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Cardiovascular Diseases Flashcards

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1
Q

What is the normal presentation of atherosclerosis?

A

Normally asymptomatic until complications. If severe, can cause angina or neurological problems.

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2
Q

In which vessels can atherosclerosis occur?

A
  • central and peripheral arteries [cerebral too]
  • coronary arteries
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3
Q

What is the normal pathology of atherosclerosis?

A
  1. Fatty streaks.
    • consist of lipid-laden macrophages [foam cells] + T-lymphocytes within the intima layer
  2. Intermediate lesions.
    • made of layers of foam cells, vascular smooth muscles cells + T-lymphocytes
  3. Fibrous plaque.
    • covered by fibrous cap that is made of collagen and elastin for strength and flexibility.
  4. Plaque rupture.
    • the fibrous cap is resorbed and redeposited in order to be maintained
  5. Plaque erosion.
    • Second most prevalent cause of coronary thrombosis
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4
Q

How is atherosclerosis normally diagnosed?

A

Patients over 40 should be assessed for their risk during their NHS health check every 5 years

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5
Q

What is a fatty streak?

A
  • The earliest lesion of atherosclerosis.
  • Aggregation of lipid-laden macrophages (foam cells), and T lymphocytes within the intima
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6
Q

What are the risk factors for atherosclerosis?

A
  • Hyperlipidaemia
  • hypertension
  • smoking,
  • poorly controlled diabetes,
  • males,
  • older age,
  • social deprivation,
  • family history,
  • south Asian African or Caribbean descent
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7
Q

What are some natural preventative measures for atherosclerosis?

A
  • Smoking cessation
  • weight reduction
  • lower alcohol consumption
  • exercise
  • managing diabetes, controlling blood pressure
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8
Q

What medications can be used to prevent progression of atherosclerosis?

A

Statins (satorvastatin, fluvastatin),
Blood pressure medications= CCB, ARBs, ACE
Low dose aspirin

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9
Q

What surgical interventions can be used for atherosclerosis?

A

PCI, Coronary angioplasty, coronary artery bypass

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10
Q

What are some possible complications of atherosclerosis?

A
  • Coronary artery disease, angina, myocardial infarction,
  • stroke, TIA,
  • peripheral artery disease
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11
Q

What is the normal presentation of hypertension?

A

Usually asymptomatic
extremely high BP can cause:
- severe headaches.
- chest pain.
- dizziness.
- difficulty breathing
- Visual changes

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12
Q

What are the risk factors for hypertension?

A

Obesity, high salt, caffeine, alcohol, low exercise, over 65s, family history, black African or Caribbean descent, some medications such as the pill, steroids, Eclampsia, renal disease, smoking

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13
Q

What are the types of hypertension?

A 
Essential / Primary= Unknown cause
Secondary= Caused by another condition
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14
Q

What is the aetiology for secondary hypertension?

A

R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)

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15
Q

What is CBP?

A

Clinic blood pressure

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16
Q

What is ABPM?

A

Ambulatory blood pressure monitoring

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17
Q

What is HBPM?

A

Home blood pressure monitoring

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18
Q

What CBP would imply stage 1 hypertension?

A

> 140/90

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19
Q

How is a diagnosis of hypertension made?

A
  • CBP of over 140/90 on two separate readings, then offered ABPM or HBPM to confirm.
  • NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.
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20
Q

What CBP would imply stage 2 hypertension?

A

> 160/100

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21
Q

What CBP would imply stage 3 hypertension?

A

> 180/120

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22
Q

What extra investigations would be offered to someone with hypertension?

A
  • Urine albumin:creatinine ratio for proteinuria and
  • dipstick for microscopic haematuria to assess for kidney damage
  • Bloods for HbA1c and lipids
  • Blood U&E for renal impairment
  • Fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities, including left ventricular hypertrophy
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23
Q

What preventative measures can be taken for hypertension?

A
  • lifestyle changes: Exercise, smoking cessation, lower salt intake, lower alcohol and caffeine, healthy BMI
  • QRISK measurement and early statins if >10%
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24
Q

What would be the first line of treatment for someone with T2DM or is under 55 and non-black, who has hypertension?

