Common CV diseases Flashcards

1
Q

ANGINA PECTORIS

A

• 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

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2
Q

Symptom characteristics of stable angina

A
• Location 
ØMid- or lower retrosternum 
• Radiation 
ØLeft arm, Throat, Epigastrium 
• Quality 
ØSqueezing, vice-like, pressure-like, suffocating, heavy 
• Duration 
Ø30 seconds to several minutes
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3
Q

Symptom characteristics of stable angina

A
• 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
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4
Q

Clinical classification of chest pain

A
• 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
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5
Q

Other manifestations of angina

A
  • 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
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6
Q

Angina –stable or unstable

A

• 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)

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7
Q

Grading of angina pectoris Canadian Cardiovascular Society (CCS)

A

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

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8
Q

Unstable Angina (USA)

A

• 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

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9
Q

ANGINA DIAGNOSIS AND TREATMENT

A
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
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10
Q

ACUTE CORONARY SYNDROME

A

• 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)

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11
Q

ACUTE MYOCARDIAL INFARCTION

A
  • 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)
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12
Q

MYOCARDIAL INFARCTION SIGNS AND SYMPTOMS

A
• 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'
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13
Q

TREATMENT

A

• Take to the hospital ASAP: ØConfirm diagnosis ØMonitoring
ØPain relief
ØPrimary Percutaneous Coronary Intervention (PPCI)

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14
Q

MANAGEMENT POST MYOCARDIAL INFARCTION

A
  • 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
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15
Q

HEART FAILURE and symptoms

A

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)

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16
Q

Systolic heart failure ( HFrEF )

A

§Impaired ventricular contractility
§Elevated afterload
§Higher than normal EDV and reduced EF
§Causes: uncontrolled systemic hypertension, MI, Idiopathic dilated cardiomyopathy, valve disease

17
Q

Diastolic heart failure (now more commonly termed HFpEF )

A

§ 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

18
Q

Responses to inadequate cardiac performance

A

-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.

19
Q

PERIPHERAL VASCULAR DISEASE

A

• 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.

20
Q

Cerebrovascular Accident

A
  • 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
21
Q

HYPERTENSION

A
  • 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)
22
Q

VALVULAR HEART DISEASE

A
Stenosis 
• Narrowed
Incompetent 
• 'Leaky‘ or 'regurgitant'
Mechanical valve 
For life Warfarin
Tissue valve 
10-15 years 
Warfarin for limited period (if at all)