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BDS2 BAMS > Cardiovascular medicine > Flashcards

Cardiovascular medicine Flashcards

1
Q

irreversible risk factors for cardiovascular disease

A
  • age
  • sex
  • family history
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2
Q

reversible risk factors for CVD

A
  • smoking
  • obesity
  • diet
  • exercise
  • hypertension
  • hyperlipidaemia
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3
Q

primary prevention of CVD

A
  • increasing exercise, eating a better diet and stopping smoking
  • altering risk factors BEFORE the onset of disease
  • opper
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4
Q

secondary prevention of CVD

A
  • reducing the risk once the disease is present

- easier to get patients to comply as they don’t want a relapse

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5
Q

antiplatelet drugs

A
  1. aspirin
  2. clopidrogel
  3. dipyridamole
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6
Q

oral anticoagulants

A

stop the coagulation pathway

WARFARIN

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7
Q

drugs to treat atherosclerosis

A

statins

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8
Q

how do diuretics help patients with CVD

A

reduce fluid volume of the blood by decreasing water retention and increasing salt retention
- reduces preload and controls blood pressure

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9
Q

nitrates

A

long or short acting
- dilate veins to reduce preload in the heart (angina)

  • dilates resistance arteries to reduce cardiac workload, oxygen consumption
  • dilates the coronary artery supply (headaches)
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10
Q

calcium channel blockers

A
  • treatment for hypertension

- blocks calcium channels in smooth muscles and some heart muscles

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11
Q

dental aspect of calcium channel blockers

A

can cause gingival hyperplasia

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12
Q

ace inhibitors

A
  • enalapril
  • inhibits conversion of angiotensin 1 to angiotensin 2
  • important vasoconstrictor, therefore reducing BP
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13
Q

dental aspect of ace inhibitors

A

can cause oral angio-oedema (top lip oedema)

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14
Q

blood vessel narrowing atherosclerosis

A
  • results in inadequate O2 delivery

- muscle cramps due to lack of oxygen, leading to lactic acid build up causing FIBROSIS

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15
Q

blood vessel occlusion atherosclerosis

A
  • no oxygen delivery due to blocking of the blood vessel
  • the tissue becomes narcotic
  • severe pain and loss of function results
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16
Q

full requirement for atherosclerosis diagnosis

A
  1. FULL medical history
  2. ECG
  • STEMI
  • nSTEMI
    3. biomarkers
  • increased coronary enzymes (troponin) levels after an MI
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17
Q

during which action is blood able to flow into the coronary arteries

A
  • disastole as the vessels are relaxed
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18
Q

why does an increased HR reduce BF to the coronary arteries

A
  • there is less time during diastole to allow blood to flow into the relaxed vessels
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19
Q

effects of narrowing/atherosclerosis in the coronary arteries

A
  • reduced O2 delivery to the heart
  • lactic acid build up
  • fibrosis of the muscle (permanent damage)
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20
Q

two types of angina

A
  1. classical

2. unstable

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21
Q

classical angina

A
  • only gets worse when the person is exerted

- symptoms decrease and stop when resting

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22
Q

unstable angina

A
  • symptoms of angina occur randomly when at rest
  • NO BIOMARKER
  • blood vessels randomly open and contract
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23
Q

angina

A

REVERSIBLE ischaemia of the heart muscle due to narrowing of one or more of the coronary arteries

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24
Q

angina pain

A
  • autonomic nerve stimulation in the heart due to low oxygen delivery
  • this registers as REFERRED PAIN in the brain
  • therefore the pain is felt in the chest, and can extend over the arm, back and jaw
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25
Q

symptoms of classical angina

A
  1. chest pain when exercising
  2. chest pain can worsen with temperature and emotion
  3. pain is relieved from rest
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26
Q

diagnosing angina

A
  1. ECG showing an area of myocardial ischaemia
  2. elimination of other potential causes
  • thyroid issues, valvular defects
    3. angiography
    4. echocardiography
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27
Q

angiography

A

dye injected into an artery to check for narrow areas

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28
Q

echocardiography

A

sound waves used to generate a live image of the heart

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29
Q

how will angina appear in an ECG?

