Chest pain Flashcards
1
Q
The basic ECG waveform:
- P wave
- QRS complex
- T wave
A
- P wave: atrial depolarisation (contraction)
- QRS complex: Ventricular depolarisation (contraction)
- T wave: ventricular re-polarisation (relaxation)
2
Q
ECG calibration spike dimensions:
A
- 10 mm tall
- 5 mm wide
3
Q
ECG heart rate measurement:
A
- Heart rate = 300 / R-R interval
4
Q
Rhythm:
- What is the rhythm
- Sinus rhythm
- Signs
A
- Where the action potential started
- Sinus rhythm: action potential starts at the sinus node
- Signs of normal sinus rhythm: P waves upright in Lead II, all P waves should be identical
5
Q
Isolated systolic hypertension:
A
- Isolated elevation in systemic pressure alone with normal diastolic pressures
- Common in elderly due to increased stiffness of large elastic vessels (aorta)
6
Q
White coat hypertension:
A
- rise in blood pressure while being examined by a physician (fight or flight response)
7
Q
Primary (essential) hypertension:
A
- ~95% of cases, no known cause identified
- BP > or = 140/90 mm Hg
8
Q
Secondary hypertension:
A
- ~ 5% of cases with a defined underlying cause
- Uncommon but important as may be treatable
9
Q
Hypertension organ damage: heart & coronary arteries (2)
A
- Left ventricular hypertrophy (LVH) in response to chronic elevation of after-load (due to high TPR) my cause congestive cardiac failure
- Accelerated coronary atherosclerosis predisposing to ischaemia and infarction
10
Q
Sign of LVH:
A
- S wave in V1 or V2 + R wave in V5 or V6 > 35mm
11
Q
Hypertension organ damage: brain (3)
- Longstanding hypertension can lead to ….
- Atherosclerotic plaques in the internal ….
- Occlusion of small penetrating branches may result in ….
A
- Longstanding Hypertension can lead to micro-aneurysms that may rupture to cause haemorrhagic stroke
- Atherosclerotic plaques in the internal carotid arteries can cause emboli that result in cerebral infarcts
- Occlusion of small penetrating branches may result in multiple tiny infarcts resulting in lacunae (cavities)
12
Q
Hypertension organ damage: aorta and peripheral vasculature (3)
A
- Peripheral vasculature disease
- Abdominal aortic aneurysm “AAA” (>6cm diameter, high risk of rupture and death)
- Aortic dissection
13
Q
Hypertension organ damage: kidney (2)
A
- All patients with hypertension should have urinalysis performed
- Nephrosclerosis (scarring), may cause proteinuria and chronic renal failure
14
Q
Hypertension organ damage: retina
A
- Damage can be directly viewed here
15
Q
Secondary hypertension signs: (5)
A
- Young age of onset
- Abrupt onset
- Signs of underlying pathology
- Sporadic (i.e. no history in first degree relatives)
- Refractory to drug treatment
16
Q
Causes of secondary hypertension: (5)
A
- Renal (chronic renal failure, renal artery stenosis)
- Mechanical (coarctation of aorta)
- Endocrine (Cushings syndrome)
- Drugs (e.g. oral contraceptives)
- Pre-eclamptic toxaemia of pregnancy
17
Q
Renal artery stenosis:
A
- Activation of renin-angiotensin-aldosterone system results in hypokalaemia
- Suspect in patients with hypertension, hypokalaemia and abdominal bruit
18
Q
Coarction of the aorta: (4)
A
- Congenital narrowing of the aorta often distal to origin of left subclavian artery
- BP in arms > legs
- Weak or absent femoral pulse
- Notched appearance of ribs on CXR due to shunting of blood through enlarged arteries
19
Q
Conn’s syndrome: (3)
A
- Adrenal tumor (adenoma) excretes excess aldosterone
- Often asymptomatic
- produces hypokalaemia
20
Q
Cushing’s syndrome: (2)
A
- Excess glucocorticoid secretion
- “Cushingoid” appearance including moonface, acne, obesity and proximal muscle wasting
21
Q
Phaeochromocytoma:
- What
- Causes
A
- Catecholamine secreting tumour (often of the adrenal medulla)
- Episodes of anxiety, sweating, palpitations and hypertension
22
Q
Pre-eclamptic toxaemia of pregnancy
A
- Placental ischaemia leads to release of agents causing endothelial dysfunction and vasoconstriction, resulting in hypertension
- Occurs in 7-10% of pregnancies and can cause fits and maternal death
23
Q
Hyperthyroidism:
A
- Produces hypertension through an increase in blood volume and cardiac output due to excessive secretion of thyroid hormones
