Cardiovascular Block > Week 2 > Flashcards

Week 2 Flashcards

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1
Q

What is considered hypertension?

A

around 140/90 mmHg

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2
Q

How is the severity of hypertension classified?

A
  • Severity is classified into three stages:
    o 1. Single reading >140/90 mmHg and average ambulatory readings >135/85 mmHg.
    o 2. Single reading >160/100 mmHg and average ambulatory readings >150/95 mmHg.
    o 3. Single reading with systolic >180mmHg or diastolic >110mmHg.
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3
Q

what is the aetiology of hypertension?

A

hypertension often occurs as a result of reduced elasticity of arteries, due to age-related and atherosclerosis-related calcification, and degradation of arterial elastin.
It may also be present in conditions associated with increased CO, such as anaemia, hyperthyroidism and aortic regurgitation.

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4
Q

Complications of untreated hypertension.

A
  • Increased risk of morbidity and mortality from all causes.
  • Coronary artery disease.
  • Heart failure.
  • Renal failure.
  • Stroke.
  • Peripheral vascular disease.
  • Retinopathy.
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5
Q

discuss the effect of the sympathetic nervous system on second-to-second blood pressure control

A
  • Sympathetic system activation produces:
    o Vasoconstriction > increases peripheral vascular resistance.
    o Reflex tachycardia > increases cardiac output.
    o Increased stroke volume > increases cardiac output.
  • Stimulates renin release which produces angiotensin II and aldosterone:
    o Angiotensin II is a vasoconstrictor.
    o Aldosterone causes salt and water retention which increases the circulating blood volume.
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6
Q

What is the function of the renin-angiotensin-aldosterone system (RAAS)?

A

maintenance of sodium balance.
control of blood volume
control of blood pressure

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7
Q

what is RAAS stimulated by?

A

fall in BP
fall in circulating volume
sodium depletion

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8
Q

what is the sequence of events following RAAS stimulation?

A
  • Renin is released from the juxtaglomerular apparatus.
  • Renin converts angiotensin to angiotensin I.
  • Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE).
  • Angiotensin II is a potent vasoconstrictor that stimulates aldosterone release from the adrenal glands.
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9
Q

what is a common treatment regime for age>55 or african/caribbean origin?

A

start CCB e.g., almlodipine
add thiazide diuretic e.g., indapamide
add ACEi/ARB e.g., ramipril or losartan
add beta blocker or alpha blocker e.g., bisoprolol or doxazosin
add less commonly used agent

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10
Q

what is the common treatment regime for age < 55 ?

A

start ACEi e.g., ramipril
add thiazide diuretic e.g., indapamide
add CCB e.g., amlodipine
add beta blocker e.g., bisoprolol
add less commonly used agent

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11
Q

what do ACE inhibitors do?

A

competitively inhibit the action of ACE.

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12
Q

ACEi contraindications

A

renal artery stenosis
impaired renal function
hyperkalaemia
fertile female (teratogenic)

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13
Q

ACEi drug-drug interactions

A

NSAIDs and potassium supplements/potassium-sparing diuretics.

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14
Q

what do angiotensin II receptor blockers (ARBs) do and whats their benefit?

A

competitively inhibit the action of angiotensin II at the angiotensin AT1 receptors.
These have fewer side effects than ACEi.

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15
Q

What are the benefits of vasodilator CCBs? give an example of two and one used in pregnant women.

A

vasodilator CCBs reduce PVR, amlodipine and felodipine can be used for age > 55, if a woman is of child-bearing age then use nifedipine.

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16
Q

CCBs adverse drug reaction

A

flushing
headache
ankle oedema
indigestion/reflux
rate limiting also cause bradycardia and constipation

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17
Q

contraindictations to CCBs

A

acute MI
Heart failure
bradycardia

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18
Q

what do thiazide-type diuretics do?

A

thiazide diuretics such as indapamide enhance urinary secretion of sodium, cause resistance vessel dilation, thereby reducing peripheral vascular resistance.