A
  • elevation i the ST segment
  • ISCHAEMIC EPISODE
  • the ST segment doesn’t reach the base line of the ECG
  • STEMI
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30
Q

treating angina

A

reducing the oxygen demand of the heart by
1. reducing after load by reducing BP

  1. reducing preload by using nitrate therapy
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31
Q

how to reduce preload for angina patients

A
  • nitrate therapy with dilate the vessels to reduce venous pressure (GTN in an emergency)
  • angioplasty to bypass narrowed vessels (CABG)
  • drugs to reduce hypertension (diuretics and ace inhibitors)
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32
Q

CABG

A
  • coronary artery bypass graft
  • vein from the leg is grafted into the heart, wrapping round the aorta to bypass narrowed vessels
  • major surgery involved, heart must be stopped
  • only lasts 10 years in good health
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33
Q

angioplasty and stenting

A
  • lowers the risk of angina
  • risks of vessels bursting
  • vessel is artificially widened
  • angioplasty = ballon with cage opened in the vessel
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34
Q

peripheral vascular disease

A

angina but in the peripheral tissues

- usually the peripheries and lower limbs

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35
Q

atheroma

A

fatty deposits and scarring in vessel walls

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36
Q

symptoms of peripheral vascular disease

A
  • pain in the limbs on exercise, improved with rest
  • limited function to peripheral tissues
  • may lead to necrosis and gangrene in severe cases
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37
Q

when does ischaemia become infarction

A

when a narrowed vessel, either by atheroma, thrombosis or platelet plug, becomes completely occluded, preventing any blood reaching the tissue

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38
Q

infarction

A

complete obstruction of a vessel causing tissue death

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39
Q

brain infarction is caused by occlusion of

A

the carotid arteries

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40
Q

heart infarction is caused by total occlusion of the

A

coronary arteries

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41
Q

symptoms of myocardial infarction

A
  1. crushing chest pain
    - clenched fist over chest is a good indicator
  2. pain radiating to the left arm
  3. nausea
  4. pale, grey skin
  5. sweating
  6. palpitations
  7. shortness of breath
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42
Q

what to do if a patient is suffering an MI in surgery

A
  1. give the patient 300mg crushed in water and spray 3 puffs of GTN under the tongue and have the patient sitting bolt upright
  2. attach defibrillator pads to the chest, they won’t shock unless the person goes into cardiac arrest
  3. attach the trauma mask to an oxygen supply and give 15L/min to the patient
  4. calm and reassure the patient as much as possible
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43
Q

types of MI

A
  1. spontaneous
  2. sudden death
  3. MI from percutaneous infection (from angioplasty or stent)
  4. MI fro CABG
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44
Q

spontaneous MI

A
  • primary coronary event

- platelet plaque plug ruptures the vessel

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45
Q

suddenly death MI

A
  • ischaemia causes STEMI or a thrombus
  • death is not from the ischaemia, but usually from ventricular fibrillation due to an interruption of the conductivity of the heart muscle from reduced BF
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46
Q

thrombolysis

A

dissolves a blood clot within 6 hours

- ideal treatment as it is non invasive

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47
Q

treating MI

A
  1. thrombolysis done within 6 hours
  2. angioplasty can be placed within 3 hours
  3. CABG must be done if other options are not appropriate
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48
Q

preventing MI

A
  1. treat patient with aspirin

2. work on risk factors

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49
Q

stroke

A

ifarction in the brain caused by an embolism
- atheroma travels into the carotid and it lodged

  • can also be caused by thrombosis in the brain (rare)
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50
Q

treatment of a stroke depends on whether it was caused by a;

A
  1. clotting or bleeding

2. embolism or thrombosis

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51
Q

transient ischaemic attacks

A

a warning sign of stroke risk
- mini strokes

  • usually last less than 24 hours before normal function returns
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52
Q

why do patients feel such sever pain during MI?

