cardio Flashcards
1
Q
What is thrombosis?
A
Blood coagulation in a vessel
2
Q
What is DVT?
deep vein thrombosis
A
The development of a blood clot within a vein deep to the muscular tissue planes
normally in a major deep vein in leg, thigh, pelvis, abdomen
3
Q
Which factors does warfarin prevent synthesis of?
A
2
7
9
10
4
Q
What scoring system is used in DVT?
A
Well’s diagnostic algorithm
5
Q
What is an aneurysm?
A
a permanent and irreversible dilatation of a blood vessel by at least 50% of the normal expected diameter
6
Q
What is the normal diameter of the abdominal aorta?
A
2cm
Increases with age
7
Q
What is the threshold diameter of an AAA?
A
3cm
8
Q
What are the different sizes of AAAs?
A
Normal: less than 3cm
Small aneurysm: 3 – 4.4cm
Medium aneurysm: 4.5 – 5.4cm
Large aneurysm: above 5.5cm
9
Q
What is a pseudoaneurysm?
A
caused by blood leaking through the arterial wall but contained by the adventitia or surrounding perivascular tissue
10
Q
What prophylaxis is offered to patients in hospital at higher risk of VTE?
A
Low molecular weight heparin
Compression stockings
11
Q
What are contraindications to giving LMWH?
A
Active bleeding
Existing anticoagulation (warfarin, DOAC)
12
Q
What is a contraindication to using compression stockings as prophylaxis for VTE?
A
Peripheral arterial disease
13
Q
What is the epidemiology for VTE?
A
1 in 1000
2/3 of these are DVT, 1/3 PE
14
Q
What is the aetiology of DVT and PE?
(and what model shows this?)
A
Virchow’s triad:
* Stasis: blood flows slowly or becomes turbulent, could be caused by immobility, long travel, varicose veins, obesity
* Hypercoagulability: blood coagulates quicker than normal, e.g. thrombophilia, oestrogen therapy, malignancy, infection and inflammation
* Endothelial injury: e.g. physical trauma, hypertension
15
Q
What makes up Virchow’s triad?
A
- Stasis: blood flows slowly or becomes turbulent
- Hypercoagulability: blood coagulates quicker than normal
- Endothelial injury
16
Q
What are the risk factors for DVT and PE?
A
Immobility
Recent surgery
Pregnancy
Long haul travel
Hormone therapy with oestrogen, combined pill or HRT
Polycythaemia
Malignancy, cancer
SLE
Thrombophilia: e.g. antiphospholipid syndrome
17
Q
Is the D-dimer test specific for VTE?
A
No
It’s sensitive so most patients with DVT will have a positive d-dimer
But not all positive d-dimers mean a DVT
18
Q
What are 2 anticoagulants used in the treatment or prophylaxis of VTE?
A
apixaban
rivaroxaban
prophylaxis after some surgeries
19
Q
What is a PE?
A
dislodged thrombi occluding the pulmonary vasculature
20
Q
What are the key presentations for DVT/PE?
A
Calf or leg swelling and pain
Chest pain
Breathlessness
21
Q
Differential diagnoses for PE
A
Angina
MI
COPD/asthma acute exacerbation
Pneumothorax
Congestive heart failure
22
Q
Differential diagnoses for DVT
A
Cellulitis
Calf muscle tear/Achilles’ tendon tear
Calf muscle haematoma
Large or ruptured popliteal cyst (Baker’s cyst)
Pelvic/thigh mass/tumour compressing venous outflow from the leg
23
Q
What investigations would you carry out for suspected DVT?
A
D-dimer
Doppler (venous) ultrasound
24
Q
What investigation would you run for suspected PE?
apart from d-dimer
A
CTPA
CT pulmonary angiogram
25
How would you manage DVT/PE?
Initial resus for PE if needed
Run tests (D-dimer must be done before starting anticoags to avoid false negative)
Start anti-coagulants immediately, even before results: apixaban or rivaroxaban, if not suitable offer LMWH
26
How long after a case of DVT/PE would a patient stay on anticoagulants?
3 months at least
27
What are some complications of DVT?
PE
Bleeding during initial treatment
Heparin induced thrombocytopenia (HIT)
28
What are some complications of PE?
Pulmonary infarction
Cardiac arrest
Death
29
What are some signs of DVT?
tenderness, swelling, warmth, discolouration
30
What are some signs of PE?
tachycardia, tachypnoea, pleural rub, hypoxia, pyrexia, elevated JVP
31
What are the symptoms of DVT?
Limb pain and tenderness
Swelling of the calf or thigh (usually unilateral).
Pitting oedema.
Distension of superficial veins.
Increase in skin temperature.
Skin discoloration
A hard, thickened palpable vein
32
What are the symptoms of PE?
Dyspnoea
Pleuritic chest pain, retrosternal chest pain.
Cough and haemoptysis.
Any chest symptoms in a patient with symptoms suggesting a deep vein thrombosis (DVT).
In severe cases, RHF causes dizziness or syncope
33
Why do you use a d-dimer test for DVT?
Acute thrombus begins to be dissolved by the body's fibrinolytic system as soon as a clot begins to form
elevated levels of breakdown products of cross-linked fibrin (D-dimer) appear in the blood soon after a clot begins to form
34
What is ischaemic heart disease?
an inability to provide adequate blood supply to the myocardium
35
When is IHD considered stable?
when symptoms, if any, are manageable and not rapidly progressive
no recent infarction, procedural intervention, or signs of significant ongoing cardiac necrosis
## Footnote
symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate
36
What are some modifiable risk factors for hypertension?
Excess weight.
Excess dietary salt intake.
Lack of physical activity.
Excessive alcohol intake.
Stress
37
What is the white coat effect?
blood pressure is raised due to the stress of being in clinic
38
What are some non-modifiable risk factors for hypertension?
Older age
Family history
Ethnicity
Gender
39
What is stage 1 hypertension?
clinic BP 140/90 mm Hg
135/85 on home or ambulatory readings
40
What is stage 2 hypertension?
Above 160/100 in clinic
Above 150/95 on home/ambulatory readings
41
What is stage 3 hypertension?
Above 180/120
42
What investigations would you do for someone with hypertension?
ECG
fasting metabolic panel with estimated GFR
lipid panel
urinalysis
Hb
thyroid-stimulating hormone
43
How would you monitor hypertension?
While adjusting medication dosage, blood pressure (BP) should be monitored every 2-4 weeks.
Once stabilised, BP should be checked and medications reviewed every 6-12 months
44
What are some secondary causes of hypertension?
- Renal disease
- Pregnancy and pre-eclampsia
- Endocrine: Conn’s, thyroid disorders
- Drugs: NSAIDs, steroids, oestrogen, liquorice, alcohol
- Obesity
45
What is primary hypertension?
develops without secondary cause
90% of cases
46
What does hypertension increase the risk of?
* IHD (angina and acute coronary syndrome)
* Cerebrovascular accident (stroke or intracranial haemorrhage)
* Vascular disease
* Hypertensive retinopathy and nephropathy
* Vascular dementia
* Left ventricular hypertrophy
* Heart failure
47
What are some differentials for hypertension?
