Cardiology Flashcards
What 4 symptoms should you always include in a cardiac history? (4)
Syncope Palpitations Chest pain (Exercise tolerance) Dyspnoea
What is a distinguishing feature between cardiac syncope and epilepsy history? (1)
Time taken to recover; very fast in cardiac, up to hours in epilepsy.
What classification can be used to grade cardiac status and associated breathlessness? (1)
New York Heart Association. Grade 1 - No breathlessness Grade 2 - breathless on exertion Grade 3 - breathless on mild exertion Grade 4 - breathless at rest
Name 4 differentials for chest pain. (4)
Central: Angina, ACS, Pericarditis, Aortic dissection, GORD, Musculoskeletal, Massive PE
Peripheral: Pneumonia, , Pneumothorax, Musculoskeletal.
Name 3 cardiac causes of syncope. (3)
Heart rate: Bradycardia, Tachycardia,
Outflow obstruction: Aortic stenosis, HOCM
Which CXR view is best for assessing cardiac size? (1)
PA
What is the definitions of bradycardia and tachycardia? (2)
What are the two types of tachycardia? (2)
Brady pulse < 60
Tachy pulse> 100
Supraventricular: arising from atrium or AV junction
Ventricular: arising from ventricles
What is the key blood investigation for the management of arrhythmias? (1)
U+E’s
What maintains the normal cardiac rhythm? (1)
How can the normal heart rate change with inspiration? (1)
Sino-atrial node, controlled by ANS, predominantly parasympathetic keeping rate slowed.
During inspiration, parasympathetic tone falls, causing quickening of pace during inspiration and slowing during expiration.
Name 4 causes of bradycardia. (4)
<60bpm
Extrinsic to the heart: drugs, hypothermia, hypothyroidism, raised ICP, cholestatic jaundice
Intrinsic to the heart: Acute ischaemia and infarction of SA node, Chronic degenerative changes (fibrosis of atrium and SA node - sick sinus syndrome)
Frank attends A+E with a pulse of 40 and signs of poor cardiac output (cold clammy extremities, hypotension, impaired consciousness, severe pulmonary oedema).
What is your immediate management? (2)
Oxygen
IV access - Bloods esp U+E’s, ?ABG for electrolyte imbalance quickly
Atropine 500mcg IV
Temporary pacing (transcutaneous or transvenous)
Permanent pacemaker
Name 4 causes of atrial arrhythmias. (4)
Cardiac: IHD, RHD, Cardiomyopathy, Wolff-Parkinson-White, ASD, Pericarditis, Cardiac surgery
Pulmonary: Pneumonia, Bronchial carcinoma, PE
Other: Thyrotoxicosis, Idiopathic (lone AF), Alcohol use, Excessive caffeine.
Name 3 signs of a haemodynamically unstable patient. (3)
Cold, clammy extremites, Hypotension, Impaired consciousness, severe pulmonary oedema.
How would you manage a haemodynamically unstable patient with AF? (3)
Immediate heparinisation Synchronised DC cardioversion IV amiodarone if DC fails or AF recurs 2nd attempt at DC cardioversion. 2nd dose amiodarone
What is the management of AF in a stable patient? (4)
Rate control: Verapamil, and beta blockers unless very sedentary then digoxin.
Rhythm control: Electrical DC cardioversion and administration of beta blockers
Pharmacological methods depend on presence or absence of heart disease.
Presence: amiodarone
Absence: sotalol, flecainide, propafenone
NB: if onset >48 hours anticoagulate for 3-4 weeks before and after cardioversion.
Which patients is it better to control rhythm rather than rate in AF? (4)
Younger <48 hours)
How are those with AF assessed for anti-coagulation and risk of stroke? (1)
CHADS2-Vasc 1= moderate risk 2= high risk CHF HTN Age 65 (1) 75(2) DM Prev stroke/tia Vascular disease Sex-female
Define heart failure. (2)
Inability of the cardiac output to meet the demands of the body despite normal venous pressure.
