Common CV diseases Flashcards
ANGINA PECTORIS
• Symptoms caused by coronary artery insufficiency leading to intermittent myocardial ischaemia
• Reduced supply from: ØStenotic atheromatous disease of epicardial coronary arteries ØThrombosis
ØSpasm of coronary arteries
ØInflammation - arteritis
• Increased demand from: ØConditions associated with increased cardiac output: exercise, stress or thyrotoxicosis
ØConditions requiring greater cardiac work to maintain an adequate output: aortic stenosis ØConditions where peripheral vessel resistance is increased hypertension
Symptom characteristics of stable angina
• Location ØMid- or lower retrosternum • Radiation ØLeft arm, Throat, Epigastrium • Quality ØSqueezing, vice-like, pressure-like, suffocating, heavy • Duration Ø30 seconds to several minutes
Symptom characteristics of stable angina
• Location ØMid- or lower retrosternum • Radiation ØLeft arm, Throat, Epigastrium • Quality ØSqueezing, vice-like, pressure-like, suffocating, heavy • Duration Ø30 seconds to several minutes • Triggered by: ØExertion or emotional stress • Relieved by: ØRest, Sublingual nitrates
Clinical classification of chest pain
• Typical angina (definite) ØMeets all three of the following characteristics: § Location/radiation and duration § Trigger § Relief • Atypical angina (probable) ØMeets two of the above characteristics • Non-cardiac chest pain ØMeets one or none of the characteristics
Other manifestations of angina
- Angina may be accompanied by: ØShortness of breath, fatigue or faintness, nausea, burping, restlessness, or a sense of impending doom
- In the elderly look for angina equivalents: ØDyspnoea, fatigue, faintness or syncope
- Equivalents are also a feature of diabetic CAD, in which classic angina may often be absent
Angina –stable or unstable
• Stable angina
ØConstant-threshold angina without any of the following characteristics
• Unstable angina (classified as an acute coronary syndrome – ACS)
ØAngina at rest (or during sleep)
ØSevere new-on set angina (Class III, CCS grading of angina) (less than 6 weeks)
ØCrescendo angina (recent destabilisation of previously stable angina – at least Class III, CCS)
Grading of angina pectoris Canadian Cardiovascular Society (CCS)
Class 1 - angina with strenuous or rapid or prolonged exertion only
Class II - angina on walking or climbing stairs rapidly
Class III - angina on walking one or two blocks on the level
Class IV - angina at rest
Unstable Angina (USA)
• One of the conditions under the umbrella term Acute Coronary Syndrome (ACS)
• Absolute contraindication to exercise testing or training
• Underlying pathophysiology:
ØRupture of an atherosclerotic plaque within the coronary artery ØThrombosis
ØRapid reduction in the lumen of the vessel
• Plasma Troponin will be assessed to differentiate from a Myocardial Infarction
ANGINA DIAGNOSIS AND TREATMENT
DIAGNOSIS • History • Resting ECG - often normal • Exercise ECG (not so common these days) and referral to cardiologist for further investigations (imaging techniques like angiogram, cardiac MRI or CT angiography) TREATMENT • Lifestyle modification • Medication
ACUTE CORONARY SYNDROME
• New terminology for acute coronary disease which incorporates:
Ø non-Q wave MI (NSTEMI) Ø Q wave MI (STEMI)
Ø unstable angina
Ø widespread sub-endocardial ischaemia
Often used in A+E prior to confirmed diagnosis of AMI
• This group includes all conditions which can result from plaque rupture
• Outcome depends on: ØRate of occlusion (e.g. slow occlusion leads to formation of collateral vessels)
ØDegree of occlusion
• The most serious of these is an Acute Myocardial Infarction (AMI)
ACUTE MYOCARDIAL INFARCTION
- The term is used for myocardial cell death secondary to ischaemia
- It is precipitated by rupture of an atherosclerotic plaque and the formation of a thrombus resulting in rapid occlusion of the vessel (may also cause vasospasm)
- Diagnosis based on symptoms, ECG evidence and blood tests (cardiac enzymes –Troponin)
MYOCARDIAL INFARCTION SIGNS AND SYMPTOMS
• Sudden severe central chest pain: Øcrushing/burning Øradiating to arms throat or jaw Øpain persists for many hours Øunrelieved by GTN • Pallor, sweating, cold and clammy • Nausea and vomiting • Agitated, Sense of “impending doom” • BUT 20-30% are 'silent'
TREATMENT
