Symptoms of subacute endocarditis
often occurs in an already abnormal valve low-grade fever non-specific symptoms fatigue night sweats weight loss Valve dysfunction or heart failure
Define acute and subacute endocarditis
Symptoms: can develop slowly over weeks/months (called subacute bacterial endocarditis) or can develop quickly over few days (acute)
Endocarditis causes
Bacterial infection - Strep. Viridans is the most common causative organism; often results in sub-acute disease. In IV drug users staph. Aureus (gram +ve commensal bacterium known to asymptomatically colonise skin) is most common causative.
Fungal infection
Endocarditis risk factors
Heart valve dysfunctions Surgery on heart valves Congenital heart defects Hypertrophic cardiomyopathy Previous infective endocarditis Injecting drugs (contaminated needles) Poor immunity (AIDS)
Endocarditis complications
Heart failure
Vegetations (breaks in to endothelial layer promote platelet adherence and formation of vegetations from fibrin, platelets which are then colonised by bacteria)
Small spots underneath fingernails, eyes etcs
Infections in other areas
Enlarged spleen
Stroke
Sudden vision loss in one eye caused by larger vegetations breaking ff and occluding arteries
Endocarditis investigations
Bloods - test for infections; ESR, CRP, WCC (white cell count), FBC (may see normochromic, normocytic anaemia)
Blood cultures: at least 3 sets of cultures taken at 30 min intervals from 3 different peripheral vein sites using sterile technique. MUST be taken before ABs are administered
Echocardiography - GOLD STANDARD to confirm endocarditis; can also detect vegetations and assess damage. Transthoracic usually first line, transesophageal echo is preferred
CXR - evidence of heart failure or septic emboli
ECG - MI from emboli or conduction defects
Urine dip - haematuria
endocarditis diagnostic criteria
Modified Duke Criteria: must meet either; 2 major criteria, 1 major and 3 minor or 5 minor criteria
Major: +ve blood cultures for infective endocarditis
typical microorganism found in two separate blood cultures in absence of primary focus (typical bacteria Strep. viridans, bovis or aureus)
single +ve culture for coxiella burnetii
evidence of endocardial involvement
abcess
new valvular regurgitation
new partial dehiscence of prosthetic valves
minor:
predisposed risk factors
fever above 38
Endocarditis treatment
Hospital admission
Antibiotics is all that’s needed in many cases
Surgery needed in up to 50% cases when infection is more severe
Medication: regular AB or antifungal doses injected directly into vein; 2-4 week courses but often given for longer (4-6 weeks IV then oral) depending on infection cause and complications. Usually needs such long administration due to ABs finding it difficult to penetrate the infection and so need longer times to diffuse and kill off bacteria.
Advice for ABs needed must be sought from the microbiology team.
Medications for complications such as heart failure also needed if applicable
Surgery: repair of replacement of damaged valve. Drainage of pus abscesses elsewhere in body
Acute pericarditis and symptoms
Inflammation of the pericardium
SYMPTOMS:
Pleuritic chest pain: usually in the middle or slightly left, feels sharp or stabbing. Can be persistent pain. May spread to neck/shoulders. Typically gets worse on deep inhalation, coughing or lying down. May be alleviated by leaning forward.
Pericardial friction rub: scratchy crunchy sound on auscultation caused by inflamed pericardium rubbing on itself. May be transient and difficult to detect.
Breathlessness
Pericardial effusion
Fever
Acute pericarditis causes
Viral Infection: several different viruses including coxackieviruses, echoviruses, influenza, mumps, HIV etc.
Bacterial infection: often causes pus between pericardial layers. Has usually spread from nearby tissues or from wounds following heart surgery. Rarely caused by syphilis or fungi
Tuberculosis usually as part of widespread TB infection in lungs etc
Uraemic pericarditis: inflammation caused by waste products build up in bloodstream in people with untreated kidney failure
MI: inflammation can occur from nearby tissue damage such as that from an MI
Surgery
Injury
Inflammatory diseases; rheumatoid arthritis, scleroderma etc.
Radiotherapy
Cancer spread from another part of the body (RARE)
Many cases are idiopathic
Acute pericarditis complications
Uncommon but include:
Pericardial effusion: fluid build up within pericardial layers
Constrictive pericarditis: thickening of pericardium contracting around heart
Cardiac tamponade
Heart failure
Acute pericarditis differential diagnosis
Viral pericarditis Bacterial pericarditis Malignancy CHF PE Ventricular aneurysm MI
Acute pericarditis investigations
Clinical examination: pericardial friction rub (grating sound)
CXR
ECG: abnormality seen in 90% of patients caused by associated epimyocarditis or inflammation in heart muscle: saddle shaped ST elevation, PR depression or inverted T waves.
