Cardiovascular medicine Flashcards
1
Q
irreversible risk factors for cardiovascular disease
A
- age
- sex
- family history
2
Q
reversible risk factors for CVD
A
- smoking
- obesity
- diet
- exercise
- hypertension
- hyperlipidaemia
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
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
5
Q
antiplatelet drugs
A
- aspirin
- clopidrogel
- dipyridamole
6
Q
oral anticoagulants
A
stop the coagulation pathway
WARFARIN
7
Q
drugs to treat atherosclerosis
A
statins
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
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)
10
Q
calcium channel blockers
A
- treatment for hypertension
- blocks calcium channels in smooth muscles and some heart muscles
11
Q
dental aspect of calcium channel blockers
A
can cause gingival hyperplasia
12
Q
ace inhibitors
A
- enalapril
- inhibits conversion of angiotensin 1 to angiotensin 2
- important vasoconstrictor, therefore reducing BP
13
Q
dental aspect of ace inhibitors
A
can cause oral angio-oedema (top lip oedema)
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
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
16
Q
full requirement for atherosclerosis diagnosis
A
- FULL medical history
- ECG
- STEMI
- nSTEMI
3. biomarkers - increased coronary enzymes (troponin) levels after an MI
17
Q
during which action is blood able to flow into the coronary arteries
A
- disastole as the vessels are relaxed
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
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)
20
Q
two types of angina
A
- classical
2. unstable
21
Q
classical angina
A
- only gets worse when the person is exerted
- symptoms decrease and stop when resting
22
Q
unstable angina
A
- symptoms of angina occur randomly when at rest
- NO BIOMARKER
- blood vessels randomly open and contract
23
Q
angina
A
REVERSIBLE ischaemia of the heart muscle due to narrowing of one or more of the coronary arteries
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
25
symptoms of classical angina
1. chest pain when exercising
2. chest pain can worsen with temperature and emotion
3. pain is relieved from rest
26
diagnosing angina
1. ECG showing an area of myocardial ischaemia
2. elimination of other potential causes
- thyroid issues, valvular defects
3. angiography
4. echocardiography
27
angiography
dye injected into an artery to check for narrow areas
28
echocardiography
sound waves used to generate a live image of the heart
29
how will angina appear in an ECG?
- elevation i the ST segment
- ISCHAEMIC EPISODE
- the ST segment doesn't reach the base line of the ECG
- STEMI
30
treating angina
reducing the oxygen demand of the heart by
1. reducing after load by reducing BP
2. reducing preload by using nitrate therapy
31
how to reduce preload for angina patients
- 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)
32
CABG
* 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
33
angioplasty and stenting
* lowers the risk of angina
* risks of vessels bursting
* vessel is artificially widened
* angioplasty = ballon with cage opened in the vessel
34
peripheral vascular disease
angina but in the peripheral tissues
| - usually the peripheries and lower limbs
35
atheroma
fatty deposits and scarring in vessel walls
36
symptoms of peripheral vascular disease
- pain in the limbs on exercise, improved with rest
- limited function to peripheral tissues
- may lead to necrosis and gangrene in severe cases
37
when does ischaemia become infarction
when a narrowed vessel, either by atheroma, thrombosis or platelet plug, becomes completely occluded, preventing any blood reaching the tissue
38
infarction
complete obstruction of a vessel causing tissue death
39
brain infarction is caused by occlusion of
the carotid arteries
40
heart infarction is caused by total occlusion of the
coronary arteries
41
symptoms of myocardial infarction
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
42
what to do if a patient is suffering an MI in surgery
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
5. calm and reassure the patient as much as possible
43
types of MI
1. spontaneous
2. sudden death
3. MI from percutaneous infection (from angioplasty or stent)
4. MI fro CABG
44
spontaneous MI
- primary coronary event
| - platelet plaque plug ruptures the vessel
45
suddenly death MI
- 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
46
thrombolysis
dissolves a blood clot within 6 hours
| - ideal treatment as it is non invasive
47
treating MI
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
48
preventing MI
1. treat patient with aspirin
| 2. work on risk factors
49
stroke
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)
50
treatment of a stroke depends on whether it was caused by a;
1. clotting or bleeding
| 2. embolism or thrombosis
51
transient ischaemic attacks
a warning sign of stroke risk
- mini strokes
- usually last less than 24 hours before normal function returns
52
why do patients feel such sever pain during MI?