24
Q
Pathophysiology of primary hypertension: (3)
A
- An imbalance between CO and TPR
- CO appears raised at first, disease progression causes LVH that compromises diastolic filling and reduces CO
- Reduction in CO causes changes to blood vessels that increases TPR long-term
25
What causes elevated TPR in primary hypertension? (2)
- Narrowing of small arteries due to hypertrophy of tunica media
- Rarefaction, reduction in no. vessels per unit volume of tissue
26
Accelerated (malignant) hypertension:
- Definition
- Effects
- KEY
- > or equal to 180/120 mmHg + papilloedema and or retinal haemorrhage
- Pathology: fibrinoid necrosis of the arterioles
- May impair function of the brain, if untreated most die within 6-12 months
- MEDICAL EMERGENCY
27
Ischaemic heart disease is a group of pathological syndromes due to imbalance of (2)
- Oxygen supply: coronary blood flow and oxygen extraction/saturation
- Oxygen demands: cardiac contractility/rate and ventricular wall tension (systolic/diastolic)
28
Coronary circulation:
- Definition
- Arteries supplying the myocardium with oxygenated blood during diastole
29
Coronary artery dominance (3)
- 70% of individuals have the posterior descending branch originating from the right coronary artery
- 20% are co-dominant
- 10% posterior descending branch originates drom the circumflex artery (LEFT BRANCH)
30
Atherosclerosis definition:
- Disease of the arterial intima featuring a slow accumulation of lipid debris (30-40 year) associated with inflammatory reaction (atheroma), causing obstruction and possible ruptures
31
Arteriosclerosis:
- Blanket term for all conditions where there is a thickening of arterial walls and loss of elasticity
- Arteriolosclerosis, medial calcific sclerosis, ATHEROSCLEROSIS
32
Ischaemic heart disease (IHD):
- Definition
- Effects
- Clinical manifestation of coronary arterial narrowing due to atherosclerosis
- Comprises of stable angina and acute coronary syndrome (unstable angina, acute MI, acute HF and sudden death)
33
Ischaemia:
- Reduced oxygen
- Reduced nutrients
- Impaired wash out of metabolic waste
34
Ischaemia causing stable angina:
- Location
- Duration
- Cause
- Obstruction
- Relief
- Pain over sternum, radiating to left shoulder/arm and jaw
- Seconds to hours
- Sharp/stabbing pain
- Triggered by exertion, cold weather, heavy meals
- Obstruction >60%
- Relieved by rest
35
Ischaemia causing unstable angina:
- Pain characteristics
- Relief??/
- Signs
- Similar to stable angina in terms of pain characteristics
- Not relieved by rest
- No cardiac biomarkers and ECG appears normal (possible ST depression)
36
Ischaemia causing myocardial infarction: (2)
- Ischaemia causes necrosis of the myocardium
- Release of cardiac biomarkers
37
ECG in ischaemia caused MI: (4)
- Normal
- ST segment depression
- T wave inversion: <
38
Percutaneous coronary intervention: (4)
- A catheter is inserted into either the groin or the arm
- Using a fluoroscopy, the catheter is threaded to the plaque build up in the coronary arteries
- It places a stent using a balloon head to compress the plaque and restore appropriate artery width
- Balloon head and catheter removed
39
Coronary artery bypass graft: (2)
- A surgical procedure where a blood vessel is taken from an arm, leg etc and then grafted above and below a blockage of the coronary artery
- This diverts the blood flow, allowing a proper supply of blood to the myocardium
40
Complications following MI:
- 80% of survivors experience some complications after an MI
SHIT LOAD OF COMPLICATIONS
41
Modifiable risk factors for Cardiovascular Disease (9)
- S
- P D
- H
- H
- I P A
- O
-D
- S
- E A C
- Smoking
- Poor diet
- Hypercholesterolaemia
- Hypertension
- Insufficient physical activity
- Obesity
- Diabetes
- Stress
- Excess alcohol consumption
42
Troponin as a biomarker for myocardial infarction:
- Troponin is detected in the blood after myocardial injury
- Specific to the heart - but not to ischaemia, so can not be used to diagnose MI on its own
43
diagnostic criteria for MI requires;
- KEY REQUIREMENT
+ one of :
- I
- ST
- Q
- loss of ....