A

ACE inhibitor or angiotensin II inhibitor (ARB)

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25
What would be the second line of treatment for someone with type II diabetes or is under 55 and non-black, who has hypertension?
Ace inhibitor or angiotensin II inhibitor + Calcium channel blocker | or ACEi/ARB + thiazide-like diuretic
26
What is the third line of treatment for anyone with hypertension?
ACE inhibitor or angiotensin II inhibitor Calcium channel blocker Thiazide diuretic
27
What is the first line of treatment for someone over 55 or black African/Caribbean with hypertension?
Calcium channel blocker
28
What is the second line of treatment for someone over 55 or black African/Caribbean with hypertension?
Calcium channel blocker | ACE inhibitor or Angiotensin II inhibitor or Thiazide diuretic
29
What are some complications of hypertension?
- Myocardial infarction, stroke, heart failure, aortic aneurysm, kidney disease, vascular dementia - CAD, malignant hypertension, cerebrovascular event [ACS/stroke], CKD, retinopathy, heart failure, LVH, aortic dissection, peripheral arterial disease
30
What is the epidemiology of patent ductus arteriosus?
Affects girls more than boys | 0.02% of live births
31
Briefly explain the pathophysiology of patent ductus arteriosus
- If the baby is premature or in cases of maternal rubella etc. the ductus ( between the pulmonary artery and aorta) does not close. - The pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery. - This creates a left to right shunt where blood from the left side of the heart crosses to the circulation from the right side. - This increases the pressure in the pulmonary vessels causing pulmonary hypertension, leading to right sided heart strain as the right ventricle struggles to contract against the increased resistance. - Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy. - The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy
32
What is the clinical presentation of patent ductus arteriosus?
- Continuous machine-whirring murmurs - Bounding pulse - If large- large heart and breathlessness - Tachycardia - Eisenmenger's syndrome Shortness of breath Difficulty feeding Poor weight gain Lower respiratory tract infections
33
How is patent ductus arteriosus diagnosed?
- CXR: With large shunt, the aorta and pulmonary arterial system may be prominent - ECG: May demonstrate left atrial abnormality and left ventricular hypertrophy - Echocardiogram: shows left to right shunt and May show right +/or left ventricle hypertrophy
34
How is patent ductus arteriosus treated?
- Duct closure surgically or trans-catheter - Low risk of complications - Venous approach may require an AV loop - Indometacin [NSAID] (prostaglandin inhibitor) can be given to stimulate duct closure as PGs keep the duct open
35
What is the epidemiology of ventricular septal defect?
Common, 20% of all congenital heart defects
36
What is the aetiology of ventricular septal defect?
Unknown, some genetic factors
37
Briefly explain the pathophysiology of ventricular septal defect?
A hole connects the ventricles, - increased pressure in the left ventricle compared to the right - Thus left to right shunt created. - Increased blood flow through the lung --> right sided overload, right heart failure and pulmonary hypertension. - **pt is NOT cyanotic as blood is passing through the lungs before the body** - Over time, the pressure in the right side of the heart may surpass that of the left --> right to left shunt and cyanosis and the lungs are bypassed and deoxygenated blood is circulated around the body. = Eisenmenger Syndrome
38
What is the clinical presentation of a large ventricular septal defect?
- Pulmonary hypertension and eventual Eisenmenger's complex - Small breathlessness baby - Increased respiratory rate - Tachycardia - CRX: Big heart - Murmur varies in intensity
39
What is the clinical presentation of small ventricular septal defect?
- Large systolic murmer - Thrill (buzzing sensation) - Well grown - Normal heart rate - Normal heart size
40
How is ventricular septal defect diagnosed?
EchoCG: Normal (small), LAD and LVH (Medium), LVH and RVH (Large) CXR: Pulmonary plethora and cardiomegaly, large pulmonary arteries
41
How is ventricular septal defect treated?
