Cardiovascular Flashcards
Define Hypertension
- 140/90mmHg on at least 2 readings on separate occasions
- Commonest cause of cardiac failure - major risk factor for cardiovascular disease
- Hypertension is major cause of premature vascular disease, leading to cerebrovascular events, IHD and peripheral vascular disease
- Mortality rises with increasing BP
What are the stages of hypertension?
Stage 1:
- BP >140/90 in clinic
White coat syndrome - BP >135/85 with ABPM/home readings
Stage 2:
- More than or equal to 160/100mmHg clinic BP
- Daytime average ABPM or HBPM greater than or equal to 150/95mmHg
Severe:
Clinic systolic BP greater than or equal to 180mmHg and/or diastolic BP greater than or equal to 110mmHg
- If there is end organ damage, start immediate anti-hypertensive drug treatment regardless of BP level
Describe the pathology of hypertension
1) VASCULAR CHANGES:
- Accelerates atherosclerosis
- Causes thickening of media of muscular arteries
HEART – major risk factor for IHD
2) NERVOUS SYSTEM
- Intracerebral haemorrhage frequent cause of death
3) KIDNEYS:
- Can cause or result from renal disease
- Kidney size often reduced and small vessels show intimal thickening and medial hypertrophy
4) Malignant:
- Characteristic features
- Markedly raised diastolic BP (usually over 120mmHg)
- Progressive renal disease
- Renal vascular changes prominent
What are the risk factors for hypertension?
Modifiable:
- Alcohol intake
- Sedentary lifestyle
- DM
- Sleep apnoea
(Smoking)
Non modifiable:
- Age (>65)
- Family History
- Ethnicity (Afro-Caribbean)
What are the causes of hypertension?
1) Essential (Primary origin) – 95% cases
2) Secondary causes:
ROPE:
- Renal disease e.g. CKD
- Obesity
- Pregnancy (pre-eclampsia)
- Endocrine (Conn’s syndrome)
- Drugs – oestrogen-containing oral contraceptives, NSAIDs, vasopressin
What are the signs and symptoms of hypertension?
- Asymptomatic – except in malignant hypertension
- May have the occasional general headache
What are the first-line investigations for the diagnosis of hypertension ?
- Take BP:
- If BP is >140/90 mmHg, then confirm using
- 24-hour ambulatory BP monitor (ABPM)
- Multiple home BP monitoring (if patient can’t tolerate ABPM)
- It is believed to be able to reduce the white coat hypertension effect in which a patient’s blood pressure is elevated during the examination process due to nervousness and anxiety caused by being in a clinical setting
How can you asses end organ-damage in hypertension?
- Urinalysis to check kidneys (protein, albumin: creatine ratio and haematuria)
- ECG/Echo for LV hypertrophy
- Fundoscopy to assess hypertension retinopathy
- Bloods
+Serum creatinine
+eGFR
+Glucose – assess diabetes risk - Clinical history – previous MI/strokes
- Others - HbA1c (DM) + Lipids
What is the first-line treatment for hypertension?
Lifestyle changes:
- Smoking cessation
- Low-fat diet + high consumption of fruit and vegetables
- Reduce alcohol and salt intake
- Increase exercise
- Loss weight if obese
What is the first-line drug treatment for hypertension?
Less than 55:
- ACEi - e.g. Ramipril
OR
- ARB e.g. Canderstan
if ACEi is contraindicated or not tolerated (e.g. due to cough)
Over 55/Afro-Caribbean:
- CCB - e.g. Amlodipine
What is the second-line treatment for HTN?
- Second line – ACE-inhibitor + CCB
- Third line – ACE-inhibitor + CCB + diuretics (e.g. Bendroflumethiazide or furosemide)
- Fourth line – ACE-inhibitor + beta blocker e.g. Bisoprolol + CCB + diuretics
A,C,D + B
What is malignant hypertension?
Rapid rise in BP leading to vascular damage
What are the symptoms of malignant hypertension?
- Headache
- Visual disturbance
What are the signs of malignant hypertension?
