Cardiology Flashcards
1
Q
What is atherosclerosis
A
combination of atheromas and sclerosis, in medium and large arteries
2
Q
What causes atherosclerosis
A
chronic inflammation and activation of the immune system in the arterial wall, which causes deposition of lipids and development of atheromatous plaques
3
Q
What do atheromatous plaques cause
A
- Stiffening of arterial wall leading to hypertension and heart strain to pump blood against resistance
- Stenosis leading to decreased blood flow(e.g. in angine)
- Plaque rupture leading to thrombus that van block a distal vessel causing ischaemia (e.g. acute coronary syndrome: coronary artery becomes ischaemic)
4
Q
Atherosclerosis non modifiable risk factors
A
- old age
- male
- family history
5
Q
Atherosclerosis modifiable risk factors
A
- smoking
- alcohol
- poor diet and exercise
- obesity
- poor sleep
- stress
6
Q
Atherosclerosis medical comorbidities
A
- diabetes
- hypertension
- Chronic kidney disease
- inflammatory conditions( e.g. rhematoid arthritis)
- Atypical antipsychotic meds
7
Q
End result of atherosclerosis
A
- angina
- MI
- TIA( transcient ischaemic attacks)
- strokes
- peripheral vascular disease
- chronic mesenteric ischaemia
8
Q
primary prevention of CVD
A
- perform a QRISK3 score : calculate percentage risk that a patient will have a stroke or MI in the next 10 years. More than 10% = start statin (20mg atorvastatin at night)
- All patients with chronic kidney disease( CDK) or t1 diabetes for more than 10 years should be started on atorvastatin 20 mg
- Checking lipids at 3 months and increasing dose to aim for a greater than 40% reduction in non HDL cholesterol
- Checking liver function test( LFT) within 3 months of starting stating and again in 12 months as it can cause a mild and transient rise in ALT and AST ( alanine and astatine aminotransferase) in the first few weeks of use
9
Q
secondary prevention of CVD
A
- Aspirin( plus a second anitplatelet such as clopidogrel for 12 months)
- Atorvastatin 80mg
- Atenolol ( or other beta blocker commonly bisoprolol) titrated to max tolerated dose
- ACE inhibitor ( ramipril) titrated to max tolerated dose
10
Q
Notable side effects of statins
A
- Myopathy
- Type 2 diabetes
- very rarely haemorragic strokes
11
Q
What is stable angina
A
- narrowing of coronary arteries reduces blood flow to the myocardium during times of high demand( insufficient supply of blood to meet the demand) relieved by rest or glyceryl trinitrate ( GTN)
12
Q
What is unstable angina
A
- narrowing of coronary arteries reduces blood flow to the myocardium randomly or whilst at rest
- ACute Coronary Syndrome
13
Q
Investigations for stable angina
A
- CT coronary angiogram
- Physical examinations
- ECG
- FBC ( check for anemia)
- U&Es ( prior to ACEi and other medications)
- LFTs prior to statins
- Lipid profile
- Thyroid function tests
- HbA1C and fasting glucose( for diabetes)
14
Q
Management for stable angina
A
- Refer to cardiology, urgently if unstable
- Advise them about the diagnosis. management and when to an ambulance
- Medical treatment
- Procedural or surgical interventions
15
Q
Medical management for angina
A
- Immediate symptomatic relief: GTN spray which causes vasodilation and relieves symptoms when symptoms start and repeat after 5 mins if required
- Long terms symptomatic relief: combination or either of beta blocker( 5mg bisoprolol once daily) and calcium channel blocker( eg amlodiphine 5mg once daily)
- Other : long acting nitrates
- 4 As of secondary prevention: aspirin, ACEi, Atorvastatin, ATonolol or other beta blocker
16
Q
Surgical procedures for angina
A