Renal artery stenosis
Chronic kidney disease
Obstructive uropathy
Obstructive sleep apnoea/hypopnoea syndrome
Obesity hypoventilation syndrome
48
What is heart failure (HF)?
a complex clinical syndrome resulting from the impaired ability of the heart to cope with the metabolic needs of the body
| heart can't meet perfusion needs
49
What is the LV ejection fraction in HF with reduced EF?
less than 40%
50
What is the LVEF in heart failure with mildly reduced EF?
41-49%
51
What is the LVEF in HF with preserved EF?
50% or more
52
What is HFrEF?
heart can't pump with enough force to push enough blood into circulation
EF less than 40%
| aka systolic HF
53
What is HFpEF?
heart can't properly fill with blood during the resting period between each beat
EF 50% or more (stroke volume is low but so is EDV)
| aka diastolic heart failure
54
What is the main cause of right sided HF?
Left sided HF
55
What is left sided heart failure?
the left side must work harder to pump the same amount of blood
HFrEF: left ventricle loses its ability to contract normally
HFpEF: Left ventricle loses its ability to relax normally because the muscle has become stiff
56
Equation for cardiac output
Heart rate (HR) x Stroke volume (SV)
57
What happens in right sided heart failure?
When the left ventricle fails and can’t pump enough blood out, increased fluid pressure is transferred back through the lungs.
This damages the heart’s right side. When the right side loses pumping power, blood backs up in the body’s veins
58
What are specific signs for heart failure?
Displaced apex beat
3rd heart sounds
Raised JVP
59
What are the NYHA classes of HF?
Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)
60
Which NYHA class of HF is:
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation or shortness of breath.
Class 1
61
Which NYHA HF class would this be:
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, shortness of breath or chest pain.
Class 2
62
Which NYHA HF Class would this be:
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, shortness of breath or chest pain
3
63
Which NYHA class of HF is this:
Symptoms of heart failure at rest. Any physical activity causes further discomfort
Class 4
64
How do you calculate ejection fraction?
stroke volume / end diastolic volume
65
Symptoms of L sided HF
- Dyspnea on exertion
- Orthopnea (shortness of breath when lying down flat)
- Paroxysmal nocturnal dyspnea (wakes up short of breath at night)
- persistent cough producing mucus
- crackling on auscultation
- fatigue (also present in R sided)
| symptoms due to pulmonary oedema
66
Symptoms of R sided HF
Peripheral oedema
Raised JVP
Tachycardia
Hepatomegaly (backup of blood into IVC)
Ascites (from increased pressure in hepatic vessels)
Fatigue
67
What is shock?
a life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to and utilisation by the cells
68
What is hypovolaemic shock?
volume of the circulatory system is too depleted to allow adequate circulation to the tissues of the body
69
What are the 4 types of shock?
Hypovolaemic
Cardiogenic
Obstructive
Distributive
70
What is cardiogenic shock?
Failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion
## Footnote
hypoperfusion and hypoxia despite adequate volume
71
What can cardiogenic shock be defined by?
Sustained hypotension
Tissue hypoperfusion
72
Risk factors for cardiogenic shock
Elderly
MI
Previous heart disease of infarction
73
What are the aetiologies of cardiogenic shock?
MI
Arrhythmias
Toxic substances
Acute mechanical causes: rupture, chest trauma, valvular incompetence
Infection
Non-adherence with meds
Excessive rise in BP
Cardiomyopathy
74
Signs and symptoms of shock
Tachycardia
Hypotension
Tachypnoea (increased RR and increased work)
Hypoxaemia
Oliguria
Skin changes: cool, clammy peripheries, cyanosis, sweating
Mental state changes
75
Signs and symptoms of cardiogenic shock
## Footnote
excluding general shock symptoms, e.g tachycardia, hypotension
Chest pain
Nausea and vomiting
Dyspnoea
Profuse sweating
Confusion/disorientation
Palpitations
Faintness/syncope
Bilateral basal pulmonary crackles or wheeze may occur
Quiet or extra heart sounds
Raised JVP/ distended neck veins
76
How would you manage shock?
ABCDE approach
Make sure airway is secure and breathing is maintained
Treat underlying cause ASAP
77
What are the vitals in hypovolaemic shock?
hypotensive
tachycardia
hypoxaemia
| increased HR, decreased CO and BP
78
What are the reversible causes of cardiac arrest?
| 4Hs & 4Ts
Hypoxia
Hypokalaemia/hyperkalaemia
Hypothermia/hyperthermia
Hypovolaemia
Tension pneumothorax
Tamponade
Thrombosis
Toxin
79
What are the 2 types of hypovolaemic shock + their causes?
Haemorrhagic: bleeding
Non-haemorrhagic: burns, DKA, severe D&V, excessive use of diuretics, pancreatitis, severe dehydration
80
What are the symptoms of hypovolaemic shock?
Tachypnoea
Long CRT
Tachycardia
Hypotension
Cold peripheries
Hypoxaemia
Cool and clammy
81
What is afterload?
force or load against which the heart has to contract to eject the blood
82
What is preload?
the initial stretching of the cardiac myocytes prior to contraction
83
What is central venous pressure?
blood pressure in the vena cava as it enters the right atrium
reflects the volume of blood returning to the heart and therefore the volume of blood the heart pumps back into the arteries
84
What can cause obstructive shock?
PE
Cardiac tamponade
Tension pneumothorax
85
What happens in distributive shock?
Extreme vasodilation, lowers BP
Capillaries can become leaky
86
What are the different types of distributive shock?
Septic
Neurogenic
Anaphylactic
87
What can cause distributive shock?
Anaphylactic: severe allergic reaction
Septic: Severe infection
Neurogenic: spinal cord injury
88
Which types of shock have a reduced preload?
Hypovolaemic
Distributive
Obstructive: PE, tension PTX
89
Which types of shock have an increased preload?
Cardiogenic
Obstructive: cardiac tamponade
90
How do you treat hypovolaemic shock?
Fluid resus
Correct hypovolaemia and hypoperfusion before irreversible organ damage
Blood transfusion in haemorrhagic
91
What is the pathophysiology of haemorrhagic shock?
- loss of blood volume from ruptured vessels
- EDV + SV decrease
- CO and BP decrease
- Baroreceptors detect
- Catecholamines, ADH and angiotensin II released to cause vasoconstriction, resistance and HR increased
92
What is obstructive shock?
Obstruction to the forward flow of blood in the great vessels or heart
93
What is the pathophysiology of distributive shock?
Septic shock: massive vasodilation in inflammatory reaction
Neurogenic: body can’t vasoconstrict so vasodilates
Anaphylaxis: IgE mediated type 1 hypersensitivity reaction, vasodilation
Vasodilation changes distribution of fluid in body
94
What investigations would you carry out in shock?
ABG (+ lactate)
Glucose
FBC + U&Es
ECG
95
How do you treat distributive shock?