- Identification of inter.....
- rise or fall in cardiac biomarker value (preferably troponin) with at least one value above 99th percentile of RR
and one of
- Ischaemia symptoms
- ST changes
- Pathological Q waves
- Imaging evidence of viable myocardium loss
- Identification of intercoronary thrombus by angiography
44
Potassium and the heart: hyperkalaemia
- Effects
- Increases cardiac excitation, increases risk of cardiac arrhythmia and heart block
45
Potassium and the heart: hyperkalaemia
- ECG signs (2)
- Tented T waves
- Reduced P wave amplitude
46
Potassium and the heart: hyperkalaemia
- causes
- Acute kidney injury/ chronic kidney disease
- Drugs (ACE-inhibitors, ARBs, NSAIDs)
- Mineralocorticoid deficiency (Addison disease)
47
Potassium and the heart: hypokalaemia
- Effects
- Increases the gradient across cardiac cell membrane, increasing AP and therefore reducing cardiac excitability
- May cause arrhythmias such as atrial fibrillation
48
Potassium and the heart: hypokalaemia
- ECG changes (3)
- Reduced T waves
- ST depression
- Prolonged PR interval
49
Potassium and the heart: hypokalaemia
- Causes:
G
E
D
I
- GI loss: diarrhoea and vomiting
- Endocrine conditions: increased mineralocorticoid activity (Conn's syndrome, Cushing syndrome)
- Non-potassium sparing diuretics
- Insulin treatment with no potassium supplementation
50
Causes of secondary hypertension:
- CKD
- RH
- P H
- C S
- A
- C of the A
- P
- Chronic kidney disease
- Renovascular hypertension
- Primary hyperaldosteronism (Conn's syndrome)
- Cushing syndrome
- Acromegaly
- Coarction of the aorta
- Pregnancy
50
Causes of secondary hypertension:
- CKD
- RH
- P H
- C S
- A
- C of the A
- P
- Chronic kidney disease
- Renovascular hypertension
- Primary hyperaldosteronism (Conn's syndrome)
- Cushing syndrome
- Acromegaly
- Coarction of the aorta
- Pregnancy
51
Mechanism of secondary hypertension :
- Cushing syndrome and Hyperaldosteronism
- Excess aldosterone causes sodium retention
52
Mechanism of secondary hypertension: Phaeochromocytoma
- Stimulation of cardiac B1- adrenoceptors
53
Mechanisms of secondary Hypertension:
Chronic kidney disease
- Fluid retention
54
Mean arterial pressure equation:
MAP = Cardiac output X total peripheral resistance
Cardiac output = Heart rate X Stroke volume
55
G-protein linked transduction: Gs
- biological agonists (3)
- receptor (3)
- 2nd messenger
- Adrenaline, adenosine, prostacyclin
- B2, A2, IP
- increase in cAMP
56
G-protein linked transduction: Gi
- Biological agonists (2)
- Receptor
- 2nd messenger
- Noradrenaline/adrenaline
- alpha 2
- Decrease in cAMP
57
G-protein linked transduction: Gq
- Biological agonists (4)
- Receptors (4)
- 2nd messenger
- Nor/adrenaline, Endothelin-1, Angiotensin 2 , Vasopressin
- a1, ETa, AT1, V1
- increase in IP3 and Rho-kinase
58
Angiotensin converting enzyme (ACE) inhibitors:
- Angiotensin role
- Effects (2)
- Angiotensin is a vasoconstrictor
- Effects in two phases:
1. Rapid due to direct anti ANG II effect
2. Slower due to blood volume effect and control of thirst
59
ACE inhibitor:
- Side effects: (6)
C
R
H
T
FDH
N
- Coughing
- Rash
- Hyperkalemia
- Taste disturbances
- First dose hypotension
- Nephrotoxicity esp in elderly
60
Ca2+ channel blockers:
- Role (2)
- Want to dilute peripheral vessels to:
1. Reduce peripheral resistance
2. Reduce filling pressure
61
Ca2+ channel blockers:
- Examples: Dihydropyridines (2)
