vascular and ischeamic heart disease Flashcards

1
Q

define hypertension

A

a disorder in which the level of sustained arterial pressure is higher than expected for the age, sex and race of the individual ie 140/90mmHg

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2
Q

what is the difference between primary and secondary hypertension

A

Primary has no obvious cause whereas secondary has an underlying disease implied eg renal disease, endocrine disease…

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3
Q

what are some underlying diseases of secondary hypertension

A
  • renal disease (reduced renal blood flow, excess renin release, salt and water overload)
  • endocrine disease
  • aortic disease
  • renal artery stenosis
  • drug therapy
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4
Q

what is benign hypertension

A
  • A cause of serious threatening morbidity
  • Asymptomatic, incidental finding often heath checks
  • Eventually causes left ventricular hypertrophy, congestive cardiac failure, increases atheroma…
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5
Q

what is left ventricular hypertrophy

A

Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart’s main pumping chamber (left ventricle)

  • increased LV load
  • poor perfusion
  • interstitial fibrosis
  • micro-infarcts
  • diastolic dysfunction
  • sudden cardiac death
  • cardiac failure
  • affects outcome of other diseases
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6
Q

what is malignant hypertension

A

Can develop from either benign primary of secondary hypertension or arise denovo. Needs urgent treatment to prevent death

  • causes cerebral oedema - seen as papilloedema
  • acute renal failure
  • acute heart failure
  • ## headache and cerebral haemorrhage
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7
Q

where do the right and left coronary arteries arise

A

base of the aorta

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8
Q

where does most coronary venous blood drain via

A

drains via the coronary sinus into the right atrium

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9
Q

what are special adaptation of coronary circulation

A
  • High capillary density
  • High basal blood flow
  • High oxygen extraction (75% compared to 25% whole body average) under resting conditions
  • This means extra O2 cannot be supplied by increasing O2 extraction
  • Can only be supplied by increasing coronary blood floe
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10
Q

what are the intrinsic mechanisms that influence coronary blood flow

A
  • A decrease in P02 causes vasodilation of the coronary arteries
  • Metabolic hyperaemia matches flow to demand
  • Adenosine (from ATP) is a potent vasodilator
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11
Q

what are extrinsic mechanisms that influence coronary blood flow

A
  • Coronary arterioles supplied by sympathetic vasoconstrictor nerves but are overridden by metabolic hyperaemia as a result of increased heart rate and stroke volume
  • So sympathetic stimulation of the heart results in coronary vasodilation despite direct vasoconstriction effect
  • Circulating adrenaline activates Beta 2 adrenergic receptors, which cause vasodilation.
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12
Q

why does most of coronary blood flow and myocardial perfusion occur during diastole

A

the subendocardial vessels from the left coronary artery aren’t compressed

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13
Q

what vessels supply the brain with blood

A

internal carotid and vertebral arteries which unite to form the basal arteries

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14
Q

what is the circle of willis

A

basilar (formed by 2 vertebral arteries) and carotid arteries anastomose to form the circle of willis

  • major cerebral arteries arise from the circle of willis
  • cerebral perfusion should be maintained even if one carotid artery gets obstructed
  • obstruction of a smaller branch of a main artery would deprive a region of the brain of its blood supply
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15
Q

what is the auto regulation of cerebral blood flow

A
  • if MABP rises the resistance vessels automatically constrict to limit blood flow
  • if MABP falls the resistance vessels dilate to maintain blood flow
  • autoregulation fails if MABP falls below 60mmHg or rises above 160mmHg
  • a MABP below 50mmHg results in confusion, fainting and brain damage if not quickly corrected
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16
Q

what does an increase and decrease in PCO2 cause in cerebral blood flow

A
increase = vasodilation 
decrease = vasoconstriction
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17
Q

what is the normal inter cranial pressure within the skull

A

8-13mmHg

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18
Q

how do you calculate cerebral perfusion pressure

A

CPP = mean arterial pressure - normal intracranial pressure

19
Q

explain why skeletal muscle blood flow increases during exercise

A
  • During exercise local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
  • Circulating adrenaline causes vasodilation (Beta2 adrenergic receptors)
  • Plus an increase in cardiac output during exercise, these could increase skeletal muscle blood flow
20
Q

what is cardiogenic shock

A

Cardiogenic shock is why people die directly of cardiac disease. It is inadequate systemic perfusion as a result of cardiac dysfunction

symptoms = chest pain

Angina is a clinical diagnosis

21
Q

what is the clinical diagnosis of angina

A
  • Visceral pain from myocardial hypoxia
  • characteristic patterns of: provocation, relief, timing ie pressing, squeezing, heaviness which can radiate to the arms, back, neck, jaw and teeth. It is provoked on exertion, stress, cold wind or after meals and is relieved after a few minutes by rest or relieved by GTN
22
Q

