Cardiology (2) Flashcards
Define deep vein thrombosis
Development of a blood clot in a major deep vein in the leg, thigh, pelvis, or abdomen, which may result in impaired venous blood flow and consequent leg swelling and pain.
Summarise the aetiology of deep vein thrombosis
- Process starts with damage to the endothelium
- Immediate vasoconstriction of blood vessel which limits amount of blood flow
- Platelets adhere to damaged vessel wall and activated by collagen and tissue factor
- Platelet plug formed - primary haemostasis
- Coagulation cascade - secondary haemostasis
What are the risk factors for DVT?
Virchow’s Triad:
- Stasis of blood - turbulence or inactivity of skeletal muscle pump
- Bed rest eg post-op
- Long haul flights
- Long car journey
- Pregnancy - Hyperoagulation state
- Genetic
- OCP
- Surgery
- Cancer - Endothelial damage
- Infection
- Chronic inflammation
- Toxins eg tobacco smoke
- Trauma
Obesity, dehydration, polycythaemia, thrombophilia
Summarise the epidemiology of DVT
Common - 1 in 1000 adults yearly
Increases with age
Slight female predominance in under 35s
What are the presenting symptoms of DVT?
Inflammed leg/unilateral leg swelling Painful leg Red or warm leg Most common in lower limbs below the knee Dilated/distended superficial veins
Very large DVT - phlegmasia cerulea dolens due to ischaemia (blue, painful LEG)
What are the signs on physical examination of DVT?
Local erythema, warmth and swelling Measure the leg circumference Varicosities (swollen/tortuous vessels) Skin colour changes Homan's Sign - forced passive dorsiflexion of the ankle causes deep calf pain
What are the appropriate investigations for DVT?
Wells’ score:
>2 - DVT is likely therefore proceed to imaging
<2 - DVT less likely so confirm with D-dimer
Scoring points:
- active cancer
- calf swelling where affected calf circumference >3cm greater than other leg
- prominent superficial veins
- recent immobility
D-dimer if Wells Score less than 2 - if normal, DVT is excluded. If elevated proceed to imaging
Doppler Ultrasound - GOLD STANDARD – inability to fully compress lumen of vein using ultrasound transducer, reduced or absent spontaneous flow, lack of respiratory variation, intraluminal echoes, colour flow patency abnormalities;
Venography - dye injected into veins, X-ray taken which identifies blockages
D-dimer - measures fibrin break-down product levels - if high suggests clot
If PE suspected: ECG, CXR, ABG
What is the management of DVT?
Prevention:
Compression stocking
Frequent calf exercises during periods of immobility/mobilisation
Prophylactic heparin
Low dose aspirin - prevent formation of clots
ANTI-COAGULATION:
Rivaroxaban
Heparin whilst waiting for warfarin to increase INR to the target range of 2-3
Don’t extend above the knee - observe and anticoagulate for 3 months
Extend beyond knee - anticoagulate for 6 months
Recurrent DVTs require long-term warfarin
Give thrombolytic enzymes to break down clot
Thrombectomy to surgically remove the clot
IVC Filter - if anticoagulation is contraindicated
What are the potential complications of DVT?
Thromboembolism leading to PE or stroke
Venous infarction (phlegmasia cerulea dolens)
Thrombophlebitis (results from recurrent DVT)
Chronic venous insufficiency
What is the prognosis of DVT?
Depends on extent of DVT:
- Below-knee DVTs have a GOOD prognosis
- Proximal DVTs have a greater risk of embolization
If patient dies from DVT, usually due to a PE
Recurrent VTE likely if: Male sex Proximal DVT Ultrasound evidence of residual clot Elevated D-dimer 1 month after stopping a 3-6 month course of oral anticoagulation Unprovoked DVT
Define dyslipidaemia and the ranges for total cholesterol, LDL and HDL
Dyslipidaemia is:
Serum Total Cholesterol, LDL-C, triglycerides concentrations above the 90th percentile
HDL-C concentrations below the 10th percentile for the general population.
Total cholesterol >5.2mmol/L
LDL >3.3mmol/L
HDL <1.55mmol/L
What is defined as hypertryglyceridaemia?
Fasting plasma triglyceride level ≥2.3 mmol/L
Explain the aetiology of dyslipidaemia
Primary:
Single or multiple gene mutations, resulting in a disturbance of LDL and triglyceride production or clearance
Mainly in children and young adults
Familial hypercholesterolaemia - AUTOSOMAL CODOMINANT (LDL >4.9mmol/L in adults and >4.1mmol/L in children)
Secondary: Sedentary lifestyle Excessive consumption of saturated fats and trans-fatty acids Chronic renal insufficiency Diabetes mellitus Abdominal obesity Hypothyroidism Alcohol dependency
Summarise the epidemiology of dyslipidaemia
12% of adult population in US have dyslipidaemia
Prevalence is 80-88% in those with coronary heart disease
Strong correlation between BMI and hyperlipidaemia
More common in industrialised countries than developing countries
What are the presenting symptoms of dyslipidaemia?