A
  • the basal ganglia picks up autonomic stimulation which is not normally recognised
  • this is passed onto the sympathetic system
  • the signals are transcribed this way confer a greater amount of anxiety coupled with the pain
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53
Q

STEMI

A

ST segment elevated myocardial infarction

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54
Q

what do abnormal Q waves on the ECG suggest

A

old MI has occurred

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55
Q

primary care of MI

A
  • get the patient into hospital
  • analgesia, aspirin, GTN
  • BLS if required
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56
Q

hospital care for MI

A
  1. PCI angioplasty and stent
  2. thrombolysis is possible, most effective if given early enough
  3. drug treatment to reduce the damage of the MI
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57
Q

complications after MI if survived

A
  1. frequent arrythmia
  2. heart failure risk due to loss of function of areas of the muscle
  3. ventricular hypofunction
    - papillary muscles can easily rupture during MI
  4. DVT or pulmonary embolism
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58
Q

preventative care of MI

A
  1. get patient on aspirin
  2. modify risk factors
  3. beta blockers
    - reduce HR
  4. ACE inhibitors
    - reduce preload and prevents vasoconstriction
  5. Statins
    - if the patient has high cholesterol
  6. diuretics
    - reduce BP
  7. Ca channel blocker
    - relaxes smooth muscle in vessels and force of the left ventricle

REMEMBER ABCD

  • aspirin, beta blocker, calcium channel blocker, diuretics
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59
Q

atherosclerosis

A
  • a build up of cholesterol in the tunica media
  • caused by NON-MODIFIABLE lifestyle factors (hyperlipidaemia)
  • chronic inflammatory response followed by incomplete healing
  • forms ATHEROMAs
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60
Q

non-modifiable risk factors of atherosclerosis

A
  1. age
  2. gender
  3. genes
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61
Q

why are males more at risk of atherosclerosis

A
  • only until the menopause

- oestrogen levels in women keep BV open

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62
Q

what defect in the genes can make a person more susceptible to atherosclerosis

A

mutation in the low density lipoprotein receptor gene
- mainly found in the liver, smooth muscles and fibroblasts

  • control cholesterol uptake and processing
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63
Q

basal state of endothelial cells

A
  • normal state
  • cells are non-adhesive and non-thrombogenic
  • the laminar flow is normal
  • there is no trauma or insult to the cells
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64
Q

activated state of endothelial cell states

A
  • change in the production of cytokine growth factor
  • encourages thrombogenic events

causes;

  1. turbulent flow
  2. hypertension
  3. bacterial productions
  4. cigarette smoke
  5. viruses
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65
Q

atheroma

A
  • chronic inflammatory response to lipoproteins, collection of monocytes which have engulfed lipid
  • endothelial cells surface becomes more permeable to lipids
  • change in adhesion so more monocytes collect and move into the tunica media
  • monocytes move in, but cannot phagocytose the lipid and therefore form a fatty deposit
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66
Q

foam cells

A

collection of pale and swollen monocytes from inability to phagocytose lipid

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67
Q

the healing response phase in the formation of an atheroma

A
  1. smooth muscle cells proliferate and fibrous tissue forms from macrophage and fibroblasts in healing
  2. this forms a fibro-fatty plaque with a central mass of lipid and necrotic tissue as the lipid cannot be phagocytosed
  3. this is covered in a thin layer of endothelial cells due to thickening of the tunica media, forming a cap over the cholesterol, forming a plug
  4. small blood vessels can form in the plug, causing haemorrhage
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68
Q

effects of atherosclerosis

A
  • decrease in blood supply to a tissue or organ (ischaemia)
  • complete obstruction of blood flow (infarction)
  • thrombosis (release of thrombogenic factors from the atheroma forms a thrombus/clot)
  • embolism may occur if the thrombus breaks off
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69
Q

periodontitis risk with atherosclerosis

A

the biofilm in the mouth causes chronic inflammation
- the inflammatory factors are released because of this