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19
Q

What are the benefits of thiazide diuretics?

A

proven benefit in reducing risk of stroke and MI.
can be used in combo with other anti-hypertensives.
commonly first-line therapy in mild-mod hypertension in people of african/caribbean origin.

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20
Q

discuss the treatment of hypertension during pregnancy.

A

centrally acting agents such as methyldopa are used to treat hypertension in pregnancy

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21
Q

define atheroma/atherosclerosis

A

atheroma/atherosclerosis is the formation of focal lesions (plaques) in the intima of large and medium sized arteries

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22
Q

describe the development of atheromatous plaques

A

o 1. Injury to the endothelial lining of an artery.
o 2. Chronic inflammatory and healing response of vascular wall to the agent causing injury.
o Chronic/episodic exposure of arterial wall to these processes > formation of atheromatous plaque.

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23
Q

what are the most important causes of endothelial injury?

A

hemodynamic disturbances (turbulent flow)
hypercholesterolemia

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24
Q

What are the components of atheromatous plaques?

A
  • Lipid.
  • Cholesterol.
  • Cellular waste products.
  • Calcium.
  • Fibrin.
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25
what are the signs of major hyperlipidaemia?
- Familial/primary vs acquired/secondary (idiopathic?). - Biochemical evidence: LDL, HDL, total cholesterol, triglycerides. - Corneal arcus (premature). - Tendon xanthomata (knuckles, Achilles). - Xanthelasmata. - Risk/premature/family history MI/atheroma.
26
what are risk factors in developing atheroma?
- Smoking. - Hypertension. - Diabetes mellitus. - Male. - Elderly. - Less strong risk factors: obesity, sedentary lifestyle, low socio-economic status, low birthweight.
27
describe the events of acute atherothrombotic occlusion
o Major complications: rupture of plaque > acute event. o Rupture exposes highly thrombogenic plaque contents (collagen, lipid, debris) to blood stream > activation of cogulation cascade and thrombotic occlusion in very short time. o Total occlusion > irreversible ischaemia > necrosis (infarction of tissues).
28
what is a thrombus?
the formation of a solid mass from the constituents of blood withing the vascular system during life
29
pathogenesis of thrombosis
o Atheromatous coronary artery. o Turbulent blood flow (fibrin deposition, platelet clumping). o Loss of intimal cells, denuded plaque. o Collagen exposed; platelets adhere. o Fibrin meshwork forms, RBCs become trapped. o Alternating bands: lines of Zahn. o Further turbulence and platelet deposition. o Propagation. o Consequences.
30
what do the consequences of thrombosis depend on?
site extent collateral circulation
31
what is virchows triad?
virchows triad are factors causing thrombosis: -changes in blood vessel wall. -change in the blood constituents. -changes in the pattern of blood flow.
32
explain the relationship between atheroma and thrombosis?
arterial thrombosis is most commonly superimposed on atheroma, virchows triad > changes in blood flow > turbulence.
33
list the factors causing thrombosis
endothelial injury stasis or turbulent flow hypercoagubility of the blood
34
whats an embolism?
The movement of abnormal material in the bloodstream and its impaction in a vessel, blocking its lumen.
35
what is an embolus?
detached intravascular solid, liquid or gaseous mass. most emboli are dislodged thrombi > thromboembolism.
36
risk factors for DVT and pulmonary thromboembolism
o Cardiac failure. o Severe trauma/burns. o Post-op/post-partum. o Nephrotic syndrome. o Disseminated malignancy. o Oral contraceptive. o Increased age. o Bed rest/immobilization. o Obesity. o PMH of DVT.
37
what is rheumatic fever?
- A disease of disordered immunity causing inflammatory changes in the heart and joints and sometimes neurological symptoms.
38