Acute pericarditis: stage 1; ST elevation and PR depressions
Stage 2: T waves flatten and invert
Stage 3: T wave inversion
Stage 4: ECG returns to normal
Echocardiogram to detect pericardial fluid and exclude wall motion abnormalities seen in MI
Infection markers from blood samples: ESR, CRP, WCC, blood/sputum cultures, vitral titres, autoantibodies
MRI/ CT scan for suspected cause other than viral such as TB or systemic inflammatory condition
Pericardiocentesis (Fluid sample for pericardial effusion) and biopsy if bacterial, TB or neoplastic disease suspected
Acute pericarditis diagnostic
2 of 4 required:
Clinical history typical of acute pericarditis
Presence of pericardial friction rub
Typical ECG changes: PR depression and saddle shaped ST interval
Pericardial effusion
Treatment of acute pericarditis
Idiopathic or viral treatment:
Anti-inflammatories like ibuprofen (600-800mg) or Aspirin (700-1000mg) for 2-3 weeks
If infection persists for more than 14 days can also be given colchicine (0.5mg for 3 months) to improve outcome and reduce recurrence
Severe pain symptoms or no improvement may also give steroids (corticosteroids can be given to those with known immunity cause)
Other causes and complications:
Antituberculosis medication
Antibiotics
Dialysis for uraemic pericarditis
Fluid drainage for effusion
Surgery to remove thickened pericardium (pericardiectomy)
Prognosis for idiopathic or viral patients usually recover within a few weeks without complications; however some cases return on and off for several months.
Pericarditis caused by MI settles within 1-2 weeks. Outlook on other forms varies depending on underlying cause
Pericardial effusion and symptoms
Collection of fluid in serous pericardial sac. Normally contains 50ml fluid but when this increases it can compromise ventricular filling and circulation; known as tamponade
Often accompanies pericarditis
SYMPTOMS:
Soft and distant heart sounds
Obscured apex beat
Friction rub (early stages) but as disease progresses will stop being heard
pericardial effusion risk factors
MI
Heart surgery
Cancer metastases
pericardial effusion investigations and management
ECGs: low voltage QRS (electrical alternans - QRS of varying heights due to heart swinging back and forwards) and sinus tachycardia
CXR: enlarged and globular heart; can see classic ‘water bottle’ shape of fluid pooling at bottom of heart
Echocardiography: confirm effusion and potential sites for fluid aspiration
MANAGEMENT:
Pain management
Treating underlying cause
cardiac tamponade
Accumulation of fluid in pericardial space. Pericardium can accommodate up to 2 litres of fluid if this occurs slowly. Volumes above 2 litres will lead to cardiac compromise
Fast fluid accumulation results in acute symptoms
Larger fluid amounts put pressure on the heart resulting in reduced ventricular filling and haemodynamic compromise leading to heart failure and shock
Can be classified into traumatic or non-traumatic:
Traumatic
Acute onset putting pressure on ventricles ability to fill via taking up large space in pericardial sac very quickly e.g. bleeding from stab wound
Caused by:
AMI with free wall rupture
Aortic thoracic dissection (stanford type A)
Coagulation disorders
Blunt force traumas
Non-traumatic: generally starts as effusion:
Gradual onset of fluid slowly building in pericardial sac adding pressure to ventricles and slowly decreasing functioning
Caused by: any cause of pericarditis, (MI, autoimmune diseases or malignancy)
cardiac tamponade symptoms
Non-specific and depend on underlying cause: Cardiogenic shock Dyspnoea Tachycardia Yachypnoea Cold and clammy extremities (hypoperfusion) Beck's triad: the 3Ds*: Distant heart sounds Decreased arterial BP Distended JVP
cardiac tamponade investigations and treatment
Investigations: Aimed at finding the underlying cause Diagnosis: Confirmed by echocardiogram Treatment: Drainage of fluid: pericardiocentesis - ultrasound guided and can attach drain Oxygen Fluid loading to provide cardiac support Surgical intervention needed in traumatic cases
Temporal arteritis/GCA
Vasculitis condition causing inflammation and necrosis to medium and large sized arteries. Abnormally large cells develop in the wall of arteries; commonly affects neck and head area in the carotid and extracranial branches from the carotid - such as the temporal artery.