  • once they are released they go into the liver and set up an acute phase response which can cause atherosclerosis
70
Q

claudication

A

relief of pain upon rest

71
Q

effects peripheral vascular diseases

A
  1. ischaemia
  2. claudication
  3. gangrene
  4. coagulation necrosis and infection
72
Q

aneurysm

A
  • abnormal dilation of the blood vessel walls
  • aortic aortic aneurysm
    • most common result of atherosclerosis
  • the lumen of the vessel widens dramatically and floods with blood as the walls become weak
    • this can rupture and cause a huge bleed
73
Q

coagulation necrosis

A
  • necrotic cells retain their outline and can be identified
  • the cytoplasm is dark but there is remnants of the nuclei in it
  • neutrophils invade the tissue and granulation tissue forms
74
Q

congestive heart failure

A
  • ventricular hypertrophy
  • causes oedema of the extremities
  • chronic venous congestion of the lung and liver can occur depending on which side of the heart fails
75
Q

pathophysiology

A
  • hypertrophy of the myocytes (parts of the muscle)
  • the heart reaches 2-3 times its weight, but capillary number stay the same
  • therefore there is an increase metabolic demand of the heart, leading to cardiac ischaemia, apoptosis and eventually heart failure
76
Q

tumours associated with the cardiac system

A
  1. hamartoma
  2. caposi sarcoma
  3. angiosarcoma
77
Q

hamartoma

A
  • found in developmental issue
  • the tissue is in its normal site
  • collection of blood vessels
  • forms a HAEMANGIOMA in newborns
78
Q

Kaposi sarcoma

A
  • blood spot
  • low grade sarcoma containing lymphatics and blood vessels
  • found on the skin and in the oral cavity
  • often associated with immune disorders (HIV, AIDS, HERPES)
79
Q

angiosarcoma

A
  • aggresive and rare
  • malignancy of the endothelial cells
  • tumour in the blood vessel
80
Q

benign cardiac tumours

A

myxoma
- tumour of connective tissue in the heart

lipoma

  • soft fatty tumour
81
Q

why may vascular malformations become more apparent in old age

A

the mucosa thins, especially in the oral cavity

82
Q

capillary vascular malformations

A
  • lots of little capillaries group together to form a haemangioma (hamartoma)
83
Q

cavernous vascular malformation

A
  • large space filled with lots of blood vessels
84
Q

storage weber syndrome

A
  • vascular malformation
  • PORT WINE STAIN
  • excessive haemangioma which tends to follow the nerves on one half of the face
85
Q

stenosis

A

injury to the valve resulting in the back flow of blood

86
Q

insufficient valvular heart disease

A

the valve doesn’t close properly

87
Q

valvular vegetations

A

lumps forming on the cusps of the valves

88
Q

valvular heart disease

A
  • congenital or acquired (from cardiac diseases)
    1. stenosis
  1. insufficiency
  2. valvular vegetations
89
Q

calcific aortic stenosis

A
  • most common valvular condition
  • calcium is deposited on the valves as a result of inflammation
  • neoplastic or dystrophic calcification
90
Q

rheumatic heart disease

A
  • comes from rheumatic fever
  • mainly affects the valves
  • host immunity attacks the strep A antigen, but also the host protein in the valves
  • type 2 and 4 hypersensitivity reaction
  • endocardium is inflamed causing fibrinoid necrosis
  • the valves thicken and fuse
  • aortic dilation from increasing volume of blood
  • makes a person very susceptible to ineffective endocarditis
91
Q

ineffective endocarditis

A

microbial infection of the heart valves

92
Q

what type of hypersensitivity causes rheumatic stenosis

A

type 2 and 4

93
Q

3 main risk factors of hypertension

A
  1. genes/environment interactions
  2. environment
  3. genes
94
Q

gene/environment interactions in hypertension risk

A
  • race

- gender

95
Q

environment risks in hypertension

A

inactivity, stress, obesity, smoking, age, salt, alcohol

96
Q

diagnosing hypertension

A
  • raised blood pressure
  • diagnosed as BP > 140/90mmHg
  • must take blood pressure at 3 different readings at rest
97
Q