- Nifedipine
- Amlodipine
62
Ca2+ channel blockers:
- Side effects (2)
- Peripheral oedema
- Dizziness
63
Classes of diuretics: Loop agents
- Examples
- Strength
- Furosemide, bumetanide
- Powerful (up to 30% filtered Na)
64
Classes of diuretics: Thiazide
- Example
- Strength
- Hydrochlorothiazide
- Mild diuretic effect (<10% filtered Na)
65
Classes of diuretics: K sparing
- Examples
- Strength
- Amiloride, Spironolactone
- Weak diuretic (<10% filtered Na)
66
Thiazides
- Roles in hypertension regulation (2)
- They block the Na+ - Cl- symporter in first part of DCT
- Direct vasodilator action
67
Thiazide side effects (3):
- Electrolyte disturbances
- Decreased glucose tolerance
- Can increase LDL and cholesterol
68
Beta-blockers: renal effects
- Blockade of B1 receptors inhibits renin release from juxta-glomerular cells reducing RAAS system activity
69
Beta-blockers: cardiac effects
- Blockade of B1-receptors in SA node reduces heart rate (-ve chronotropic effect) and in myocardium decreases cardiac contractility (-ve inotropic effect)
70
Beta blockers: CNS and PNS
- Blockade of peripheral and brainstem b-receptors inhibits neurotransmitter release and decreases SNS activity
71
Beta-blockers:
- Role
- Examples (2)
- Used for uncomplicated hypertension where ACD has failed to achieve BP control
- Atenolol: more B1-selective
- Carvedilol: also blocks a-receptors
72
Chronic heart failure is a syndrome characterised by progressive cardiac dysfunction leading to:
- B
- T
N D
Raised ....
O
S D
- Breathlessness
- Tiredness
- Neurohormonal disturbances
- Raised CVP
- Oedema
- Sudden death
73
Causes of heart failure: volume overload
- Valve regurgitation
74
Causes of HF: pressure overload (2)
- Systemic hypertension
- Outflow obstruction
75
Causes of HF: loss of muscle (4)
- Post MI
- Chronic ischemia
- Connective tissue diseases
- Infection/injury
76
Causes of HF: restricted filling (3)
- Pericardial diseases
- Restrictive cardiomyopathy
- Tachyarrhythmia
77
Causes of HF: chronic heart failure
- Affects 2-5% of population with a poor prognosis - 5 year mortality of 50% rising to 80% for some
78
Nitrates:
- NO role
- NO production
- Endothelium-derived relaxing factor (EDRF)
- Breakdown of organic nitrate
79
NO effects (4):
1. General vasodilation giving pre-/after-load reduction
2. Coronary artery vasodilation
3. Enhancement of coronary collateral flow
4. Anti-platelet and anti-thrombotic effects
80
NO:
- Examples (2): N , I M
- Side effects (4)
- Nitroglycerin sl (fast acting), isosorbide mononitrate
- Headache, flushing, palpitations, tolerance
81
What is a pulmonary embolism?:
How do they occur?:
- A thrombus within pulmonary arterial circulation
- Usually arises from embolisation of proximal DVT from lower limb (through right side heart)
82
What is a pulmonary embolism?:
How do they occur?:
- A thrombus within pulmonary arterial circulation
- Usually arises from embolisation of proximal DVT from lower limb (through right side heart)
83
Virchow's triad: a summary of developmental factors for VTE
(3)
- Hypercoagulability
- Venous stasis
- Endothelial inury
84
VTE symptoms:
B
C
H
S
F
ULS
P
- Breathlessness (dyspnoea)
- Chest pain (pleuritic or non pleuritic)
- Haemoptysis (coughing blood)
- Syncope/pre-syncope (fainting)
- Fever (low grade)
- Unilateral leg swelling
- Palpitations
85
Signs of pulmonary embolism (6)
- Tc
- Tp
- H
- H
- F
- RHS
- Tachycardia