Can cause damage to skin, kidneys, lung, heart, brain and GIT
GCA symptoms
Headache: typically occipital or temporal
Tenderness of scalp over temporal arteries; can feel inflammation under skin
Pain in jaw muscles (jaw claudication) while talking, eating.
Visual disturbances: permanent partial or complete vision loss in one/both eyes occurs in up to 1 in 5 people and is often an early symptom. Urgent treatment needed
Tiredness
Depression
Night sweats
Fever
Loss of appetite; weight loss
Polymyalgia rheumatica: up to 50% also develop this related condition. Causes pain, tenderness/stiffness in shoulders or upper arms and sometimes in hips and neck. Due to inflammation of affected muscles, cause is unknown. Treatment is similar to GCA.
GCA risk factors and complications
Risk factors: 50+ years of age Complications: Loss of vision MI Aortic aneurysm Stroke Damage to nerves Tissue ischaemia Deafness (block arteries to brain)
GCA investiigations
Bloods; test for inflammation
Erythrocyte sedimentation rate (ESR) test: high levels indicate inflammation
CRP: same as above
FBC: normochromic, normocytic anaemia
Ultrasound of vessels
Biopsy of temporal artery to confirm diagnosis: definitive diagnostic test must be taken within 7 days of commencing steroids. Negative biopsies are possible as vasculitis produces ‘skip lesions’ within vessel
GCA treatment
Usually started before biopsy conformation due to need to prevent further damage
Glucocorticoid Steroids: prednisolone is usual; reduce inflammation and ease symptoms. Starts on high dose 60-100mg prednisolone per day (with visual symptoms) or 40-60mg without visual symptoms and reduces to maintenance dose 10mg per day. Condition usually goes away after 2-3 years allowing steroid treatment to be gradually withdrawn.
Low-dose aspirin: 75mg daily to prevent MI/stroke risk
Proton pump inhibitor (PPI): steroid and aspirin can increase risk of stomach ulcers therefore this mediation reduces acid in the stomach aiming to prevent bleeding stomach ulcer from developing. End in ‘azole’; esomeprazol.
Medication to prevent osteoporosis
Long term steroid side effects
Osteoporosis Increased risk of infection Weight gain Increased BP High blood glucose Skin problems - poor healing; thinning etc. Mood and behavioural changes Increased risk of cataracts Increased risk of duodenal and stomach ulcers
Takayasu’s arteritis and risk factors
Pulseless disease - present with decreased pulse strength or no pulse at all
Pathology:
Predominantly affects aorta and great vessels
Similar pathology to GCA but lumen narrowing is common
Pulmonary and abdominal arteries affected in 50% cases
Risk factors:
Typically affects young women (40 below)
Prevalent in asian population
Takaasu’s arteritis investigations and treatment
Investigations and diagnosis: Difference in BP in arms of 10mmHg Subclavian steel syndrome - reduced left subclavian blood flow steals blood from carotid artery through circle of willis Biopsy is impractical Abdominal Bruits Incidentally found on CT scans Angiography MRI shows stenosis Raised ESR and CRP support diagnosis
Treatment
Glucocorticoids
Alternative for steroid resistance
Angioplasty with balloon assist symptom relief improve circulation
Heart failure
Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder (IHD, valvulopathies etc) impairing the ability of the heart to function and maintain CO to meet the body’s demands.