age and hypertension risk

A
  • BP rises naturally with age
  • the aorta stretches to accommodate high pressure but cannot cope in the elderly
  • age itself is not a cause, must be in conjunction with other factors
98
Q

obesity and hypertension

A

higher risk of atherosclerosis resulting in higher pressure flow

99
Q

target BMI

A

below 25

100
Q

drugs which can cause hypertension

A
  • NSIDs
  • corticosteroids
  • oral contraceptives
  • sympathomimetics
101
Q

what other diseases or conditions can result from hypertension

A
  1. cerebrovascular accident (stroke)
  2. renal damage
  3. congestive heart failure
  4. end organ damage

these diseases are brought on or caused by pressure

  • treatment of hypertension can therefore greatly reduce the risk
102
Q

essential hypertension

A
  • no identified triggers

- occurs without being able to identify the exact cause

103
Q

triggers of hypertension

A
  1. renal syndromes
    - raise BP due to issues controlling fluid and angiotensin levels
  2. endocrine issues
    - tumours, cushings, hyperthyroidism, high cortisol, hyperaldosterone
104
Q

renal artery stenosis

A
  • blockage in the renal artery

- rare cause of hypertension due to problems controlling blood pressure

105
Q

phaeochromocytoma

A
  • tumous of the adrenal gland
  • sits just above the kidney
  • can cause hypertension fro too much adrenaline production and increase HR
106
Q

cuhsing’s

A
  • retaining a lot more water and salt than normal

- increases fluid pressure and therefore causes hypertension

107
Q

signs and symptoms of hypertension

A
  • often there is no presentation
  • only some people show symptoms
  1. headaches
    - only if systolic pressure is above 300mmHg
  2. transient ishaemic attack
    - TIA “mini stoke”
    - full neurological function returns 24h after the stroke
108
Q

resistant hypertension

A

an inability to get the BP stable, with use of medication

109
Q

accelerated hypertension

A

a recent significant increase over the baseline BP that is associated with target organ damage

110
Q

renal artery stenosis

A

the renal artery is smaller than it should be
- not getting enough BF due to narrowing of the vessel and it is therefore underdeveloped

  • over activates angiotensin release as it senses lower BP
111
Q

bilateral renal artery stenosis

A
  • caused by atherosclerosis of the aorta

- renal arteries come off of the aorta at right angles, resulting in more turbulent flow in there

112
Q

investigations into hypertension

A
  1. urinalysis
  2. serum biochemistry
  3. ECG
  4. renal ultrasound
  5. angiography
113
Q

urinalysis

A
  • determines the efficiency of renal function
114
Q

serum biochemistry

A
  • tests the elctrolyte, urea and creatinine levels in the blood
  • important as these levels can be upset due to more retention, indicating hypertension
115
Q

treatment of hypertension

A
  1. modify the risk factors
  2. single daily drugs
  • requires patient compliance
  • beta blockers, calcium channel blockers, diuretics, ace inhibitors
116
Q

side effects of thiazide diuretics

A

can cause gout and painful joints

117
Q

side effects of beta blockers

A
  • can interfere with patients with asthma and COPD
118
Q

side effects of calcium channel antagonists/blockers

A
  • may reduce cardiac output, but doesn’t do anything to reduce constriction of the blood vessels
119
Q

side effects of ace inhibitors

A

can make peripheral vascular disease worse by reducing bf back to the heart

120
Q

heart failure

A

when the ability of the heart to prodce cardiac output necessary for bodily function is compromised and therefore cannot meet the demand of the tissues to keep them alive

121
Q

types of heart failure

A
  1. high output failure

2. low output failure

122
Q

high output heart failure

A

very rare form of heart failure

- caused by anaemia or thyrotoxicosis (hyperthyroidism causing an increased in O2 demand)

123
Q

low output failure

A
  • more common form of heart failure

- caused by MI or valve disease

124
Q

systolic disfunction

A
  • the heart has enlarged ventricles which fill with blood

- the ventricles pump out less than 40-50% od the blood filling them, resulting in a low cardiac output

125
Q

diastolic function

A
  • the ventricles become stiff and therefore cannot fill with as much blood
  • the amount of blood in the ventricles may be lower than normal
126
Q

what does the body think the reason is for low BP? how does this result in heart failure?