- Surgical closure - Medical initially since many will spontaneously close - If small, no intervention required - Prophylatic antibiotics - If moderately sized lesion; ACE inhibitor, Furosemide
42
What are some possible complications of ventricular septal defect?
- Aortic regurgitation - Cardiac Failure - Infundibular stenosis - Infective endocarditis - Subacute bacterial endocarditis - Pulmonary hypertension
43
What is the epidemiology of abdominal aortic aneurysm?
- Present in 5% of population over 60 | - More common in men
44
What is abdominal aortic aneurysm?
- dilation of the vessel wall >50% -> a diameter of >3cm - A diametre of over 3cm | - Most occur below renal arteries
45
What are the causes/ risk factors of abdominal aortic aneurysm?
- Normally no identifiable cause - Men are affected significantly more often and at a younger age than women - Increased age - Smoking - Hypertension - Family history - Existing cardiovascular disease
46
Briefly explain the pathophysiology of abdominal aortic aneurysm
- The collagen and elastin within the tunica media and adventitia are destroyed and smooth muscle cells lost - The dilation affects all 3 layers of the vascular tunic Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss
47
What are the clinical features of unruptured abdominal aortic aneurysm?
- Often asymptomatic- only picked up via abdominal examination/ x ray - Pain in abdomen, back, loin or groin - Pulsatile, expansile abdominal swelling
48
What are the clinical features of ruptured abdominal aortic aneurysm?
- Intermittent or continuous abdominal pain (radiates to back, iliac fossa or groin) - Pulsatile abdominal swelling - Collapse - Shock:hypotension + tachycardia, - profound anaemia, - sudden death - Grey-Turner's sign: Flank bruising secondary to retroperitoneal haemorrhage
49
How is abdominal aortic aneurysm diagnosed?
- Abdominal ultrasound | - CT angiogram gives a more detailed picture of the aneurysm and helps guide elective surgery to repair the aneurysm.
50
How is abdominal aortic aneurysm treated?
- Small aneurysms are generally just monitored - Treat underlying cause - Modify risk factors (diet, smoking) - Vigorous BP control - Lowering of lipid in blood - Surgery; open surgical repair, endovascular repair= stent inserted via femoral or iliac arteries
51
What is the epidemiology of aortic dissection?
- Affects men more than women | - Most common between 50-70 yrs
52
What are the causes of aortic dissection?
- Atherosclerosis - uncontrolled hypertension - Trauma - Connective tissue disorders - Ehlers-Danlos Syndrome + Marfan’s Syndrome - Bicuspid aortic valve - Coarctation of the aorta
53
Briefly explain the pathophysiology of aortic dissection
- A tear in the intima of the aorta allows a column of blood to enter the aortic wall, creating a false lumen - This extends for a variable distance in either direction; anterograde (Towards bifurcations) or retrograde (towards aortic root) - narrows the true lumen
54
What are the clinical features of aortic dissection?
- Sudden onset of severe, central chest pain that radiates to back and down the arms - Differences in blood pressure between the arms (more than a 20mmHg difference is significant) - Patients may be shocked and have neurological symptoms - Chest and abdominal pain - Radial pulse deficit (the radial pulse in one arm is decreased or absent and does not match the apex beat) - Absent peripheral pulses - Hypertension - Complications: May develop aortic regurgitation, coronary ischaemia, cardiac tamponade
55
How is aortic dissection diagnosed?
- CT angiography = GS - confirms the diagnosis and can generally be performed very quickly | - MRI angiography will confirm - Chest X-ray + ECG: may demonstrate a widened mediastinum and rule out other potential causes - Ultrasound - Indicates site/extent
56
How is aortic dissection treated?
- Blood pressure and heart rate need to be well controlled to reduce the stress on the aortic walls. This usually involves beta-blockers - Adequate analgesia - MORPHINE - Surgery to replace aortic arch OR repair the tear depending on type A or B - Endovascular intervention with stents - Long term follow up with CT or MRI
57
What are the 3 acute coronary syndromes?