Presence of risk factors Consumption of saturated fats and trans-fatty acids Abdominal obesity Angina pain Claudication pain
What are the signs on physical examination of dysplipidaemia?
Xanthelasma
Tendinous xanthoma
Corneal arcus
Obesity
What is the management of dyslipidaemia?
Lifestyle: Exercise Weight loss Stop smoking Decreased saturated fats consumption
Pharmacological:
Statins - 10-20mg atorvastatin if no previous CVS event (increase to 40-80mg if needed)
- Decrease LDL and triglycerides, increase HDL
- Side effects: muscle pain, myopathy, increase diabetes risk, increase AST and ALT
2nd line = selective cholesterol absorption inhibitors eg ezetimibe
- Decrease LDL by preventing cholesterol absorption
- Side effects: diarrhoea
Fibrates (side effects = myopathy, increase AST and ALT)
Bile acid sequestrants (side effects = diarrhoea)
Niacin (side effects = facial flushing therefore taken with 300mg aspirin 30 mins before)
LDL apheresis - blood passed through apparatus which removed LDL and remaining then returned to circulation
Liver transplantation
What are the possible complications of dyslipidaemia?
Ischaemic heart disease Peripheral vascular disease Acute coronary syndrome Stroke Erectile dysfunction
What is the prognosis of dyslipidaemia?
Statins significantly reduce adverse events
Cholesterol reduction is useful as coronary heart disease risk-reduction strategy
Once plasma lipid levels have achieved goals and are stable they can be monitored along with liver function tests every 6 months
Define gangrene
A complication of necrosis characterised by the decay of body tissues. The two major categories are infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene). It may result from ischaemia due to arterial or venous compromise, infection, or trauma (or a combination of these processes).
Summarise the aetiology of gangrene
Tissue ischaemia and infarction
Physical trauma
Thermal injury
Infectious gangrene:
Necrotising fasciitis - mainly group A beta-haemolytic Streptococcus species
Gas gangrene: caused by Clostridium perfringens
Ischaemic gangrene: Atherosclerosis Diabetes-associated microangiopathy Hypercoagulable states Vasospasm associated with Raynaud's phenomenom and cocaine Venous obstruction
What are the risk factors of gangrene?
Diabetes mellitus Renal disease Drug and alcohol abuse Malignancy Leg ulcers Immunosuppression Steroid use Puncture/surgical wounds
Ischaemic gangrene: Atherosclerosis Smoking Hypercoagulable states Prolonged application of torniquets
Infectious gangrene:
Trauma or abdominal surgery
Contaminated wounds
Malnutrition
Summarise the epidemiology of gangrene
Relatively common
Occurs equally in men and women
Type I necrotising fasciitis more common in diabetics and those with peripheral vascular disease
Gas gangrene often predisposed by severe penetrating trauma and crush injuries associated with interruption of blood supply
What are the presenting symptoms of gangrene?
Pain - sudden onset in infectious gangrene, long history of claudication pain in ischaemic gangrene
Swelling and redness of the area
Low grade fever and chills for infectious gangrene
Discolouration of affected area
Usually extremities or areas subject to high pressures affected
What are the signs on physical examination of gangrene?
Oedema and erythema of affected region
Skin discolouration
Crepitus - gentle palpation of gas gangrene causes abnormal popping or crackling sound
Diminished pedal pulses and ankle-brachial index in ischaemic gangrene
Painful area = erythematous region around gangrenous tissue
Gangrenous tissue = BLACK because of haemoglobin break down products
Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
What are the appropriate investigations for gangrene?
Bloods:
FBC - leukocytosis if infectious gangrene
U&Es
Glucose
CRP - elevated if infectious gangrene
Blood culture - positive for infective organism
Metabolic panel - metabolic acidosis, liver derangement, liver failure
Imaging:
X-ray - may show gas if gas gangrene
CT/MRI - reveal abscess formation or evidence of enhancement, oedema, or thickening in the fascia
Doppler ultrasound - presence and severity of arterial or venous obstruction
Wound Swab, Pus/Fluid Aspirate - MC&S
Define heart block - 1st, 2nd and 3rd degree
Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.
1st degree heart block - signals from the atria are delayed in passing to the ventricles, resulting in a prolonged PR interval >200ms due to prolonged conduction through AV node
2nd degree heart block Mobitz I - signals from the atria and progressively more and more delayed until eventually a signal is unable to pass into the ventricles, resulting in progressively lengthening PR intervals followed by a dropped beat. The cycle then begins again
2nd degree heart block Mobitz II - signals from the atria are delayed in passing to the ventricles, resulting in some intermittent, random dropped beats - intermittent failure of conduction through the AV node
3rd degree/complete heart block - signals from the atria are not transmitted to the ventricles and are completely blocked. Ventricular contraction is only due to ventricular escape beats. NO RELATIONSHIP BETWEEN ATRIAL AND VENTRICULAR CONTRACTION.