A
  • haemorrhage
  • all systems work to increase fluid level
  • the heart pumps faster to increase fluid levels, however because the heart has failed the lungs and tissues build up with fluid
127
Q

causes of low output failure

A
  1. heart muscle disease
    - MI, myocarditis
  2. pressure overload
    - hypertension
    - aortic stenosis
  3. volume overload
    - mortal or aortic incompetence
  4. arrythmias
    - heart block or AF
  5. drugs
    - beta blockers, corticosteroids
128
Q

signs and symptoms of left heart failure

A
  • lung and systolic effects
    1. tachycardia
  1. low blood pressure and volume
  2. dyspnoea (shortness of breath)
129
Q

signs and symptoms of right heart failure

A
  • elevated venous pressure
  • peripheral and sacral oedema
  • enlarged liver
  • fluid build up in the abdomen
  • raised jugular venous pressure
130
Q

classic symptoms of heart failure reported by patients

A
  • shortness of breath
  • swollen extremities
  • chronic lack of energy
  • difficulty breathing when lying down
  • swollen and tender abdomen
  • loss of apatite
  • cough
  • confusion
131
Q

treating acute heart failure

A
  • emergency
  • hospital treatment
  • oxygen, morphine and frusemide loop diuretic to help reduce fluid volume
132
Q

treating chronic heart failure

A
  • improve myocardial function in general practice

- where possible, treatment of the cause is most effective

133
Q

treatable causes of heart failure

A
  • hypertension
  • valve disease
  • arrythmias
  • anaemia
  • thyroid disease
134
Q

drugs to treat heart failure

A
  • diuretics to increase salt and water loss
  • ace inhibitors to reduce salt and water retention
  • nitrates to reduce venous filling pressure (preload)
135
Q

“tachy” arrhythmia are …

A

FAST
- atrial fibrillation

  • ventricular tachycardia
136
Q

“brady” arrhythmia are…

A

SLOW

- blockage in the AV node or drug induced reduced rate (beta blockers)

137
Q

pacemakers

A
  • used to treat brady arrythmias
  • keeps the HR at a minimum level
  • if HR is too slow, the PM delivers a shock to increase myocardial beating rate
138
Q

P wave of ECG

A

atrial depolarisation

139
Q

QRS complex of ECG

A

ventricular depolarisation

140
Q

T wave of ECG

A

ventricular depolarisation

141
Q

ventricular fibrillation

A
  • unstable electrical activity in the heart
  • no P wave in the ECG
  • extremely irregular rhythm
  • patients needs defibrillated
142
Q

asystole

A
  • lack of ventricular movement
  • heart rate and rhythm are absent
  • wandering line on ECG
  • patient is dead
143
Q

atrial fibrillation

A
  • regularity of heart hbeatis gone
  • inconsistent gaps between beats
  • managed with anticoagulants
144
Q

left cardiac valve disease effects which valves

A

mitral and aortic

145
Q

mitral valve

A

betwen LA and LV

146
Q

aortic valve

A

between LA and aorta

147
Q

right valve disease effects

A

tricuspid and pulmonary valves

148
Q

tricuspid valve goes between

A

right atrium and right ventricle

149
Q

pulmonary valve goes between the

A

right ventricle and the pulmonary artery

150
Q

the heart valves are composed of…

A

cusplets of collagen tied onto papillary muscles

151
Q

stenosis

A
  • narrowing of a valve
  • results in blood and pressure filling up in a chamber as it doesn’t open properly
  • blood is released at higher pressure into the system as it is ejected at a higher pressure
152
Q