- ST-elevation myocardial infarction (STEMI) - Non-ST-Elevation myocardial infarction (NSTEMI) - Unstable angina
58
What causes a STEMI?
- A complete occlusion of a major coronary artery previously affected by atherosclerosis - Causes a full thickness damage of heart muscle due to infarction
59
What causes a NSTEMI?
- A complete occlusion of a minor or a partial occlusion of a major coronary artery affected by atherosclerosis - Partial thickness damage of heart muscle
60
What is the difference between Unstable Angina and a NSTEMI?
In a NSTEMI, there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatinine kinase- MB
61
What are the clinical features of mitral stenosis?
- Left atrial dilation and AF - RV hypertrophy and palpitations - Malar flush due to low CO - diastolic murmer - Haemoptysis - Pulmonary hypertension leading to dyspnoea and pink frothy sputum tapping apex beat
62
What causes mitral stenosis?
- infections: esp Rheumatic valvular disease (usually strep pyogenes) causes thickening of the mitral valve, obstructing normal flow. age via annular calcification - This raises the left atrium pressure, causing left atrium hypertrophy and dilation, causing palpitations. - Raised left atrial pressure also leads to pulmonary hypertension thus RV failure.
63
How is mitral stenosis diagnosed?
- ECG= AF, LA enlargement, RV hypertrophy - Echocardiography= Definitive diagnosis, measure mitral orifice
64
How is mitral stenosis treated?
- Diuretics (furosemide)= rate control and anticoagulation - Valvotomy - Excise segments of valve, or valve replacement - Infective endocarditis prophylaxis - BB for rate control
65
What are the clinical features of mitral regurgitation?
- Dyspnoea - AF  - Oedema - Malar flush - Haemoptysis - Diastolic murmur - Tapping apex beat – palpable with a prominent S1.
66
What causes mitral regurgitation?
- Mitral valve fails to prevent blood pressure reflux due to inability to shut properly, caused by infective endocarditis or rheumatic valvular disease. - IHD + HTN also - Regurgitation into the left atria, causes a raise in LA pressure. This increases the pulmonary pressure, causing pulmonary oedema.
67
How is mitral regurgitation diagnosed?
- Echocardiography
68
How is mitral regurgitation treated?
- Repair preferred over replacement - treat underlying AF + HF
69
What is the epidemiology of atrial flutter?
- More common in men | - Prevelance increases with age
70
What is atrial flutter?
- An organised atrial rhythm with an atrial rate typically between 250-350 bpm = tachycardia - caused by a re-entrant circuit that allows propagation of the signal repeatedly through the right atrium.
71
What are the causes of atrial flutter?
- causes are often pulmonary: COPD, PE, pulmonary hypertension. - Also: IHD, sepsis and alcohol - Atrial flutter is caused by a re-entrant rhythm in either atrium. - The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria without interruption - each signal doesn't enter the AV node due to the refractory period -> a conduction ratio of 2:1 or 3:1 etc.
72
What are the clinical features of atrial flutter?
- asymptomatic - Palpitations - Breathlessness - Chest pain - Dizziness - Syncope - Fatigue
73
How is atrial flutter diagnosed?
- ECG: Regular sawtooth-like atrial flutter waves (repeated P waves) between QRS complexes due to continuous atrial depolarisation
74
How is atrial flutter treated?
- Rate control - beta blockers, CCB and digoxin. - Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide. - Electrical cardioversion but anticoagulate beforehand - Catheter ablation
75
What is sinus tachycardia?
- Heart rate greater than 100bpm
76
What causes sinus tachycardia?
- Anaemia - Anxiety - Exercise - Pain - Infection - Heart failure - Pulmonary embolism
77
How is sinus tachycardia treated?
- Treat causes. If necessary, beta blockers can be used.
78
Briefly explain the pathophysiology of supraventricular tachycardia?
- Supraventricular tachycardia is caused by the electrical signal re-entering the atria from the ventricles. 3 types of SVT - The gating mechanism of the AV node is being bypassed. - 1) In re-entrant, a bypass tract exists to go around the node (Wolff-Parkinson-White syndrome) - 2) In automatic, an impulse is created that never encounters the AV node - 3) The signal passes back through the AV node into the atria in AV-node re-entrant tachycardia