Fluid resus
Septic: antibiotics
Neurogenic: vasopressors, corticosteroids
Endocrine: corticosteroids
Anaphylactic: adrenaline, antihistamines
96
Risk factors for an AAA
smoking
family history
increased age
hypertension
male sex (prevalence)
female sex (rupture)
aortic degeneration accelerated in marfans and pregnancy
97
What should you suspect in a patient with hypotension and atypical abdo pain?
Ruptured AAA
98
Key presentations of an AAA
Pulsatile and expansile mass in abdomen
Pain in abdo, back, loin and groin
99
Signs of a ruptured AAA
Hypotension
Atypical abdo symptoms
Syncope, collapse
Shock
100
What investigation would you do for a suspected AAA?
aortic ultrasound
101
Differentials for AAA
GI haemorrhage
Mesenteric AA
IBS/IBD
Diverticulitis
Ureteric colic
102
How do you manage a AAA?
Ruptured or symptomatic: urgent surgical repair
Unruptured: surveillance and treatment of modifiable risk factors
103
How often would you do an aortic ultrasound for a known AAA?
Annually if the AAA measures 3.0 to 4.4 cm
Every 3 months if the AAA measures 4.5 to 5.4 cm
104
What are some possible complications of AAA repair?
- Abdominal compartment syndrome
- AKI
- Colitis
105
What is the screening for AAA?
Routine screening for AAA for all men aged 65 years
106
What is pericarditis?
inflammation of the pericardium
107
What is the function of the pericardium?
Restrains volume of heart so it can't overfill
Protects heart
Provides fluid layer in pericardial cavity to avoid friction
108
What is acute pericarditis?
new-onset inflammation of pericardium lasting <4 to 6 weeks
109
What 3 signs characterise pericarditis?
Chest pain
Pericardial friction rub
Serial ECG changes
110
How does a pericardial effusion occur from pericarditis?
Pericardium inflammation causes cytokines to be released. This causes blood vessels to become more permeable and fluid leaks into pericardial cavity.
111
Can pericarditis exist without pericardial effusion?
Yes
Majority of time some effusion, but not always
112
When does cardiac tamponade occur?
When pericardial effusion inhibits stretch of pericardium or happens rapidly
113
What can cause pericarditis?
- Infectious: viral (EBV, CMV, SARS Cov2), bacterial (TB)
- Autoimmune (Sjorgen, rheumatoid arthritis, SLE)
- neoplastic (secondary metastatic tumours)
- metabolic
- trauma + iatrogenic
- post MI, dressler's syndrome
- uraemia
| viral causes or idiopathic are responsible for 90%
114
What is Dressler's syndrome?
late-onset post-myocardial infarction pericarditis
Can occur anywhere up to 3 months after MI
115
What are the risk factors for pericarditis?
Male
Age 20-50
Transmural MI
Cardiac surgery
Infections
Uraemia or dialysis
Autoimmune disorders
116
What is chronic constrictive pericarditis?
chronically thickened pericardium
116
What is chronic pericarditis and its subtypes?
long-lasting, gradual inflammation of the pericardium
signs and symptoms lasting longer than 3 months
subtypes: effusive, constrictive
117
What is chronic effusive-constrictive pericarditis?
combination of tense effusion in the pericardial space and constriction by the thickened pericardium
118
What are the clinical criteria for diagnosing acute pericarditis?
| At least 2 must be present
- Characteristic chest pain; typically sharp, pleuritic, and relieved by sitting forwards
- Pericardial friction rub
- New widespread concave upwards ST elevation or PR depression on ECG
- Pericardial effusion (new or worsening)
119
What are the symptoms of pericarditis?
Acute onset, sharp, pleuritic chest pain
Pericardial rub
Chest pain relieved on sitting forward
Fever
Signs of effusion
120
What investigations should be done for pericarditis?
ECG: saddle shape on ST segment, PR depression
FBC: increase in white cell count
CXR
Echocardiogram
121
What ECG changes are seen in pericarditis?
Saddle-shaped ST-elevation
PR depression
122
What are the differentials for pericarditis?
MI
Pneumonia
Pleurisy
PE
Aortic dissection
Pneumothorax
Myocarditis
123
How would you manage pericarditis?
Give NSAIDs and Colchicine
Check for tamponade
124
What are the possible complications of pericarditis?
Pericardial effusion
Cardiac tamponade
Chronic constrictive pericarditis
125
What is a pericardial effusion?
excess fluid collects within the pericardial sac
126
What can cause pericardial effusion?
Malignancy
Infections (from pericarditis)
Iatrogenic (post surgery)
127
What is cardiac tamponade?
the accumulation of pericardial fluid, blood, pus, or air within the pericardial space that creates an increase in intra-pericardial pressure, restricting cardiac filling and decreasing cardiac output
128
What normally happens during inspiration in the RV?
inhaling causes negative pressure, pulling blood into heart. RV expands into pericardial space so it doesn’t affect left heart volume
129
What happens in cardiac tamponade when the RV can't expand into the pericardial space?
RV can’t move into pericardial space, so pushes into left instead.
Causes reduction in LV diastolic volume, lower SV and drop in systolic BP during inspiration.
Decrease in systolic BP of greater than 10mmHg is called pulsus paradoxus
130
What makes up Beck's triad in diagnosing cardiac tamponade?
Hypotension
Elevated JVP
Muffled heart sounds
131
What are the signs of cardiac tamponade?
Becks triad
Fall in systolic BP (pulsus paradoxus)
Kaussmaul’s sign
ECG changes
132
What are the symptoms of cardiac tamponade?
Dyspnoea
Tachycardia
Hypotension
Cold and clammy peripheries
Elevated JVP
Signs of pericardial effusion
133
What are the differentials for cardiac tamponade?
Constrictive pericarditis
Restrictive cardiomyopathy
Cardiogenic shock
134
How do you treat cardiac tamponade?
Pericardiocentesis (not as great in smaller effusions or constrictive causes)
NSAIDS + Colchicine (pericarditis)
| main point is drain the pericardium
135
What are the possible complications of cardiac tamponade?
Cardiac arrest
Organ hypoperfusion
136
What is the action of ACE inhibitors?
inhibit the conversion of angiotensin I to angiotensin II
137
What drugs can be used to treat hypertension?
ACE inhibitors
Angiotensin II receptor blockers (ARBs)
CCBs
Beta-adrenoreceptor blockers
Diuretics
## Footnote
others: Alpha-1 adrenoreceptor blockers
Centrally acting anti-hypertensives
Direct renin inhibitors
138
Examples of ACE inhibitors?
Ramipril
Perindopril
Enalapril
139
What are the indications for ACE inhibitors?
HF
Hypertension
Diabetic nephropathy
140
What are some possible adverse effects of ACE inhibitors cause by inhibting the breakdown of bradykinin?
Persistent dry cough
Rash
Anaphylactoid reactions
141
What are some adverse effects of ACE inhibitors?
Hypotension (related to AGT 2)
Acute renal failure (AGT 2)
Hyperkalaemia (AGT 2)
Teratogenic in pregnancy (AGT2)
Cough (related to kinins)
Rash (kinins)
Anaphylactoid reactions (kinins)
142
What are the contraindications of ACE inhibitors?