- Severe hypertension
Systolic > 200 mmHg
Diastolic > 130 mmHg - Bilateral renal haemorrhage = exudates = papilloedema
- Papilledema is optic disc swelling that is caused by increased intracranial pressure due to any cause.
- The swelling is usually bilateral and can occur over a period of hours to weeks.
- Unilateral presentation is extremely rare.
What are the complications of malignant hypertension?
- Hypertensive emergencies e.g. acute kidney injury, HF and encephalopathy
- Cardiac failure with LV hypertrophy and dilatation
- Blurred vision and retinal haemorrhages
- Haematuria and renal failure due to fibrinoid necrosis of glomeruli
- Severe headache and cerebral haemorrhage
What is the treatment of malignant hypertension?
Sodium nitroprusside
Define Ischaemia
An imbalance between the supply of oxygen to cardiac muscle and cardiac demand
What is Atherosclerosis
- Atherosclerosis causes narrowing of coronary arteries 🡪 ischaemia and pain i.e. Angina
Describe the process of Atherosclerosis
1) INITATION – endothelial injury 🡪 lipid accumulation 🡪 local cellular proliferation 🡪 mural thrombi on surface and subsequent healing and repeat of cycle
2) ADAPTATION – as plaque progresses to 50% of vascular lumen size, vessel can no longer compensate by re-modelling and becomes narrowed 🡪 new matrix surfaces and degradation of matrix 🡪 can progress to unstable plaque.
3) CLINICAL STAGE –
- Plaques continues to impinge on lumen, running risk of haemorrhage or exposure of tissue HLA-DR antigens 🡪 T cell accumulation
PATHOLOGICAL:
Fatty Streak:
- Show macrophages filled with foam cells
- As smooth muscle cells with fat
Intimal cell mass:
- Collections of muscle cells and connective tissue without lipid “cushions”
The atheromatous plaque:
- Characterised by distorted endothelial surface containing lymphocytes, macrophages, smooth muscles cells and variably complete endothelial surface
What are the complications of an atherosclerotic plaque?
- Acute occlusion due to thrombus
- Chronic narrowing of vessel with healing of local thrombus
- Aneurysm change
- Embolism of thrombus ± plaque lipid content
What are the causes of IHD?
MOST COMMON CAUSE:
- Coronary artery atheroma (atherosclerotic plaques consisting of accumulations of lipids, macrophages and smooth muscle cells in the intima)
- Results in reduced blood flow or a fixed obstruction to coronary blood flow
- LV hypertrophy – increased distal resistance
- Anaemia – reduced O2 carrying capacity
- Hypoxia – reduced availability of O2
- Coronary artery thrombosis
- Coronary artery spasm
- Arteritis
What are the Modifiable (reversible) risk factors
for IHD?
- Smoking
- Obesity
- Exercise
- Diet:
- High in fats (particularly saturated fat intake)
- Low in antioxidant intake (fruit and veg)
- Alcohol intake
- Sedentary lifestyle
What are the Clinical risk factors for IHD?
- Hypertension
- Diabetes
- Hyperlipidaemia
- Hypercholesterolaemia
- Depression
What are the Non-modifiable risk factors for IHD?
- Age
- Family history (genetics)
- Gender – M>F
- Ethnicity
What are the psychosocial risk factors for IHD?
- High demand, low control jobs have high stress
- Low social interaction
- Lack of support network
What does the QRISK2 score predict?
- The QRISK2 score predicts risk of CVD in next 10 years
It considers:
- BP
- Age
- Smoking status
- Cholesterol
- Rheumatoid Arthritis
- Diabetes Mellitus
- Anti-hypertensives
- BMI
- Ethnicity
Define Angina Pectoris (Stable Angina)
Descriptive term for chest pain/discomfort arising from the heart as a result of myocardial ischaemia
What are the different types of Angina?
- Stable – induced by effort and relieved by rest
- Unstable (crescendo) - increases in severity, occurs at rest or is of recent onset (less than 1 month)
- Variant (Prinzmetal’s) angina – caused by coronary artery spasm and results in angina that occurs without provocation, usually at rest
- Decubitus angina – occurs lying down
- Nocturnal angina – occurs at night and may wake patient from sleep
What are the symptoms of Angina?