- Percutaneous Coronary Intervation (PCI) with coronary angioplasty ( dilating the blood vessel with a ballon and/or inserting a stent ) is offered to patients with proximal or extensive disease on CT coronary angiography. This involves putting a catheter into the patients brachial or femoral artery, feeding it up to the coronary arteries under x-ray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highligted
- Coronary artery bypass graft( CABG): for patients with severe stenosis. This normally involves opening chest along the sternum causing a midline sternotomy scar, taking a graft vein from the patients leg( usually the greater saphenous vein) and sewing it on the affected coronary artery to bypass the stenosis. Slower recovery and higher complication rate
17
Q
Pathophysiology of acute coronary disease
A
- usually result of thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets
18
Q
what parts does the right coronary artery supply
A
- RA
- RV
- Inferior aspect of left ventricle
- Posterior septal area
19
Q
what parts does the circumflex artery supply
A
- LA
- Posterior aspect of LV
20
Q
what parts does the left anterior descending artery supply
A
- Anterior aspect of LV
- Anterior aspect of Septum
21
Q
what are the 3 types of acute coronary syndrome
A
1) Unstable angina
2) ST-elevation myocardial infarction ( STEMI )
3) Non ST-elevation myocardial infarction ( NSTEMI)
22
Q
Making a diagnosis for ACS
A
- Perform ECG: if there is ST elevation or new left bundle branch block diagnosis a STEMI. If there is no ST elevation perform troponin blood tests. Raised troponim and/ or other ECG changes( ST depression or T wave inversion or pathological G waves)= NSTEMI. If troponin levels are normal and the ECG does not show pathological changes: unstable angina or another cause such as musculoskeletal chest pain
23
Q
ACS symptoms
A
- central, constricting chest pain
- Nausea and vomiting
- Sweating and clamminess
- Feelings of impedending doom
- SHotness of breath
- Palpitations
- Pain radiating to the jaw or arms
- For diabetics: might not experience typical chest pain= SIlent MI
24
Q
ECG changes in STEMI
A
- ST segment elevation in leads is consistent with an area of ischaemia
- New left Bundle Branch Block
25
Q
ECG changes in NSTEMI
A
- ST segment depression in a specific region
- Deep T wave inversion
- Pathological Q waves : deep infract and is a late sign
26
Q
What leads show the anterolateral side of the heart
A
I, aVL, V3-V6
27
Q
What leads show the Anterior side of the heart
A
V1-V4
28
Q
What leads show the Lateral side of the heart
A
I,aVL, V5-V6
29
Q
What leads show the inferior side of the heart
A
II, III, aVF
30
Q
What are troponins and their connection to ACS
A
- Proteins in myocardium. A diagnosis for ACS requires serial troponins ( e.g. at baseline and 6 or 12 hours after the onsset of symptoms). A rise is consistent with Myocardial ischaemia as the proteins are released from the ischaemic muscle
31
Q
DD for raised troponins
A
- Chronic renal failure
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
32
Q
Other investigations for stable angina
A
- Chest x ray
- ECG
- CT coronary angiogram
33
Q
Acute STEMI treatment
A
- Within 12 hours of onset should be urged for PCI is available within 2 hours or thrombolysis which involves injecting a fibrinolytic medication to break down fibrin and dissolve the clot. There is a significant risk of bleeding. Some example of thrombolytic agents are streptokinase, alteplase and tenecteplase
34
Q
Acute NSTEMI treatment
A
- Beta blockers
- Aspirin 300 mg stat dose
- Ticagrelor 180 stat dose or clopidogrel 300mg is an alternative
- Morphine titrated to control pain
- Anticoagulant: low molecular weight heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days )
- Nitrates(e.g. GTN) to relieve coronary artery spasm
- Give oxygen is sats are below 95 %
35
Q
GRACE score to assess for PCI in NSTEMI
A
- Gives 6 month risk of death or repeat MI after having NSTEMi