79
What are the clinical features of supraventricular tachycardia?
- Paroxysmal attacks - May be minimal - Syncope and palpitations - Tachycardia
80
How is supraventricular tachycardia treated?
- Haemodynamically unstable= Cardioversion - Haemodynamically stable= Carotid massage/ Valsalva manoeuvre
81
What are the risk factors for supraventricular tachycardia?
- Previous MI - Mitral valve prolapse - Rheumatic heart disease - Pericarditis Heart disease. Heart failure. Other heart conditions, such as Wolff-Parkinson-White syndrome. Chronic lung disease. A lot of caffeine. Drinking too much alcohol. Drug misuse, including cocaine and methamphetamine.
82
How is supraventricular tachycardia diagnosed? | what are the results
- ECG= P waves may not be visible. Pre-excitation on resting ECG, and rapid and paroxysmal regular palpitations. **Short PR interval**
83
What causes supraventricular tachycardia?
- Drugs - Alcohol - Caffeine - Congenital - Stress - Smoking
84
What are the general clinical features of bundle branch block?
- Asymptomatic usually | - Possible syncope
85
What causes a right bundle branch block?
- Right ventricular hypertrophy - Pulmonary embolism - Ischaemic heart disease - Congenital heart disease (ASD) - Normal variant
86
How is right bundle branch block diagnosed?
- ECG= maRRow QRS looks like a M in lead V1 QRS looks like a W in leads V5 and V6
87
How is right bundle branch block treated?
- May require pacemaker
88
What causes a left bundle branch block?
- IHD - Aortic valve stenosis - MI - Hyperkalaemia - Left ventricular hypertrophy
89
How is left bundle branch block diagnosed?
- ECG= wiLLiam W= QRS looks like a W in leads V1 and V2 M= QRS looks like an M in leads V4-V6 Also abnormal Q waves
90
How is left bundle branch block treated?
- Treat underlying cause
91
What are the two types of acute myocardial infarction?
STEMI NSTEMI
92
What are the clinical features of acute myocardial infarction?
- Chest pain= severe ongoing pain which may radiate into the left arm, jaw or neck - Nausea, vomitting, dyspnoea, fatigue and/or palpitations - Distress and anxiety - Pale, clammy and marked swelling - Significant hypotension
93
How is a STEMI diagnosed?
Can be diagnosed on presentation by ECG - ST elevation - Tall T waves - L bundle branch block - T wave inversion and pathological Q waves follow - After afew days, the ST segment returns to normal, but the Q wave remains
94
How is a NSTEMI diagnosed?
Diagnosed retrospectively by ECG - ST depression - T wave inversion Also troponin I or T increased
95
What is ventricular ectopics?
Premature ventricular contraction
96
What are the clinical features of ventricular ectopics?
- May be uncomfortable especially when frequent - Pulse is irregular owing to the premature beats - Usually asymptomatic - Can feel faint or dizzy
97
How are ventricular ectopics diagnosed?
ECG= Widened QRS complex (greater than 0.12 seconds)
98
How are ventricular ectopics treated?
- Reassure patient | - Give beta blockers e.g. bisoprolol if symptomatic
99
What is ventricular tachycardia?
Pulse of more than 100bpm with at least 3 irregular heart beats in a row
100
Briefly explain the pathophysiology of ventricular tachycardia?
- Rapid ventricular beating so inadequate blood filling between beats - Therefore decreased cardiac output, and thus a decrease in the amount of oxygenated blood circulating
101
What are the clinical features of ventricular tachycardia?
- Breathlessness - Chest pain - Palpitations - Light headed/ dizzy
102
How is ventricular tachycardia treated?
Beta blockers e.g. bisoprolol
103
What is sustained ventricular tachycardia?
Ventricular tachycardia for longer than 30 seconds
104
What is intermittent claudication?
- Ischaemic leg pain | - When exercising, there is lactic acid build up, causing pain
105
What is the epidemiology of aortic stenosis?
- Primarily a disease of the old - Congenital= 2nd most common cause - Most common valvular disease
106
What are the causes of aortic stenosis?
- Calcific aortic valvular disease - Calcification of the congenital bicuspid aortic valve - Rheumatic heart disease
107