- Central crushing retrosternal chest pain that radiates to arms, jaw and neck
- Dyspnoea
- Palpitations
- Syncope
What are the signs of Angina?
- Chest pain comes on with exertion and rapidly resolved by rest and/or GTN
- Exacerbated by cold weather, anger and excitement
How would you score Angina?
- Central tight chest pain radiating to arms, neck and jaw
- Precipitated by exertion
- Relieved by rest or GTN spray
3/3 – typical angina
2/3 – atypical angina
1/3 – non-anginal pain
What is the differential diagnosis for Angina?
- Pericarditis/Myocarditis
- Pulmonary embolism
- Chest infection
- GORD
- Dissection of the aorta
What are the first-line investigation for Angina?
- First-line = 12 Lead ECG:
- Usually normal
- May show ST depression and T wave inversion
What is the gold-standard investigation for Angina?
- CT angiography
- Shows narrowing of a coronary artery
- Once narrowing is shown it is then possible to go in and open with a stent or balloon
What other tests can you do for Angina?
- Stress ECG (ischaemia inducing exercise stress test)
Bloods:
- FBC – anaemia
- Cardiac enzymes
- Glucose
- Lipid profile
- CXR – check heart size and pulmonary vessels
How can you manage Angina?
- Lifestyle
- Weight loss
- More exercise
- Quit smoking
- Treat underlying conditions
- HTN and DM
What is the pharmacological treatment of Angina?
+Symptomatic relief:
- GTN spray
+Long term symptomatic relief:
- Beta blocker or CCB
+Secondary prevention:
- Aspirin
- Atorvastatin
- ACEi
…………………………….
+Percutaneous Coronary Intervention (PCI)
- Stenting or ballooning the narrow artery
- Risk of restenosis (re-narrowing) or thrombosis
- Drug-eluting stents reduces risk of restenosis
- Less invasive, shorter recovery
- Coronary artery bypass graft (CABG)
Describe the mechanism of action of the drugs used to treat Angina
1) Glyceryl Trinitrate (GTN) spray – 1st line anginal:
- Dilates systemic veins (venodilator) –> reduces venous return to right heart –> reduces preload –> reduces work of heart and oxygen demands
- Also dilates coronary arteries
Common side effect is headache
…………………………..
2) Beta blockers (e.g. bisoprolol, atenolol, propranolol):
- Act on B1 receptors in heart as part of adrenergic sympathetic pathway
- Reduce HR and force of contraction (negatively chronotropic and inotropic)
- Contraindicated in asthma or in patients with heart block/heart failure/hypotension
- Use a Calcium channel blocker instead e.g. amlodipine
………………………………..
3) CCB (E.G. amlodipine)
Dilates systemic arteries (arterodilator) –> BP drop –> reduces afterload –> less energy required for same cardiac output
- Relax coronary arteries and reduce force of LV contraction
- Ca2+ channel blocker – Arterodilators e.g. amlodipine
………………………………………….
4) Anti-platelet - 75mg Aspirin (inhibits platelet aggregation by inhibiting COX)
± Clopidogrel if aspirin is contraindicated
…………………………………………..
- Statins – reduce cholesterol e.g. atorvastatin, simvastatin
HMG-CoA reductase inhibitor
………………………………………….
- ACE inhibitors for BP control e.g. Ramipril, lisinopril
- If severe consider angiotensin receptor blocker e.g. Candesartan or Losartan
………………………………………….
- Ivabradine – inhibits pacemaker current in the SAN and therefore reduces heart rate
………………………………………….
- Another option if beta blockers are contraindicated
What is the treatment when meds fail or when high risk disease identified?
- Percutaneous Coronary Intervention (PCI):
- Stenting or ballooning the narrow artery
- Convenient and less invasive
- Shorter recovery
- Risk of stent thrombosis
- Coronary artery bypass graft (CABG):
- CABG – LIMA used to bypass narrowing in LAD – good prognosis but invasive + longer recovery, risk of stroke/bleeding
What is Acute coronary Syndrome?