- Tachypnoea
- Hypotension
- Hypoxia
- Low grade fever
- Right heart strain
86
Aims of clinical assessment for PE: (4)
1. Does this patient have a PE
2. Severity of the PE
3. Cause of PE
4. Cautions or contraindications of using anticoagulants
87
Scans for PE diagnosis:
- CXR
- CTPA
- CXR: usually normal or non specific but may contain some signs (reduced vascularity in peripheral lung, central pulmonary artery enlargement, wedge shaped infarct)
- CTPA: confirmatory
88
Haemodynamic instability definition: (4)
- Cardiac arrest
- Systolic BP <90 mmHg
- Vasopressers required to achieve BP >90 mmHg
- Systolic BP drop >40 mmHg for > 15 mins
89
Risk adjusted management strategy for acute PE: (4)
1. Assessment of haemodynamic instability
2. Diagnosis of PE severity
3. sPESI (risk of mortality)
4. Asses for RV dysfunction
90
PE management options: (3)
- Anticoagulation: mainstay of treatment
- Thrombolysis: only in high risk PE
- Thrombectomy: high risk PE with high bleeding risk
91
Anticoagulation dose and duration for VTE:
- Initial treatment: 3 - 6 months, therapeutic dose with 'front loading'
- After this, risk of recurrence must be weighed against risk of bleeding on anticoagulants
92
Treatment of serious anticoagulant related bleeding: (6)
1. Estimate source and severity of bleeding
2. Estimate how much drug is on board
3. STOP anitcoagulant drug
4. Simple local measures and resuscitation
5. Tranexamic acid (coagulant)
6. Specific reversal agent if available for severe cases
93
Surgeries and bleeding risks:
- Low
- Significant
- High
- Dental extraction, joint injection, cataract surgery, low risk endoscopies
- Most surgery
- Neurosurgery
94
Investigation and management of non cardiac chest pain (NCCP):
- Investigations (4)
- Management
- History and examination
- ECG
- Blood tests (inc. cardiac biomarkers)
- CXR
- Depends on underlying cause
94
Investigation and management of non cardiac chest pain (NCCP):
- Investigations (4)
- Management
- History and examination
- ECG
- Blood tests (inc. cardiac biomarkers)
- CXR
- Depends on underlying cause
95
Investigation and management of non cardiac chest pain (NCCP):
- Investigations (4)
- Management
- History and examination
- ECG
- Blood tests (inc. cardiac biomarkers)
- CXR
- Depends on underlying cause
96
Causes of NCCP: (5)
- Lung pathologies
- MSK chesty pain
- Abdominal pathology
- Systemic inflammatory disorders
- Medically unexplained chest pain
97
MSK chest pain characteristics: (5)
- Worse with movement
- Reproducibility
- Chest wall tenderness
- Pleuritic
- Little/no physiological compromise
98
MSK chest pain causes: (3)
- Strains/sprains
- Costochondritis
- Tietze syndrome
99
Abdominal pathology causing chest pain: (6)
PUD
PV
C
P
BC
OS
- Peptic ulcer disease
- Perforated viscus
- Cholecystisis
- Pancreatitis
- Biliary colic
- Oesophageal spasm
100
Peptic ulcer disease:
- Definition
- Causes (2)
- Mucosal break in the oesophagus, stomach or duodenum
- Helicobacter pylori infection
- NSAIDs
101
How does helicobacter pylori infection cause peptic ulcer disease:
- The pathogen secretes urease to create an alkaline environment, gastric mucosal irritation, inflammation and ucleration ensues
102
How does NSAID cause peptic ulcer disease:
- Protective mucous secretion os stimulated by prostaglandins
- NSAIDs, corticosteroids and aspirin interfere with prostaglandin synthesis
103