valve deformation factors

A
  • very common in elderly and people with downs syndrome
  • rheumatic fever can cause heart disease, immunological response from the infection targeting STREP A but also the host proteins in the valves
153
Q

causes of valve disease

A
  1. congenital defects
    - valve is formed incorrectly during growth
  2. stretching of the aorta
    - valve is pulled apart
  3. myocardial infection
    - papillary muscles rupture
  4. rheumatic fever
    - immunological reaction to strep a
  5. dilation of the aortic root
    - syphilis side effect, causes aortic aneurysm
154
Q

investigating valve diseases with an ultrasound

A
  • shows the heart moving in real time
  • technology shows the blood moving in the direction it should and the direction it shouldn’t (colour doppler flow assessment)
155
Q

mechanical valve replacement

A
  • metal valve
  • patient needs to be on anticoagulants for life (warfainised) to prevent the blood clotting on the abnormal tissue
  • must also be on dual anti platelets (aspirin and clopidrogel)
156
Q

tissue valve

A
  • usually a pig valve
  • lasts about 10 years
  • don’t need to be on anticoagulants as the blood won’t stick to the collagen leaflets
157
Q

INR

A

international normalised ratio
- a cohort of results resulting in an average value for how long it takes for blood to clot

  • warfarin will increase a patients INR as it is an anticoagulant
158
Q

why are patients who have received valve replacements encourages to regularly visit the dentist

A

they are at a higher risk of ineffective endocarditis, due to the risk of streptococci from the oral cavity entering the blood stream
- these patients must be given prophylactic care and must maximise their oral health

159
Q

overfusion

congenital heart defects

A
  1. atrial septal defects

2. ventricular septal defects

160
Q

atrial septal defects

A
  • creates a lower pressure system
  • only a small amount of blood goes back into the lungs, therefore some blood is oxygenated twice
  • right atrium may be enlarged as it has to pump more blood each time
161
Q

ventricular septal defects

A
  • blood is squirted into the left atrium at high pressure then into the right ventricle as well as the left ventricle
  • this can cause right heart failure as the heart has to pump at a much higher pressure
162
Q

co-arctation of the aorta

A
  • incomplete closure of the ductus venosus after birth
  • blood therefore travels to the aorta from the RV without passing through the pulmonary circulation
  • sometimes overclosure may result in narrowing of the aorta
163
Q

central cyanosis

A
  • congenital heart disease
  • core tissue are starved, resulting in blue mucosa
  • exists when there is 5g/decilitre or more deoxygenated Hb in the blood

signs;

  1. finger clubbing
  2. blue mucosa and peripheries
164
Q

peripheral cyanosis

A
  • occurs when a person is cold
  • cold from the outside
  • peripheral system shuts down to prevent heat loss
165
Q

ineffective endocarditis

A
  • infection of the endocardium
  • usually on the valves
  • many organisms implicated
  • often there is no known predisposing factors
  • thrombi form on the platelets due to surface abnormalities causing turbulent blood flow
  • these thrombi form VALVULAR VEGETATIONS which microbes attach to and multiply
166
Q

symptoms of ineffective endocarditis

A
  1. fever
  2. heart murmur
  3. skin manifestations (petachie, splinter haemorrhages)
  4. septic complications (pneumonia)
167
Q

organisms involved in inefective endocarditis

A
  1. streptococci
  2. staphylococci
  3. fungi
168
Q

treating I. endocarditis

A

4+ weeks of bactericidal treatment often combined with other drugs
- potential for valve replacement if there is sufficient damage

169
Q

montgomery issues of ineffective endocarditis

A
  • patient must be informed about antibiotic prophylaxis
  • consequences of no ABP
  • patient can discuss this this with their cardiac team
170
Q

drug regime for prophylaxis against ineffective endocarditis

A
  • 3g of oral amoxycillin 1 hour before procedure, even if used recently
  • if allergic to penicillin or high risk, 1.5g clinamycin can be taken

BDS2 BAMS (57 decks)

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