- 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
53
STEMI
ST segment elevated myocardial infarction
54
what do abnormal Q waves on the ECG suggest
old MI has occurred
55
primary care of MI
- get the patient into hospital
- analgesia, aspirin, GTN
- BLS if required
56
hospital care for MI
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
57
complications after MI if survived
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
58
preventative care of MI
1. get patient on aspirin
2. modify risk factors
3. beta blockers
- reduce HR
4. ACE inhibitors
- reduce preload and prevents vasoconstriction
4. Statins
- if the patient has high cholesterol
5. diuretics
- reduce BP
6. Ca channel blocker
- relaxes smooth muscle in vessels and force of the left ventricle
REMEMBER ABCD
- aspirin, beta blocker, calcium channel blocker, diuretics
59
atherosclerosis
- 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
60
non-modifiable risk factors of atherosclerosis
1. age
2. gender
3. genes
61
why are males more at risk of atherosclerosis
- only until the menopause
| - oestrogen levels in women keep BV open
62
what defect in the genes can make a person more susceptible to atherosclerosis
mutation in the low density lipoprotein receptor gene
- mainly found in the liver, smooth muscles and fibroblasts
- control cholesterol uptake and processing
63
basal state of endothelial cells
- normal state
- cells are non-adhesive and non-thrombogenic
- the laminar flow is normal
- there is no trauma or insult to the cells
64
activated state of endothelial cell states
- 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
65
atheroma
* 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
66
foam cells
collection of pale and swollen monocytes from inability to phagocytose lipid
67
the healing response phase in the formation of an atheroma
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
68
effects of atherosclerosis
- 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
69
periodontitis risk with atherosclerosis
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
claudication
relief of pain upon rest
71
effects peripheral vascular diseases
1. ischaemia
2. claudication
3. gangrene
4. coagulation necrosis and infection
72
aneurysm
* 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
coagulation necrosis
- 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
congestive heart failure
- 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
pathophysiology
- 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
tumours associated with the cardiac system
1. hamartoma
2. caposi sarcoma
3. angiosarcoma
77
hamartoma
- found in developmental issue
- the tissue is in its normal site
- collection of blood vessels
- forms a HAEMANGIOMA in newborns
78
Kaposi sarcoma
- 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
angiosarcoma
- aggresive and rare
- malignancy of the endothelial cells
- tumour in the blood vessel
80
benign cardiac tumours
myxoma
- tumour of connective tissue in the heart
lipoma
- soft fatty tumour
81
why may vascular malformations become more apparent in old age
the mucosa thins, especially in the oral cavity
82
capillary vascular malformations
- lots of little capillaries group together to form a haemangioma (hamartoma)
83
cavernous vascular malformation
- large space filled with lots of blood vessels
84
storage weber syndrome
- vascular malformation
- PORT WINE STAIN
- excessive haemangioma which tends to follow the nerves on one half of the face
85
stenosis
injury to the valve resulting in the back flow of blood
86
insufficient valvular heart disease
the valve doesn't close properly
87
valvular vegetations
lumps forming on the cusps of the valves
88
valvular heart disease
- congenital or acquired (from cardiac diseases)
1. stenosis
2. insufficiency
3. valvular vegetations
89
calcific aortic stenosis
- most common valvular condition
- calcium is deposited on the valves as a result of inflammation
- neoplastic or dystrophic calcification
90
rheumatic heart disease
- 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
ineffective endocarditis
microbial infection of the heart valves
92
what type of hypersensitivity causes rheumatic stenosis
type 2 and 4
93
3 main risk factors of hypertension
1. genes/environment interactions
2. environment
3. genes
94
gene/environment interactions in hypertension risk
- race
| - gender
95
environment risks in hypertension
inactivity, stress, obesity, smoking, age, salt, alcohol
96
diagnosing hypertension
- raised blood pressure
- diagnosed as BP > 140/90mmHg
- must take blood pressure at 3 different readings at rest
97
age and hypertension risk
- 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
obesity and hypertension
higher risk of atherosclerosis resulting in higher pressure flow
99
target BMI
below 25
100
drugs which can cause hypertension
- NSIDs
- corticosteroids
- oral contraceptives
- sympathomimetics
101
what other diseases or conditions can result from hypertension
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
essential hypertension
- no identified triggers
| - occurs without being able to identify the exact cause
103
triggers of hypertension
1. renal syndromes
- raise BP due to issues controlling fluid and angiotensin levels
2. endocrine issues
- tumours, cushings, hyperthyroidism, high cortisol, hyperaldosterone
104
renal artery stenosis
- blockage in the renal artery
| - rare cause of hypertension due to problems controlling blood pressure
105
phaeochromocytoma
- tumous of the adrenal gland
- sits just above the kidney
- can cause hypertension fro too much adrenaline production and increase HR
106
cuhsing's
- retaining a lot more water and salt than normal
| - increases fluid pressure and therefore causes hypertension
107
signs and symptoms of hypertension
- 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
resistant hypertension
an inability to get the BP stable, with use of medication
109
accelerated hypertension
a recent significant increase over the baseline BP that is associated with target organ damage
110
renal artery stenosis
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
bilateral renal artery stenosis
- caused by atherosclerosis of the aorta
| - renal arteries come off of the aorta at right angles, resulting in more turbulent flow in there
112
investigations into hypertension
1. urinalysis
2. serum biochemistry
3. ECG
4. renal ultrasound
5. angiography
113
urinalysis
- determines the efficiency of renal function
114
serum biochemistry
- tests the elctrolyte, urea and creatinine levels in the blood
- important as these levels can be upset due to more retention, indicating hypertension
115
treatment of hypertension
1. modify the risk factors
2. single daily drugs
- requires patient compliance
- beta blockers, calcium channel blockers, diuretics, ace inhibitors
116
side effects of thiazide diuretics
can cause gout and painful joints
117
side effects of beta blockers
- can interfere with patients with asthma and COPD
118
side effects of calcium channel antagonists/blockers
- may reduce cardiac output, but doesn't do anything to reduce constriction of the blood vessels
119
side effects of ace inhibitors
can make peripheral vascular disease worse by reducing bf back to the heart
120
heart failure
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
types of heart failure
1. high output failure
| 2. low output failure
122
high output heart failure
very rare form of heart failure
| - caused by anaemia or thyrotoxicosis (hyperthyroidism causing an increased in O2 demand)
123
low output failure
- more common form of heart failure
| - caused by MI or valve disease
124
systolic disfunction
- 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
diastolic function
- 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
what does the body think the reason is for low BP? how does this result in heart failure?