Pregnancy
History of angio-oedema
Diabetics on aliskiren with a eGFR below 60mL/minute
143
What are angiotensin II receptor antagonists (ARBs) used for?
Hypertension
HF when ACEi is contraindicated
Diabetic nephropathy
144
What are the contraindications of ARBs?
Pregnancy
History of angio-oedema
Diabetics on aliskiren with a eGFR below 60mL/minute
Breastfeeding women
145
What are some adverse effects of ARBs?
Hypotension (esp if volume depleted)
Rash
Potential for renal dysfunction
Hyperkalaemia
Angio-oedema
146
What is the action of ARBs?
Block angiotensin 2 by acting on AT-1 receptor
147
Examples of calcium channel blockers
Dihydropyridine:
- Amlodipine
- Felodipine
Benzothiazepines:
- Diltiazem
Phenylalkylamine:
- Verapamil
148
What are calcium channel blockers used for?
Hypertension
IHD – angina
Arrhythmia (tachycardia)
149
What are some contraindications of CCBs?
HF
Cardiac outflow obstruction
Cardiogenic shock
Avoid within 1 month of MI (amlodipine fine)
150
What are the actions of CCBs?
Act on L-type calcium channels
Dihydropyridines are arterial vasodilators and have little direct cardio effects
Verapamil mostly affects heart
Diltiazem has cardiac and peripheral effects
151
What are the adverse effects of CCBs?
Flushing (related to vasodilation)
Headaches (vasodilation)
Oedema (vasodilation)
Palpitations (vasodilation)
Bradycardia
AV block
Worsening of cardiac failure
Verapamil causes constipation
152
Examples of beta-adrenoceptor blockers
Propanolol
Bisoprolol
Atenolol
153
What are the indications fo beta-adrenoceptor blockers?
IHD – angina
Heart failure
Hypertension
Arrhythmia
154
What are the contraindications of beta-adrenoceptor blockers?
Asthma and COPD
2nd and 3rd degree AV block
Phaeochromcytoma
155
What are the different classes of diuretics?
Thiazides
Loop diuretics
Potassium-sparing diuretics
Aldosterone antagonists
156
Examples of thiazide diuretics
- Bendroflumethiazide
- Hydrochlorothiazide
157
Examples of aldosterone antagonist diuretics
Spironolactone
Eplerenone
158
What are thiazides used for?
used to relieve oedema due to chronic heart failure and, in lower doses, to reduce blood pressure
159
What are loop diuretics used for?
used in pulmonary oedema due to left ventricular failure and in patients with chronic heart failure
160
What are the main indications of diuretics?
HF
Hypertension
161
What are some adverse effects of diuretics?
Hypovolaemia (loops)
Hypotension
Loss of electrolytes
Hyperuricaemia – gout
Impaired glucose tolerance
Erectile dysfunction
162
What are the actions of nitrates?
Arterial and venous dilators
Reduction of preload and afterload
Lower BP
163
What are the indications of nitrates?
IHD - angina
HF
164
How much aspirin is used to treat an acute event? (e.g. TIA, MI)
300mg
165
What effect does aspirin have on platelets?
Blocks synthesis of thromboxane A2
Low dose inhibits COX 1
High dose inhibits both COX 1 and 2
166
Is aspirin used in primary or secondary prevention of CVD?
secondary
not recommended in primary prevention
167
What is the dosage for aspirin in secondary prevention of cardiovascular disease?
75mg daily
168
How does clopidogrel work?
inhibits the binding of ADP to its platelet receptor, blocking amplification of platelet aggregation
169
What are some antiplatelet drugs?
Aspirin
Clopidogrel
170
What is clopidogrel used for?
prevention of atherothrombotic events in patients with a history of symptomatic ischaemic disease
171
When are clopidogrel and aspirin used in combo?
in patients with AF and at least 1 risk factor to prevent thromboembolic event when warfarin isn't suitable
## Footnote
however does increase risk of bleeding
172
What should be controlled before giving aspirirn?
Hypertension
173
When could you prescribe 75mg aspirin?
Angina
AF with 75mg of clopidogrel for patients who don't want anticoags
ACS
Patients undergoing CABG + tricagelor or prasugrel
174
What is the preferred antiplatelet for secondary prevention of stroke/TIA?
Clopidogrel 75mg
175
What is the main risk of antiplatelets?
Increase risk of bleeding
176
What are the acute coronary syndromes?
Unstable angina
NSTEMI
STEMI
177
What can cause acute coronary syndrome?
Rupture/erosion
thrombus from an atherosclerotic plaque blocking a coronary artery
178
What's atrial fibrillation?
a supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction
179
What's the pathophysiology of AFib?
Electrical activity is disorganised, causing atrial contraction to become uncoordinated, rapid and irregular.
It passes to ventricles, resulting in irregularly irregular ventricular contraction
Uncoordinated atrial activity means the blood can stagnate in the atria, forming a thrombus, which may lead to an ischaemic stroke
180
What is an acute myocardial infarction?
myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand
181
What does the RCA supply?
Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area
182
What do the branches of the LCA supply?
Circumflex artery;
- L atrium
- Posterior L ventricle
Left anterior descending (LAD):
- Anterior L ventricle
- Anterior septum
183
What are the risk factors for an MI?
smoking
HTN
diabetes
obesity
high cholesterol
physical inactivity
renal insufficiency
established coronary artery disease
family Hx of premature coronary artery disease
cocaine use
male sex
age >50 years
female after menopause
184
What typically causes a STEMI?
complete atherothrombotic occlusion of a coronary artery due to atherosclerotic plaque rupture
185
What's the difference in aetiology for a STEMI and NSTEMI?
STEMI: complete occlusion
NSTEMI: transient/ near complete occulsion, e.g. plaque or thrombus
186
What can cause an NSTEMI?
- Plaque rupture with non-occlusive thrombus
- Dynamic obstruction, such as in vasospasm
- Progressive luminal narrowing
- Inflammatory mechanisms (i.e., vasculitis)
- Extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia, or hypoxia)
187
How is troponin related to an MI?
Troponin is a protein in cardiac muscle (myocardium) and skeletal muscle.
A rise in troponin is consistent with myocardial ischaemia, as they are released from the ischaemic muscle tissue
Non-specific marker for MI
## Footnote
used in diagnosis for NSTEMI
188
How does an MI present?
- **central heavy chest pain**
- **may radiate to the left arm, neck, or jaw**
- nausea, vomiting
- dyspnoea
- lightheadedness/ syncope
- palpitations
189
What are the ECG changes for an MI?
STEMI: ECG showing ST elevation or new LBBB
NSTEMI: ECG with no ST elevation, may show ST depression or T wave inversion
190
What investigations should be done for a suspected MI?
Troponin: elevated
ECG
191
What are some of the possible differentials for an MI?
Unstable angina
NSTEMI/STEMI (whichever it isn't)
Ptx
PE
GORD
Aortic dissection
192
What's the initial management for an MI?