Defined as when CO is inadequate for body requirements
Prognosis is poor – 25-50% mortality rate within 5 years diagnosis
Occurs in about 1-3% general population and greater than 10% in 65+
HF causes
Most common cause in UK is IHD
In Africa is HTN
Causes: Any factor increasing myocardial work Main causes are IHD, cardiomyopathy and hypertension Other causes: Arrhythmias Anaemia Hyperthyroidism Pregnancy Obesity Severe brady/tachycardia Pericardial disease Infections
HF ejection fraction types and causes
systolic Heart failure with EF less than 40% (HFrEF) causes: IHD, MI, cardiomyopathy
ventricles cannot contract normally and so CO is reduced
usually left sided HF
diastolic Heart failure with normal EF (HFpEF) causes: hypertension, LV hypertrophy, cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis
inability of LV to relax and fill enough causing high filling pressures in atria and ejection fraction is above 50%, but SV is still too low
usually right sided HF
LVF causes and symptoms
Causes: IHD, HTN, MI, cardiomyopathy
Signs and symptoms: due to congestion behind LV; exertional dyspnoea, orthopnoea, PND, fatigue, nocturnal cough (with or without pink frothy sputum), wheeze, nocturia, cold peripheries, poor exercise tolerance
RVF causes and symptoms
Causes: LVF, COPD, pulmonary stenosis, left to right shunt
Signs and symptoms: due to congestion behind RV; peripheral oedema (ankles, thighs, sacrum, abdo wall), enlarged JVP, hepatosplenomegaly, hepatojugular reflex, cardiac cirrhosis, ascites, nausea, anorexia
Congestive cardiac failure (CHF) and presentation
Congestive cardiac failure:
LVF and RVF occurring together
CHF
Presentation of CHF Cough (+/- pink sputum) Tired Pulmonary oedema Pleural effusion Swelling of abdomen Ankle oedema Sacral oedema
CHF diagnosis
Framingham criteria:
Need at least 2 major criteria OR 1 major and 2 minor Major criteria: PND – paroxysmal nocturnal dyspnoea Neck vein engorgement (high JVP) Hepatojugular reflux Increased CVP* >16cmH2O at RA S3 gallop – associated with ventricular dilation Crepitations in basal lungs, bilaterally Cardiomegaly (cardiothoracic ratio >50% on CXR) Acute Pulmonary Oedema (APE) Weight loss in response to treatment (Tx) >4.5kg in 5 days [i.e. presence of oedema in body, before Tx] Minor criteria: Bilateral Ankle Oedema Dyspnoea on ordinary exertion Tachycardia (>120/min) Hepatomegaly Pleural effusion Nocturnal cough Decrease in Vital Capacity (VC) by ⅓ from maximum recorded normal CVP values – 4-12 cmH2O reflects amount of blood returning to the heart (preload)
HF investigations
FBC, U+E, BNP; raised in HF; may drop if treatment is working
CXR
ECG – may indicate cause (MI, etc)
Echocardiography – may indicate cause and can confirm presence/absence of LV dysfucnion. Will only be performed if indicated by ECG and BNP; if not then look into alternative diagnosis for dyspnoea first
Endomyocardial biopsy (rarely needed)
ABCDE of HF CXR
things to look for in CXR
- alveolar oedema (bats wings)
- Kerley B lines (interstitial oedema)
- cardiomegaly
- Dilated vessels
- Pleural Effusion
NYHA classification of HF:
1 – no dyspnoea
2 – dyspnoea on ordinary activity
3 – dyspnoea on less than ordinary activities
4 – dysponea at rest
HF management
Lifestyle changes – smoking, alcohol, weight and nutrition
Treat underlying cases of HF (HTN, IHD etc.)
Medications – diuretics, vasoldilatory (ACEi), beta blockers, digoxin (increase heart contractility)
Revascularisation – coronary artery graft
Implantable cardioverter debfib
Replace valves
Repair CHD
Heart transplantation
wolff parkingson white syndrome ecg signs
slurred upstroke into the QRS complex (delta wave), short PR interval, QRS complexes may be slightly broad, dominant R wave in V1 (because the accessory pathway is left-sided)
brugada syndrome ECG signs
(cardiac sodium channelopathy): RBBB with ST elevation V1-3
Perfusion abnormalities
previous infarct ECG trace
T wave inversion (last weeks-months) and pathological Q waves (permanent)
Left ventricular hypertrophy ECG trace
R wave taller than 5 big squares in V5/6, increased S wave depth, T wave inversion in lateral leads/ST Depression
Right ventricular hypertrophy ECG trace
dominant R wave in V1, T wave inversion in right chest leads (V1-3), right axis deviation
Hypertrophic cardiomyopathy ECG signs
left ventricular hypertrophy signs + dramatic T wave inversion in lateral leads (maximal in V4 rather than V6)
Metabolic conditions and ECG changes
Hyperkalaemia: low flat P waves, wide bizarre QRS, slurring into ST segment, tall tented T waves
Hypokalaemia: small flattened T waves, prolonged PR, depressed ST, prominent U wave
Hypercalcaemia: short QT
Hypocalcaemia: prolonged QT
Anterior STEMI ECG changes
ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
Reciprocal ST depression in the inferior leads (mainly III and aVF).
Anterior-inferior STEMI due to occlusion of a “wraparound” LAD shows simultaneous ST elevation in the precordial and inferior leads due to occlusion of a variant (“type III”) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left ventricle.
left main coronary artery occlusion in ECG
widespread ST depression with ST elevation in aVR ≥ V1
Wellens syndrome ECG and indication
deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)
De Winter T waves ecg and indication
upsloping ST depression with symmetrically peaked T waves in the precordial leads; a “STEMI equivalent” indicating acute LAD occlusion.