- 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
causes of low output failure
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
signs and symptoms of left heart failure
- lung and systolic effects
1. tachycardia
2. low blood pressure and volume
3. dyspnoea (shortness of breath)
129
signs and symptoms of right heart failure
- elevated venous pressure
- peripheral and sacral oedema
- enlarged liver
- fluid build up in the abdomen
- raised jugular venous pressure
130
classic symptoms of heart failure reported by patients
- shortness of breath
- swollen extremities
- chronic lack of energy
- difficulty breathing when lying down
- swollen and tender abdomen
- loss of apatite
- cough
- confusion
131
treating acute heart failure
- emergency
- hospital treatment
- oxygen, morphine and frusemide loop diuretic to help reduce fluid volume
132
treating chronic heart failure
- improve myocardial function in general practice
| - where possible, treatment of the cause is most effective
133
treatable causes of heart failure
- hypertension
- valve disease
- arrythmias
- anaemia
- thyroid disease
134
drugs to treat heart failure
- diuretics to increase salt and water loss
- ace inhibitors to reduce salt and water retention
- nitrates to reduce venous filling pressure (preload)
135
"tachy" arrhythmia are ...
FAST
- atrial fibrillation
- ventricular tachycardia
136
"brady" arrhythmia are...
SLOW
| - blockage in the AV node or drug induced reduced rate (beta blockers)
137
pacemakers
- 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
P wave of ECG
atrial depolarisation
139
QRS complex of ECG
ventricular depolarisation
140
T wave of ECG
ventricular depolarisation
141
ventricular fibrillation
- unstable electrical activity in the heart
- no P wave in the ECG
- extremely irregular rhythm
- patients needs defibrillated
142
asystole
- lack of ventricular movement
- heart rate and rhythm are absent
- wandering line on ECG
- patient is dead
143
atrial fibrillation
- regularity of heart hbeatis gone
- inconsistent gaps between beats
- managed with anticoagulants
144
left cardiac valve disease effects which valves
mitral and aortic
145
mitral valve
betwen LA and LV
146
aortic valve
between LA and aorta
147
right valve disease effects
tricuspid and pulmonary valves
148
tricuspid valve goes between
right atrium and right ventricle
149
pulmonary valve goes between the
right ventricle and the pulmonary artery
150
the heart valves are composed of...
cusplets of collagen tied onto papillary muscles
151
stenosis
- 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
valve deformation factors
- 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
causes of valve disease
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
investigating valve diseases with an ultrasound
- 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
mechanical valve replacement
- 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
tissue valve
- 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
INR
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
why are patients who have received valve replacements encourages to regularly visit the dentist
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
overfusion
| congenital heart defects
1. atrial septal defects
| 2. ventricular septal defects
160
atrial septal defects
- 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
ventricular septal defects
- 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
co-arctation of the aorta
- 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
central cyanosis
- 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
peripheral cyanosis
- occurs when a person is cold
- cold from the outside
- peripheral system shuts down to prevent heat loss
165
ineffective endocarditis
- 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
symptoms of ineffective endocarditis
1. fever
2. heart murmur
3. skin manifestations (petachie, splinter haemorrhages)
4. septic complications (pneumonia)
167
organisms involved in inefective endocarditis
1. streptococci
2. staphylococci
3. fungi
168
treating I. endocarditis
4+ weeks of bactericidal treatment often combined with other drugs
- potential for valve replacement if there is sufficient damage
169
montgomery issues of ineffective endocarditis
- patient must be informed about antibiotic prophylaxis
- consequences of no ABP
- patient can discuss this this with their cardiac team
170
drug regime for prophylaxis against ineffective endocarditis
- 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
