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Old Y3 Sofia Notes > Cardiology 2 > Flashcards

Cardiology 2 Flashcards

1
Q

Define constrictive pericarditis

A

Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.

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2
Q

Explain the aetiology/risk factors of constrictive pericarditis

A
  • NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure
  • Can occur after any pericardial disease process
  • More common causes of pericarditis:

o Idiopathic

o Virus

o TB

o Mediastinal irradiation

o Post-surgical

o Connective tissue disease

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3
Q

Summarise the epidemiology of constrictive pericarditis

A
  • RARE
  • Documented in all ages
  • 9% of patients with acute pericarditis will develop constrictive pericarditis
  • TB has the HIGHEST TOTAL INCIDENCE out of all causes
  • More common in MALES
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4
Q

Recognise the presenting symptoms and signs of constrictive pericarditis

A
  • Gradual-onset of symptoms
  • EARLY - symptoms and signs may be very subtle
  • ADVANCED - jaundice, cachexia, muscle wasting
  • Right Heart Failure Signs

o Dyspnoea

o Peripheral oedema

o Raised JVP

o Kussmaul’s sign (paradoxical rise in JVP on inspiration)

o Pulsatile hepatomegaly

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5
Q

Identify appropriate investigations for constrictive pericarditis

A
  • CXR - may show calcification of the pericardium
  • Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy
  • MRI - allows assessment of thickness of pericardium
  • CT - same role as MRI
  • Pericardial biopsy - may be indicated (especially if suspected infective cause)
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6
Q

Define Deep Vein Thrombosis

A

Formation of a thrombus within the deep veins (most commonly in the calf or thigh)

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7
Q

Explain the aetiology/risk factors of DVT

A
  • Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (look up Virchow’s triad)
  • Risk Factors

o COCP

o Post-surgery

o Prolonged immobility

o Obesity

o Pregnancy

o Dehydration

o Smoking

o Polycythaemia

o Thrombophilia (e.g. protein C deficiency)

o Malignancy

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8
Q

Summarise the epidemiology of DVT

A
  • VERY COMMON

* Especially in hospitalised patients

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9
Q

Recognise the presenting symptoms of DVT

A
  • Swollen limb

* May be painless

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10
Q

Recognise the signs of DVT on physical examination

A
  • Examination of the Leg

o Local erythema, warmth and swelling

o Measure the leg circumference

o Varicosities (swollen/tortuous vessels)

o Skin colour changes

o NOTE: Homan’s Sign - forced passive dorsiflexion of the ankle causes deep calf pain

  • Risk is stratified using the WELLS CRITERIA (NOTE: this is

different from the PE Wells criteria)

o Score 2 or more = high risk

  • Examine for PE

o Check respiratory rate, pulse oximetry and pulse rate

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11
Q

Identify appropriate investigations for DVT

A
  • Doppler Ultrasound - GOLD STANDARD
  • Impedance Plethysmography - changes in blood volume results in changes of electrical resistance
  • Bloods

o D-dimer: can be used as a negative predictor

o Thrombophilia screen if indicated

  • If PE suspected

o ECG

o CXR

o ABG

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12
Q

Generate a management plan for DVT

A
  • ANTICOAGULATION

o Heparin whilst waiting for warfarin to increase INR to the target range of 2-3

o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months

o DVTs extending beyond the knee require anticoagulation for 6 months

o Recurrent DVTs require long-term warfarin

  • IVC Filter

o May be used if anticoagulation is contraindicated and there is a risk of embolisation

  • Prevention

o Graduated compression stockings

o Mobilisation

o Prophylactic heparin (if high risk e.g. hospitalised patients)

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13
Q

Identify possible complications of DVT

A
  • PE
  • Venous infarction (phlegmasia cerulea dolens)
  • Thrombophlebitis (results from recurrent DVT)
  • Chronic venous insufficienc
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14
Q

Summarise the prognosis for patients with DVT

A
  • Depends on extent of DVT
  • Below-knee DVTs have a GOOD prognosis
  • Proximal DVTs have a greater risk of embolisation
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15
Q

Define gangrene and necrotising fasciitis

A
  • Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene
  • Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes
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16
Q