- Aspirin 300mg immediately
- IV morphine/ other pain relief
- IV nitrate
193
What's the management of a STEMI?
| after initial
- Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
- Thrombolysis if no PCI
194
How is a NSTEMI managed?
- Unstable: angiography + revascularisation
- Aspirin 300mg
- Ticagrelor 180mg (clopidogrel if bleeding risk)
- Morphine for pain relief
- Heparin or fondaparinux
195
What are some possible complications of an MI?
post-infarction pericarditis (Dressler's syndrome)
congestive heart failure
ventricular arrhythmias
recurrent ischaemia and infarction
196
What is peripheral arterial disease (PAD)?
the narrowing of the arteries supplying the limbs and periphery, reducing the blood supply to these areas
197
What is intermittent claudication?
| PAD
- symptom of ischaemia in a limb, occurring during exertion and relieved by rest.
- typically a crampy, achy pain in the calf, thigh or buttock muscles associated with muscle fatigue when walking beyond a certain intensity.
198
What is critical limb ischaemia?
- end-stage of peripheral arterial disease, where there is an inadequate supply of blood to a limb to allow it to function normally at rest.
- There is a significant risk of losing the limb.
- features are pain at rest, non-healing ulcers and gangrene.
- Pain is worse at night when the leg is raised, as gravity no longer helps pull blood into the foot.
199
What is acute limb ischaemia?
- rapid onset of ischaemia in a limb.
- Typically due to a thrombus (clot) blocking the arterial supply of a distal limb, similar to a thrombus blocking a coronary artery in myocardial infarction.
200
What is gangrene?
refers to the death of the tissue, specifically due to an inadequate blood supply
201
What are the features of acute limb ischaemia?
| 6 Ps
Pain
Pallor
Pulseless
Paralysis
Paraesthesia (abnormal sensation or “pins and needles”)
Perishing cold
202
What is Leriche syndrome?
occlusion in the distal aorta or proximal common iliac artery. clinical triad of:
- Thigh/buttock claudication
- Absent femoral pulses
- Male impotence
203
What is the main cause of PAD?
atherosclerosis
204
What is the epidemiology of PAD?
Increases with age
Affects men and women equally
205
What is the ankle-brachial index?
| used to diagnose PAD
the ratio of systolic BP in the ankle compared with the systolic blood pressure in the arm
206
What are the main features of PAD?
intermittent claudication
thigh or buttock pain with walking that is relieved with rest
diminished or absent pulses
## Footnote
most patients are asymptomatic
207
What are the risk factors for PAD?
smoking
diabetes
HTN
hyperlipidaemia
age >40 years
hx of coronary artery disease/cerebrovascular disease
low levels of exercise
208
What investigations should be done for PAD?
resting ankle-brachial index: ABI ≤0.90
Duplex ultrasound – ultrasound that shows the speed and volume of blood flow
Angiography (CT or MRI) – using contrast to highlight the arterial circulation
209
What are the management options for PAD?
aggressive risk factor control
lifestyle limiting claudication: supervised 12-week exercise programme
anti-platelet therapy: aspirin or clopidogrel
statins: Atorvastatin
surgical:revascularisation
210
What are the differentials of PAD?
Spinal stenosis
Arthritis
Venous claudication
Chronic compartment syndrome
Symptomatic Baker's cyst
Nerve root compression
211
What are the complications of PAD?
leg/foot ulcers
gangrene
permanent limb weakness/numbness
permanent limb pain
212
What causes the first heart sound?
closing of the atrioventricular valves (mitral and tricuspid) at start of systolic contraction of ventricles
213
What causes the second heart sound?
closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete
214
What causes aortic stenosis?
## Footnote
and what does it often follow?
calcification and fibrosis of aortic valve
congenital bicuspid aortic valve
## Footnote
aortic sclerosis
215
What is aortic stenosis?
obstruction of blood flow across the aortic valve due to aortic valve fibrosis and calcification
216
What are the main symptoms in a patient presenting with aortic stenosis?
fatigue
decreased exercise capacity
exertional dyspnoea
exertional chest pain (angina)
syncope
## Footnote
decades long subclinical phase
217
What is the murmur like in aortic stenosis?
ejection-systolic, high-pitched murmur with a crescendo-decrescendo pattern
218
What would an ecg show for aortic stenosis?
left ventricular hypertrophy and absent Q waves, may have a bundle block
219
What investigations should be done for aortic stenosis?
Doppler transthoracic echocardiography (TTE): elevated aortic pressure gradient
ECG: left ventricular hypertrophy and absent Q waves, may have a bundle block
CXR
220
What are the differentials for aortic stenosis?
Aortic sclerosis
Ischaemic heart disease
Hypertrophic cardiomyopathy (HCM)
221
How is aortic stenosis treated?
aortic valve replacement
222
What is aortic regurgitation?
diastolic leakage of blood from the aorta into the left ventricle (LV)
223
What causes aortic regurgitation?
inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.
## Footnote
can be acute or chronic, acute is medical emergency
224
How can acute AR present?
sudden onset of pulmonary oedema and hypotension or in cardiogenic shock
225
What are some symptoms of chronic AR?
dyspnoea
fatigue
weakness
orthopnoea
paroxysmal nocturnal dyspnoea
## Footnote
often asymptomatic
226
What investigations should be done for aortic regurgitation?
ECG: non-specific ST-T wave changes, left axis deviation, or conduction abnormalities
CXR
**Echocardiogram**
## Footnote
colour flow doppler can also be done
227
What are the differentials for aortic regurgitation?
Mitral regurgitation (MR)
Mitral stenosis
Aortic stenosis
Pulmonary regurgitation
228
What are the management options for aortic regurgitation?
Reassurance and monitoring for asymptomatic and good LV function
Symptomatic patients: aortic valve replacement (AVR) or repair
229
What is mitral stenosis?
narrowing of the mitral valve orifice
230
What can cause mitral stenosis?
Rheumatic fever leading to rheumatic heart disease (main cause)
congenital deformity of the valve
carcinoid syndrome
231
What is the pathophysiology of mitral stenosis?
valve orifice reduced in mitral stenosis, flow between left atrium and left ventricle is progressively impeded
pressure in the left atrium remains higher than left ventricle.
- Increased left atrial pressure is referred to the lungs, leading to congestion
- Restricted orifice limits filling of the left ventricle, limiting cardiac output.
232
What are the risk factors for mitral stenosis?
streptococcal infection (rheumatic fever)
female sex (3x more likely)
233
What does the murmur for mitral stenosis sound like?
Diastolic low-pitched rumbling murmur with opening snap
234
What are the symptoms of mitral stenosis?
Dyspnoea
Orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
neck vein distension
235
What investigations would be done for mitral stenosis and what would they show?
Trans-thoracic echocardiography (TTE) showing typical valve deformities
ECG: AF, LA enlargement, RV hypertrophy
CXR: Kerley B lines
236
What's the management for mitral stenosis?
Furosemide diuretic
balloon valvotomy, valve replacement or repair
| no therapy required for mild or asymptomatic, this is for severe
237
What's mitral regurgitation?
incompetent mitral valve, allowing blood to flow back from the left ventricle to the left atrium during systolic contraction of the left ventricle.