Name 4 causes of low output cardiac failure. (4)
LHF: IHD, HTN, cardiomyppathy, aortic valve disease, MR
RHF: secondary to LHF, infarction, cardiomyopathy, chronic lung disease, pulmonary hypertension/embolus/valve disease, tricuspid regurgitation.
Name 3 causes of high output cardiac failure. (3)
Anything that increases myocardial work.
Anaemia, hyperthyroidism, pregnancy, obesity.
When the heart fails to maintain cardiac output sufficiently to meet the body’s demands, there are compensatory mechanisms that occur.
Name 2. (2)
Activation of sympathetic nervous system- increases HR and contractility. Constriction of venous vessels to increase venous return (pre-load).
(Also causes arteriolar constriction which increases after-load and reduces CO.)
Renin-Angiotensin System- reduced CO and increased sympathetic tone causes decreased renal perfusion => RAS activation and fluid retention => increases venous pressure and maintains stroke volume.
(As salt and flud is retained => peripheral and pulmonary congestion => oedema and dyspnoea)
Natriuretic peptides- ANP, BNP.
Ventricular dilatation- failure of pump => more blood left in ventricle during diastole => increased volume => stretching of myocardial fibres => increased contractility.
(Flattening of Starling’s curve limits compensatory effect)
Ventricular remodelling- hypertrophy, loss of myocytes, increased interstitial fibrosis.
Name 4 symptoms of heart failure. (4)
Exertional dyspnoea, orthopnoea, PND, fatigue.
LHF: tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles, third heart sound.
RHF: Raised JVP, hepatomegaly, ascites, ankle/sacral pitting oedema
How is heart failure classified? (1)
New York Heart Association of Heart failure.
Class I - no limitation
Class II - mild limitation. Normal physical activity causes fatigue, dyspnoea of palpitations.
Class III - Marked limitation. Comfortable at rest but gentle physical activity causes marked symptoms.
Class IV - symptoms occur at rest and are exacerbated by any physical activity.
Name 3 investigations that you would perform in a patient with heart failure. (3)
Bedside: ECG,
Bloods: BNP (normal excludes HF), FBC (anaemia), LFTs (?hepatic congestion), Glucose (DM), U+E’s (diuretics and ACEi), TFTs (elderly and AF)
Imaging: Echo, CXR
What vaccinations should be offered to a patient with chronic heart failure? (2)
Annual flu
one off pneumococcal
What drugs are used in the management of chronic heart failure? (5)
Which improve prognosis? (2)
ACEi and Beta-blocker first line and improve prognosis.
ARB, Aldosterone antagonist, Hydralazine with nitrate are all second line options.
Digoxin third line
Loop diuretics for symptomatic relief
Why are ACEi’s first line and ARB’s second line? (2)
ACEi block conversion of Angiotensin I to angiotensin II which is a vasconstrictor, additionally they allow the increase in bradykinin (a vasodilator). ARB’s only block the AT2 receptor and so have no effect on bradykinin.
Why is hydralazine and ISMN given together? (1)
ISMN is a vasodilator (reduces preload), hydralazine is arteriolar vasodilator (reduces afterload).
Why are beta blockers first line in the management of heart failure? (1)
Name one licensed for heart failure. (1)
Blockade of chronically activated sympathetic system.
Bisoprolol, carvedilol, nebivolol
Which calcium channel blockers should be avoided in heart failure? (2)
Diltiazem and verapamil
Name 2 invasive treatments for heart failure? (2)
Revascularisation - CAD is most common cause of HF
Cardiac resynchronisation therapy - improve atria and ventricular coordination.
Implantable cardioverter-defibrillator (ICD)
Cardiac transplantation - in younger patients with severe disease (transplanted hearts are at risk of accelerated coronary atherosclerosis of unknown cause)
What is acute heart failure? (1)
Medical emergency with left or right heart failure developing over minutes to hours.
Name 3 drugs that are used in acute heart failure. (3)
Oxygen Furosemide GTN Dobutamine Enoxaparin Diamorphine
A 65-year-old man is found to have an ejection systolic murmur and narrow pulse pressure on examination. He has experienced no chest pain, breathlessness or syncope. An echo confirms aortic stenosis and shows an aortic valve gradient of 40 mmHg. How should this patient be managed? (1)
Regular outpatient review.