Explain the aetiology/risk factors of necrotising fasciitis

A
  • Gangrene

o Tissue ischaemia and infarction

o Physical trauma

o Thermal injury

o Gas gangrene is caused by Clostridia perfringens

  • Necrotising Fasciitis

o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms

  • Risk Factors

o Diabetes

o Peripheral vascular disease

o Leg ulcers

o Malignancy

o Immunosuppression

o Steroid use

o Puncture/surgical wounds

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17
Q

Summarise the epidemiology of gangrene and necrotising fasciitis

A
  • Gangrene - relatively COMMON

* Necrotising fasciitis and gas gangrene - RARE

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18
Q

Recognise the presenting symptoms of gangrene and necrotising fasciitis

A
  • Gangrene

o Pain

o Discolouration of affected area

o Often affects extremities or areas subject to high pressure

  • Necrotising Fasciitis

o Pain

  • Often seems SEVERE and out of proportion to the apparent physical signs

o Predisposing event (e.g. trauma, ulcer, surgery)

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19
Q

Recognise the signs of gangrene and necrotising fasciitis on examination

A
  • Gangrene

o Painful area = erythematous region around gangrenous tissue

o Gangrenous tissue = BLACK because of haemoglobin break down products

o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes

o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)

  • Necrotising Fasciitis

o Area of erythema and oedema

o Haemorrhagic blisters may be present

o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)

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20
Q

Identify appropriate investigations for gangrene and necrotising fasciitis

A
  • Bloods - FBC, U&Es, glucose, CRP and blood culture
  • Wound Swab, Pus/Fluid Aspirate - MC&S
  • X-ray of affected area - may show gas produced in gas gangrene
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21
Q

Define heart block

A
  • 1st Degree AV Block: prolonged conduction through the AV node
  • 2nd Degree AV Block:

o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle ten begins again.

o Mobitz Type II: intermittent or regular failure of conduction through the AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1)

  • 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle
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22
Q

Summarise the epidemiology of heart block

A

250,000 pacemakers are implanted every year and they are mostly for heart block

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23
Q

Explain the aetiology/risk factors of heart block

A
  • MI or ischaemic heart disease (MOST COMMON)
  • Infection (e.g. rheumatic fever, infective endocarditis)
  • Drugs (e.g. digoxin)
  • Metabolic (e.g. hyperkalaemia)
  • Infiltration of conducting system (e.g. sarcoidosis)
  • Degeneration of the conducting system
24
Q

Recognise the presenting symptoms of heart block

A
  • 1st Degree - asymptomatic
  • 2nd Degree - usually asymptomatic
  • Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole)

o May also cause dizziness, palpitations, chest pain and heart failure

25
Q

Recognise the signs of heart block on physical examination

A
  • Often NORMAL
  • Check for signs of a potential cause of heart block
  • Complete Heart Block

o Slow large volume pulse

o 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
  • Mobitz Type II and 3rd Degree Heart Block

o Signs of reduced cardiac output (e.g. hypotension, heart failure)

26
Q

Identify appropriate investigations for heart block

A
  • ECG - GOLD STANDARD

o First Degree - fixed prolonged PR interval (> 0.2 s)

o Mobitz Type I (Wenckebach) - progressively prolonged PR interval, culminating in a P wave that is NOT followed by a QRS complex. The pattern then begins again. ‘Going, going, gone’.

o Mobitz Type II - intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)

o Complete Heart Block - no relationship between P waves and QRS complexes. If QRS is initiated in the:

  • Bundle of His - narrow complex
  • More distally - wide complex and slow rate (~ 30 bpm)
  • CXR

o Cardiac enlargement

o Pulmonary oedema

  • Bloods

o TFTs

o Digoxin level

o Cardiac enzymes

o Troponin

  • Echocardiogram

o Wall motion abnormalities

o Aortic valve disease

o Vegetations

27
Q

Generate a management plan for heart block

A
  • Chronic Block

o Permanent pacemaker is recommended in:

  • Complete heart block
  • Advanced Mobitz Type II
  • Symptomatic Mobitz Type I
  • Acute Block

o If associated with clinical deterioration use IV atropine

o Consider temporary (external) pacemaker

28
Q

Identify the possible complications of heart block

A
  • Asystole
  • Cardiac arrest
  • Heart failure
  • Complications of any pacemaker inserted
29
Q

Summarise the prognosis for patients with heart block

A

Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease

30
Q

Define hypertension

A
  • Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions.
  • Malignant Hypertension: BP > 200/130 mm Hg
31
Q