Acute Rheumatic fever
Pharyngeal infection with Lance field group A beta haemolytic streptococci triggers rheumatic fever roughly 2-4 weeks post infection onset. May cause permeant damage to heart valves
Peak incidence is 5-15years
Tends to reoccur unless prevented
Acute rheumatic fever diagnosis
Use revised jones criteria: must be evidence of recent strep infection plus two major criteria OR one major and two minor Major criteria: Carditis Arthritis Subcutaneous nodules Erythema marginatum Sundenhams chorea
Minor criteria: Fever Raised ESR or CRP Arthralgia (not if arthritis is present) Prolonged PR interval Previous rheumatic fever
Acute rheumatic fever management
Bed rest until CRP is normal for 2 weeks (May be three months)
Benzylpenicillin 0.6-1.2g IV
Then phenoxymethylpenicillin 250-500mg 4 times daily for ten days (for allergies give erythromycin)
Analgesia for carditis/arthritis: 100mg/kg/d aspirin in divided doses for two days, then 70mg for 6 weeks
Monitor salicylate levels- toxicity causes tinnitus, hyperventilation and metabolic acidosis
Immobilise joints in severe arthritis
Haloperidol 0.5mg/8h PO or diazepam for chorea
Leriche’s syndrome/triad
Leriche’s syndrome is the term used for a group of symptoms that are caused by a certain type of peripheral arterial disease of the legs. In Leriche’s syndrome, blood flow in the aorta is blocked in the stomach area. This blocks blood flow to the legs. In men, blood flow to the penis is also blocked
The following symptoms happen:
Leg weakness or numbness.
Pain in the thighs, hips, and buttocks (intermittent claudication).
Erectile dysfunction (impotence).
Weak pulse in the thigh arteries (femoral arteries).
Instructing patient use of GTN
Use in case of angina
Use before planned exercise or exertion
Administration:
Sublingual tablet: 300,500,600micrograms place under tongue takes 1-3 mins to work
Spray: 400mocrograms/dose; spray once under tongue and close mouth immediately
Side effects: headache, lightheaded ness, flushing (vasodilators)
Pheochromocytoma and symptoms
Rare, usually noncancerous (benign) tumor that develops in an adrenal gland
Usually, develops in only one adrenal gland. But tumors can develop in both.
Tumor releases hormones that may cause:
high blood pressure,
headache,
sweating
symptoms of a panic attack.
Most common between the ages of 20 and 50. But the tumor can develop at any age.
If young patient comes to you with malignant hypertension - suspect this immediately!!
Pheochromocytoma treatment and complications
Surgery to remove a pheochromocytoma usually returns blood pressure to normal.
If a pheochromocytoma isn’t treated, severe or life-threatening damage to other body systems can result.
complications: Heart disease Stroke Kidney failure Problems with the nerves of the eye
Acute pulmonary oedema and causes
accumulation of fluid in lung parenchyma leading to decreased gaseous exchange causes: cardiac: ACS arrhythmia valvular heart disease HTN cardiomyopathy cardiac tamponade Non-cardiac: non-compliance with medication negatively inotropic medication fluid overload high output cardiac failure: anaemia, thyrotoxicosis, sepsis ARDS acute respiratory distress syndrome renal artery stenosis RAS
Pulmonary oedema signs and symptoms
fatigue worsening dyspnea progressing from exercise tolerance of dyspnoea on exertion to at rest orthopnoea PND cough producing pink, frothy sputum ankle swelling (pitting oedema)
Pulmonary oedema investigations
ABG FBC U+Es Mg Ca TFTs 12 lead ECG: shows ischaemia, infarction, LVH, arrhythmia CXR: ABCDE signs (alveolar oedema, bats wings and kerley B lines, cardiomegaly, diversion to upper lobes, effusions; blunting of costophrenic angles) echocardiogram if needed
Pulmonary oedema management
Initial management:
assess patient ABCDE
sit upright and attach monitoring: BP, oximeter, 3 lead cardiac monitor
maintain airway; suctions
oxygen if needed; 15L non-rebreathing mask
IV access and blood tests
consider troponin if concerned about cardiac event
Furosemide 40mg IV (diuretic)
Morphine 2.5-10mg IV (dilate venous system; decrease preload and improve breathing)
GTN 1mg/ml at 2ml/hour or give sublingually if fails IV
start CPAP if severe oedema (continuous positive airway pressure)
Further management:
continuing CPAP or inotropic support needs referral to HDU for continuous BP, ABG, CVP, oxygen, cardiac monitoring and urine output monitoring
Broad complex tachycardias
Regular:
Ventricular tachycardia: generated by single ventricular focus
SVT with BBB: rare
Irregular:
Polymorphic VT (torsades de pointes): usually due to abnormal ventricular repolarization (long QT)
AF with BBB
Narrow complex tachycardias
Regular rhythm:
Sinus tachycardia: physiological response
Atrial tachycardia: aberrant atrial focus independent of SAN
AVNRT: re-entry circuit within AVN
AVRT: re-entry circuit with AVN and accessory pathway
WPW syndrome: AVRT condition
Atrial flutter: re-entry circuit within atria
Irregular rhythm:
Atrial fibrilltion: atrial twitch in uncoordinated manner
congenital heart disease
heart condition or defect that develops in the womb, before a baby is born. There are many different types of congenital heart disease.