<5 % low risk
5-10% medium risk
>10% high risk
If there is medium or high risk they are considered for early PCI ( within 4 days of admission) to treat underlying coronary artery disease
36
Q
Complications of MI ( DREAD)
A
Death Rupture of the heart septum or papillary muscles oEdemia( heart failure) Arrhytmias and Aneurysm Dresslers syndrome
37
Q
What do you know about dressler’s syndrome
A
- Post MI syndrome, normally 2-3 weeks after an MI
- Caused by localised immune response and cause pericarditis ( inflammation of the pericardium )
- Presents with pleuritic chest pain, low grade fever and pericardial rub on auscultation. It can cause a pericardial effusion and rarely pericardial tamponade
- Diagnosis: ECG= global ST elevation and T wave inversion, echocardiogram : pericardial effusion and raised inflammatory markers: CRP and ESR
- Management : NSAIDs ( apsirin/ ibuprofen) and in more severe cases steroids ( prednisolone ). They made need pericardiocentesis to remove fluid
38
Q
Secondary prevention medical management ( 6 As)
A
- Asprin 75 mg once daily
- Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
- ATorvastatin 80 mg once daily
- ACEi ( ramipril triturated as tolerated to 10 mg once daily )
- Atenolol or other beta blocker titrated as high as tolerated
- Aldosterone antagonist for those with clinical heart failure ( i.e. eplerone titrated to 50 mg once daily )
39
Q
Secondary prevention lifestyle advice
A
- stop smoking
- reduce alcohol consumption
- Mediterranean diet
- Cardiac rehabilitation
- optimise treatment of other medical conditions
40
Q
Types of MI (4)
A
- T1: due to acute coronary event
- T2: Ischaemia secondary to increased demand or reduced supply or O2 ( e.g. 2ry to every anaemia , tachycardia or hypotension )
- T3: suddent cardiac death or cardiac arrest suggestive of an ischaemic event
- T4: MI associated with procedures such as PCI, coronary stenting or CABG
41
Q
What is Acute LVF?
A
- when LV can push blood around the heart
- This causes backlog of blood that increases the amount of blood left stuck in the LA, pulmonary veins and lungs
- As the vessels are engorged with blood due to increased volume and pressure they leak fluid and are unable to rebasorb fluid from the surrounding tissues which causes pulmonary oedema ( lung tissue and alveoli become full of interstitial fluid). This interferes with normal gas exchange in the lungs, causing shortness of breath , reduced O2 saturation and other
42
Q
Triggers of Acute LVF
A
- Iatrogenic
- Sepsis
- MI
- Arrhtmias
43
Q
Symptoms of acute LVF
A
- shortness of breath
- Looking and feeling unwell
- COugh with frothy white or pink sputum
- Chest pain in ACS
- Fever in sepsis
- Palpitations with arrhythmias
44
Q
Physical examination findings for acute LVF
A
- Increased RR
- Low O2 sats
- Tachycardia
- 3rd heart sound
- Bilateral basal ‘wet’ crackles
- Hypotension in severe cases such as cardiogenic shock
- If there is also RHS heart failure there could be raised JVP and peripheral oedema in ankles, legs and sacrum
45
Q
Work up for Acute LVF
A
- History
- CLinical examination
- ECG to look for ischaemias and arrhythmias
- Arterial blood gas (ABG)
- Chest x-ray
- Routine bloods for infection, kidney function, BNP and consider troponin if suspecting MI
- Echocardiogram
46
Q
What is a BNP blood test
A
- B-type natriuretic peptide is a hormone released form the heart by the ventricles when the cardiac muscle is stretched beyond the normal range. High result: heart is overloaded with blood beyond its normal capacity
- BNP is to relax the smooth muscle in blood vessels. This reduced systemic resistance and acts on the kidneys as. diuretic to promote the exretion of more water in the urine
