Cardiovascular Flashcards
How are atherosclerotic plaques distributed?
- found in peripheral and coronary arteries
- focal distribution (small area) along artery length
- change in flow alters endothelial cell function
- wall thickness changed leading to neointima (scar tissue)
- altered gene expression in key cell types
What are fatty streaks and when do they appear?
- earliest type of lesion < 10 years
- aggregations of lipid laden macrophages and T lymphocytes in the intimal layer of the vessel wall
What is an intermediate lesion?
- no symptoms and walled off
- foam cells and T lymphocytes
- vascular smooth muscle cell proliferation from media > intima
- adhesion and aggregation of platelets to vessel wall
What is a fibrous plaque?
- impedes blood flow
- prone to rupture
- covered by dense fibrous cap made of ECM proteins inc collagen, elastin overlying lipid core and necrotic debris
- may experience symptoms e.g. angina
Describe plaque rupture
- Plaques grow and recede
- fibrous cap is resorbed and redeposited in order to be maintained
- if balance shifts in favour of inflammatory conditions, cap becomes weak and plaque ruptures
What is the difference between red and white thrombus?
- Red: contains red blood cells and fibrins
- White: platelets and fibrinogen
What drugs are commonly used in treatment of atherosclerosis?
- aspirin
- clopidogrel/ticagrelor - inhibits P2Y12 ADP receptor on platelets
- statins: reduce cholesterol synthesis by inhibiting HMG CoA reductase
How is acute MI diagnosed?
- ST elevation MI can be diagnosed on ECG
- Non ST elevation MI is diagnosed retrospectively made after troponin results
What are the 3 acute coronary syndromes?
- STEMI: ST elevation MI
- NSTEMI: Non-ST elevation MI
- Unstable angina: prolonged, severe angina, usually at rest possibly with ECG changes
Describe unstable angina:
- occlusion
- infarction
- ECG
- troponin
- partial occlusion of minor coronary artery
- no infarction: ischaemia only
- normal ECG, may show ST depression or T wave inversion
- normal troponin
Describe NSTEMI:
- occlusion
- infarction
- ECG
- troponin
- partial occlusion of major coronary artery/total occlusion of minor coronary artery
- sub endothelial infarction so area distal to occlusion dies
- ST depression, T wave inversion, new LBBB
- elevated troponin
Describe STEMI:
- occlusion
- infarction
- ECG
- troponin
- total occlusion of major c.a.
- transmural infarction (full thickness of myocardium)
- ST elevation in local leads,
- elevated troponin
What are the causes of ACS?
- most common: rupture of an atherosclerotic plaque + consequent arterial thrombosis
What are the risk factors for ACS/IHD?
- age
- smoking
- family history
- diabetes
- hyperlipidaemia + htn
- obesity
- stress
- male 1.5:1
What are the symptoms of MI?
- unremitting cardiac chest pain radiating to left arm, neck, jaw (crushing/squeezing)
- usually severe but may be mild or absent
- associated with sweating, breathlessness, nausea/vomiting
- dyspnoea
What are the symptoms of unstable angina and how can it be diagnosed?
- cardiac chest pain at rest, with crescendo pattern
- new onset angina
- diagnosed by history, ECG and troponin
What is the first line investigation for ACS?
12 lead ECG
What is seen on an ECG after an MI?
- hyperactive T waves
- pathologically steep Q waves
- LBBB (left bundle branch block - electrical impulse disrupted) (prolonged QRS complex)
What is the gold standard investigation for ACS?
CT coronary angiogram
How is ACS managed?
- MONAC if acute
- coronary reperfusion: PCI (<12h) or thrombolysis w alteplase (>12h)
- patient should be given aspirin, β blocker
- 2nd antiplatelet agent e.g. clopidogrel
- atorvastatin + ACEi
What should patients be offered for secondary prevention of ACS/stable angina?
- lifestyle advice firstly
- ACE inhibitor/ARB
- β blocker
- dual anti platelet therapy
- statin
How are MIs managed?
- oxygen therapy if hypoxic
- pain relief (opiates/nitrates)
- Aspirin (and maybe P2Y12 inhibitor)
- potentially β blocker, antianginal therapy, angoigraphy
What is troponin?
- protein complex regulating actin:myosin contraction
- highly sensitive marker of cardiac muscle injury
- may not represent permanent muscle damage
What is the pathophysiology of stable angina?
- oxygen supply ≠ demand
- most commonly attributed to IHD
- impairment of blood flow by proximal arterial stenosis
- increased distal resistance
- reduced oxygen carrying capacity of the blood
What are the criteria for stable angina?