What are the types of aortic stenosis?
- Supravalvular - Subvalvular - Valvular
108
Briefly explain the pathophysiology of aortic stenosis?
- Obstructed left ventricular emptying - Results in increased afterload - This causes increased left ventricular pressure - In turn, this results in relative ischaemia of the LV myocardium, and consequent angina, arrythmias and LV failure
109
What are the clinical features of aortic stenosis?
- Syncope - Angina - Heart failure - Dyspnoea on exertion - Sudden death - Slow rising carotid pulse - Heart sounds= soft or absent 2nd heart sound, prominent 4th heart sound, ejection systolic murmer-crescendo-decrescendo character
110
How is aortic stenosis diagnosed?
- Echocardiogram= LV hypertrophy, dilation and ejection fraction. Doppler derived gradient and valve area. Doppler ultrasound to assess pressure gradient across the valve during systole - ECG= LV hypertrophy, left atrial delay, LV strain pattern due to pressure overload= ST depression, T wave invesion - CXR= LV hypertrophy, calcified aortic valve
111
How is aortic stenosis treated?
Surgery - Valve replacement - Balloon valvuloplasty - Transcatheter aortic valve replacement - Surgical valvuloplasty TAVI= Transcathater aortic valve implantation
112
What are the 2 causes of acute lower limb ischaemia?
- Embolitic or thrombotic disease
113
What are the symptoms of acute lower limb ischaemia?
- Pain - Pallor - Perishing cold - Pulseless - Paralysis - Paraestesia
114
What is critical limb ischaemia?
- Blood supply is barely adequate to allow basal metabolism - Rest pain that is typically nocturnal - Risk of gangrene and/or infection - Critical condition, and most severe clinical manifestation of peripheral vascular disease
115
What are the clinical features of severe chronic lower limb ischaemia?
- Infarction - Gangrene - General symptoms= Absent femoral, popliteal or foot pulses, cold white legs
116
What is the most common cause of peripheral vascular disease?
- Atherosclerosis
117
What are the risk factors for peripheral vascular disease?
- Smoking - Diabetes - Hypercholesterolaemia - Hypertension - Physical inactivity - Obesity
118
What are the signs of peripheral vascular disease?
- Absent femoral, popliteal or foot pulses | - Cold, white legs
119
How is peripheral vascular disease diagnosed?
- ECG: 60% of claudication patients have evidence of coronary artery disease. - Doppler ultrasonography: Confirm diagnosis. Site, degree and length. - ABPI
120
How is peripheral vascular disease treated?
Modify risk factors - Revascularisation for critical ischaemia - Surgical treatment for acute ischaemia
121
What are the 4 types of angina?
- Stable - Unstable - Decubitus - Prinzmetals-vasopastic
122
What is stable angina?
- Angina that is induced by effort and relieved by rest - An attack lasts less than 20 mins - Subendocardium is most commonly affected
123
What is unstable angina?
- Continuous pain of increasing severity/ frequency - Minimal exertion - Can also happen at rest
124
What is decubitus angina?
- Pain when lying flat
125
What is Prinzmetals-Vasopastic angina?
- Pain during rest | - Likely involves vasoconstriction factors like platelet thromboxane A2. All layers are affected
126
What causes stable, unstable or decubitus angina?
Atheroma obstructing or narrowing coronary vessels. Due to aortic stenosis, atheroma or hypertension
127
What causes Prinzmetals-Vasopastic angina?
Coronary artery spasm. Doesn't correlate with exertion
128
What are the clinical features of angina?
- Tightness or heaviness in chest or exertion/rest/cold/emotion - May radiate to one or both arms/jaw/neck or teeth - Dyspnoea - Nausea - Sweatiness - Faintness
129
What are the complications of angina?
Increased risk of MI
130
How is angina diagnosed?
ECG= Normally normal, flat or inverted T waves - ST depression for stable and unstable angina - ST elevation in Prinzmetals-Vasopastic
131
How is Angina treated?
- Modify risk factors - Aspirin - Beta blockers - Nitrates - Long acting calcium channel blockers - K+ channel activators - Nitroglycerine - Calcium channel blockers
132
What is the epidemiology of atrial fibrillation?
- Most common sustained cardiac arrythmia - Males more than females - Affects around 5-15% of patients over age 75