Summarise the epidemiology of hypertension

A
  • VERY COMMON

* 10-20% of adults in the Western world

32
Q

Explain the aetiology/risk factors of hypertension

A
  • Primary

o Essential or idiopathic hypertension

o Responsible for > 90% of cases

  • Secondary

o Renal

  • Renal artery stenosis
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • Polycystic kidney disease
  • Chronic renal failure

o Endocrine

  • Diabetes mellitus
  • Hyperthyroidism
  • Cushing’s syndrome
  • Conn’s syndrome
  • Hyperparathyroidism
  • Phaeochromocytoma
  • Congenital adrenal hyperplasia
  • Acromegaly

o Cardiovascular

  • Coarctation of the aorta
  • Increased intravascular volume

o Drugs

  • Sympathomimetics
  • Corticosteroids
  • COCP

o Pregnancy

  • Pre-eclampsia
33
Q

Recognise the presenting symptoms of hypertension

A
  • Often ASYMPTOMATIC
  • Symptoms of complications
  • Symptoms of the cause
  • Accelerated or Malignant Hypertension

o Scotomas (visual field loss)

o Blurred vision

o Headache

o Seizures

o Nausea and vomiting

o Acute heart failure

34
Q

Recognise the signs of hypertension on physical examination

A
  • Blood pressure should be measured on 2-3 different occasions before diagnosing hypertension
  • The lowest reading should be recorded
  • Examination may reveal information about causes:

o Radiofemoral delay = coarctation of the aorta distal to the left subclavian artery

o Renal artery bruit = renal artery stenosis

o Fundoscopy to detect hypertensive retinopathy

Keith-Wagner Classification of Hypertensive Retinopathy

i. Silver wiring
ii. As above + arteriovenous nipping
iii. As above + flame haemorrhages + cotton wood exudates
iv. As above + papilloedema

35
Q

Identify appropriate investigations for hypertension

A
  • Bloods:

o U&Es

o Glucose

o Lipids

  • Urine Dipstick

o Blood and protein (e.g. if glomerulonephritis)

  • ECG

o May show signs of left ventricular hypertrophy or ischaemia

  • Ambulatory blood pressure monitoring

o Excludes white coat hypertension

  • Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram)
36
Q

Generate a management plan for hypertension

A
  • Conservative

o Stop smoking

o Lose weight

o Reduce alcohol intake

o Reduce dietary sodium

  • Investigate for secondary causes (mainly in young patients)
  • Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage. Multiple drug therapies often needed.

o ACE Inhibitors or Angiotensin Receptor Blockers - first line if:

  • < 55 yrs
  • Diabetic
  • Heart failure
  • Left ventricular dysfunction

o CCBs - first line if:

  • > 55 yrs
  • Black
  • NOTE: thiazide diuretics can be used if CCBs are not tolerated

o Beta-Blockers

  • Not preferred initial therapy
  • May be considered in younger patients
  • CAUTION: combining with thiazide diuretic may increase risk of developing diabetes
  • May increase risk of heart failure

o Alpha-Blockers

  • 4th line
  • May be used in patients with prostate disease
  • Target BP

o Non-Diabetic: < 140/90 mm Hg

o Diabetes without proteinuria: < 130/80 mm Hg

o Diabetes WITH proteinuria: < 125/75 mm Hg

  • Severe Hypertension Management (Diastolic > 140 mm Hg)

o Atenolol

o Nifedipine

  • Acute Malignant Hypertension Management:

o IV beta-blocker (e.g. esmolol)

o Labetolol

o Hydralazine sodium nitroprusside

o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction

  • This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high
  • Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted
  • A rapid drop in blood pressure with constricted vessels will cause an infarction
37
Q

Identify the possible complications of hypertension

A
  • Heart failure
  • Coronary artery disease
  • Cerebrovascular accidents
  • Peripheral vascular disease
  • Emboli
  • Hypertensive retinopathy
  • Renal failure
  • Hypertensive encephalopathy
  • Posterior reversible encephalopathy syndrome (PRES)
  • Malignant hypertension
38
Q

Summarise the prognosis for patients with hypertension

A
  • Good prognosis if well controlled
  • Uncontrolled hypertension is associated with increased mortality
  • Treatment reduces incidence of renal damage, stroke and heart failure
39
Q

Define infective endocarditis

A

Infection of intracardiac endocardial structures (mainly heart valves)

40
Q

Explain the aetiology/risk factors of infective endocarditis

A
  • Most common organisms causing infective endocarditis:

o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis

o Staphylococci (35%) - S. aureus and S. epidermidis

o Enterococci (20%) - usually E. faecalis

o Other organisms:

  • Haemophilus
  • Actinobacillus
  • Cardiobacterium
  • Coxiella burnetii
  • Histoplasma (fungal)
  • Pathophysiology

o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia

o The vegetations are made up of platelets, fibrin and infective organisms

o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities

o Activation of the immune system can lead to the formation of immune complexes –> vasculitis, glomerulonephritis, arthritis

  • Risk Factors

o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)

o Prosthetic heart valves

o Turbulent blood flow (e.g. patent ductus arteriosus)

o Recent dental work/poor dental hygiene (source of S. viridans)

41
Q

Summarise the epidemiology of infective endocarditis

A
  • UK Incidence: 16-22/1 million per year
42
Q

Recognise the presenting symptoms of infective endocarditis

A
  • Fever with sweats/chills/rigors

o NOTE: this might be relapsing and remitting

  • Malaise
  • Arthralgia
  • Myalgia
  • Confusion
  • Skin lesions
  • Ask about recent dental surgery or IV drug use
43
Q

Recognise the signs of infective endocarditis on physical examination

A
  • Pyrexia
  • Tachycardia
  • Signs of anaemia
  • Clubbing
  • New regurgitant murmur or muffled heart sounds
  • Frequency of heart murmurs:

o Mitral > Aortic > Tricuspid > Pulmonary

  • Splenomegaly
  • Vasculitic Lesions

o Roth spots on retina

o Petechiae on pharyngeal and conjunctival mucosa

o Janeway lesions (painless macules on the palms which blanch on pressure)

o Osler’s nodes (tender nodules on finger/toe pads)

o Splinter haemorrhages

44
Q

Identify appropriate investigations for infective endocarditis

A
  • Bloods

o FBC - high neutrophils, normocytic anaemia

o High ESR/CRP

o U&Es

o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive

  • Urinalysis

o Microscopic haematuria

o Proteinuria

  • Blood Culture

o Do microscopy and sensitivities as well

  • Echocardiography

o Transthoracic or transoesophageal (produces better image)

  • Duke’s Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs
45
Q

Generate a management plan for infective endocarditis

A
  • Antibiotics for 4-6 weeks
  • On clinical suspicion = EMPIRICAL TREATMENT

o Benzylpenicillin

o Gentamicin

  • Streptococci - continue the same as above
  • Staphylococci

o Flucloxacillin/vancomycin

o Gentamicin

  • Enterococci

o Ampicillin

o Gentamicin

  • Culture Negative

o Vancomycin

o Gentamicin

  • SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics
46
Q

Identify the possible complications of infective endocarditis

A
  • Valve incompetence
  • Intracardiac fistulae or abscesses
  • Aneurysm
  • Heart failure
  • Renal failure
  • Glomerulonephritis
  • Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
47
Q

Summarise the prognosis for patients with infective endocarditis

A
  • FATAL if untreated

* 15-30% mortality even WITH treatment

48
Q

Define ischaemic heart disease

A
  • Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome.
  • ACS can be further subdivided into:

o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury

o NSTEMI

o STEMI - ST elevation with transmural infarction

o NOTE: MI = cardiac muscle necrosis resulting from ischaemia

(Laz page 75 has a good picture)

49
Q

Summarise the epidemiology of ischaemic heart disease

A
  • COMMON
  • Prevalence: > 2 %
  • More common in males
  • Annual incidence of MI in the UK ~ 5/1000
50
Q

Explain the aetiology/risk factors of ischaemic heart disease

A
  • Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
  • This is usually due to atherosclerosis
  • Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli
  • Atherosclerosis pathophysiology

o Endothelial injury leads to migration of monocytes into the subendothelial space

o These monocytes differentiate into macrophages

o Macrophages accumulate LDL lipids and become foam cells

o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans

o This leads to the formation of an atherosclerotic plaque

  • Risk Factors

o Male

o Diabetes mellitus

o Family history

o Hypertension

o Hyperlipidaemia

o Smoking

51
Q

Recognise the presenting symptoms of ischaemic heart disease

A
  • ACS

o Acute-onset chest pain

o Central, heavy, tight, crushing pain

o Radiates to the arms, neck, jaw or epigastrium

o Occurs at rest

o More severe and frequent pain that previously occurring stable angina

o Associated symptoms:

  • Breathlessness
  • Sweating
  • Nausea and vomiting
  • SILENT INFARCTS occur in the elderly and diabetics
  • Stable Angina

o Chest pain brought on by exertion and relieved by rest

52
Q

Recognise the signs of ischaemic heart disease on physical examination

A
  • Stable Angina

o Check for signs of risk factors

  • ACS

o There may be NO CLINICAL SIGNS

o Pale

o Sweating

o Restless

o Low-grade pyrexia

o Check both radial pulses to rule out aortic dissection

o Arrhythmias

o Disturbances of BP

o New heart murmurs

o Signs of complications (e.g. acute heart failure, cardiogenic shock)

53
Q

Identify appropriate investigations for ischaemic heart disease

A
  • Bloods

o FBC

o U&Es

o CRP

o Glucose

o Lipid profile

o Cardiac enzymes (troponins and CK-MB)

o Amylase (pancreatitis could mimic MI)

o TFTs

o AST and LDH (raised 24 and 48 hours post-MI, respectively)

  • ECG

o Unstable Angina or NSTEMI:

  • May show ST depression or T wave inversion

o STEMI:

  • Hyperacute T waves
  • ST elevation (> 1 mm in limb leads, > 2 mm in chest leads)
  • New-onset LBBB
  • Later changes:
  • T wave inversion
  • Pathological Q waves

o Relationship between ECG leads and the side of the heart

  • Inferior: II, III, aVF
  • Anterior: V1-V5/6
  • Lateral: I, aVL, V5/6
  • Posterior: Tall R wave and ST depression in V1-3
  • CXR

o Check for signs of heart failure

  • Exercise ECG

o Indications

  • Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
  • Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
  • NOTE: digoxin is associated with giving a false-positive result

o Results:

  • Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
  • Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
  • NOTE: beta-blockers reduce heart rate and so should be stopped before the test
  • Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
  • Radionuclide Myocardial Perfusion Imaging (rMPI)

o Uses Technetium-99m sestamibi or tetrofosmin

o Can be performed under stress or at rest

o Stress testing shows low uptake in ischaemic myocardium

  • Echocardiogram

o Measures left ventricular ejection fraction

o Exercise or dobutamine stress echo may detect regional wall motion abnormalities

  • Pharmacological Stress Testing

o This is used in patients who are unable to exercise

o Pharmacological agents can be used to induce a tachycardia, such as:

  • Dipyridamole
  • Adenosine
  • Dobutamine

o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium

o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease

  • Cardiac Catheterisation/Angiography

o Performed if ACS with positive troponin or if high risk on stress testing

  • Coronary Calcium Scoring

o Uses specialised CT scan

o May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia

54
Q

Generate a management plan for ischaemic heart disease

A
  • Stable Angina

o Check for signs of risk factors

  • ACS

o There may be NO CLINICAL SIGNS

o Pale

o Sweating

o Restless

o Low-grade pyrexia

o Check both radial pulses to rule out aortic dissection

o Arrhythmias

o Disturbances of BP

o New heart murmurs

o Signs of complications (e.g. acute heart failure, cardiogenic shock)

Identify appropriate investigations for ischaemic heart disease

  • Bloods

o FBC

o U&Es

o CRP

o Glucose

o Lipid profile

o Cardiac enzymes (troponins and CK-MB)

o Amylase (pancreatitis could mimic MI)

o TFTs

o AST and LDH (raised 24 and 48 hours post-MI, respectively)

  • ECG

o Unstable Angina or NSTEMI:

  • May show ST depression or T wave inversion

o STEMI:

  • Hyperacute T waves
  • ST elevation (> 1 mm in limb leads, > 2 mm in chest leads)
  • New-onset LBBB
  • Later changes:
  • T wave inversion
  • Pathological Q waves

o Relationship between ECG leads and the side of the heart

  • Inferior: II, III, aVF
  • Anterior: V1-V5/6
  • Lateral: I, aVL, V5/6
  • Posterior: Tall R wave and ST depression in V1-3
  • CXR

o Check for signs of heart failure

  • Exercise ECG

o Indications

  • Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease
  • Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender
  • NOTE: digoxin is associated with giving a false-positive result

o Results:

  • Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex
  • Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)
  • NOTE: beta-blockers reduce heart rate and so should be stopped before the test
  • Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm
  • Radionuclide Myocardial Perfusion Imaging (rMPI)

o Uses Technetium-99m sestamibi or tetrofosmin

o Can be performed under stress or at rest

o Stress testing shows low uptake in ischaemic myocardium

  • Echocardiogram

o Measures left ventricular ejection fraction

o Exercise or dobutamine stress echo may detect regional wall motion abnormalities