- central crushing chest pain radiating to neck/jaw
- brought on with exertion e.g. walking up hill, cold weather, heavy meal
- relieved with 5 mins rest/ GTN spray
What are the symptoms of stable angina?
- central crushing chest pain radiating to neck/jaw (worsens with time)
- nausea
- sweating
- fatigue
- dyspnoea
What is the gold standard investigation for stable angina?
CT coronary angiography to highlight any narrowing
What is the management strategy for immediate symptomatic relief of angina?
- GTN spray used as required to cause vasodilation and ease symptoms
- a second dose is taken after 5 mins if pain hasn’t subsided
- call an ambulance after another 5 mins if pain hasn’t gone
What medications are used for long term symptomatic relief of angina?
- β blockers (contraindicated by asthma)
- calcium channel blockers (CCB)
- lifestyle changes
How do calcium channel blockers work and in which disease are they contraindicated?
- reduce afterload
- relax smooth muscle cells in arterial walls
- contraindicated by heart failure
What is a CABG?
- coronary artery bypass graft
- for multi vessel disease
- a graft vein is taken from the leg (usually great saphenous vein) or internal mammary artery and sewn on to bypass the stenosis
What is PCI?
- Percutaneous coronary intervention with coronary angioplasty
- putting a catheter into the brachial or femoral artery
- contrast injected so stenosis is evident
- balloon stent can be inserted
Describe the anatomy of the pericardium
- great vessels lie within pericardium
- 2 layers are continous
- LA is mainly outside pericardium
- parietal layer uses fibrous attachments to fix heart in thorax
What is acute pericarditis?
- an inflammatory pericardial syndrome with or without effusion
What factors are used in diagnosis of acute pericarditis and how many factors are needed?
- diagnosis made with 2 of 4 factors:
- chest pain
- friction rub
- ECG changes
- pericardial effusion
What is the epidemiology of pericarditis?
- 80-90% is idiopathic + seasonal with viral trends
- higher in young, previously healthy patients
What are the infectious causes of pericarditis?
- MAINLY viral: enteroviruses, herpesviruses (EBV, CMV, HHV-6), adenoviruses
- bacterial: mycobacterium tuberculosis
What are the non-infectious causes of pericarditis?
- autoimmune: Sjogren, rheumatoid arthritis, scleroderma
- neoplastic (most common): secondary metastatic tumours
- trauma (most common): PCI, pacemaker insertion
- other (rare): amyloidosis, aortic dissection
How does pericarditis present?
- severe chest pain, sharp and pleuritic (not constricting + crushing like IHD)
- KEY: relieved by sitting forward and exacerbated by lying down
- rapid onset
- left ant chest/epigastrium
- breathlessness, coughing, hiccups
How can pericarditis be investigated?
- pericardial rub: heard around 2nd heart sound, sounds like crunching snow
- ECG, bloods, CXR, Echo
What is seen on the ECG in pericarditis?
- PR depression
- concave (saddle shaped) ST elevation
- similar ECG to acute STEMI
Describe the management of pericarditis
- restricting physical activiity
- NSAIDs + PPIs
- colchicine
- 2nd line: corticosteroids if NSAIDs or colchicine fail
What is cardiomyopathy and what is hypertrophic cardiomyopathy the cause of?
- disease of the heart muscle
- caused by autosomal dominant mutation of sarcomeric protein genes
- HCM = most common cause of sudden cardiac death in young people
What is the pathology behind HCM?
- thickening of the cardiac muscle leads to impaired filling of the ventricles (esp LV)
- this leads to decreased cardiac output
- can lead to diastolic heart failure
- may be white areas of fibrosis/scarring of the heart muscle + septum becomes asymmetrically thickened
- patients with troponin T mutation at greatest risk
What are the risk factors for HCM?
- young + asymptomatic
- family history of sudden cardiac death
- history of arrhythmia
- playing competitive sport
How does HCM present?
- exertion chest pain, dyspnoea
- palpitations
- fatigue
- exertion syncope: suggests LV outflow tract obstruction
What is seen on ECG for HCM?
- diagnosed by ECG: sharp, deep Q waves > 40ms
- wide P waves
- T wave inversion
How is HCM managed?
- control arrhythmias with amiodarone
- control LV function: β blockers and verapamil
What is the cause of dilated cardiomyopathy?
