CPC 4 Chest pain and hypertension Flashcards
Atypical presentations of myocardial infarction
Back, shoulder or jaw pain. Sweating Nausea Lightheaded/dizzy, fatigued Breathless Anxiety ALL THESE ARE MORE COMMON IN WOMEN.
Differential diagnoses of chest pain, by anatomy: Pleura Lung GIT Aorta Musculoskeletal Heart.
Pleura: effusion, pneumothorax, malignancy Lung: infection, tumour, infarct, PE. GIT: stomach, perforation, oesophagitis. Aorta: aneurysm, dissection Musculoskeletal Heart.
Differential diagnoses of chest pain, by anatomy - anatomical areas.
Pleura Lung GIT Aorta Musculoskeletal Heart.
Cause of interscapula pain
Aortic dissection
Cause of pleuritic pain
Pulmonary embolus
Cause of positional pain
Pericarditis
Signs of aortic dissection
Unequal BP L/R UL, absent pulse
Signs of congestive heart failure
Raised JVP, gallop S3, Pulmonary oedema
How to establish the diagnosis of an MI
a rise or fall in cTn between first assessment and repeat 3-6hr later, coupled with a strong pre-test likelihood.
What are D-dimers?
Fibrin degradation products released from thrombi by
fibrinolysis
When are D-dimers raised
PE, DVT, pregnancy, after surgery, inflammation or
malignancy etc
Used to rule out PE as high negative predictive value.
Where do fibrofatty plaques occur?
At sites of decreased haemodynamic shear stress e.g artery bifurcations.
Clinical events caused by fibrofatty plaques
Renal failure and hypertension, intestinal angina (mesenteric), angina pectoris (coronary), carotid stenosis, aortic aneurysm.
Pleural causes of chest pain
Effustion, pneumothorax, malignancy
Lung tissue causes of chest pain
Infection, tumour, infarct, PE
GIT causes of chest pain
Stomach ulcer/perforation, GORD, oesophagitis.
Aortic causes of chest pain
aneurysm, dissection
Name the key coronary arteries
Left anterior descending artery, the circumflex artery, the right coronary artery.
Causes of pansystolic murmurs
MR, VSD
Cause of pericardial rub
pericardial effusion
Other name for costochondritis
Tietze’s Syndrome
Name all the cardiac biomarkers in blood
Trop I and Trop T (good)
CK-MB and myoglobin (fall rapidly).
CK and LDH (slight rise)
Most important risk factors for CVD: non-modifiable, behavioural, medical
Non-modifiable: age, gender, PMH, FH.
Behavioural: Smoking
Medical: Htn, DM, high LDL, low HDL.
How does smoking cause CVD
Endothelial damage
Incr. thrombus formation/platelet activation.
What is a lipoprotein
A macromolecular complex of lipids and proteins held together by non-covalent forces. They are required for transport of lipids both intra- and extra-vascularly.
Secondary causes of hypercholesterolaemia
Hypothyroidism Nephrotic syndrome Immunoglobulins Cholestasis Anorexia Cyclosporins, sirolimus, anti-epileptics.
Secondary causes of mixed hyperlipidaemia
Nephrotic syndrome
Hypothyroidism
Secondary causes of hypertriglyceridaemia
T1 and 2 DM CRF Obesity Alcohol Hypothyroidism Immunoglobulins Oestrogens, corticosteroids, progestogens, protease inhibitors, retinoids.
How can you split primary dyslipidaemias?
Disorders of synthesis and secretion.
Disorders of metabolism.
What is familial hypoercholesterolaemia?
An inherited genetic defect leading to raised LDL-C levels from birth and hence premature atherosclerosis. Underdiagnosed.
Complications of fibrofatty plaques
Fissuring or ulceration
Calcification
Mural thrombus
Rupture
What can cause coronary artery occlusion?
Thrombus Plaque haemorrhage Coronary artery dissection Vasospasm Embolic (vegetations, mural thrombus, paradoxical emboli)
Ischaemia effects on the myocardium
ATP depletion within seconds
Loss of contractility in under 2 minutes.
ATP 60 minutes.