what are some differential diagnoses of chest pain

A
  • GI tract
  • Musculoskeletal
  • Pericarditis
  • Pleuritic pain
23
Q

what are the pros and cons for exercise testing

A
  • pros = cheap, reproducible, risk stratification

- cons = poor diagnostic accuracy in important subgroups, submaximal tests

24
Q

what are the pros and cons of perfusion imaging

A
  • pro = non invasive, pharmacological stress in less mobile patients, more precision than ETT, risk stratification
  • cons = radiation, false positives and negatives
25
Q

what are the pros and cons of a CT angiography

A
  • pro = non invasive, anatomical data and risk stratification
  • cons = radiation, less precise than angiography, particularly when calcium present, cost
26
Q

how is an angiography carried out

A
  • Sheath inserted into artery
  • catheter advanced from wrist / groin to coronary osmium
  • X-ray contrast agent injected to outline coronaries
  • Video fluoroscopy recorded images in multiple views
27
Q

how do you manage coronary heart disease

A
  1. reduce risk = drugs, lifestyle, revascularisation
  2. relieving symptoms
    - drugs = aspirin (anti platelet), beta blocker (slow heart rate, reduce O2 demand, reduce BP), statin ( reduces cholesterol), ACE inhibitor (reduces blood pressure)
28
Q

what is the technique for PCI (percutaneous coronary intervention)

A
  • vascular access
  • anti platelet drugs, anticoagulation
  • catheter to osmium of coronary
  • guide wire down vessel
  • balloons threaded over wire
  • stents(s) implanted
  • balloon, catheter, wires removed
29
Q

what are acute coronary syndromes grouped into

A
  • stable angina
  • unstable angina
  • STEMI
  • NSTEMI
30
Q

what is claudication

A

pain/cramping in the lower leg due to inadequate blood flow to the muscles on exercise

31
Q

what is ankle brachial pressure index

A

ankle pressure / brachial pressure

  • normal = 0.9-1.2
  • claudication = 0.4-0.85
  • severe = 0-0.4
32
Q

what are clinical features of chronic limb threatening ischaemia

A
  • rest pain = toe/foot ischaemia (nerve ending damage)
  • ulcers / gangrene = severe ischaemia and damage
  • cold to touch
  • absence of peripheral pulses
  • colour change
  • poor tissue nutrition
  • venous fluttering
33
Q

what are varicose veins

A

dilated, torturous superficial veins, due to the abnormal transmission of deep vein pressure

34
Q

what is the management for chronic limb threatening ischaemia

A
  • gradual compression ie 4 layer bandaging or stockings
  • foam sclerotherapy
  • endogenous ablation
  • surgical
35
Q

define aneurysm

A

dilation of a vessel by more than 50% of its normal diameter normal = 1.2-2

36
Q

true vs false aneurysm

A

true aneurysm = the vessel wall is intact

false aneurysm = there is a breach in vessel wall

37
Q

what are the 3 morphologic appearances of aneurysm

A
  • saccular
  • fusiform
  • mycotic
38
Q

what is a duplex ultrasound

A

A duplex ultrasound is a test to see how blood moves through your arteries and veins

39
Q

what is acute limb ischaemia

A

sudden loss of blood supply to a limb - occlusion of native artery or bypass graft which can be caused by embolism, atheroembolism, arterial dissection, trauma

40
Q

what are the clinical features of acute limb ischaemia

A
  • pain
  • pallor
  • pulseless
  • perishingly cold
  • paraesthesia
  • paralysis
  • no prior history of claudication
  • known cause for embolism
  • full complement of contra-lateral pulses
41
Q

what is the problem of diabetic foot sepsis and what are the clinical features

A

if the build up of pus cannot escape the pressure builds up in the rigid compartment rapidly leading to impairment of capillary blood floe and further ischaemia and tissue damage

systemic clinical findings =

  • pyrexia
  • tachycardia
  • tachypnoeic
  • confused
  • kussmauls breathing
42
Q

what are the three clinical entities of limb ischaemia

A
  • acute limb ischaemia
  • acute-on-chronic limb ischaemia
  • chronic limb threatening ischaemia
43
Q

what is acute limb ischaemia

A

sudden deterioration in arterial supply to the limb due to embolism, thrombus, trauma, iatrogenic

clinically presents with the 6 P’s

examination findings

  • 6 P’s
  • pulses may help determine level of occlusion- beware of water hammer pulse
  • contralateral pulses often present
  • look for signs pointing to aetiology

management

  • IV heparin
  • IV fluids
  • Analgesia