Incidence:
8 in 1000 births
Most common congenital abnormality
Prognosis:
Severe cases result in miscarriage or early death
Mild cases have shorter life expectancy and higher risk of arrhythmias, HF and infective endocarditis
VACTERL disorders
a disorder affecting many systems causing multiple birth defects; often patients have at least three of these abnormalities V - Vertebral anomalies A - Anorectal malformations C - Cardiovascular anomalies T - Tracheoesophageal fistula E - Esophageal atresia R - Renal (Kidney) and/or Radial anomalies L - Limb defects
Eisenmenger’s complex/syndrome
process in which a long standing left to right cardiac shunt caused by a congenital heart defect (typically VSD, ASD or PDA) causes pulmonary HTN and eventually reversal of the shunt to a R to L shunt causing ischaemia to organs and tissues
life threatening condition
Eisenmenger’s complex/syndrome symptoms
Bluish or grayish skin color (cyanosis)
Large, rounded fingernails or toenails (clubbing)
Easily tiring and shortness of breath with activity
Shortness of breath while at rest
Chest pain or tightness
Skipped or racing heartbeats (palpitations)
Fainting (syncope)
Coughing up blood (hemoptysis)
Dizziness
Numbness or tingling in the fingers or toes
Headaches
Abdominal swelling
Eisenmenger’s complex/syndrome complications
Cyanosis erythrocytosis: high RBC arrhythmias sudden cardiac arrest HF Hemoptysis (coughing up blood) stroke kidney problems Pregnancy risks: due to strain on mums heart and lungs women with this complex should not become pregnant as there is high risk of death for mother and baby
Eisenmenger’s complex/syndrome investigations and diagnosis
ECG CXR: pulmonary artery enlargement echo: look for CHDs blood tests: FBC, TFTs, LFTs CT MRI cardiac catheterisation walking test: 6 min walking test to check exercise tolerance
Eisenmenger’s complex/syndrome treatment
aimed at controlling symptoms and managing the condition. NO CURE medications may help improve your quality of life and prevent serious complications. Anti-arrhythmias iron supplements aspirin or anticoagulants vasodilators antibiotics
heart transplant or lung transplant may be needed eventually
Don’t generally recommend surgery to repair defects as surgery may be life-threatening.
needs referral to specialist immediately
Ischaemic limits on vital organs
brain - 4 mins without O2
heart - 8 mins
muscle and nerves - 4-6 hours
skin- several days without oxygen
Atrial septal defect
Acyanotic defect: does not bypass lungs
Causes increased O2 saturation in RA, RV and pulmonary artery
Is 7% of CHD cases (10-15% all CHD cases?)