Valve replacement if symptomatic or if valvular gradient > 50mmHg with signs of LVF.
Name a rate limiting calcium channel blocker used in management of angina. (1)
Why should these not be co-prescribed with a beta-blocker? (1)
If a patient with angina is already on atenolol, what calcium channel block may be started? (1)
Diltiazem or Verapamil
Increased risk of heart block.
Long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine)
What is the management of chronic angina? (3)
1st: beta blocker or calcium channel block (dilt or vera)
2nd line:increase dose to maximum daily
3rd line: beta blocker and MR nifedipine
If patient unable to tolerate addition of second line therapy then a long-acting nitrate, ivabradine, nicorandil or ranolazine may be used.
Describe the process of atherosclerosis. (3)
1: Damage to the endothelium (endothelial dysfunction)
2: Increased permeability and accumulation of oxidised lipoproteins into tunica intima.
3: Macrophages take up lipoproteins to form “foam cells”
4. These are called “fatty streaks”
5. Release of cytokines causes further accumulation of macrophages and migration and proliferation of smooth muscle cells.
6. Smooth muscle produces collagen to form a fibrous cap. it is now an “advanced plaque”.
Give 3 reversible and 3 non-reversible risk factors for atherosclerosis. (6)
Non-reversible: Age, male, FH.
Reversible: Smoking, Hypercholesterolaemia, Diabetic control, BP control, Obesity, Diet and Alcohol intake.
At what 10 year cardiovascular risk should patients be offered preventative measures? (1)
Asymptomatic patients with over 20% risk.
Which artery is commonly used to bypass stenoses in the LAD or RCA? (2)
LAD, Left internal mammary artery
RCA, Right internal mammary artery.
What is thromboxane A2? (1)
What drug inhibits it? (1)
When plaques rupture, the platelet rich clot releases TA2, which is a vasconstrictor.
Aspirin
When should troponin T be measure in a patient with severe central chest pain? (2)
What does a positive test indicate? (1)
On arrival and at 12 hours after start of symptoms.
Raised trop T indicates myocardial damage and suggests NSTEMI or STEMI.
What features on an ECG may suggest NSTEMI or unstable angina? (2)
Evidence of myocardial ischaemia, eg ST depression or T wave inversion
ST elevation is a sign of infarction and STEMI.
What drugs should be started in a patient following a NSTEMI? (5)
Aspirin Clopidogrel Beta blocker Acei Statin GTN
What is the management of a patient presenting with acute central chest pain? (5)
IV access (bloods) Pain relief: GTN, diamorphine IV with anti-emetic Oxygen Aspirin 300mg chewed Clopidogrel 300mg ECG if NSTEMI... LMWH 1mg/kg bd sc Risk assessment using TIMI or GRACE scores for risk of further STEMi and death. Med/high risk = PCI
Which patients are most at risk of “silent” MI’s? (3)
Elderly, diabetics, hypertensives
Describe the characteristic pattern of ECG in STEMI. (4)
ST segment elevation (>1mm in 2 or more contiguous leads) and T wave flattening or inversion.
Pathological Q waves are broad (>1mm) and deep (>2mm) negative deflections.
New LBBB is also an indicator.
Which leads would you expect to show changes in an inferior infarct? (1)
Which leads would you expect to show changes in a lateral infarct? (1)
Which leads would expect to show changes in an anterior infarct? (1)
Inf: Leads II, III, AVF
Lat: I, II, AVL
Ant: V2-6
After suffering a STEMI, how long will a patient not be driving for? (1)
1 month.
Rex attends A+E with severe, central, crushing chest pain. ECG shows ST elevated MI.
His blood glucose is 12.3 and his pulse is 125, bp in 140/90.
What is your management? (5)
Oxygen, pain relief, aspirin, clopidogrel.