238
What is going wrong in mitral regurgitation?
mitral valve dysfunction leads to backflow of blood into L atrium during contraction
reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart
resulting in congestive cardiac failure
239
What are the main causes of secondary mitral regurgitation?
cardiomyopathy or coronary artery disease
| primary MR caused be degeneration of mitral valve
240
What are some possible presenting symptoms of MR?
dyspnoea on exertion
orthopnoea
paroxysmal nocturnal dyspnoea
lower extremity oedema
palpitations
fatigue
sweating
241
What can be heard in mitral regurgitation?
pan-systolic, high-pitched “whistling” murmur, radiates to the left axilla
diminished S1
S3 present (third heart sound)
242
What investigations should be done for MR?
Transthoracic echo
ECG
243
What are the surgical options for MR?
Mitral valve repair
Mechanical valve replacement + anticoags
244
What are the complications of MR?
AF
Pulmonary HTN
LV dysfunction and CHF
245
What are the common causes of AF?
| SMITH pneumonic
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
246
What are the typical symptoms of AF?
Palpitations
SOB
Fatigue
chest pain
dizziness
247
What are the risk factors for atrial fibrillation?
increasing age
HTN
heart failure
diabetes mellitus
male
obstructive sleep apnoea
obesity + alcohol abuse
coronary artery disease
valve disease
other atrial arrhythmias
previous stroke/TIA
hyperthyroidism
248
What would an ECG show for AF?
absent P wave
irregularly irregular QRS
249
What is paroxysmal AF?
episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm.
These episodes can last between 30 seconds and 48 hours.
250
What investigations should be done for atrial fibrillation?
ECG
Echocardiogram
electrolytes, urea, and creatinine
TFTs
251
What are the differentials for atrial fibrillation?
Atrial flutter.
Supraventricular tachyarrhythmias.
AVNRT
Wolff-Parkinson-White syndrome.
Ventricular tachycardia.
252
What are the management options for AF?
DOACs: rivaroxaban, apixaban for thrombi prevention
Beta-blockers: bisoprolol, metoprolol for rate control
Antiarrhythmics: amiodarone
Consider a DC cardioversion or ablation
253
What are the complications of AF?
Stroke
MI
Congestive heart failure
Bradycardia
254
What does the HAS-BLED score assess?
bleeding risk on an DOAC in AF
255
What does the CHA2DS2-VASc score assess?
stroke risk for AF patients
256
What is atrial flutter?
macro re-entrant atrial tachycardia with atrial rates usually above 250 bpm up to 320 bpm
257
What is going wrong in atrial flutter?
Re-entrant rhythm starts in atrium, looping back and overriding SAN, causing atria to contract at fast rates (around 300bpm)
often results in two atrial contractions for every one ventricular contraction
258
What are the risk factors for atrial flutter?
increasing age
valvular dysfunction
atrial septal defects
atrial dilation
recent cardiac or thoracic procedures
heart failure
hyperthyroidism
Resp: COPD, asthma, pneumonia
259
What can cause atrial flutter?
structural or functional conduction abnormalities of the atria
- atrial dilation
- incisional scars
- toxins and metabolic: thyrotoxicosis, alcoholism, pericarditis
- antiarrhythmics converting AF to flutter, e.g. amiodarone
260
What are some symptoms that could suggest atrial flutter?
Palpitations
Dypnoea
Fatigue
Light-headedness
Chest discomfort
Altered consciousness
Polyuria
261
What would an ECG show for atrial flutter?
saw tooth pattern, regular
atria 300bpm
ventricles 150bpm
262
What investigations should be done for atrial flutter?
ECG
transthoracic echocardiography (TTE)
fbc
tfts
263
How is atrial flutter managed?
Beta-blocker for rate control
Electrical cardioversion for rhythm control
264
What is the pathophysiology of WPW?
an extra electrical pathway connecting the atria and ventricles (bundle of Kent)
The additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the AV node
Ventricles can then contract slightly early, pre-excitation
265
What causes the issues in WPW?
presence of an accessory pathway between atria and ventricles
266
How might WPW present?
Palpitations
Dizziness
SOB
chest pain
syncope (rare)
sudden cardiac death (rare)
arrthymias: atrioventricular re-entrant tachycardia (AVRT)
267
What are the differences on an ECG for type A and B WPW?
type A (left-sided pathway): dominant R wave in V1, right axis deviation
type B (right-sided pathway): no dominant R wave in V1, left axis deviation
268
What are the ECG findings for WPW?
ECG: Short PR interval, Wide QRS complex, Delta wave
269
What are the management options for WPW?
radiofrequency ablation of the accessory pathway
amiodarone
270
What is AV nodal re-entrant tachycardia?
supraventricular tachy where the re-entry point is back through the atrioventricular node
271
What is aortic dissection?
a break or tear forms in the inner layer of the aorta, allowing blood to flow between the layers of the wall of the aorta
272
What are type A and B aortic dissection?
Type A dissection involves the ascending aorta with or without involvement of the arch and descending aorta
**Type B does not involve the ascending aorta,** and predominantly involves only the descending thoracic and/or abdominal aorta
273
What are the risk factors for aortic dissection?
HTN
male sex
smoking
atherosclerotic aneurysmal disease
Marfan syndrome
Ehlers-Danlos syndrome
bicuspid aortic valve
274
What does aortic dissection result from?
results from an intimal tear that extends into the media of the aortic wall
275
What is the pathophysiology of aortic dissection?
With aortic dissection, blood enters between the intima and media layers of the aorta.
A false lumen full of blood is formed within the wall of the aorta
276
How does aortic dissection typically present?
abrupt onset chest, back, or abdominal pain that is severe in intensity or is described as 'sharp' or 'stabbing'
blood pressure differential between the two arms
pulse differences
277
What investigations should be done for aortic dissection?
**CT angiogram**
transthoracic echocardiography: intimal flap
ECG to rule out STEMI
278
What are the differentials for aortic dissection?
Acute coronary syndrome
Pericarditis
Aortic aneurysm
MSK pain
PE
Mediastinal tumour
279
How is an aortic dissection managed?
IV labetalol
Surgical repair urgently
280
What are some complications of an aortic dissection?
MI
Cardiac tamponade
Aortic valve regurgitation
Aneurysmal degeneration
Stroke
281
In cardiac arrest which rhythms are shockable?
V tachycardia
V fib
282
What rhythms are not shockable in cardiac arrest?
Electrical activity that isn't vfib or v tachycardia without a pulse
asystole
| pulseless electrical activity
283
What is long QT syndrome?
congenital or acquired condition that is characterised by a prolonged QT interval
associated with a high risk of sudden cardiac death due to ventricular tachyarrhythmias
| mean age at diagnosis is 14
284
How does LQTS typically present?
young people with cardiac arrest or unexplained syncope
285
What does LQTS show on an ECG?