133
What are the risk factors for atrial fibrillation?
- Over 60 - Diabetes - Prior MI
134
Briefly explain the pathophysiology of atrial fibrillation?
- Atrial activity is chaotic and mechanically ineffective and stagnation of blood in the atria causes thrombus formation - Reduction in cardiac output causes heart failure - Higher risk of thromboembolic events
135
What are the causes of atrial fibrillation?
- Idiopathic - Any condition that results in increased atrial pressure - Hypertension - Heart failure - Coronary artery disease - Valvular heart disease - Cardiac surgery - Cardiomyopathy - Rheumatic heart disease - Acute excess alcohol intake
136
What are the clinical features of atrial fibrillation?
- Variable symptoms - May be asymptomatic - Palpitations - Dyspnoea and chest pains - Fatigue - Apical pulse is greater than radial rate - 1st heart sound is of variable intensity
137
How is atrial fibrillation diagnosed?
ECG - Absent P waves - Irregular and rapid QRS complex
138
How is atrial fibrillation treated?
- Treat underlying cause - Drugs for rate control (calcium channel blocker, beta blockers, digoxin, anti arrhythmic) - AV nodal slowing agents - Cardioversion - Anticoagulation
139
What causes long QT syndrome?
- Jervell-Lange-Nielsen syndrome - Romano-Ward syndrome - Hypokalaemia - Hypocalcaemia - Certain drugs - Bradycardia - Acute MI - Diabetes
140
What are the clinical features of long QT syndrome?
- Syncope | - Palpitations
141
How is long QT syndrome diagnosed?
ECG
142
How is long QT syndrome treated?
- Treat underlying cause | - IV isoprenaline
143
What causes acute pericarditis ?
- Viral= Enteroviruses, adenoviruses - Bacterial= Myocardium TB - Neoplastic - Autoimmune conditions - Pericardial injury syndromes - Iatrogenic trauma
144
What are the clinical features of acute pericarditis?
- Chest pain: severe, sharp and pleuritic. Rapid onset. Worse on inspiration or lying flat. Pain may radiate to arm - Fever or lymphocytosis if due to infection - Pericardial friction rub present on ausiculation - Tachycardia - Dyspnoea, cough, hiccups
145
How is acute pericarditis treated?
- Restrict physical activity until resolution of symptoms - NSAIDs for 2 weeks - Colchicine for 3 weeks
146
How is acute pericarditis diagnosed?
- ECG: Saddle shaped ST elevation, PR depression - CXR: Cardiomegaly, pneumonia is common - FBC: Slight increase in WCC, anti neutrophil antibody in young females, SLE - ESR/CRP= increased ESR if autoimmune
147
What are the differentials for acute pericarditis?
- Angina - MI (most important to rule out) - Pleural pain - GI reflux
148
What are the two types of second degree AV block?
Mobitz I and Mobitz II
149
What is first degree AV block?
Prolongation of the PR interval to greater than 0.22s.
150
What is second degree AV block?
Occurs when some P waves conduct and others do not
151
What is third degree AV block?
Complete heart block. When all atrial activity fails to conduct to the ventricles
152
What are the 4 types of cardiomyopathy?
- Restrictive - Dilated - Hypertrophic - Arrhythmogenic right ventricular
153
What are the most common organisms that cause infective endocarditis?
- Staph. Aureus (Most common) - P. Aeruginosa - Strep. Viridans
154
What are the risk factors for infective endocarditis?
- IV Drug use - Poor dental hygiene - Skin and soft tissue infection - Dental treatment - IV cannula - Cardiac surgery - Pacemaker
155
What are the clinical features of infective endocarditis?
- Fever plus prosthetic material inside the heart, RF for infective endocarditis, newly developed ventricular arrhythmias or conduction disturbances - Headache, fever, malaise, confusion and night sweats - Heart failure - Splinter hemorrhages on nail beds, embolic skin lesions, osler nodes, Janeway lesions, roth spots
156
How is infective endocarditis diagnosed?
- Blood cultures - Blood test: CRP&ESR raised. Normochromic normocytic anaemia. Neutrophilia - Urinalysis- look for haematuria - CXR: Cardiomegaly - ECG: Long PR interval at regular intervals - Echo (normally transoesophageal echo)
157
How is infective endocarditis treated?
- Antibiotic treatment for 4-6 weeks - If not staph. then use penicillin - If staph then use vancomycin and rifampicin - Surgery= removing valve and replacing with prosthetic