- cytoskeletal gene mutations
- enlarged ventricular size and systolic dysfunction
- thin cardiac muscle walls contract poorly > dec CO
How does DCM present?
- dyspnoea
- fatigue
- peripheral oedema
- loud 3rd and 4th heart sounds
How is DCM diagnosed?
- ECG: sinus tachycardia, T wave inversion, ST depression, LBBB
- CXR: enlarged heart, pleural effusion
How is DCM managed?
- treat reversible causes
- prophylactic anticoagulation
- consider pacemaker
- treat as heart failure
What is restrictive cardiomyopathy?
- reduced compliance of ventricular walls during diastolic filling
- Commonly affects the LV, but can often affect both.
- Causes high diastolic filling pressures > pulmonary hypertension
- reduced CO
What are the symptoms of RCM?
- dyspnoea
- fatigue
- pulmonary oedema
- loud 3rd heart sound
- AF in 75% of patients
How is restrictive cardiomyopathy diagnosed and managed?
- ECG: T wave and ST changes, pathological Q waves
- echocardiogram: may have dilated atria or myocardial hypertrophy
- no treatment, maybe transplant
What is tetralogy of fallot and its 4 features ?
- key issue: interior dislocation of the septum which partially obstructs RVOT and PA
1. ventricular septal defect: leading to equal ventricular pressures
2. pulmonary stenosis
3. overriding aorta
4. RV hypertrophy
What is the presentation of tetralogy of fallot?
- cyanosis
- dyspnoea on feeding, crying, exertion
- failure to thrive
- murmur
- fallot spells: sudden onset dyspnoea/cyanosis
- inc venous return to RV and severe spells > death
How is tetralogy of fallot managed?
- VSD patched
- PV widened or replaced
What is a ventricular septal defect?
- most common form of congenital heart disease
- malformation of ventricular septum
- if LV pressure > RV then blood flows LV to RV
- inc blood flow through lungs
How does a VSD present?
- loud systolic murmur
- severe: breathlessness, poor feeding, failure to thrive, tachycardia
- mild: small inc in pulmonary blood flow, endocarditis risk, asymptomatic
How is a VSD diagnosed and managed?
- gold standard: echocardiogram
- CXR, ECG
- percutaneous/open heart surgery, patch application
What is an atrial septal defect?
- congenital heart defect causing a shunting of blood from L to R atria
- inc flow into right heart and lungs
- secundum ASD: patent foramen ovale
- leads to right heart dilation in severe
How does an ASD present?
- pulmonary flow murmur
- split S2 heart sound due to delayed closure of PV and inc blood volume
- big pulmonary arteries and heart on CXR
What is an atrio-ventricular septal defect (AVSD)?
- Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
- Can be complete or partial
What is a patent ductus arteriosus (PDA)?
- Persistence of the connection between the aorta and pulmonary artery
- normally rise in PaO2 and decline in prostaglandins close the duct
How does a patent ductus arteriosus present?
- tachycardia and tachypnoea
- continuous murmur at left sternal edge
- failure to thrive
- poor feeding
- risk of endocarditis
How is PDA diagnosed and managed?
- diagnosis: echocardiogram
- management: usually closed via cardiac catheterisation
What is coarctation of the aorta and how does this present in severe and mild patients?
- narrowing of the aorta at the site of the ductus arteriosus
- presents with htn and murmur
How does coarctation of the aorta present?
- right arm hypertension
- bruits over scapulae and back
- murmur
How is coarctation of the aorta managed?
- repaired by surgical or percutaneous intervention - narrow section removed
What is an abdominal aortic aneurysm and what is the pathophysiology?
- permanent dilation of the abdominal aorta with a diameter of more than 3cm
- mostly originate below the renal arteries
- smooth muscle, elastic and structural degeneration in all 3 layers of the vascular tunica
What are the risk factors for an AAA/TAA?
- men more than women, and at a younger age
- smoking
- hypertension
- family history
- existing CVD
What is the aetiology of AAAs?
- coarctation of the aorta
- Marfan’s syndrome
- aortic surgery
- 3rd trimester pregnancy
How does AAA present?
- mostly asymptomatic and detected on rupture
- non-specific abdominal pain
- Pulsatile and expansile mass in the abdomen when palpated with both hands
- incidental finding on x-ray, ultrasound or CT
What is the diagnostic investigation for AAA?
ultrasound then CT angiogram to guide elective surgery
How are AAAs managed?
- treating reversible risk factors
- screening yearly/3 monthly
- surgical: artificial graft: open repair or EVAR (endovascular aneurysm repair) stent