ECG showing prolonged QT and changes in T waves
286
How does torsade present on an ecg?
appearance that the QRS complex is twisting around the baseline
heights get progressively larger then smaller etc
287
What are ventricular ectopics?
premature ventricular beats caused by random electrical discharges outside the atria
288
What does an ECG with ventricular ectopics show?
isolated, random, abnormal, broad QRS complexes
bigeminy is when every other beat is an ectopic
289
What's the management for ventricular arrthymias?
non-selective beta-blockers, e.g. nadolol
290
What pathophysiologically causes angina?
atherosclerosis in coronary arteries, narrowing the lumen and reducing blood flow to the myocardium
During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand
Causes symptoms of angina
291
When is angina unstable?
appear randomly whilst at rest
this is a form of ACS and requires urgent management
292
How does stable IHD (angina) typically present?
chest pressure or squeezing lasting several minutes
provoked by exercise or emotional stress
relieved by rest or glyceryl trinitrate
| may radiate to jaw or arm
293
What are the risk factors for developing angina?
advancing age
smoking
HTN
elevated LDL or low HDL cholesterol
diabetes
inactivity
obesity
illicit drug use
male sex
294
What are the two diagnostic tests for angina?
Cardiac stress testing: assessing the patient’s heart function during exertion, e.g. walking on a treadmill or giving dobutamine
Coronary computed tomography angiography (CCTA): injecting contrast in CT to find narrowing
295
Apart from stress testing and CCTA, what other investigations should be done for angina?
resting ECG: can be normal or abnormal
haemoglobin: possible anaemia
lipid profile: elevated LDL is risk, HDL is protective
fasting blood glucose or HbA1c: diabetes important risk factor
296
What are some differentials for angina?
MI - unstable angina
Pleuritis - unstable angina
PE
GORD
Ptx
Aortic dissection
Pericarditis
Biliary disease
297
What medications are used for secondary prevention of stable angina?
A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief
298
How is stable angina managed?
Immediate symptomatic relief:
- sublingual glyceryl trinitrate (GTN) spray or tablets. GTN causes vasodilation
Long-term symptomatic relief:
- Beta blocker (e.g., bisoprolol)
- Calcium-channel blocker (e.g. amlodipine)
Lifestyle management
299
Complications of angina
MI
Stroke
PAD
HF
300
What is unstable angina?
myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis
301
What characterises unstable angina?
prolonged (>20 minutes) angina at rest
new onset of severe angina
angina that is increasing in frequency, longer in duration, or lower in threshold
angina that occurs after a recent MI
302
What's the most common cause of unstable angina?
coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque and is usually non-occlusive
303
What investigations should be done for unstable angina?
ECG: no evidence of STEMI, may be normal or show ST-segment depression, transient ST-segment elevation, or T-wave inversion
Troponin: no dynamic elevation
FBC, U&Es, LFTs, BM, CRP
304
How should unstable angina be managed?
Acute management includes antiplatelet and anticoagulant therapy
- Aspirin
- Fondaparinux
- Morphine/ GTN
Ongoing management
- Beta blockers, e.g. bisoprolol
- GTN
305
What is prinzmetal's angina?
intense vasospasm of a coronary artery
306
What is paroxysmal nocturnal dyspnoea?
suddenly waking at night with a severe attack of shortness of breath, cough and wheeze
307
What can be used in the management of HFrEF?
ACE inhibitor + Beta-blockers first line
Second line Aldosterone antagonists, e.g. spironolactone
SGLT2 inhibitor, e.g. dapagliflozin
308
What investigations are done for heart failure?
Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test: elevated
ECG: evidence of underlying disease
Transthoracic echocardiogram: accurate determination of biventricular systolic and diastolic function
Bloods
CXR: abnormal
309
What are the differential diagnoses for heart failure?
Ageing/ inactivity
COPD
PE
Pneumonia
Post-partum cardiomyopathy
Nephrotic syndrome
310
What can cause chronic heart failure?
Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
HTN
Arrhythmias (commonly atrial fibrillation)
Cardiomyopathy
311
How is HFpEF treated?
SGLT2 inhibitors (e.g., dapagliflozin)
Lifestyle changes and treatments
## Footnote
focused on reducing congestion, identification and treatment of underlying causes and comorbidities, implementing lifestyle
312
What are the complications of heart failure?
pleural effusion
chronic kidney disease
anaemia
acute decompensation of chronic heart failure
AKI
sudden cardiac death
hyperkalaemia
313
What are the CXR findings for heart failure?
A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly
D: dilated upper lobe vessels
E: effusions
314
What is cor pulmonale?
right-sided heart failure caused by respiratory disease
315
What happens in cor pulmonale?
increased pressure and resistance in the pulmonary arteries (pulmonary HTN) limits RV pumping blood into the pulmonary arteries.
This causes back-pressure into the RA, VC and systemic venous system
316
What are the symptoms of cor pulmonale?
Shortness of breath
Peripheral oedema
Breathlessness of exertion
Syncope (dizziness and fainting)
Chest pain
317
What can cause AV blocks?
fibrosis and calcification of the conduction system
coronary artery disease
medication: beta-blockers, CCB, digitalis, antiarrhythmics
cardiomyopathy
318
How does a first degree heart block present on an ecg?
Fixed prolongation of the PR interval >0.2 seconds (5 small squares) with no failure of AV conduction.
319
What are second degree heart blocks?
some atrial impulses do not make it through the AV node to the ventricles, some P waves not followed by QRS
Mobitz type 1 and 2
320
How does a second degree mobitz type 1 heart block show on an ECG?
increasing PR interval until a P wave is not followed by a QRS complex.
PR interval then returns to normal, and the cycle repeats itself
321
What is a second degree mobitz type 2 heart block?
intermittent failure of conduction through AV node, with an absence of QRS complexes following P waves.
There is usually a set ratio of P waves to QRS complexes, e.g. three P waves for each QRS complex (3:1 block).
The PR interval remains normal.
risk of asystole with Mobitz type 2
322
How does a 2nd degree Mobitz type 2 block present on an ECG?
occasional loss of AV conduction for 1 beat preceded and followed by fixed
unchanging PR intervals
2:1 block = two P waves for each QRS complex
323
What is a 3rd degree (complete) heart block?
also called complete heart block.
There is no observable relationship between the P waves and QRS complexes.
There is a significant risk of asystole
324
What's a bundle branch block?
electrical signal gets completely blocked or held up along one of the bundle branches
| caused by fibrosis, or scarring
325
How do bundle branch blocks appear on an ecg?
LBBB there is a 'W' in V1 and a 'M' in V6
RBBB there is a 'M' in V1 and a 'W' in V6
| WiLLiaM MaRRoW
326
What happens in a RBBB?
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal.
The left ventricular wall depolarises as normal.
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway
327
What does a LBBB look like on an ECG?
Broad QRS complex: >120 ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads: I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave >60ms in leads V5-V6
| WiLLiaM
328
What does a RBBB look like on an ECG?
Broad QRS complex: >120 ms (3 small squares)
RSR’ pattern in V1-V3: small upward deflection (R wave), a larger downward deflection (S wave), then another large upward deflection (a second R wave, which is indicated as R’)
Wide, slurred S wave in lateral leads: I, aVL, V5-V6
| MaRRoW
329
What happens in a LBBB?
Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway
330
What can cause a LBBB?
conduction system degeneration or myocardial pathologies such as ischaemic heart disease, cardiomyopathy and valvular heart disease.
LBBB may also occur after cardiac procedures
## Footnote
ALWAYS PATHOLOGICAL
331
What should you consider in an ecg with broad complexes?
BBB
332
What is infective endocarditis?
infection of the endothelium (the inner surface) of the heart.
Most commonly, it affects the heart valves.
acute, subacute or chronic
333
What are the risk factors for infective endocarditis?
Hx of infectious endocarditis
IV drug use
Structural heart pathology: valvular or congenital, hypertrophic cardiomyopathy, implantable cardiac devices
CKD (particularly on dialysis)
Immunocompromised
334
What causes infective endocarditis?
- Staphylococcus aureus.
- Streptococcus (notably the viridans group of streptococci): biggest cause of native IE
- Enterococcus (e.g., Enterococcus faecalis)
335
What are the symptoms of infective endocarditis?
Fever
Fatigue
Night sweats
Muscle aches
Anorexia
SOB
336
What are the signs of infective endocarditis?
New or “changing” heart murmur
Splinter haemorrhages (thin red-brown lines along the fingernails)
Petechiae
Janeway lesions
Osler’s nodes
Roth spots
337
What is the Duke Criteria for diagnosing endocarditis?
Major:
- persistently positive blood cultures
- Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800
- Evidence of endocardial involvement (abscess, vegetation, valvular)
Minor:
- Predisposition
- Fever above 38°C
- Vascular phenomena
- Immunological phenomena
- Microbiological phenomena
## Footnote
2 major or 1 major and 3 minor or 5 minor
338
What investigations should be done for infective endocarditis?
3 sets of blood cultures from different venepuncture sites taken at 30-minute intervals
Echocardiography
FBC and CRP
339
What's the management for infective endocarditis?
IV broad-spectrum Abx
Abx for staph: beta-lactams: flucloxacillin
Abx for strep: benzylpenicillin or amoxicillin + gentamicin
Surgery: to remove infected tissue completely and repair/replace the affected valves
340
What are some of the complications of infective endocarditis?
acute HF
systemic embolization (including stroke)
AKI
anterior mitral valve vegetation
splenic abscess
mycotic aneurysms
341
What is cardiomyopathy?
disorders of the heart muscle
342
What is hypertrophic cardiomyopathy?
development of a hypertrophied, non-dilated left ventricle in the absence of another predisposing condition
## Footnote
characteristically age-related
343
What are common features of hypertrophic cardiomyopathy?
atrial arrthymias
diastolic dysfunction
higher risk of thromboembolism
344
What investigations are done for cardiomyopathy?
ECG and Echo
345
What tends to cause hypertrophic CM?
autosomal dominant defect in the genes for sarcomere proteins
346
How can patients with hypertrophic CM present?
SOB
Fatigue
Dizziness
Syncope
Chest pain
Palpitations
## Footnote
mostly asymptomatic
347
What might be found on examination for hypertrophic CM?
Ejection systolic murmur at the lower left sternal border
Fourth heart sound
Thrill at the lower left sternal border
348
What is dilated cardiomyopathy?
presence of left ventricular dilatation and systolic dysfunction in the absence of abnormal loading conditions or significant coronary artery disease
| RV dilation often present too
## Footnote
genetic cause
349
What is restrictive cardiomyopathy?
presence of a restrictive ventricular filling pattern
| heart becomes rigid and stiff, causing impaired V filling in diastole
350
How is hypertrophic cardiomyopathy treated?
Beta-blockers
CCBs
avoid strenous exercise (risk of sudden cardiac death)
351
What are some complications of hypertrophic cardiomyopathy?
Sudden cardiac death
Arrhythmias: supraventricular (especially atrial fibrillation) and ventricular in origin
Heart failure
Infective endocarditis
352
What is rheumatic fever?
autoimmune condition triggered by streptococcus bacteria
a multi-system disorder that affects the joints, heart, skin and nervous system
353
Why is rheumatic fever rare in the UK?
early treatment of streptococcus with Abx
354
What are the main manifestations of rheumatic fever?
carditis
arthritis
chorea
erythema marginatum
subcutaneous nodules
355
What causes rheumatic fever?
group A beta-haemolytic streptococcal, typically strep pyogenes causing tonsillitis
antibodies created that also match and attack body cells, e.g. myocardium
356
What type of hypersensitivity reaction is rheumatic fever?
type 2
357
What investigations are done for rheumatic fever?
Throat swab for bacterial culture
ASO antibody titres
Echocardiogram, ECG and chest xray
358
What criteria is used to diagnose rheumatic fever?
Jones
359
What are the symptoms (not signs) of rheumatic fever?
Fever
Joint pain
Recent sore throat
Rash
360
How is rheumatic fever treated?
single injection of benzathine benzylpenicillin
NSAIDs
Aspirin and steroids are used to treat carditis
361
What are the complications of rheumatic fever?
Recurrence of rheumatic fever
Valvular heart disease, most notably mitral stenosis
Chronic heart failure
362
What are L to R shunts?
- Lesions that allow blood to shunt from the left side to the right side of the heart
- Increased pulmonary blood flow and are typically acyanotic
- Cyanosis occurs only if the lesions are large and not repaired in childhood
363
What are some examples of L-R shunts?
atrial septal defect
patent ductus arteriosus
364
What is the recommended imaging and primary intervention for left to right shunts?
Echocardiography
cardiac catheterisation primary intervention
365
What are R to L shunts?
Lesions that result in de-oxygenated blood reaching the aorta
associated with an increased or decreased pulmonary blood flow
366
What is tetralogy of fallot?
a congenital condition where there are four coexisting pathologies:
- Ventricular septal defect (VSD)
- Overriding aorta
- Pulmonary valve stenosis
- Right ventricular hypertrophy
| right to left shunt
367
What are the symptoms of TOF?
- Cyanosis (blue discolouration of the skin due to low oxygen saturations)
- Clubbing
- Poor feeding
- Poor weight gain
- Ejection systolic murmur heard loudest in the pulmonary area
- “Tet spells” (cyanotic episodes due to shunt worsening)
368
What is ventricular septal defect?
- 20% of congenital heart diseases
- a congenital hole in the septum between the two ventricles, can be big enough to form one ventricle
369
What can happen in a left to right shunt?
A left to right shunt leads to right sided overload, right heart failure and increased flow into the pulmonary vessels.
370
What can cause a pan-systolic murmur?
ventricular septal defect
mitral regurgitation
tricuspid regurgitation
371
What is coarctation of the aorta?
a congenital condition where there is narrowing of the aortic arch, usually around the ductus arteriosus
## Footnote
weak femoral pulses in neonates
372
What is seen on an ECG for cardiac tamponade?
low QRS voltage
electrical alternans
373
What can cause cor pulmonale?
COPD (the most common cause)
Pulmonary embolism
Interstitial lung disease
Cystic fibrosis
Primary pulmonary hypertension
374