158
How is shock recognised?
- Skin is pale, sweaty and vasoconstricted - Pulse is weak and rapid - Pulse pressure is reduced - Reduced urine output - Confusion, weakness, collapse and coma
159
What are the causes of shock?
- Hypovolaemic shock - Cardiogenic shock - Distributive shock - Anaemic shock - Cytotoxic shock
160
How is shock treated?
ABC
161
What are the 4 features of tetralogy of fallot?
- A large, maligned ventricular septal defect - An overriding aorta - RV outflow obstruction - RV hypertrophy
162
What are the clinical features of tetralogy of fallot? -
- Central cyanosis - Low birthweight and growth - Dyspnoea on exertion - Delayed puberty - Systolic ejection murmers - CXR: boot shaped heart
163
How is tetralogy of fallot treated?
- Full surgical treatment during first 2 years of life due to progressive cardiac debility and cerebral thrombosis risk - Often get pulmonary valve regurg in adulthood and require redo surgery
164
What is Cor Pulmonale?
Right sided heart failure due to chronic pulmonary arterial hypertension
165
What are the causes of Cor Pulmonale?
- Chronic lung disease - Pulmonary vascular disorders - Neuromuscular and skeletal disease
166
What are the clinical features of Cor Pulmonale?
- Dyspnoea - Fatigue - Syncope - Cyanosis - Tachycardia - Raised JVP - Pan systolic murmur due to tricuspid regurg - RV heave - Hepatomegaly - Oedema
167
How is Cor Pulmonale diagnosed?
ABG- Hypoxia +/- hypercapnia
168
How is Cor Pulmonale treated?
- Treat underlying cause - Give oxygen to treat resp failure - Treat cardiac failure - Consider venesection if haemocrit >55 - Consider heart-lung transplant in young patients
169
What are the causes of Wolff-Parkinson-White syndrome?
- Congenital - Hypokalaemia - Hypocalcaemia - Drugs; amiodarone, tricyclic antidepressants - Bradycardia - Acute MI - Diabetes
170
What are the clinical features of Wolff-Parkinson-White syndrome?
- Usually benign but can make some arrythmias more severe - Palpitations - Severe dizziness - Dyspnoea
171
How is Wolff-Parkinson-White syndrome diagnosed?
ECG= Pre-excitation, short PR interval, Wide QRS complex that begins slurred (Delta wave)
172
How is Wolff-Parkinson-White syndrome treated?
- Vagal manoeuvre= Breath holding, carotid massage, valsalva manoeuvre - IV adenosine - Surgery
173
What are the causes of aortic regurgitation?
- Congenital bicuspid valves - Rheumatic fever - Infective endocarditis
174
What are the risk factors for aortic regurgitation?
- SLE - Marfan's and Ehler's-Danlos syndrome - Aortic dilation - IE or aortic dissection
175
What are the clinical features of aortic regurgitation?
- In chronic regurg, patients remain symptomatic for many years - Exertional dyspnoea and syncope - Palpitations, angina - Apex beat displaced laterally - Heart sounds; Early diastolic low pitched rumbling murmer, and Austin Flint murmer
176
How is aortic regurgitation diagnosed?
- Echo: evaluation of the aortic valve and valve root. Measurement of left ventricle dimensions and function - CXR: Enlarged cardiac silhouette and aortic root enlargement. LV enlargement - ECG: Signs of LV hypertrophy, tall R waves and deeply inverted T waves
177
How is aortic regurgitation treated?
- Infective endocarditis prophylaxis - Vasodilators such as ACE-I will improve stroke vol and reduce regurgitation - Serial echos for monitoring - Surgery for valve replacement
178
What is the immediate management of acute coronary syndrome?
``` MONAC Morphine Oxygen Nitrate Aspirin 300mg stat Clopidogrel ```
179
How is STEMI treated?
- PCI (clopidogrel and aspirin) if treated in 120 mins - Fibrinolysis (alteplase) - Prevention
180
How is NSTEMI/ Unstable angina treated?
- GRACE score for risk of NSTEMI - Fondaparinux - Prevention
181
How is acute coronary syndrome prevented?
ACAAB - ACE I - Clopidogrel - Aspirin - Atorvastatin - Beta blocker
182
What are the complications of acute coronary syndrome?
DREAD - Death - Rupture of myocardium - Edema (Heart failure) - Arrhythmia - Dressler's syndrome
183
What is a common side effect of calcium channel blockers?
Ankle swelling
184
What is a common side effect of ACE-I?
Cough
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