Reperfusion: PCI, GPIIb/IIIa inhibitor, thrombolysis (if in 12 hours of onset)
Metoprolol 5mg
Insulin infusion to aim for 7-10mmol/L
Name some complications of myocardial infarction. (5)
HF
Rupture of free wall of infarcted ventricle
Rupture of interventricular septum (VSD)
MR
Arrhythmias (bradycardia, AF, VEB’s, VT, VF)
Heart block
Pericarditis
Thromboembolism
Dressler’s (may occur weeks-months after MI)
Ventricular aneurysm (weeks-months after MI)
What is Dressler’s syndrome? (2)
Rare complication of MI, where auto-antibodies cause pericarditis, with a fever and effusion.
Give 2 examples of causes of innocent murmurs. (2)
Describe an innocent murmur. (2)
Pregnancy, thyrotoxicosis, anaemia, fever in childhood
Short, soft, systolic, non radiating.
Give one advantage and one disadvantage of a bioprosthetic valve over a mechanical valve. (2)
Adv: no need for anti-coagulation
Dis: only last 10 years (used most in elderly), increased risk of infection (endocarditis)(all prosthetic valves)
mechanical valves are longer lasting but are thrombogenic so require long term anti-coagulation.
What is the most common cause of mitral stenosis? (1)
Rheumatic heart disease
Why is mitral stenosis linked with atrial fibrillation? (2)
Mitral stenosis restricts blood flow from LA to LV. This causes build up of pressure within the left atrium and dilatation and AF.
Why is mitral stensosis linked with respiratory symptoms? (1)
Name 3 respiratory symptoms. (3)
Name 3 other symptoms/signs. (3)
Restriction of blood flow from LA to LV, causes increased pressure in LA and consequently pulmonary hypertension.
Progressive exertional dyspnoea, productive cough, blood-tingued sputum, frank haemoptysis.
AF, pulmonary oedema, fatigue and lower limb oedema (RHF), malar flush (severe), Tapping apex beat, mid-diastolic murmur.
You suspect a diagnosis of mitral stenosis. Name 3 investigations that may aid your diagnosis? (3)
CXR- enlarged LA, calcified mitral valve, pulmonary venous hypertension, pulmonary oedema if severe
ECG- AF
Echo- confirms diagnosis and assess severity
What is the management of mitral stenosis. (2)
Mild: treat complications eg beta blocker and warfarin for AF, diuretic for HF.
Moderate symptoms: percutaneous balloon valvotomy or replacement.
Name 3 causes of mitral regurgitation. (3)
Rheumatic heart disease, mitral valve prolapse, Infective endocarditis, Rupture of papillary muscle (MI), HOCM, Marfan’s, Ehler-Danlos, SLE.
Why does only acute mitral regurgitation cause pulmonary oedema? (1)
Chronic MR has a compensatory dilated LA. Acutely there is a sudden rise in LA pressure resulting in increased pulmonary venous pressure and pulmonary oedema.
Which murmur-causing valve defect is most likely to be caused by infective endocarditis? (1)
Which valve disease is most likely to cause an thromboembolic event? (1)
Endocarditis: Mitral regurgitation
Thromboembolic: Mitral stenosis (AF)
How is the apex beat affected in:
a) mitral stenosis
b) mitral regurgitation
c) aortic stenosis
d) aortic regurgitation
a) tapping (due to inferior displacement)
b) displaced laterally
c) thrusting and displaced laterally
d) thrusting and displaced laterally
What is the management of mitral valve regurgitation? (2)
Asymptomatic: serial echos every 1-5 years Moderate symptoms (fatigue/exertional dyspnoea, lethargy) or LV dysfunction: Mitral valve replacement or repair.
What valve disease commonly affects young women? (1)
Prolapsing mitral valve.
What are the three causes of aortic stenosis? (3)
Degeneration and calcification of normal valve.
Calcification of congenital bicuspid valve.
Rheumatic heart disease.
What is the triad of symptoms typically associated with aortic stenosis? (3)
Chest pain
Dyspnoea
Syncope
What is the prognosis of a patient with aortic stenosis who has become symptomatic? (1)
Once the valve is reduced to 1/3 of its patency, then they will become symptomatic. This is moderately-severely stenosed an patients will die within 3 years if not treated.
