Chest pain Flashcards
The basic ECG waveform:
- P wave
- QRS complex
- T wave
- P wave: atrial depolarisation (contraction)
- QRS complex: Ventricular depolarisation (contraction)
- T wave: ventricular re-polarisation (relaxation)
ECG calibration spike dimensions:
- 10 mm tall
- 5 mm wide
ECG heart rate measurement:
- Heart rate = 300 / R-R interval
Rhythm:
- What is the rhythm
- Sinus rhythm
- Signs
- 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
Isolated systolic hypertension:
- Isolated elevation in systemic pressure alone with normal diastolic pressures
- Common in elderly due to increased stiffness of large elastic vessels (aorta)
White coat hypertension:
- rise in blood pressure while being examined by a physician (fight or flight response)
Primary (essential) hypertension:
- ~95% of cases, no known cause identified
- BP > or = 140/90 mm Hg
Secondary hypertension:
- ~ 5% of cases with a defined underlying cause
- Uncommon but important as may be treatable
Hypertension organ damage: heart & coronary arteries (2)
- 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
Sign of LVH:
- S wave in V1 or V2 + R wave in V5 or V6 > 35mm
Hypertension organ damage: brain (3)
- Longstanding hypertension can lead to ….
- Atherosclerotic plaques in the internal ….
- Occlusion of small penetrating branches may result in ….
- 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)
Hypertension organ damage: aorta and peripheral vasculature (3)
- Peripheral vasculature disease
- Abdominal aortic aneurysm “AAA” (>6cm diameter, high risk of rupture and death)
- Aortic dissection
Hypertension organ damage: kidney (2)
- All patients with hypertension should have urinalysis performed
- Nephrosclerosis (scarring), may cause proteinuria and chronic renal failure
Hypertension organ damage: retina
- Damage can be directly viewed here
Secondary hypertension signs: (5)
- Young age of onset
- Abrupt onset
- Signs of underlying pathology
- Sporadic (i.e. no history in first degree relatives)
- Refractory to drug treatment
Causes of secondary hypertension: (5)
- Renal (chronic renal failure, renal artery stenosis)
- Mechanical (coarctation of aorta)
- Endocrine (Cushings syndrome)
- Drugs (e.g. oral contraceptives)
- Pre-eclamptic toxaemia of pregnancy
Renal artery stenosis:
- Activation of renin-angiotensin-aldosterone system results in hypokalaemia
- Suspect in patients with hypertension, hypokalaemia and abdominal bruit
Coarction of the aorta: (4)
- 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
Conn’s syndrome: (3)
- Adrenal tumor (adenoma) excretes excess aldosterone
- Often asymptomatic
- produces hypokalaemia
Cushing’s syndrome: (2)
- Excess glucocorticoid secretion
- “Cushingoid” appearance including moonface, acne, obesity and proximal muscle wasting
Phaeochromocytoma:
- What
- Causes
- Catecholamine secreting tumour (often of the adrenal medulla)
- Episodes of anxiety, sweating, palpitations and hypertension
Pre-eclamptic toxaemia of pregnancy
- 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
Hyperthyroidism:
- Produces hypertension through an increase in blood volume and cardiac output due to excessive secretion of thyroid hormones
Pathophysiology of primary hypertension: (3)
- 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
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
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
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)
Coronary circulation:
- Definition
- Arteries supplying the myocardium with oxygenated blood during diastole
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)
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
Arteriosclerosis:
- Blanket term for all conditions where there is a thickening of arterial walls and loss of elasticity
- Arteriolosclerosis, medial calcific sclerosis, ATHEROSCLEROSIS
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)
Ischaemia:
- Reduced oxygen
- Reduced nutrients
- Impaired wash out of metabolic waste
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
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)
Ischaemia causing myocardial infarction: (2)
- Ischaemia causes necrosis of the myocardium
- Release of cardiac biomarkers
ECG in ischaemia caused MI: (4)
- Normal
- ST segment depression
- T wave inversion: «risk of acute total occlusion of main artery
- ST segment elevation: acute occlusion of one of the three main coronary arteries