  • Pharmacological Stress Testing

o This is used in patients who are unable to exercise

o Pharmacological agents can be used to induce a tachycardia, such as:

  • Dipyridamole
  • Adenosine
  • Dobutamine

o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium

o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease

  • Cardiac Catheterisation/Angiography

o Performed if ACS with positive troponin or if high risk on stress testing

  • Coronary Calcium Scoring

o Uses specialised CT scan

o May be useful in outpatients with atypical chest pain or in acute chest pain that isn’t clearly due to ischaemia

55
Q

Identify the possible complications of ischaemic heart disease

A
  • STABLE ANGINA

o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes)

  • All patients should receive aspirin 75 mg/day unless contraindicated

o Immediate symptom relief (e.g. GTN spray)

o Long-term management

  • Beta-blockers
  • Contraindicated in:
  • Acute heart failure
  • Cardiogenic shock
  • Bradycardia
  • Heart block
  • Asthma
  • Calcium channel blockers
  • Nitrates

o Percutaneous coronary intervention (PCI)

  • Performed in patients with stable angina despite maximal tolerable medical therapy

o Coronary artery bypass graft (CABG)

  • Occurs in more severe cases (e.g. three-vessel disease)
  • UNSTABLE ANGINA/NSTEMI

o Admit to coronary care unit

o Oxygen, IV access, monitor vital signs and serial ECG

o GTN

o Morphine

o Metoclopramide (to counteract the nausea caused by morphine)

o Aspirin (300 mg initially, followed by 75 mg indefinitely)

o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk)

o LMWH (e.g. enoxaparin)

o Beta-blocker (e.g. metoprolol)

o Glucose-insulin infusion if blood glucose > 11 mmol/L

o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients:

  • Undergoing PCI
  • At high risk of further cardiac events

o If little improvement, consider urgent angiography with/without revascularisation

o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH

  • Morphine
  • Oxygen
  • Nitrates
  • Anticoagulants (aspirin + clopidogrel)
  • Beta-blockers
  • ACE inhibitors
  • Statins
  • Heparin
  • STEMI

o Same as UAP/NSTEMI management except:

  • Clopidogrel
  • 600 mg if patient is going to PCI
  • 300 mg if undergoing thrombolysis and < 75 yrs
  • 75 mg if undergoing thrombolysis and > 75 yrs
  • MAINTENANCE: 75 mg daily for at least 1 year
  • If undergoing primary PCI:
  • IV heparin (plus GlpIIb/IIIa inhibitor)
  • Bivalirudin (antithrombin)

o Primary PCI

  • Goal < 90 min if available

o Thrombolysis

  • Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase)
  • Only considered if within 12 hours of chest pain with ECG changes and not contraindicated
  • Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis

o Secondary Prevention

  • Dual antiplatelet therapy (aspirin + clopidogrel)
  • Beta-blockers
  • ACE inhibitors
  • Statins
  • Control risk factors

o Advice

  • No driving for 1 month following MI

o CABG

  • Considered in patients with left main stem or three-vessel disease

Identify the possible complications of ischaemic heart disease

  • Increased risk of MI and other vascular disease (e.g. stroke, PVD)
  • Cardiac injury from an MI can lead to heart failure and arrhythmias
  • Early Complications (within 24-72 hrs)

o Death

o Cardiogenic shock

o Heart failure

o Ventricular arrythmias

o Heart block

o Pericarditis

o Myocardial rupture

o Thromboembolism

  • Late Complications

o Ventricular wall rupture

o Valvular regurgitation

o Ventricular aneurysms

o Tamponade

o Dressler’s syndrome

o Thromboembolism

  • MNEMONIC for Complications of MI

o Death

o Arrhythmias

o Rupture

o Tamponade

o Heart failure

o Valve di

o Aneurysm

o Dressler’s syndrome

o Embolism

56
Q

Summarise the prognosis for patients with ischaemic heart disease

A
  • TIMI score (0-7) can be used for risk stratification

o NOTE: TIMI = thrombolysis in myocardial infarction

o High scores are associated with high risk of cardiac events within 30 days of MI

  • Killip Classification of acute MI can also be used:

o Class I: no evidence of heart failure

o Class II: mild to moderate heart failure

o Class III: over pulmonary oedema

o Class IV: cardiogenic shock

Old Y3 Sofia Notes (9 decks)

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