Timescale of morphological changes post-MI: 0.5-4 hr 4-12 hr 12-24 hr 1-3 days 3-7 days 7-14 days 2-8 weeks > 2 months
0.5-4 hr - No change 4-12 hr - Faint mottling 12-24 hr - Dark mottling 1-3 days - Yellow infarct centre 3-7 days - Hyperaemic border 7-14 days - Yellow core, red margin. 2-8 weeks - Scar formation > 2 months - Scar complete
Risks of reperfusion after MI
Reperfusion injury
Myocardial stunning
Haemorrhage
Early rupture
Causes of acute ischaemia
Inadequate supply: coronary artery stenosis, thrombus, dissection & spasm, microcirculatory dysfunction, anaemia.
Excessive demand: LV hypertrophy, LV dilatation.
MI complications (immediate)
Contractile dysfunctions
Arrhythmias
Myocardial ruptures
How much fluid is needed in the pericardium to cause acute tamponade
200-300 ml
MI complications (chronic)
Pericarditis Infarct expansion Mural thrombus Ventricular aneurysm Progressive heart failure.
When is secondary hypertension likely to be the cause of asymptomatic hypertension?
In a patient
What are the causes of secondary hypertension
Renal (>80%) Endocrine disease Coarctation of the aorta (in young) Pre-eclampsia Drugs
What are some renal causes of hypertension
Chronic glomerulonephritis, chronic pyelonephritis, congenital polycystic kidneys, renal artery stenosis
What are some endocrine causes of hypertension?
Conn’s syndrome, Cushing’s syndrome, phaeochromocytoma, acromegaly, diabetes, hyperparathyroidism
What suggests a renal cause of hypertension
History of renal disease
Recurrent urinary tract infection
Certain drugs (inc losartan and aspirin)
What is accelerated hypertension and what are its symptoms?
BP>200/130 : visual impairment, nausea, vomiting, fits, headaches
What cause of secondary hypertension can also give you palpitations and sweating episodes?
Phaeochromocytoma.
What test would you do to check renal impairment or Conn’s syndrome as a cause of hypertension?
Urea (renal impairment)
Electrolytes (hypokalaemia in Conn’s syndrome)
Why would you do an ECG in someone with hypertension?
for left ventricular hypertrophy myocardial or ischaemia
Why would you do a urine dipstick in someone with hypertension?
To check for haematuria/proteinuria
Why would you do an MSSU and cytology for someone with hypertension?
To check for renal damage due to a possible infection and/or red cell casts.
Why would you do a renal ultrasound in someone with hypertension?
To check the kidneys.
Why would you do a CXR in someone with hypertension?
To look for heart failure and/or rib notching.
Why would you do an echo in someone with htn?
For left ventricular hypertrophy.
Which hypertensive patients would you do a urinary catecholamines or a magnetic resonance image of the renal arteries?
In those under 35 yr or where a secondary cause is suspected.
What is carotid sinus syndrome?
A condition (generally in the elderly) where increased responsiveness of the carotid baroreceptors leads to arrhythmia or a drop in blood pressure.
What is orthostatic hypotension
A greater than 20 mmHg drop in systolic blood pressure on standing.
Chest pain relieved by nitrates
Fast: angina
Slow: oesophageal spasm
Chest pain caused by meals
angina or oesophageal spasm
Precipitating factors for pain from oesophageal disease
Food, lying flat, hot drinks, alcohol.
Initial management of acutely ill patients with chest pain
Admit, check pulse and BP in both arms, JVP, heart sounds, check legs for DVT. Give O2 as necessary. IV line. Relieve pain (morphine + anti-emetic). Cardiac monitor, 12 lead ECG, CXR, ABG
If a patient presents with shock and a raised JVP, what are they likely to have?
Cardiac tamponade.
Questions if you suspect heart failure.
Orthopnoea, paroxysmal nocturnal dyspoea and peripheral oedema.
What is cardiac catheterisation used for in coronary artery disease?
Diagnostic
Therapeutic (angioplasty, stent insertion)
What is cardiac catheterisation used for in valvular disease?
Diagnostic
Therapeutic valvuloplasty
What is cardiac catheterisation used for in congenital heart disease?
Diagnostic
Therapeutic - balloon dilatation or septostomy.
Pre-procedural checks for cardiac catheterisation
Peripheral pulses, bruits, aneurysms FBC, U&Es, LFTs, clotting screen, CXR, ECG Consent for all possibly eventualities IV access Nil by mouth for 6 h prior
Indications for trans-oesophageal echocardiography
Diagnosing aortic dissection, assessing prosthetic valves, finding cardiac source of emboli
Contra-indications for trans-oesophageal echo
Oesophageal disease or cervical spine injury.