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
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
Complications following MI:
- 80% of survivors experience some complications after an MI
SHIT LOAD OF COMPLICATIONS
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
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
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
Potassium and the heart: hyperkalaemia
- Effects
- Increases cardiac excitation, increases risk of cardiac arrhythmia and heart block
Potassium and the heart: hyperkalaemia
- ECG signs (2)
- Tented T waves
- Reduced P wave amplitude
Potassium and the heart: hyperkalaemia
- causes
- Acute kidney injury/ chronic kidney disease
- Drugs (ACE-inhibitors, ARBs, NSAIDs)
- Mineralocorticoid deficiency (Addison disease)
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
Potassium and the heart: hypokalaemia
- ECG changes (3)
- Reduced T waves
- ST depression
- Prolonged PR interval
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
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
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
Mechanism of secondary hypertension :
- Cushing syndrome and Hyperaldosteronism
- Excess aldosterone causes sodium retention
Mechanism of secondary hypertension: Phaeochromocytoma
- Stimulation of cardiac B1- adrenoceptors
Mechanisms of secondary Hypertension:
Chronic kidney disease
- Fluid retention
Mean arterial pressure equation:
MAP = Cardiac output X total peripheral resistance
Cardiac output = Heart rate X Stroke volume
G-protein linked transduction: Gs
- biological agonists (3)
- receptor (3)
- 2nd messenger
- Adrenaline, adenosine, prostacyclin
- B2, A2, IP
- increase in cAMP
G-protein linked transduction: Gi
- Biological agonists (2)
- Receptor
- 2nd messenger
- Noradrenaline/adrenaline
- alpha 2
- Decrease in cAMP
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
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
ACE inhibitor:
- Side effects: (6)
C
R
H
T
FDH
N
- Coughing
- Rash
- Hyperkalemia
- Taste disturbances
- First dose hypotension
- Nephrotoxicity esp in elderly
Ca2+ channel blockers:
- Role (2)
- Want to dilute peripheral vessels to:
1. Reduce peripheral resistance
2. Reduce filling pressure
Ca2+ channel blockers:
- Examples: Dihydropyridines (2)
- Nifedipine
- Amlodipine
Ca2+ channel blockers:
- Side effects (2)
- Peripheral oedema
- Dizziness
Classes of diuretics: Loop agents
- Examples
- Strength
- Furosemide, bumetanide
- Powerful (up to 30% filtered Na)
Classes of diuretics: Thiazide
- Example
- Strength
- Hydrochlorothiazide
- Mild diuretic effect (<10% filtered Na)
Classes of diuretics: K sparing
- Examples
- Strength
- Amiloride, Spironolactone
- Weak diuretic (<10% filtered Na)
Thiazides
- Roles in hypertension regulation (2)
- They block the Na+ - Cl- symporter in first part of DCT
- Direct vasodilator action
Thiazide side effects (3):
- Electrolyte disturbances
- Decreased glucose tolerance
- Can increase LDL and cholesterol
Beta-blockers: renal effects
- Blockade of B1 receptors inhibits renin release from juxta-glomerular cells reducing RAAS system activity
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)
Beta blockers: CNS and PNS
- Blockade of peripheral and brainstem b-receptors inhibits neurotransmitter release and decreases SNS activity
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
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
Causes of heart failure: volume overload
- Valve regurgitation
Causes of HF: pressure overload (2)
- Systemic hypertension
- Outflow obstruction
Causes of HF: loss of muscle (4)
- Post MI
- Chronic ischemia
- Connective tissue diseases
- Infection/injury
Causes of HF: restricted filling (3)
- Pericardial diseases
- Restrictive cardiomyopathy
- Tachyarrhythmia
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
Nitrates:
- NO role
- NO production
- Endothelium-derived relaxing factor (EDRF)
- Breakdown of organic nitrate
NO effects (4):
- General vasodilation giving pre-/after-load reduction
- Coronary artery vasodilation
- Enhancement of coronary collateral flow
- Anti-platelet and anti-thrombotic effects
NO:
- Examples (2): N , I M
- Side effects (4)
- Nitroglycerin sl (fast acting), isosorbide mononitrate
- Headache, flushing, palpitations, tolerance
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)