• Take to the hospital ASAP: ØConfirm diagnosis ØMonitoring
ØPain relief
ØPrimary Percutaneous Coronary Intervention (PPCI)
MANAGEMENT POST MYOCARDIAL INFARCTION
- Hospital 3-5 days normally (uncomplicated MI)
- Medications considered
- Advice on discharge - lifestyle modification
- Sometimes (but not usually) Exercise ECG - if positive (+ve) may be referred for Angiogram
- If negative (-ve) referred for Cardiac Rehabilitation
HEART FAILURE and symptoms
Inability of the heart to provide sufficient cardiac output to meet the body’s metabolic needs
Symptoms include:
• Shortness of breath, fatigue, swollen ankles (pitting oedema), pulmonary oedema, weight gain (fluid retention)
Systolic heart failure ( HFrEF )
§Impaired ventricular contractility
§Elevated afterload
§Higher than normal EDV and reduced EF
§Causes: uncontrolled systemic hypertension, MI, Idiopathic dilated cardiomyopathy, valve disease
Diastolic heart failure (now more commonly termed HFpEF )
§ 30-50% of all cases
§ Common in the elderly and women
§ Reduced EDV caused by inappropriate relaxation of the ventricle, reduced compliance (increased ‘stiffness’) OR BOTH
§ Causes: LVH, myocardial ischaemia, and HCM
Responses to inadequate cardiac performance
-Activation of the adrenergic nervous system § This may result in peripheral vasoconstriction which helps redistribute the blood to vital organs (brain/heart) by constricting the circulation in the skin and muscles
§ More lactic acid may be produced in muscles which leads to fatigue and weakness
-Stimulation of the renin - angiotensin system (RAS)
§ Drop in renal perfusion (renal arterial BP) activates the baroreceptors in the renal arterioles and leads to release of renin which catalyses the production of angiotensin I (from angiotensinogen). This then converts to angiotensin II (a powerful vasoconstrictor) with help from the Angiotensin Converting Enzyme – ACE
-Angiotensin II causes:
§ Vasoconstriction
§ Sympathetic activation
§ Release of endothelin (another vasoconstrictor)
§ Production of aldosterone (hence the other name for RAS which is RAAS – renin-angiotensin-aldosterone system)
§ Aldosterone
§ Produced by the adrenal cortex
§ Promotes Na+ reabsorption
-Increased production of antidiuretic hormone (ADH) (aka vasopressin) § Secreted by the posterior pituitary gland when its osmoreceptors sense a drop in BP or blood volume § ADH is a powerful vasoconstrictor and increases BP by increasing the reabsorption of water in the renal tubules
-Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) § These cause sodium excretion and result in water excretion. Also cause peripheral vasodilation and reduce cardiac load. Their levels are increased in cardiac failure and they are thought to play a protective role.
PERIPHERAL VASCULAR DISEASE
• Intermittent claudication -Atheromatous plaques cause diminished blood supply to the legs causing ischaemic pain. The paincomes on with exercise and disappears with rest
Aneurysms -may be caused by atheromatous plaques which can weaken the arterial wall. The wall becomes distended and may burst with catastrophic results.
Cerebrovascular Accident
- Thrombosis - Clot forms in artery wall blocking supply
- Embolism - Clot formed in another part of body, travels in blood supply
- Haemorrhage - Sudden burst in artery wall
- Transient ischaemic attack (TIA) - mimics a stroke - resolves in 24 hours
HYPERTENSION
- Blood pressure elevated above 140/90
- Over 95% of the cases are idiopathic (termed ‘essential hypertension‘)
- Silent killer
- Heart has to work harder to overcome increased resistance (afterload)
- Enlarged heart, hardening of arteries
- Heart Failure, stroke, IHD, PVD and kidney failure
- Increased BP can result from increase in cardiac output or peripheral resistance or both ØBP = Cardiac Output X TPR
- TPR can be modified by the nervous system, metabolic factors, hormones, and local vascular factors
- Alteration of baroreceptor sensitivity can lead to increased BP
- LVH may result since myocardial workload is increased (LVH may lead to ischaemia, ventricular arrhythmias, and congestive heart failure)
VALVULAR HEART DISEASE
Stenosis • Narrowed Incompetent • 'Leaky‘ or 'regurgitant' Mechanical valve For life Warfarin Tissue valve 10-15 years Warfarin for limited period (if at all)