Thrombus from an atherosclerotic plaque blocking a coronary artery, causing:
1) Unstable Angina (Ischaemia)
- Cardiac chest pain with crescendo pattern
- Deterioration in previously stable angina
- Symptoms frequently occurring at rest
2) STEMI (complete occlusion)
- Develops after occlusion of a MAJOR coronary artery previously affected by atherosclerosis
- Causes FULL thickness cardiac muscle damage
- Can usually be diagnosed on ECG at presentation
3) NSTEMI (partial occlusion → subendocardial infarction)
- Occurs by developing a COMPLETE occlusion of a MINOR coronary artery or PARTIAL occlusion of a MAJOR coronary artery previously affected by atherosclerosis
- Causes infarction distally and ischaemia proximally
- Causes partial thickness cardiac muscle damage
- Usually a retrospective diagnosis after troponin results and other investigations
Describe the Pathology of Acute coronary syndromes
- All have same mechanism
- Rupture or erosion of the fibrous cap of a coronary artery atheromatous plaque –> subsequent formation of a platelet-rich clot (thrombosis) –> inflammation and vasoconstriction produced by platelet release of serotonin and thromboxane A2
- Unstable angina differs from NSTEMI in that in NSTEMIs the occluding thrombus is sufficient to cause myocardial damage (necrosis) and an elevation in serum markers of myocardial injury (troponin and creatine kinase)
- Rarely due to emboli, coronary spasm or vasculitis
How can you differentiate between the three different types of ACS?
1) Stable Angina
- Pain develops when there is increased demand in the setting of a stable atherosclerotic plaque
- The vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand - Ischaemia BUT no infarct
- ECG = Normal
- Troponins = Normal
2) Unstable Angina
- The plaque ruptures and a thrombus forms around the ruptured plaque, causing PARTIAL occlusion of the vessel
- Angina pain occurs at rest or progresses rapidly over a short period of time
- ECG = Normal, inverted T waves, ST depression
- Troponins = Normal
3) NSTEMI
- The plaque ruptures and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium (subendocardial infarct)
- ECG = Normal, inverted T waves, ST depression
- Troponins = Elevated
4) STEMI
- Complete occlusion of the blood vessel lumen = transmural injury and infarct to the myocardium
- This is reflected by ECG changes and a rise in troponins
- ECG = Hyperacute T waves or ST elevation
- Troponins = Elevated
Describe the ECG changes in Acute coronary syndrome (Unstable angina, STEMI & MSTEMI).
1) Unstable Angina:
- ECG = Normal, inverted T waves, ST depression
2) NSTEMI:
- ECG = Normal, inverted T waves and / or ST depression
3) STEMI:
- ST elevation and tall T waves
- Will produce pathological Q waves some time after an MI
- There may be a new LBBB in larger MIs (WiLLiaM)
V1 – W shape
V6 – M shape
What ECG changes can ischaemia cause?
- ST depression
- T wave flattening or inversion
What does a Q wave on an ECG show?
- Pathological Q wave
- Evidence of previous infarction
- Pathological Q waves are deeper and wider than normal (>35% QRS height and wider than one small square)
- The larger the infarction is, the more likely it will result in pathological Q waves
If you see ST depression in an ECG of someone who has had an STEMI, why must this have occurred?
- A posterior STEMI will show ST depression in V1 to V4 as the view of the heart on the ECG is inverted.
- V7-V9 are additional leads that can be placed on someone’s back to check for a posterior MI
What are the causes of ACS?
- Rupture of atherosclerotic plaque and consequent arterial thrombosis
- Uncommon causes include coronary vasospasm without plaque rupture, drug abuse (amphetamines, cocaine), dissection of the coronary artery related to defects of the vessel connective tissue, and thoracic aortic dissection
What are the first line investigations for ACS?
1) ECG
Acute STEMI:
- Tall T waves
- ST elevation
- New LBBB
NSTEMI:
- ST depression and/or T wave inversion
Bloods:
- FBC
- U&E
- Glucose
- Lipids
What other tests can be done to detect ACS?
