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Clinical Physiology > Hypertension and Coronary Heart Disease > Flashcards

Hypertension and Coronary Heart Disease Flashcards

1
Q

Definition of Blood Pressure

A

force exerted by circulating blood on artery walls

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2
Q

BP =

A

cardiac output x peripheral vascular resistance

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3
Q

Cardiac Output =

A

volume of blood pumped out of the heart (stroke volume) x heart rate

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4
Q

Why do we check blood pressure?

A

hypertension damages blood vessels

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5
Q

What is systolic and diastolic?

A

systolic: contraction of left ventricle
diastolic: relaxation of ventricles

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6
Q

What increases vascular resistance?

A

increased blood viscosity, reduced blood vessel length, reduced vessel radius

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7
Q

What are the stages to measure BP?

A
  1. normal blood flow
  2. occlusion of blood
  3. release cuff - hear systolic pressure
  4. no pulse - diastolic pressure
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8
Q

Primary cause of hypertension?

A

essential/idiopathic

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9
Q

Secondary causes of hypertension?

A
  • Renal or renovascular disease
  • Endocrine disease
    • Phaeochomocytoma
    • Cushing’s syndrome
    • Conn’s syndrome
    • Acromegaly and hypothyroidism
  • Coarctation of the aorta
  • Pregnancy
  • Medications
    • Hormonal / oral contraceptive/ steroids
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10
Q

Stages of RAAS pathway

A
  1. low BP
  2. kidney releases renin
  3. angiotensinogen in liver activated
  4. angiotensinogen -> angiotensin 1
  5. ACE (angiotensin converting enzyme) angiotensin 1 -> angiotensin 2
  6. BP increased
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11
Q

What does Angiotensin 2 do?

A

vasoconstriction, increases blood volume

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12
Q

How does angiotensin 2 increase blood volume?

A
  1. adrenal cortex gland releases aldosterone
  2. kidneys retain water and salt and excrete potassium
  3. pituitary gland activated to release ADH (anti - diuretic hormone) causing kidneys to retain water
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13
Q

What is ABPM?

A

Ambulatory blood pressure monitoring - patient wears cuff for 24hrs and BP measured every 30 mins

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14
Q

Why do patients not tolerate ABPM and what is a suitable alternative?

A

ABPM interrupts sleep, home blood pressure measurement - first thing and before bed for 7 days and average (ignore day 1)

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15
Q

Stage 1 Hypertension

A

BP in clinic is ≥140/90 mm Hg and ambulatory blood pressure monitoring (ABPM) or home blood pressure monitoring (HBPM) is ≥135/85 mm Hg.

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16
Q

Stage 2 Hypertension

A

BP in clinic is ≥160/100 mm Hg and ABPM or HBPM is ≥150/95 mm Hg.

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17
Q

Severe Hypertension

A

BP in surgery/clinic is ≥180/110 mmHg or higher.

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18
Q

Systolic or Diastolic important for diagnosis?

A

systolic

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19
Q

difference between urgent and emergent?

A

Urgent: needs treatment but no end organ damage

Emergent: end organ damage likely, patient not behaving normally/ displaying symptoms

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20
Q

What lifestyle interventions can help manage hypertension?

A
  • Healthy diet
  • Stop smoking
  • Encouraging exercise
  • Encourage weight loss if overweight or obese
  • Reduce alcohol intake
  • Reduce salt intake
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21
Q

Treatment for under 55 (first line)?

A

ACE inhibitor or low cost angiotensin 2 receptor blocker

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22
Q

any age (black african/carribean) or over 55 (first line)?

A

calcium channel blocker (CCB)

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23
Q

Second line hypertension treatment?

A

ACE inhibitor + CCB

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24
Q

Third line hypertension treatment?

A

ACE inhibitor + CCB + thiazide like diuretic (normally referred to cardio clinic)

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25
Q

Treatment for resistant hypertension?

A

ACE inhibitor + CCB + thiazide like diuretic + further diuretic or alpha/beta blockers
expert advice advised

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26
Q

Why should Afro-Caribbean patients not be given ACE inhibitors?

A

They are at risk of angioedema

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27
Q

How do beta blockers reduce hypertension?

A

reduces heart rate so reduces cardiac output

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28
Q

How do alpha blockers reduce hypertension?

A

relaxes arteries, alpha blockers are not cardio selective so can reduce PVR

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29
Q

What are the effects of ACE inhibitors?

A

Decrease aldosterone secretion, decrease angiotensin 2 production, induce pulmonary bradykinin accumulation

30
Q

What does decreased aldosterone secretion do?

A

high potassium retention, high sodium/water excretion

31
Q

What does decrease in angiotensin 2 production do?

A

lower systemic vascular resistance

32
Q

Hyperkalaemia is a side effect of _____ from ACE inhibitors

A

decreased aldosterone secretion

33
Q

Hypotension is a side effect of ______ from ACE inhibitors

A

decreased aldosterone secretion and decreased angiotensin 2 production

34
Q

Headache is a side effect of ______ from ACE inhibitors

A

decreased angiotensin 2 production

35
Q

Non productive cough is a side effect of ______ ACE inhibitors

A

induced pulmonary bradykinin accumulation

36
Q

What is GTN spray?

A

vasodilator - reduces blood pressure

37
Q

What type of drug is aspirin?

A

antiplatelet - reduces risk of clot

38
Q

How does aspirin work?

