Cardio Flashcards
What are the clinical manifestations of acute coronary syndromes?
KEY: Acute, central, crushing chest pain.
SYMPTOMS:
- Acute, central, crushing chest pain, often radiating to the jaw or left shoulder, lasting >15 minutes
- Pain often associated with sweating, nausea, dyspnoea and palpitations
- “Silent” MI symptoms include syncope, pulmonary oedema, epigastric pain and vomiting
- New onset or recently destabilised angina
SIGNS:
- Distress and anxiety
- Pallor and sweating
- Tachycardia/bradycardia
- Hypotension/hypertension
- 4th heart sounds
- Signs of heart failure (increased JVP, 3rd heart sound, basal crepitations) or pansystolic murmur
- Low grade fever may be present
- Later on, pericardial friction rub or peripheral oedema may develop
How are acute coronary syndromes investigated?
- Resting 12-lead ECG:
- Must be done in first instance to determine cardiac origin
- Ischaemic changes include ST-segment changes (elevation in STEMI, depression in NSTEMI), T-wave depression/inversion, LBBB or pathological Q-waves if evolved disease
- Unstable angina may not show any abnormality, do not rule out ACS if ECG normal
- Be aware of pre-existing abnormalities - Blood troponin tests:
- High sensitivity troponin test should be conducted - sensitive indicator of ischaemia - Detailed history is essential.
- Monitoring until firm diagnosis/plan is made (usually by pulse oximetry, BP, repeat 12-lead)
GOLD STANDARD/ DIAGNOSTIC:
Angiography is ultimately the gold standard however diagnostic criteria is cardiac biomarker changes above 99th percentile and one of the following:
- Coronary angiography changes
- Symptoms of ischaemia
- New ST/T changes or LBBB
- Newly developed pathological Q waves
- Imaging evidence of new loss of viable myocardium
How are STEMIs managed?
- Immediately assess eligibility for coronary reperfusion therapy (either PPCI or fibrinolysis) and deliver ASAP
- Aspirin 300mg (single loading dose) in first instance for all STEMI patients unless allergic. Nitrates and oxygen if hypoxic.
- If fibrinolysis, give antithrombin at the same time
- If PPCI, DAPT in the first instance
- Assess LV function (if failure, treat with aldosterone antagonist eg spironolactone)
- Long term DAPT, ACE-i, beta-blocker and sometimes statins and CCBs
- Cardiac rehabilitation
How are NSTEMIs/Unstable angina managed?
- Aspirin 300mg (single loading dose) in first instance unless allergic. Nitrates and oxygen if hypoxic.
- Fondaparinux (antithrombin therapy) unless patient undergoing immediate angiography or have high bleeding risk. Consider unfractionated heparin as alternative if significant renal impairment (dose adjustment is essential)
- Consider coronary angiography and PCI within 72hrs of admission if condition is unstable (give DAPT concurrently)
- Consider revascularisation by CABG or PCI
- Long term DAPT, ACE-i, beta-blocker and sometimes statins and CCBs
- Assess LV function (if failure, treat with aldosterone antagonist)
- Cardiac rehabilitation
What are the clinical manifestations of chronic coronary syndrome?
KEY: Discomfort in the chest on exertion which may radiate to the jaw, arm or shoulder and be relieved by rest or sublingual nitrates.
SYMPTOMS:
- Discomfort (pain, pressure or tightness) in the chest which lasts <10 mins.
- Fatigue/faintness
- Exertional dyspnoea
- Nausea
Pain is usually worse after a heavy meal or after waking up, is worse in cold weather and is exacerbated by exertion. It is relieved by GTN spray and rest.
How is chronic coronary syndrome investigated?
FIRST LINE:
A thorough history is essential
1. Assess symptoms and perform clinical investigations to exclude ACS.
2. Resting ECG, bloods (FBC, U&E, TFT, lipids, HbA1c), ambulatory ECG, CXR and resting echocardiography should be carried out and LVEF assessed.
3. Assess pre-test probability and clinical likelihood of CAD (age, risk factors, etc).
GOLD STANDARD/ DIAGNOSTIC:
Offer diagnostic testing depending on pre-test probability of CAD. Exercise tolerance testing is often done.
Low risk - CT coronary angiography (CTCA)
High risk - testing for ischaemia +/- invasive angiography (+/- FFR).
How is chronic coronary syndrome managed?
Management aims to decrease angina symptoms and prevent future cardiovascular events.
Lifestyle modification:
- Smoking cessation
- Weight loss if overweight
- Increase exercise
- Taking medication as advised
- Healthy diet
- Cardiac rehabilitation
Pharmacological management:
- 1 or 2 antianginal drugs: usually beta blocker(-olol)/calcium channel blocker (verapamil, diltiazem)
- GTN or other short acting nitrates for relief of anginal symptoms
- Nitroglycerine/isosorbide dinitrate/isosorbide mononitrate or other long acting nitrates can be used as angina prophylaxis as 2nd line management
- Dihydropyridine agents (nifedipine, amlodipine) can be used additionally if first line BB/CCB are ineffective
ADDITIONAL MANAGEMENT:
Revascularisation via PCI or CABG can be used additionally to medical management to improve symptoms and prognosis. It is typically indicated after other treatments have been unsuccessful, or if ischaemia has been documented following investigations.