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)
Virchow’s triad: a summary of developmental factors for VTE
(3)
- Hypercoagulability
- Venous stasis
- Endothelial inury
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
Signs of pulmonary embolism (6)
- Tc
- Tp
- H
- H
- F
- RHS
- Tachycardia
- Tachypnoea
- Hypotension
- Hypoxia
- Low grade fever
- Right heart strain
Aims of clinical assessment for PE: (4)
- Does this patient have a PE
- Severity of the PE
- Cause of PE
- Cautions or contraindications of using anticoagulants
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
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
Risk adjusted management strategy for acute PE: (4)
- Assessment of haemodynamic instability
- Diagnosis of PE severity
- sPESI (risk of mortality)
- Asses for RV dysfunction
PE management options: (3)
- Anticoagulation: mainstay of treatment
- Thrombolysis: only in high risk PE
- Thrombectomy: high risk PE with high bleeding risk
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
Treatment of serious anticoagulant related bleeding: (6)
- Estimate source and severity of bleeding
- Estimate how much drug is on board
- STOP anitcoagulant drug
- Simple local measures and resuscitation
- Tranexamic acid (coagulant)
- Specific reversal agent if available for severe cases
Surgeries and bleeding risks:
- Low
- Significant
- High
- Dental extraction, joint injection, cataract surgery, low risk endoscopies
- Most surgery
- Neurosurgery
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
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
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
Causes of NCCP: (5)
- Lung pathologies
- MSK chesty pain
- Abdominal pathology
- Systemic inflammatory disorders
- Medically unexplained chest pain
MSK chest pain characteristics: (5)
- Worse with movement
- Reproducibility
- Chest wall tenderness
- Pleuritic
- Little/no physiological compromise
MSK chest pain causes: (3)
- Strains/sprains
- Costochondritis
- Tietze syndrome
Abdominal pathology causing chest pain: (6)
PUD
PV
C
P
BC
OS
- Peptic ulcer disease
- Perforated viscus
- Cholecystisis
- Pancreatitis
- Biliary colic
- Oesophageal spasm
Peptic ulcer disease:
- Definition
- Causes (2)
- Mucosal break in the oesophagus, stomach or duodenum
- Helicobacter pylori infection
- NSAIDs
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
How does NSAID cause peptic ulcer disease:
- Protective mucous secretion os stimulated by prostaglandins
- NSAIDs, corticosteroids and aspirin interfere with prostaglandin synthesis
Symptoms of peptic ulcer disease: (5)
- Epigastric pain: upper abdo, related to mealtime
- Bloating
- Waterbrash
- Nausea
- Loss of appetite
Gastric ulcer haemorrhage:
- Symptoms (4)
- Treatment
- Haematemesis
- Melaena
- Syncope
- Breathlessness
- Endoscopic treatment
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
Acute pancreatitis causes:
- >80% GE
- TSMASHED
- > 80% caused buy alcohol and gallstones
- Trauma
- Steroids
- Mumps (viruses)
- Autoimmune
- Scorpion venom
- Hyperlipidaemia, hyperparathyroidism, hypothermia
- ERCP
- Drugs
Pancreatitis effects:
- Local (3)
- Autodigestion of pancreas & abdominal viscera]
- Fat necrosis and saponification
- Complications include abscess and cyst formation
Pancreatitis (distant) effects: (4)
- Hypocalcaemia
- Volume depletion
- Renal failure
- Respiratory failure & ARDS
Pancreatitis symptoms: (3)
- Epigastric or central abdominal pain
- Nausea and vomiting
- Other symptoms depending on complications and severity
Pancreatitis;
- management (3)
- prognosis
- IV fluids, pain control, monitoring
- Early feeding
- May require ICU in severe cases
- Mortality up to 10%
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%)
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
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
FMF management: (2)
- Acute attacks: self-limiting, treatment is supportive; analgesia, antipyretics, fluids
- Prophylaxis: colchicine - reduces attack frequency and amyloid deposition
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
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
Acute chest syndrome: effects (2)
- Initially results in hypoxaemia and HbS polymerisation
- Vaso-occlusion causes further falls in pulmonary blood flow and oxygen levels
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
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