A hole between the atria; in 80% this hole is high in the septum (ostium secundum type; second hole in atrial septum embryology)
20% is ostium primum type (first hole in embryo development); hole is towards endocardial cushion (bottom of atria)
Associated with downs syndrome and fetal alcohol syndrome
ASD symptoms
Usually none in childhood
Widely split fixed S2 + systolic murmur (due to pulmonary flow murmur)
Ages 40-60 show signs of dyspnoea/HF due to LV compliance decreasing with age causing large L to R shunt of blood causing symptoms
Chest pains
Palpitations
Arrhythmias (including AF)
ASD complications and treatment
Complications:
Reversal to L to R shunt, Eisenmengers complex
Paradoxial emboli: DVT breaks off travels to heart as venous embolus, through atrial septal defect and into carotid resulting in stroke (very rare)
Treatment:
May close spontaneously
Needs repair especially if symptomatic via transcatheter closure (more common than surgical closure)
Ventricular septal defect and symptoms
Accounts for 25% CHD cases Acquired VSD can occur post septal MI; necrosis and perforation causes acute presentation Symptoms usually seen in childhood Usually mild Harsh loud pansystolic blowing murmur with/without thrill Smaller holes will give louder murmurs Lack of normal growth (FFT) Pulmonary symptoms
VSD investigations and treatment
Echo
ECG: normal while young; later shows left or combined ventricular hypertrophy
CXR: pulmonary engorgement
Maladie de roger (small asymptomatic VSD) in 20% cases close spontaneously by 9 months
Larger defects require endovascular closure preferred over surgery
VSD complications
Aortic regurgitation Pulmonary HTN Infectious endocarditis Eisenmenger’s complex HF
Coarctation of aorta
Congenital narrowing of the descending aorta; usually occurs just distal to origin of left subclavian artery
More common in boys
Associated with bicuspid aortic valve and turner’s syndrome
Infants about 70% cases; occurs before ductus arteriosus on arch of aorta; can be fatal causing cyanosis
In adults (30% cases) no patent ductus arteriosus is fibrosed to ligamentum arteriosum
Coarctation of aorta symptoms and signs
Symptoms: Headache Low exercise capacity Intermittent leg cramps Signs: Radiofemoral delay High BP in head and upper limbs; due to high pressures above constriction point Low BP beneath constriction point; causes weak femoral pulse and claudication Scapular bruit, systolic murmur best heard over left scapula Weak femoral pulse Intermittent claudication Cold feet
Coarctation of aorta complications
HF
Infectious endocaritis
Intracerebral haemorrhage; increased risk in berry aneurysms
Aortic dissections increased risk
Coarctation of aorta investigations and treatment
CT/MRI or aortogram is 1st line GOLD STANDARD
CXR may show rib notching: blood diverts down ICA to reach lower body causing vessels to dilate and erode local rib bone
Treatment:
Balloon dilation with/without stenting
Surgery to remove narrowed section and correct hyper/hypotension
Patent ductus arteriosus
Ductus arteriosus remains open (patent) after birth.
Normally closes within few hours and fibrosis keeps closed
Common in premature newborns
Respiratory problems in premature babies causes hypoxia and lack of DA closure post birth
Creates higher pressure within the pulmonary artery and congestion in the lung leading to long term complication of HF
PDA signs and symptoms
Failure to thrive Pneumonia CCF Infectious endocarditis Collapsing pulse Systolic pulmonary area murmur or continuous machinery humming
PDA investigations and treatment
Investigations:
CXR: increased vascular markings and large aorta
ECG: LVH
Management:
Indometacin first line pre-term.
Ibuprofen
Surgery - open or video assisted thoracoscopic surgery (VATS)
Tetralogy of fallot
Most common cyanotic CHD (3-6 in 10,000)
Most common cyanotic heart defect surviving to adulthood
Is a combination of four heart defects:
VSD
Pulmonary stenosis
Overriding aorta: Aortic valve enlarged and opens from both ventricles; sits directly on top of VSD
Right Ventricular hypertrophy
Tetralogy of fallot presentation
severity depends on degree of pulmonary stenosis
Acyanotic at birth as they also often have PDA, become cyanotic after DA closes
During hypoxic spell; restless and agitated
Toddlers may squat (typical feature) as this increases peripheral vascular resistance; decreasing degree of R to L shunt
Adults often asymptomatic although cyanosis and hypoxic spells are common
Tetralogy of fallot investigations and management
ECG; RVH and RBBB
CXR: normal or boot shaped heart
Echocardiography: first line Ix
Cardiac CT/MRI: planning surgery info
Hyperoxia test: giving O2 supplementation would improve symptoms in any other heart or lung condition but not ToF
Management:
Prostaglandin infusion to help keep the infant asymptomatic by keeping the PDA open
Surgery usually before age 1 to close VSD and correct pulmonary stenosis
Acute HF
medical emergency caused by either left or right HF developing over minutes or hours and heart can no longer pump enough blood to meet the bodys demands
Acute HF clinical features
Acute decompensation of CHF Hypertensive HF Acute pulmonary oedema Cardiogenic shock high output cardiac failure Right HF
Acute HF symptoms
Can present in numerous ways depending on major underlying cause pulmonary oedema: breathless, tachycardia, profuse sweating, wheezes and crackles throughout chest, hypoxia in ABG Cardiogenic shock: hypotension tachycardia oliguria: decreased urine output cold extremities High output CF: warm peripheries pulmonary congestion blood pressure low Right HF: elevated JVP Hepatomegaly Hypotension
Acute HF investigations
blood tests; TFTs, LFTs, troponin, DDIMER, ABG
ECG
CXR: look for pulmonary oedema
Echo
Acute HF management
In many cases, patient is so unwell treatment begins before diagnosis
Transfer patient to HDU
Prophylactic anticoagulation e.g. enoxaparin
Oxygen if needed
IV line diuretics (furosemide 50mg)
GTN nitrates
Inotropic support for those not responding to initial therapy
Arteriovenous malformations overview
Occur in less than 1% general population
More common in males
Usually congenital
Symptoms: Intracranial haemorrhage Seizures Headaches Difficulty with movement, speech and vision
Investigations:
CT scan
MRI
Angiogram
Treatments:
Treatment depends on symptoms and size of malformation
Lifestyle: avoid triggers like excessive exercise
Anticoagulants (warfarin)
Surgery if there is a bleed
Stereotactic radiosurgery
Interventional neuroradiology/endovascular neurosurgery
cellulitis, when it needs medical attention and common organisms
bacterial skin infection
can spread if severe
Most common organism is Strep. Pyogenes gain entry to dermal and subcutaneous tissues via cuts etc.