If revascularisation is performed, patients should follow the specified pharmacological regimen (DAPT, ACE-i, etc).
What are the clinical manifestations of heart failure?
KEY: SOBOE, fatigue, ankle oedema.
SYMPTOMS:
- Dyspnoea on exertion and fatigue which may limit exercise tolerance
- Orthopnoea (breathlessness on lying flat)
- Paroxysmal nocturnal dyspnoea
- Fluid retention
- Nocturnal cough (+/- pink frothy sputum) or wheeze
- Light headedness/syncope
- Anorexia
SIGNS:
- Tachycardia at rest
- Low systolic BP
- Displaced apex beat (LV dilatation)
- Narrow pulse pressure or pulsus alternans
- Raised JVP
- Gallop rhythm due to presence of S3 or murmurs of mitral/aortic valve disease
- Bilateral basal end inspiratory crackles +/- wheeze (‘cardiac asthma’)
- Tachypnoea
- Pleural effusions
- Tender hepatomegaly (pulsatile in tricuspid regurgitation with ascites)
- Extensive peripheral oedema
- In acute failure, the patient may look ill and exhausted and may be cyanosed
How is heart failure managed?
Lifestyle modification:
1. Stop smoking, drinking alcohol and eating salty food.
2. Optimise weight and nutrition.
Treat the cause if appropriate eg dysrhythmias/valvulopathies. Treat exacerbating factors (anaemia, thyroid disease, infection, hypertension).
Avoid exacerbating factors including NSAIDs (fluid retention) and verapamil (negative inotrope). Give flu vaccine and one of pneumococcal vaccine.
Pharmacological management:
- DIURETICS: give loop diuretics to relieve symptoms eg furosemide/bumetanide. Increase dose as necessary but watch K+ and renal impairment - add K+ sparing diuretic (eg spironolactone) if necessary. If refractory oedema, consider adding thiazide diuretic. Diuretics relieve symptoms but do not benefit mortality.
- ACE INHIBITORS: consider in all patients with LV systolic dysfunction, improves symptoms and prolongs life. Can be substituted for ARB if kinin cough. Monitor for hyperkalaemia.
- BETA-BLOCKERS: eg carvedilol, decreases mortality in heart failure, benefit additional to that of ACE-i in patients with systolic dysfunction. Use with caution - ‘start low and go slow’. Wait >2 weeks between each dose increase.
- MINERALOCORTICOID RECEPTOR ANTAGONISTS: (potassium sparing diuretics) eg spironolactone are known to decrease mortality by 30% when added to conventional therapy. Use when patients are still symptomatic despite optimal therapy and in all post MI patients with LV systolic dysfunction.
- DIGOXIN: helps symptoms even in those with sinus rhythm and should be considered for all patients with LVSD with symptoms of HF whilst receiving standard therapy or in patients with AF.
- VASODILATORS: dual therapy of hydralazine and isosorbide dinitrate should be used if intolerant of ACE-i/ARB as it reduces mortality. Can also reduce mortality when added to standard therapy in black patients with HF.
Which BP defines hypertension?
high blood pressure is considered to be from 140/90mmHg or more if your reading was taken at a pharmacy, GP surgery or clinic (or an average of 135/85mmHg if it was taken at home)
if you’re over the age of 80, high blood pressure is considered to be from 150/90mmHg or more if your reading was taken at a pharmacy, GP surgery or clinic (or an average of 145/85mmHg if it was taken at home)
How is hypertension managed?
LIFESTYLE MODIFICATIONS should be advised for all patients with or at risk of hypertension. This consists of addressing any risk factors which the patient may have.
TREAT UNDERLYING CAUSE for secondary hypertension.
Goals of treatment: <140/90mmHg (130/80 in diabetes, 150/90 if over 80yrs). BP should be reduced slowly as rapid reductions can be fatal, particularly by causing acute stroke.
DRUG THERAPY
Monotherapy:
- If >55yrs/any black patients, 1st choice is CCB or thiazide
- If <55yrs, 1st choice is ACE-i (or ARB if intolerant)
- Beta-blockers are not recommended as 1st line but consider in younger people especially women of childbearing potential
Combination therapy:
- ACE-i + CCB or thiazide is logical and has been used in many trials
- There is little evidence surrounding use of 3 drugs but recommendations for triple therapy is ACE-i + CCB + thiazide
- If still uncontrolled on 3 drugs, consider spironolactone as a 4th drug OR increase thiazide dose, but monitor U&E closely. Also consider a beta blocker.
How is heart failure investigated?
- NT-proBNP: should be done in all patients with suspected HF as a first line investigation. If NT-proBNP is normal then heart failure is unlikely, but if it is positive then it does not necessarily confirm diagnosis of HF. Other investigations are required.
- ECG: should be done in all patients with suspected HF. Identifies potential aetiological factors (MI/arrhythmias) but is also necessary for treatment decisions eg rate control/anticoagulation for AF/pacing for bradycardia. A normal ECG makes HF very unlikely.
- CXR: classic ABCDE findings of alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessels, pleural effusion.
DIAGNOSTIC:
- Echocardiography is the definitive diagnostic investigation. All patients should have transthoracic echocardiogram done within 2-6 weeks depending on NT-proBNP level in suspected chronic HF.
If acute HF suspected then should be done within 48hrs of admission