Summarise the aetiology of heart block
Fibrosis or damage eg calcification to conduction system of the heart
Most common = Ischaemic Heart Disease or MI
Myocarditis
Cardiomyopathies
Infection (e.g. rheumatic fever, infective endocarditis)
Metabolic (e.g. hyperkalaemia)
Infiltration of conducting system (e.g. sarcoidosis)
Coronary Artery Disease
AV-nodal blocking agents - beta-blockers, calcium-channel blockers, digitalis, adenosine
Anti-arrhythmic medications eg sodium channel blockers
Post-catheter ablation
Post-surgery
Summarise the epidemiology of heart block
Majority of the 250,000 pacemakers implanted annually are for heart block
What are the presenting symptoms of heart block?
Type 1 usually asymptomatic
Type 2 Mobitz I usually asymptomatic, sometimes lightheaded, dizzy, syncope
Type 2 Mobitz II: Chest pain Fatigue Syncope Dyspnoea
Type 3: Severe chest pain Syncope Confusion Dyspnoea Increased risk of sudden death
Palpations, nausea and vomiting
What are Stokes-Adams attacks?
Syncope caused by ventricular asystole which is a symptom of Type 2 Mobitz I and Type 3
What are the signs on physical examination of heart block?
Often NORMAL
Heart rate <40bpm
Hypoxaemia
Complete Heart Block:
Slow large volume pulse
JVP may show cannon a waves
Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously. Reflect the contraction of the right atrium against a closed tricuspid valve.
Mobitz Type II and 3rd Degree Heart Block:
Signs of reduced cardiac output (e.g. hypotension, heart failure)
What are the appropriate investigations for heart block?
Bloods:
Troponin - may be elevated if due to ischaemia
Cardiac enzymes
Potassium - electrolyte imbalances can be reversible causes of heart block
Calcium - electrolyte imbalances can be reversible causes of heart block
pH - pH imbalances can be reversible causes of heart block
Digoxin level
TFTs
12 lead ECG:
1st degree - prolonged PR interval >200ms
2nd degree Mobitz I - progressively prolonged PR intervals followed by a dropped beat (p wave with missing QRS complex). Cycle then continues
2nd degree Mobitz II - intermittent dropped beats shown by random missing QRS complexes. May be
a regular pattern of P waves not followed by a QRS (e.g. two P waves per QRS, indicating 2:1 block)
3rd degree - no relationship between P waves and QRS complexes. Regular P and R waves.
CXR: Cardiac enlargement, pulmonary oedema.
Echocardiogram: Wall motion abnormalities, aortic valve disease, vegetations.
What is the management of heart block?
Asymptomatic - monitoring
Acute:
Medication to increase heart rate eg atropine
Transcutaneous temporary pacing using electrodes on the skin
Chronic:
Permanent pacing with implanted device - monitor rhythm and send impulse to ventricle if detects delay
Permanent pacing = type 3, type 2 Mobitz II and SYMPTOMATIC Mobitz I
What are the possible complications of heart block?
Asystole
Cardiac arrest
Heart failure
Complications of inserted pacemaker - bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade
What is the prognosis of heart block?
Mobitz type II and third degree heart block usually indicate serious underlying cardiac disease.
Prognosis is related to the degree of AV block, the severity of associated symptoms and the underlying condition.
Permanent pacing improves survival in patients with third degree heart block
Define hypertension
Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions.
Summarise the aetiology of hypertension
Primary/essential hypertension - 90% of cases
- NO CLEAR CAUSE
Secondary hypertension - 10% of cases
- Low renal blood flow
- Vasculitis
- Fibromuscular dysplasia (young women, thickens artery walls)
- Tumour secreting excess aldosterone
- Obstructive sleep apnoea
Renal: Renal artery stenosis, chronic glomerulonephritis, pyelonephritis, polycystic kidney disease, chronic renal failure
Endocrine: Diabetes mellitus, Hyperthyroidism, Cushing’s syndrome, Conn’s syndrome, Hyperparathyroidism, Phaeochromocytoma, Congenital adrenal hyperplasia, Acromegaly
Cardiovascular: Coarctation of the aorta, Increased intravascular volume, atherosclerosis, aortic dissection
Drugs: Sympathomimetics, Corticosteroids, COCP
Pregnancy: Pre-eclampsia
What are the risk factors for hypertension?
Increasing age High salt diet Obesity Sedentary lifestyle Family history Smoking Alcohol
Summarise the epidemiology of hypertension
Very common - 10-20% of the Western world population
What are the presenting symptoms of hypertension?
Primary hypertension is ASYMPTOMATIC
Secondary hypertension has symptoms associated with underlying cause
Emergency hypertensive crisis: Confusion Drowsiness Chest pain Breathlessness
Accelerated or Malignant Hypertension - Scotomas (visual field loss), Blurred vision, Headache, Seizures, Nausea and vomiting, Acute heart failure
