Cardio Flashcards
Give 5 complications of atherosclerosis.
Angina MI TIA Stroke Peripheral vascular disease Mesenteric ischemia
Describe the primary prevention of cardiovascular disease.
QRISK3 score - calculates risk of stroke/MI in next 10 years.
If >10%, or CKD/T1DM for more than 10 yrs, offer a statin eg atorvastatin 20mg nocte
Check lipids at 3 months and increase the dose to aim for >40% in non-HDL cholesterol.
Check LFTs within 3 months of statin and then at 12 months. statins can cause transient and mild rise in ALT/AST in first few weeks of use, often don’t need stopping though if the rise is less than 3 times the upper limit of normal.
Describe the secondary prevention of cardiovascular disease.
(after cvd)
Aspirin 75mg daily + clopidogrel 12 months
Atorvastatin 80mg
Beta blocker eg bisoprolol titrated to max tolerated dose
ACE inhibitor eg ramipril titrated to max tolerated dose
Give 3 side-effects of statins.
Myopathy - check creatinine kinase in patients with muscle pain or weakness
Type 2 diabetes
Haemorrhagic strokes (rare)
Give 3 modifiable and 3 non-modifiable risk factors for atherosclerosis.
Modifiable: smoking, alcohol, diet (high in sugar and trans fats, low in fruit and veg and omega 3), exercise, obesity, poor sleep, stress
Non modifiable; age, family history, male sex
Medical comorbidities: diabetes, htn, CKD, inflammatory conditions eg RA, atypical antipsychotics
What is angina? How is it classified?
Symptoms of chest pain due to narrowing of the coronary arteries reduces blood flow to the myocardium.
Stable = symptoms always relieved by rest or GTN
Unstable = symptoms at rest (ACS)
Also can be classified as typical or atypical.
What investigations would you do for ?angina?
gold standard = CT coronary angiogram. would show stenosis.
Baseline investigations:
ECG, FBC, U+Es, LFTs, lipid profile, TFTs, HbA1C
How is angina managed?
Think RAMP:
Refer to cardiology (urgently if unstable)
Advice about diagnosis, management and when to call 999
Medical:
-symptomatic: GTN, b-blocker, CCB
-secondary prevention of CVD: aspirin, statin, ACEI
Procedures:
- PCI with coronary angioplasty if proximal or extensive disease on CTCA
- GABG if severe stenosis.
When should a patient with anginal chest pain call an ambulance?
Try the GTN, wait 5 mins
Try GTN again, wait 5 mins
Call ambulance
What is a CABG and how does it work?
Coronary artery bypass graft.
Chest opened up along sternum, graft vein harvested from leg usually great saphenous vein, sewn on to the affected coronary artery to bypass the stenosis.
The recovery is slower and complication rate is higher than PCI
What is acute coronary syndrome?
A thrombus from an atherosclerotic plaque blocks a coronary artery, so heart is not perfused causing sx such as chest pain.
Includes unstable angina, STEMI and NSTEMI
What does the right coronary artery supply? Which ECG leads correspond?
Right atrium, right ventricle, inferior left ventricle, posterior septal area
Leads I, II and aVL
What are the branches of the left coronary artery and what do they supply? Which ECG leads correspond?
Circumflex - Left atrium Posterior left ventricle Leads I, aVL, V5-6 Left anterior descending - Anterior left ventricle anterior septum Leads v1-4
What investigations would you do for acute chest pain?
ECG - ST elevation/new LBBB = STEMI.
serial troponin eg baseline and 6hrs after symptoms. raised = NSTEMI (but also raised in CKD, sepsis, myocarditis, aortic dissection, PE)
Both normal = unstable angina or non-cardiac cause.
ECG, FBC, U+E, LFT, lipid profile, TFTs, HbA1c, fasting glu.
CXR
Echocardiogram after the event
CTCA
How does acute coronary syndrome present?
Central constricting chest pain, N+V, sweating, clamminess, impending doom feeling, SOB, palpitations, pain radiating to jaw or arms
Sx at rest for 20 mins.
Silent MI eg in diabetic pts - no chest pain
What ECG changes would be seen in an MI?
STEMI- ST elevation, new LBBB
NSTEMI - ST depression, deep T wave inversion, pathological Q waves (late sign)
What is the acute management of a STEMI?
Within 12 hrs onset:
1st line: Primary PCI if available within 2hrs of presentation
Thrombolysis if this is not possible. eg streptokinase
PCI (catheterisation and balloon stenting)
What is the acute management of an NSTEMI?
BATMAN Beta blockers Aspirin 300mg stat dose Ticagrelor 180mg stat dose Morphine for pain Anticoagulant - LMWH treatment dose (Nitrates?) Oxygen if sats <95%
When would you do PCI for someone with an NSTEMI?
GRACE score gives 6 month risk of death or repeat MI after NSTEMI. If medium/high risk they are considered for PCI within 4 days of admission to treat underlying CAD
Give 5 complications of MI.
DREAD Death Rupture of heart septum/papillary muscle Edema/ Heart failure Arrhythmia, aneurysm Dressler's syndrome (pericarditis due to localised immune response, 2-3 weeks after MI)
Describe the secondary prevention of MI.
Aspirin 75mg daily
another Antiplatelet eg clopidogrel <12 months
Atorvastatin 80mg OD
ACEI eg ramipril titrated to 10mg OD
Atenolol
Aldosterone antagonist if heart failure, ie eplerenone 50mg OD
Lifestyle - smoking, alcohol, diet, cardiac rehabilitation, optimise treatment of other medical conditions.
What is the pathophysiology of acute left ventricular failure?