what are the presenting features of rheumatic fever?
- Presenting feature: ‘flitting’ (painful) polyarthritis of large joints (wrists, elbows, knees, ankles) plus skin rashes and fever. - Pancarditis (inflammation affecting the endocardium, myocardium, and pericardium) in the acute phase; heart murmurs are common.
39
What can pancarditis in acute rheumatic fever progress to?
Can progress over time to chronic rheumatic heart disease, mainly manifesting as valvular abnormalities.
40
Valvular heart disease pathologies
- Valvular stenosis: valve thickened/calcified and obstructs normal blood flow into chamber/vessel. - Valvular incompetence/regurgitation/incompetency: valve loses normal function and fails to prevent reflux of blood after contraction of cardiac chamber. - Vegetations: infective or thrombotic nodules develop on valve leaflets impairing normal valve mobility; may embolise.
41
what is stable angina?
Angina is a discomfort if the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis.
42
what causes stable angina?
It is caused by a mismatch between the supply of oxygen and metabolite to the myocardium and the myocardial demand for them. - Most commonly due to a reduction in coronary artery blood flow to the myocardium, caused by Obstructive coronary atheroma (very common).
43
what are non-modifiable risk factors in developing stable angina?
age male gender family history of CAD genetic predisposition
44
what are modifiable risk factors in developing stable angina?
smoking high blood pressure high cholesterol - LDL diabetes lifestyle - exercise and diet.
45
What is a possible complication of stable angina?
- An established obstructive atheromatous plaque (causing stable angina) can spontaneously rupture, and local thrombosis can occur, causing further occlusion. - This can lead to acute coronary syndromes.
46
clinical presentation of stable angina: classify the pain and its aggravating factors
- Site of pain: retrosternal. - Character of pain: often tight band/pressure/heaviness. - Radiation sites: neck and/ or into jaw, down arms. - Aggravating e.g., with exertion, emotional stress and relieving factors e.g. rapid improvement with GTN or physical rest.
46
clinical presentation of stable angina
- Site of pain: retrosternal. - Character of pain: often tight band/pressure/heaviness. - Radiation sites: neck and/ or into jaw, down arms. - Aggravating e.g., with exertion, emotional stress and relieving factors e.g. rapid improvement with GTN or physical rest.
47
Discuss relevant investigations of stable angina.
- bloods. - CXR. - ECG. - exercise tolerance test myocardial perfusion imaging ct coronary angiography invasive angiography cardiac catheterisation/coronary angiography
48
radionucleotide tracer criteria
if radionucleotide tracer is seen at rest but not after stress = ischaemia. if radionucleotide is seen neither at rest or after stress = infarction.
49
discuss the disease-altering medical treatment of stable angina
o Statins: if cholesterol > 3.5mmol/L. o ACE-I if increased CV risk and atheroma. o Aspirin, 75mg or Clopidogrel if intolerant of aspirin.
50
medical treatment for relief of symptoms of stable angina
o Beta-blockers to achieve resting hr < 60bpm. o CCBs to achieve resting hr < 60bpm, produce vasodilation. o Ik channel blockers to achieve resting hr < 60 bpm. o Nitrates to produce vasodilation. o K+ channel blockers.
51
discuss percutaneous coronary intervention
PCI, also known as coronary angioplasty, is a minimally invasive procedure in which a catheter is inserted into an artery in the groin or wrist and guided to blocked or narrowed coronary arteries using x-ray imaging. A small balloon is inflated to widen the artery and a stent may be inserted to keep it open. PCI is used to relieve symptoms and improve blood flow to the myocardium in patients with stable angina or acute coronary syndrome.
52
discuss coronary artery bypass surgery
During CABG, a surgeon creates a new route for blood to flow around blocked or narrowed coronary arteries by taking a blood vessel from another part of the body (usually the long vein in the leg) and grafting it onto the heart. This new vessel bypasses the blocked or narrowed artery and restores blood flow to the heart muscle.