- Cardiac enzymes – released into blood stream when cardiac muscle is damaged
- Troponin T and I – highly sensitive and specific markers of cardiac muscle injury but not diagnostic:
- Rise within 3-12 hours
- Peak at 24-48 hours
- Return to baseline by 5-14 days
- <14g/l normal = no MI, 14-30 ng/l = possible MI, >30ng/l = definite MI
- Creatine kinase – catalyses conversion of creatine and utilises ATP to create phosphocreatine (PCr) and ADP
- 3 different types found in skeletal muscle, brain and the heart
- CK-MB rise within 3-12 hours of onset of pain and can be used to determine re-infarction as levels drop back to normal after 36-72 hours
- Myoglobin
Rises within 1-4 hours of onset of pain
Highly sensitive but not specific - CT angiography
What are the causes of raised troponin?
Cardiac causes:
- Congestive heart failure
- Acute or chronic stable coronary artery disease
- Myocarditis (and endocarditis and pericarditis)
- Tachy/bradyarrhythmia’s
- Heart block
Non-cardiac causes:
- PE
- Gram negative sepsis
- Severe pulmonary
- Hypertension
- Renal failure
- COPD
- Diabetes
- Drugs
- Acute neurological events
Define Unstable Angina
- An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage
- Classified by:
1. Cardiac chest pain at rest
- May have crescendo pattern (it gets worse and worse more readily)
- New onset angina
- 50% of patients with unstable angina will get an infarction within 30 days if left untreated
What are the diagnosis and investigations for Unstable Angina?
- History
- FBC – anaemia aggravates it
- Cardiac enzymes (troponin normal) – excludes infarction
- ECG – ST depression when patient is in pain
- CT Coronary angiography
- Risk assessment (QRISK2)
– if low risk do an elective stress test
What is the management of Acute Coronary Syndrome?
Risk Factor modification:
- Stop smoking
- Lose weight
- Healthy diet
- Exercise
What is the Pharmacological treatment for STEMI (ACS)?
1) Percutaneous coronary intervention (PCI) within 120 mins
- Clopidogrel or prasugrel and aspirin
2) Fibrinolysis (anti-coagulant treatment) (if PCI not possible in <120 mins)
e. g. Alteplase
- Ticagrelor and aspirin
What is the Pharmacological treatment for NSTEMI (Unstable Angina)?
- Use GRACE score to predict 6 month mortality + risk of further cardio events
- Fondaparinux
Low risk:
-Ticagrelor and aspirin
Med/high risk:
- Angiography + PCI + CABG
- Prasugrel and aspirin
What is the secondary pharmacological treatment for ACS?
ABAS:
- ACEi
- Beta blocker
- Aspirin + Clopidogrel
- Statin
Explain the pharmacology of the drugs used to treat ACS
Anti-platelet therapy:
1) Aspirin (300mg initially then 75mg daily) – irreversibly inhibits COX-1 🡪 less production of thromboxane A2 🡪 less platelet aggregation
2) Dual therapy with P2Y12 receptor inhibitors - Clopidogrel (300 mg initially then 75mg for 12 months), ticagrelor (180 mg initially then 90 mg twice daily) or prasugrel
- Inhibits ADP-dependant activation of IIb/IIIa glycoproteins preventing the amplification response of platelet aggregations
- Platelet glycoprotein IIb/IIIa receptor inhibitor for high risk patients e.g. abciximab
- Anti-coagulants – Heparin interferes with thrombus formation at site of plaque rupture by inhibiting factors II (prothrombin), VII, IX and X and reduces risk of ischaemic events and death
- LMWH e.g. enoxaparin has better efficacy than unfractionated heparin
- Fondaparinux (synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin
- Nitrates – GTN spray or IV infusion
- Beta blockers – metoprolol, bisoprolol
- Statins – Reduce cholesterol e.g. atorvastatin, simvastatin
- ACE inhibitors - Ramipril
- Calcium channel blockers (if beta blocker contraindicated) – amlodipine
What is the difference between NSTEMI and unstable angina?