- Testing is sensitive but not specific. This means that when the result is negative its is useful in ruling out heart failure but it can be positive due to other causes such as tachycardia, sepsis, Pulmonary embolism, renal impairment, COPD
47
Q
What is an echocardiography
A
- Useful to assess the function of the LV and any structural heart abnormalities
- for the LV the measure is the ejection fraction. Above 50% it is considered normal
48
Q
Chest X ray findings
A
- Cardiomegaly on an xray it is defined as a cardiothoracic ration of more than 0.5: the diameter of the widest part of the heart is more than half of the diameter of the widest part of the lung fields
- Upper lobe venous diversion may also be seen. Normally when standing erect the lower lobe veins contain more blood and the upper lobe veins less so they are smaller. LVF there is such a back pressure where the upper lobe veins also fill and become engorged. This is visible as increased prominence and diameter of the upper lobe vessels
- Fluid licking from oedematous long tissue causes additional x-ray findings of bilateral pleural effusions, fluid in interlobar fissures, fluid in septal lines
49
Q
Management of Acute LVF (Poor SOD)
A
- Pour away (stop) IV fluids
- SIt up : the lungs when lying flat spread to a large are. When upright gravity takes it to the bases leaving the upper lungs free for gas exchange
- Oxygen : is O2 sats are below 95%
- Diuretics: e.g. furosemide 40 mg sat. This reduces circulating volume
- Other options: intravenous opiates( such as morphine that act as vasodilators), Non invasive ventilation and continuous positive airway pressure ( tight fittings mask to forcefully blow air into the lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV doesn’t work they may need full intubation and ventilation), Ionotrope( like infusion of noradrenaline, as they strengthen the force of heart contractions and improve heart failure )
50
Q
What is chronic heart failure
A
Chronic version of acute heart failure. It is caused by either impaired left ventricular contraction( systolic heart failure) or left venticular relaxation ( diastolic heart failure)
51
Q
Presentation of chronic heart failure
A
- Breathlessness worsened by exertion
- Cough: they may produce frothy white/ pink sputum
- Orthopnoea: sensation of shortness of breathing when lying flat relieved by sitting or standing
- Paroxysmal Nocturnal Dyspnoea
- Peripheral Oedema
52
Q
What is Paroxysmal Nocturnal Dyspnoea
A
- Severe attack of shortness of breath and cough when waking up at night
Caused by 3 mechanisms:
1) lying flat means that fluid is settling across a wider surface area of the lungs so sitting or standing allows freedoms for the upper lung lobes
2) The respiratory centre of the brain slows down during sleep so doesn’t compensate for reduced O2 sats
3) less adrenaline is released and therefore the myocardium is more relaxed
53
Q
Diagnosis of chronic heart failure
A
- Clinical presentation
- BNP blood tests specifically N-terminal pro-B-type natriuretic peptide
- Echocardiogram
- ECG
54
Q
Causes of chronic heart failure
A
- Ischaemic heart disease
- Aortic stenosis
- hypertension
- Arrhytmias commonly atrial fibrillation
55
Q
Management of chronic heart failure
A
- Reffer to specialist
-Surgical treatment in severe aortic stenosis or mitral regurgitation - Yearly flu and pneumonococcal vaccine
- Stop smoking
- Optimise co morbidities
-Exercise as tolerated - Medical: (ABAL)
1) ACEi e.g. ramipril titrated as tolerated up to 10 mg daily
2) beta blocker bisopropol titrated as tolerated up to 10 mg daily
3) Aldosterone antagonist if A and B don’t work e.g. spironolactone or eplerenone
4) Loop diuretics e.g. furosemide 40 mg once daily
Extra medical: angiotensin receptor blocker if Acei are not tolerated e.g. candesartan up to 32 mg daily