53
what is acute coronary syndrome? subtypes
- Acute coronary syndrome is a constellation of symptoms and clinical finding which results from impaired cardiac perfusion at rest. - Subtypes of ACS: o Unstable angina. o Non-ST-elevation myocardial infarction. o ST-elevation myocardial infarction.
54
What causes myocardial infarction
under-perfusion of the myocardium leading to the death of myocardial tissue
55
What causes MI type I and type 2s
- MI type 1: plaque rupture with thrombus. - MI type 2: vasospasm or endothelial dysfunction. - MI type 2: fixed atherosclerosis and supply-demand imbalance. - MI type 2: supply-demand imbalance alone.
56
What is the second most common cause of death in scotland?
Coronary artery disease
57
What is the typical clinical presentation of MI chest pain using SOCRATES?
SITE - central/left-sided ONSET- usually sudden CHARACTERISTIC- crushing pain ('like someone is sitting on your chest'). RADIATION- left arm, neck and jaw. ASSOCIATED SYMPTOMS- nausea, sweating, clamminess, SOB, sometimes vomiting or syncope. TIMING- constant. EXACERBATING/RELIEVING FACTORS- worsened by exercise/exertion and may be improved by GTN. SEVERITY- often extremely severe.
58
NSTEMI ECG changes and other diagnostic aids?
o Cardiac chest pain. o Newly abnormal ECG which is not ST-elevation. o Raised troponin (with no other reasonable explanation).
59
STEMI ECG changes and other diagnostic aids
o ST-elevation >2mm in the adjacent chest leads. o ST-elevation >1mm in adjacent limb leads. o New left bundle branch block (LBBB) with chest pain or suspicion of MI.
60
Outline the management of MI
- Mechanical > percutaneous coronary intervention (PCI) = angioplasty and stenting, performed in the cardiac catheterization lab. - Pharmacological > using strong blood thinner to cause thrombolysis. - If a patient suffering from a STEMI can get to the cath lab within 2 hours, then a primary PCI is the preferred treatment. However, if they cannot get there in two hours then thrombolysis is performed first.
61
define atypical angina
- Atypical angina: stable angina but with symptoms not clearly identifiable as ischaemic chest pain such as breathlessness and burning/reflux/burping.
62
describe the mechanism of action of thrombolytic therapy
- Recombinant tissue plasminogen activator (rtPA). - Works by converting plasminogen to plasmin (a natural fibrinolytic agent- clot buster). - Plasmin lyses clot by breaking down fibrinogen and fibrin within a clot.
63
benefits of thrombolytic therapy
- Benefits: o 23% reduction in mortality. o 39% reduction in mortality when used with aspirin (ISIS-3 trial).
64
What is aspirin and what are the benefits of aspirin therapy in patients with ischaemic heart disease
- Aspirin is a thromboxane-A2 inhibitor that inhibits platelet activation and recruitment. - Reduces cardiac events/MI/death when utilised correctly.
65
Discuss the use of beta-blockers
beta-blockers reduce the workload on the heart by slowing the heart rate and reducing blood pressure. they are used to control symptoms, prevent further damage to the heart and reduce the risk of future events.
66
beta blockers contraindications
asthma acute heart failure bradycardia or heart block
67
how do CCBs help
o Reduced heart rate – exclusively NDHP CCBs like verapamil/diltiazem. o Reduced contractility (NDHP). o Reduce afterload (DHP). o Increases diastolic prefusion time (NDHP).
68
CCB contraindications
bradycardia/heart block (NDHP) reduced LV function
69
CCB side effects
peripheral oedema (DHP) hypotension headache flsuhing
70
what are the possible side effects of daily aspirin therapy?
- Possible side effects of daily aspirin therapy: o Stroke caused by a burst blood vessel. o GI bleeding. o Allergic reaction.
71
selective BB example
bisoprolol
72
non-selective BB example
propanolol
73
DHP CCB example
amlodipine, felodipine and nifedipine
74
N-DHP CCB example
verapamil and diltiazem
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