The LV is unable to adequately move blood through the left side of the heart and out into the body –> backlog of blood in L atrium, pulmonary veins and lungs –> leak fluid –> pulmonary oedema = interstitial fluid in lungs. This interferes with normal gas exchange causing SOB, hypoxia etc.
Can be triggered by iatrogenic stuff eg IV fluids, sepsis, MI, or arrhythmia
How does acute LFV present?
Rapid onset breathlessness worse on lying flat.
T1 resp failure (hypoxia eithout hypercapnia)
SOB, unwell, cough with frothy white/pink sputum
Signs:
Tachypnoea, tachycardia, hypoxia, 3rd heart sound, bilat basal crackles (sounds wet on auscultation
What investigations would you do for ?acute LVF and what would they show?
ECG (ischemia, arrhythmias)
ABG
CXR - cardiomegaly, venous diversion (prominent upper lobe vessels), Kerley lines (fluid in the septal lines), pleural effusions, fluid in interlobar fissures)
bloods - infection, CKD, BNP, troponin if ?MI
Echo - ejection fraction.
If clinically acuter LVF don’t let the Ix delay treatment.
What is BNP? What does raised BNP indicate?
B-type natriuretic peptide is a hormone released from ventricles when myocardium stretched. Therefore high BNP indicates overload (also raised in tachycardia, sepsis, PE, renal impairment, and COPD)
BNP relaxes smooth muscle in blood vessels –> reduces systemic vascular resistance –> easier for heart to pump blood.
Also diuretic action in kidneys, reducing circulating volume.
How is acute LVF managed?
Pour SOD:
Stop (pour away) IV fluids, measure input and output, U+E, daily weight.
Sit up
Oxygen if <95%. Be cautious in pts with COPD
Diuretics IV furosemide 40mg stat
What is chronic heart failure and how is it classified?
LV failure to pump blood around the body, due to either impaired LV contraction (systolic) or relaxation (diastolic).
Reduced ejection fraction: EF <40%
Preserved ejection fraction: EF >40%
Can be caused by ischemic heart disease, valvular heart disease (commonly aortic stenosis), htn and arrhythmias (commonly atrial fibrillation)
How does chronic heart failure present?
SOB worse on exertion Cough, frothy white/pink sputum Orthopnoea (SOB when lying flat) Paroxysmal nocturnal dyspnoea (waking up acutely SOB at night with cough and wheeze) Peripheral oedema
Describe the pathophysiology of paroxysmal nocturnal dyspnoea.
- More fluid on lungs
- less active respiratory centre in brain, so does not respond to reduced O2 saturation like it does when awake
- less adrenalin, myocardium more relaxed, lower cardiac output
How is chronic heart failure diagnosed?
Clinical
NT-proBNP blood test
echocardiogram
ECG
How is chronic heart failure managed?
- Refer to specialist - urgently if NT-proBNP >20,000ng/l
- Discuss and explain the condition
- Medical (start low go slow)
- ACEI ramipril 10mg OD/ ARB if ACEI not tolerated or CI due to valvular heart disease
- BB bisoprolol 10mg OD
- aldosterone antagonist eg spironolactone - in HFREF not controlled with A and B
- loop diuretics eg furosemide - lowest dose needed to control symptoms - Surgical rx in severe AS or MR
- HF specialist nurse.
- yearly flu+ pneumococcal vaccine, stop smoking, optimise treatment of co-morbidities, exercise as tolerated.
Why do you need to monitor U+Es in patients with heart failure?
ACE inhibitors, aldosterone antagonists and diuretics all cause electrolyte disturbances.
What is cor pulmonale? Describe the pathophysiology.
Right sided heart failure caused by respiratory disease - the increased pressure and resistance in the pulmonary arteries (pulmonary htn) results in the RV being unable to effectively pump blood out of the ventricle and into the pulmonary arteries, leading to back pressure of blood in the R atrium, vena cava and systemic venous system.
Causes:
COPD, PE, interstitial lung disease, CF, primary pulmonary htn.
How does cor pulmonale present?
Asymptomatic SOB (but this could be due to the causative respiratory disease) Peripheral oedema SOBOE syncope chest pain
Give 5 signs of cor pulmonale.
Hypoxia
Cyanosis
Raised JVP due to backlog of blood in jugular veins
peripheral oedema
3rd heart sound
murmurs (eg pan-systolic in TR)
hepatomegaly due to backpressure in hepatic vein (pulsatile in TR)
What is the management and prognosis of cor pulmonale?
Treat symptoms and underlying cause
long term oxygen therapy (LTOT)
poor prognosis as often underlying cause is irreversible such as COPD
How is hypertension diagnosed and staged?
stages:
1. BP >140/90 in clinic or 135/85 at home
2. >160/100, home 150/95
3. >180/120
diagnostic process:
1. screen every 5 yrs for everyone, every year in patients with T2DM or borderline.
2. confirm BP reading with 24hr ambulatory BP/home reading to exclude white coat htn - defined at >20/10 mmHg difference between clinic and home readings.
3. Assess for end organ damage: bloods for HbA1c, renal function and lipids, urine albumin creatinine ratio and dipstick for haematuria (kidney damage), fundoscopy, ECG
What causes hypertension?
95% of htn is due to essential or primary htn.
Secondary causes:
Renal artery stenosis
Obesity
Pregnancy/pre-eclampsia
Endocrine - esp hyperaldosteronism (Conns syndrome) - Renin aldosterone ratio blood test.
Give 5 complications of hypertension.
Ischemic heart disease CVA eg stroke, heamorrhage hypertensive retinopathy hypertensive nephropathy heart failure