Symptoms of peptic ulcer disease: (5)
- Epigastric pain: upper abdo, related to mealtime
- Bloating
- Waterbrash
- Nausea
- Loss of appetite
104
Gastric ulcer haemorrhage:
- Symptoms (4)
- Treatment
- Haematemesis
- Melaena
- Syncope
- Breathlessness
- Endoscopic treatment
105
Gastric ulcer perforation:
- Definition
- Pain type
- Management
- Full-thickness ulceration through GI wall, contents leak into abdominal cavity
- Severe, sharp and unremitting abdominal pain
- Emergency surgery
106
Acute pancreatitis causes:
- >80% GE
- TSMASHED
- >80% caused buy alcohol and gallstones
- Trauma
- Steroids
- Mumps (viruses)
- Autoimmune
- Scorpion venom
- Hyperlipidaemia, hyperparathyroidism, hypothermia
- ERCP
- Drugs
107
Pancreatitis effects:
- Local (3)
- Autodigestion of pancreas & abdominal viscera]
- Fat necrosis and saponification
- Complications include abscess and cyst formation
108
Pancreatitis (distant) effects: (4)
- Hypocalcaemia
- Volume depletion
- Renal failure
- Respiratory failure & ARDS
109
Pancreatitis symptoms: (3)
- Epigastric or central abdominal pain
- Nausea and vomiting
- Other symptoms depending on complications and severity
110
Pancreatitis;
- management (3)
- prognosis
- IV fluids, pain control, monitoring
- Early feeding
- May require ICU in severe cases
- Mortality up to 10%
111
Systemic inflammatory disorders: Familial Mediterranean Fever (FMF)
- What is it?
- Where?
- Mutation?
- inherited disorder of pyrin
- found in granulocytes, mediates inflammatory cytokine release
- Gain-of-function mutations cause hyper-stimulation and high interleukin levels, autosomal recessive (20%)
112
Familial Mediterranean Fever (FMF):
- Effects (3)
- Attacks of painful inflammation of various organs
- Accompanied by fever
- First attack usually by age 20, last 1-3 days with variable quiescent intervals
113
FMF chest attacks: (2)
- Pleuritis: pleuritic chest pain, often worse when lying flat with dyspnoea and fever
- Pericarditis: central chest pain, often pleuritic and relieved by sitting forward, ECG changes
114
FMF management: (2)
- Acute attacks: self-limiting, treatment is supportive; analgesia, antipyretics, fluids
- Prophylaxis: colchicine - reduces attack frequency and amyloid deposition
115
Sickle cell disease:
- what is it?
- Under normal conditions
- Under hypoxic conditions
- Inherited abnormality of haemoglobin A beta subunit (HbS)
- No effect, same function & structure
- HbS polymerises, forming sickle-shaped RBC which do not return to normal. Loss of elasticity, RBC occludes small vessels and have shorter lifespan
116
Acute chest syndrome (sickle crisis):
- What is it?
- Stats
- Effects (5)
- Vaso-occlusive crisis of the pulmonary vasculature
- Second most common crisis type, accounts for 25% of deaths in SCD
- Pleuritic chest pain, dyspnoea, fever, cough, spectrum of presentation severity
117
Acute chest syndrome: effects (2)
- Initially results in hypoxaemia and HbS polymerisation
- Vaso-occlusion causes further falls in pulmonary blood flow and oxygen levels
118
Acute chest syndrome: management (5)
O T
I F
Ana
Ant
E T & I V
- Oxygen therapy
- IV fluids
- Analgesia
- Antibiotics
- Exchange transfusion and invasive ventilation if necessary
119
Chest pain: anxiety and panic disorder
- Relevancy
- Aetiology
- Common symptom of panic attacks (40-70% during acute attacks)
- Aetiology: unclear but muscular, coronary and somatosensory mechanisms proposed