- NSTEMI and unstable angina have similar management, only difference is that an NSTEMI is an acute infarction and will not involve the whole of the heart wall like a STEMI. Both are due to a narrowing of the coronary artery lumen rather than a total occlusion like a STEMI
What are common Post-MI Complications?
DREAD:
- Death
- Rupture of heart septum/papillary muscles
- Edema (heart failure)
- Arrhythmias and Aneurysm:
- Tachycardia – Sinus, VF, AF
- Brachycardia – Sinus, AV block
- Dressler’s syndrome
= pericarditis following cardiac intervention/surgery
Define Myocardial Infarction?
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to COMPLETE occlusion of an artery by thrombus.
- Most common cause of death in developed countries
- 1/3 cases occur at night
Describe the pathology of an MI?
- Almost always due to a rupture of an atherosclerotic plaque which leads to clot formation which then occludes one of the coronary arteries causing myocardial cell death and inflammation
- So basically, plaque rupture –> development of thrombosis –> total occlusion of coronary artery –> myocardial cell death
What are the signs of an MI on an ECG?
1) STEMI:
- ST elevation
- Tall T waves
- Might present as a new LBBB (WilliaM)
- Pathological Q waves
2) NSTEMI:
- ST depression and/or T wave inversion
What are the risk factors for an MI?
- Age
- Male
- History of premature coronary heart disease
- Diabetes mellitus
- Hypertension
- Hyperlipidaemia
- Family history
What are the symptoms of an MI?
- Crushing central chest pain similar to that occurring in angina – described as “elephant sitting on chest:
- Sweating
- SOB/Dyspnoea
- Fatigue
- Nausea
- Vomiting
What are the signs of a heart attack?
- Occurs at rest
- Last longer than 20 minutes
- Not relived by GTN spray
- Pain may radiate to left arm, neck and/or jaw
- Pulse and BP may vary between being up or down
- Patient appears pale, sweaty and grey
- 4th heart sound – due to forceful contraction of the atria to overcome a stiff or dysfunctional ventricle
- Pansystolic murmur – due to papillary muscle dysfunction or rupture
Who are silent infarctions more present in?
- Silent infarctions either go unnoticed or present with hypotension, arrhythmias or pulmonary oedema.
- This occurs most commonly in elderly patients, diabetics or those with hypertension.
What is the differential diagnosis for an MI?
- Stable/unstable angina
- Pericarditis
- Aortic aneurysm
- Endocarditis
- Pulmonary Embolism
- Pneumothorax
What are the investigations for an MI?
- Clinical history
- ECG
1) STEMI:
- ST elevation
- Tall T waves
- LBBB
- Pathological Q waves follow
2) NSTEMI:
- ST depression and/or T wave inversion
- Cardiac enzymes – troponin T, creatine kinase, myoglobin
- CT angiography
- CXR
- FBC
- U&E
- Blood glucose and lipids
What is the acute (initial management) of an MI?
- Get to hospital immediately
MONA:
- Morphine
- Oxygen (if sats are <94%)
- Nitrates – typically fondaparinux in Sheffield
- Aspirin 300mg – chewed in order to increase absorption
- 12 lead ECG and cardiac monitor
- Beta blocker IV – contraindicated in hypotension, HF, bradycardia and asthma
- Refer for PCI, thrombolysis (IV alteplase) or CABG ASAP as long as it’s not contraindicated
What is the subsequent (secondary prevention) of an MI?
Modification of risk factors:
- Diabetes
- Smoking
- Hypertension
- Hypercholesterolaemia
- Exercise
- Diet – high in oily fish, fruit and veg, low in saturated fats
What is the subsequent pharmacological (secondary prevention) of an MI?
- Aspirin – 75mg daily
- Clopidogrel/ticagrelor (for dual antiplatelet therapy)
- Statins
- Beta blocker if contraindicated give ACEi
- ACE inhibitors – use angiotensin receptor blocker if intolerant e.g. valsartan