A
  • inhibits cyclooxygenase (cox) irreversibly
  • Cox produces prostanoids which cause platelets to stick together
  • blocks production of thromboxane a2 in platelets
  • platelet half life is 7 days
39
Q

Management of acute coronary syndrome

A

bisoprolol - reduce HR

aspirin, ticagrelor - platelets

ramipril - BP control

omeprazole - PPI - reduces risk of GI bleeds caused by ticagrelor + aspirin

40
Q

What is coronary heart disease?

A

coronary arteries become narrowed resulting in reduced blood supply to heart muscle. These arteries supply heart muscle with oxygen-rich blood.

41
Q

What is the most common cause of CHD?

A

atherosclerosis

42
Q

What is atherosclerosis?

A

Over time, a fatty material called atheroma can build up inside coronary arteries.Eventually, arteries may become so narrow that they can’t get enough oxygen rich blood to the heart.

43
Q

What is the risk of atherosclerosis?

A

If a piece of atheroma breaks off, it can cause a blood clot form. This clot can block your coronary artery and cut off the supply of blood and oxygen to your heart muscle. This is known as a heart attack.

44
Q

What is the progression of atherosclerosis?

A

Initial lesion
fatty streak
intermediate lesion
atheroma
fibroatheroma
complicated lesion

45
Q

What are the types of coronary artery disease?

A

stable ischemic heart disease - chronic angina
acute coronary syndrome - acute chest pain

46
Q

What is a STEMI and what defining factors does it have?

A

ST elevated myocardial infarction
ST elevations
elevated troponin

47
Q

What is a NSTEMI and what defining factors does it have?

A

Non ST elevated myocardial infarction
no ST elevation
troponin +ve

48
Q

Defining factors of unstable angina

A

-ve troponin
no ST elevation
no ECG changes

49
Q

Risk factors for atherosclerosis

A
  • Abdominal obesity
  • Type 2 Diabetes mellitus
  • High alcohol intake
  • High blood pressure
  • High cholesterol
  • Not eating fruits and vegetables
  • Not exercising regularly
  • Smoking
  • Stress
  • Family history
  • Age
  • Ethnic background
50
Q

Symptoms of coronary artery disease

A
  • angina
  • palpitations
  • sweating
    -weakness
  • shortness of breath
  • rapid heartbeat
  • dizziness
  • nausea
51
Q

Why do diabetics not experience pain in the same way as non diabetics?

A

peripheral nerve damage - neuropathy

52
Q

Treatment for CAD

A
  • Drug therapies
  • Thrombolytic therapy
  • Percutaneous coronary intervention
  • Coronary artery bypass grafting
  • Lifestyle changes
53
Q

How is coronary artery disease diagnosed?

A

Coronary angiogram

54
Q

What is an angiogram?

A

An angiogram (also known as a cardiac catheterisation) is a special type of x-ray which uses contrast dye to allow your doctor to look at your coronary arteries (the blood vessels that supply your heart).

55
Q

Drug therapies for coronary artery disease?

A
  • ACE inhibitors
  • angiotensin 2 antagonists
  • antiarrhytmic medicine
  • anticoagulant medicine
  • anti-platelet
  • beta blockers
  • CCB
  • cholesterol lowering
  • diuretics
  • nitrates
56
Q

Why do steroids increase BP?

A

they have a mineralic corticoid effect causing retention

57
Q

Why does diabetes contribute to high BP?

A

kidney damage which can cause high BP

58
Q

What is metabolic syndrome?

A

presence of a cluster of risk factors specific for cardiovascular disease. Metabolic syndrome greatly raises the risk of developing diabetes, heart disease, stroke, or all three.

59
Q

Metabolic factors of metabolic syndrome?

A

central obesity
high glucose
retention
high triglyceride
low LDL

60
Q

Risk of high BP in pregnancy?

A

preeclampsia - serious blood pressure condition that develops during pregnancy. People with preeclampsia often have high blood pressure (hypertension) and high levels of protein in their urine (proteinuria). Preeclampsia typically develops after the 20th week of pregnancy.

61
Q

is high BP in pregnancy normal?

A

no. vasodilation in pregnancy. the secondary circulation to the baby lowers the PVR. high BP is more significant

62
Q

what cofactors making hypertension more harmful?

A

diabetes

overweight

haemorrhage

chronic high BP main risk - stroke - ischemia in the brain caused by thrombosis or haemorrhage

In reality a massive pressure is required to rupture a small vessel wall. The pressure from high BP weakens the wall gradually and then it ruptures, it is not immediate.

smoking

63
Q

examples of ACE inhibitors

A

ramipril, namipril

64
Q

side effects of ACE inhibitors

A

clots since bradykinin production increased, dry cough, hyperkalaemia

65
Q

examples of CCB

A

amlodipine, nifedipine

66
Q

side effects of CCB

A

reduce PVR resulting in compensatory CO but ultimately lowering BP. intravascular volume reduced, more fluids retained - water retention → peripheral oedema, headaches from vasodilatory effects

67
Q

side effect of GTN

A

headache

68
Q

What are the 4 coronary arteries?

A

right
left main
circumflex
left anterior descending

69
Q

How is an MI diagnosed?

A

ECG 12-lead
inferior myocardial infarction affects leads 2,3, AVF - right coronary artery

70
Q

How does atorvastatin work?

A

Statins block 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase). HMG-CoA reductase is involved with mevalonate synthesis which is used in the body to make sterols including cholesterol

71
Q

What is a PCI?

A

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis.

72
Q

Why is PCI not done from the arm?

A

Blood vessels are small and so blood supply to the rest of the arm would be stopped.

Clinical Physiology (11 decks)

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