Uses of echocardiography
Quantification of global LV function, right hear haemodynamics (e.g regurg), congenital heart disease, endocarditis, pericardial effusion and HCM.
Causes of angina pectoris
Common: atheroma
Rarely: anaemia, AS, tachyarrhythmias, HCM, arteritis or small vessel disease.
Types of angina
Stable, unstable, decubitus and Prinzmetal’s.
Angina on ECG
Usually normal, can show ST depression, flat or inverted T waves, signs of past MI.
Angina management
Lifestyle changes Aspirin B-blockers Nitrates Long acting calcium antagonists (amlodipine, diltiazem) Nicorandil
Indications for an angina referral
New angina of sudden onset, recurrent if past MI or CABG, uncontrolled by drugs, or unstable.
Indications for percutaneous transluminal coronary angioplasty
Poor repsonse or intolerance to medial therapy, refractory angina in patients not suitable for CABG, previous CABG, post-thrombolysis if severe stenosis, symptoms or positive stress test.
Should PTCA be accompanied by stenting?
Usually yes and with clopidogrel.
What investigations should you do with a patient with known CAD and typical pain?
No further investigation needed.
What investigations should you do with a patient with known CAD and atypical pain?
Either exercise testing or functional limitation
What investigations should you do with a patient with unknown CAD?
Stratify likelihood of CAD.
Low risk - reconsider
Low-middle risk - CT with cororanry artery calcification scor.
Middle risk - functional imaging
High-ish risk angiography
Very high risk, treat as CAD (smoking, diabetic, hyperlipidaemia, over 45).
Treatment for Prinzmetal’s angina
Calcium channel blockers and long-acting nitrates. Avoid aspiring and B-blockers.
Who presents with silent MI?
The elderly and diabetics.
How does silent MI normally present?
Syncope, pulmonary oedema, epigastric pain and vomiting, post-operative hypotension, oliguria, confusion, stroke and diabetic hyperglycaemic states.
Blood tests for suspected ACS
FBCs, U&Es, glucose, lipids.
Cardiac enzymes - cardiac troponin, creatine kinase, myoglobin.
Differentials for ACS
Angina, pericarditis, myocaarditis, aortic dissection, pulmonary embolism and oesophageal reflux.
Management of ACS without ST segment elevation - MANABA(CW)
Admit to CCU Monitor O2 stats and administer if necessary Analgesia Nitrates Aspirin B-blocker Antithrombotic e.g. fondaparinux or LMWH (Clopidogrel, or if high risk GPIIb/IIIa antagonist e.g. tirofiban. Warfarin)
If a patient with ACS comes in, and during monitoring proves to be high risk (rise in trop, changes to ECG, upon history taking), what do you do?
Infuse a GPIIb/IIIa antagonist and refer for angiography
If a patient with ACS comes in, and during monitoring proves to be low risk, what do you do?
Discharge if repeat trop is negative. Arrange further investigation.
Pre-hospital ACS management
Ambulance, 300mg aspirin chewed, GTN sublingual, analgesia and metoclopramide.
Management of ACS with ST elevation. ABACW
Angioplasty or thrombolysis B-blocker ACE inhibitor Clopidogrel Warfarin
What kind of MI is most commonly followed by 1st degree heart block?
An inferior MI.
What is Dressler’s syndrome?
Recurrent pericarditis, pleural effusions, fever, anaemia and raised ESR post MI.
Causes of myocarditis
Idiopathic, viral, bacterial, spirochaetes, protozoa, drugs (herceptin, penicillin, chloramphenicol).
Symptoms and signs of myocarditis
Fatigue, dyspnoea, chest pain, fever, palpitations, tachycardia.
Associations with dilated cardiomyopathy
Alcohol, increased BP, haemochromatosis. Many others.
Hypertrophic cardiomyopathy - inheritance and presentation.
Autosomal dominant inheritance - commonest cause of sudden cardiac death in the young. Can present with angina, dyspnoea, palpitation, syncope
Clinical features of pericardial effusion
Dyspnoea, raised JVP, bronchial breathing at left base.
Most common type of oesophageal cancer
Adenocarcinoma