56
Q
What is cor pulmonale
A
- RHS heart failure caused by respiratory disease
- Increased pressure and volume in the pulmonary veins= strain to the RV= back presssure to the RA= to the vena cava and pulmonary arteries
57
Q
Respiratory causes of cor pulmonale
A
- COPD
- Pulmonary embolism
- Interstitial lung disease
- Cystic fibrosis
- Primary pulmonary hypertension
58
Q
Presentation of cor pulmonale
A
- Normally asymptomatic. They might complain about shortness of breath however this is normally caused by the underlying lung disease. They might also present syncope, chest pain , peripheral oedema and increased breathlessness
59
Q
Signs of cor pulmonale on examination
A
- Hypoxia
- Cyanosis
- Raised JVP
- Peripheral oedema
- 3rd heart sound( pan systolic in tricuspid regurgitation)
- Murmurs
- Hepatomegaly( increased pressure from the back flow in the hepatic vein )
60
Q
Management of cor pulmonale
A
- Treating symptoms
- Treating underlying cause
- Sometimes long term O2 therapy
- poor prognosis
61
Q
Causes of Hypertension ( ROPE)
A
- 1ry hypertension: developed on its own no secondary cause
-2ry hypertension:
Renal disease ( such as renal artery stenosis when the pressure is very high or doesn’t respond to treatment)
Obesity
Pregnancy induced/ pre eclampsia
Endocrine: majority is hyperaldosteronism( Conn’s syndrome )
62
Q
Complications of hypertension
A
- Ischaemic heart disease
- Cerebrovascular accident ( stroke or haemorrhage )
- hypertensive retinopathy
- hypertensive nephropathy
- Heart failure
63
Q
Stage 1 and 2 hypertension
A
- Stage 1: >140/90 clinic reading
- Stage 2: >160/100 clinic reading
64
Q
Medications for hyper tension
A
- Acei ramipeil 1.25 mg to 10 mg daily
- Beta blocker bisopropol 5mg to 20 mg
- Calcium channel blocker amlodipine 5mg to 10 mg
- Thiazide like diuretic indapamide 2.5 mg
- Angiotensin II Receptor blocker candesartan 8mg to 32 mg if a person can’t tolerate ACEi commonly with African or Caribbean descent
65
Q
Initial hypertension management
A
- Investigate causes and end organ failure
- Advice on lifestyle
66
Q
Medical management for hypertension (4 steps)
A
Step 1: aged less than 55 and non back use ACEi. Aged over 55 or black use Calcium channel blocker
Step 2: Non black use ACEi and Calcium channel blocker. If black use Angiotensin II receptor blocker instead of A
Step 3: ACEi, Calcium channel blocker , thiazide like diuretic
STep 4 : ACEi, Calcium channel blocker and 2 doses of thiazide like diuretic
67
Q
Potassium balance and hypertension meds
A
- If potassium is more than 4.5 use thiazide like diuretic as thiazide like diuretics can cause hypokalaemia
- If potassium is less or equal to 4.5 use potassium sparing diuretic such as spironolactone as it blocks the action of aldosterone and causes Na secretion and K reabsorption
- Very close monitoring because ACEi can cause hyperkalaemia
68
Q
Treatment optimum targets
A
- <80 : <140/<90
- >80: <150/<90
69
Q
S1 and S2 sounds
A
S1: closing of atrioventricular valves( tricuspid and mitral) at the start of systolic ventricular contraction
- S2: Closing of semilunar valves( pulmonary and aortic) when systolic contraction is complete
70
Q
S3 sound
A
- Can be normal for 15-40 year olds, lasts about 0.1 seconds after the S2 sound and is because of rapid ventricular filling causing the chord tendinae to stretch
71
Q
S4 sound
A
- Directly before S1, always abnormal and rare, caused by a stiff or hypertrophic ventricle when the atria contracts blood into a non compliant space
72
Q
What does mitral stenosis cause
A
Left atrial Hypertrophy
73
Q
What does aortic stenosis cause
A
Left ventricular hypertrophy
74
Q
What does mitral regurgitation cause
A
Left atrial dilation
75
Q
What does aortic regurgitation cause
A
Left ventricular dilation