Needs immediate medical attention if involved area grows rapidly, blisters or abcesses form or if you develop a fever or flu-like symptoms
Cellulitis risk factors and possible complications
risk factors: skin trauma, ulceration and obesity complications: necrotizing fasciitis sepsis persistent leg ulceration recurrent celluitis
Cellulitis investigations and differentials
usually made on clinical exam alone: show red and warm skin around infected area, can draw pen line around the infection site to monitor if the infection is spreading/getting worse etc. may need swap culture for open wounds differentials: DVT septic arthritis acute gout ruptured backers cyst
Cellulitis treatment
Flucloxacillin 500-1000mg 4x daily for 5-7 days
If allergic to penicillin - clarithromycin 500mg 2xdaily 5-7 days
If patient is systemically unwell the refer to specialist
PVD symptoms
Erectile dysfunction Intermittent claudication buttock/thigh pain while walking Diminished or absent pulse Poor wound healing
PVD severity stages
stage 1: Asymptomatic stage 2: Mild claudication stage 3: Mod-severe claudication stage 4: Ischaemic pain at rest stage 5: Ulceration and gangrene
PVD investigations
Clinical exam: diminished pulse
BP: HTN
ABPI
Duplex ultrasound
PVD management
Plan:
Lifestyle changes
Drugs for HTN
Statins for cholesterol (10mg primary; 20mg QRISK >10%; 80mg previous CVD event)
Follow ups:
Smoking cessation clinics
BP monitoring
Medication monitoring (ACEi 2wks then annually/after dose change)
QRISK calculation regularly with lifestyle alterations
Duckett Jones criteria (J<3NES) for diagnosing acute rheumatic fever
major: Joints (arthritis) <3 Carditis Nodules Erythema marginatum Sydenham's chorea (St Vitus' dance)
minor: fever raised ESR arthralgia prolonged PR interval
key points on administering adenosine for SVT:
Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
Warn patient about the scary feeling of dying / impending doom when injected
Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
Initially 6mg, then 12mg and further 12mg if no improvement between doses
Bradycardia/AVN blocks treatment
Stable: Observe
Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
First line: Atropine 500mcg IV
No improvement: Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
Other inotropes (such as noradrenalin)
Transcutaneous cardiac pacing (using a defibrillator)
In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
Temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
Permanent implantable pacemaker when available
Note. Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. This leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation.
Venticular ectopics management
Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
WPW syndrome overview
Wolff-Parkinson White Syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.
The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway.
ECG Changes:
Short PR interval (< 0.12 seconds) Wide QRS complex (> 0.12 seconds) “Delta wave” which is a slurred upstroke on the QRS complex
Note: If the person has a combination of atrial fibrillation or atrial flutter and WPW there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.
Cardiovascular causes of finger clubbing
All Cardiac Ends Poorly
Atrial myxoma
Cyanotic heart disease
Endocarditis
Pericarditis
ECG changes summary
Saddle ST elevation - acute pericarditis
ST elevation - STEMI
inverted T wave - ischaemia
Tall Tented T wave - hyperkalaemia
U wave - hypokalaemia
J wave - hypothermia
A waves - atrial myxoma
Delta waves - WPW syndrome
Bifid P wave - mitral regurgitation
Fibrillation waves - atrial fibrillation
