Cardiovascular Disease Flashcards
(194 cards)
1
Q
irreversible risk factors for CVD?
A
age <older
sex <male
family history
2
Q
reversible risk factors for CVD by patient?
A
smoking - damage blood vessels -> clots
obesity - fatty material damage and clog vessels
diet
exercise
3
Q
reversible risk factors for CVD by medication?
A
hypertension - damage to heart and blood vessels
hyperlipidemia (high cholesterol) - fatty deposits
diabetes - damage blood vessels and nerves
4
Q
define primary prevention for cardiovascular disease
A
preventing the disease
5
Q
define secondary prevention for cardiovascular disease?
A
preventing further disease following diagnosis
6
Q
define claudication
A
cramping pain in leg following exercise caused by obstruction of arteries
7
Q
how is cardiovascular disease prevented 4
A
lifestyle changes
control cholesterol
control hypertension
anti-platelet drugs (aspirin)
8
Q
what lifestyle changes are required to prevent cardiovascular disease?
A
exercise, diet, smoking
9
Q
what level is controlled cholesterol?
A
<5.00mmol/L or 25%
10
Q
how is cholesterol controlled
A
statin treatment
11
Q
what level is controlled hypertension?
A
Reduce blood pressure to <140/85
12
Q
when are antiplatelet drugs used in cardiovascular disease?
A
if have cvd
if high risk of developing cvd
13
Q
what is hypertension?
A
high blood pressure
14
Q
Blood pressure at which harm occurs
A
140/90mmHg
15
Q
how is blood pressure taken? 2
A
3 measurements at 3 times sitting and rested
Ambulatory measuring -> see how blood pressure changes over 24 or 72hrs
16
Q
why is age a risk factor for hypertension?
A
stiffer arteries - high blood pressure
17
Q
why is race a risk factor for hypertension?
A
racism - stress
salt sensitivity
body mass index
18
Q
why is obesity a risk factor for hypertension?
A
fatty build up in arteries
increased heart work
19
Q
why is alcohol a risk factor for hypertension?
A
increase in hormone renin which causes vasoconstriction
20
Q
why is pregnancy a risk factor for hypertension?
A
placenta issues and increase heart work
21
Q
why is stress a risk factor for hypertension?
A
sympathetic nervous system response causing vasoconstriction and increased heart rate
22
Q
what are the possible outcomes of hypertension? 2
A
accelerated atherosclerosis -> MI, stroke, peripheral vascular disease
renal damage - renal failure makes hypertension worse
23
Q
causes of hypertension? 3
A
commonly none
renal artery stenosis -> constriction of arteries to kidney, kidney thinks drop in blood pressure, releases aldosterone so water is retained
endocrine tumours
- Phaeochromocytoma (Adrenergic tumour -> releases adrenaline which causes vasoconstriction and hypertension)
- Conn’s syndrome (Aldosterone = increases the circulating blood volume)
- Cushing’s syndrome (too much cortisol - Salt and water retention increases the circulating blood volume)
24
Q
signs and symptoms of hypertension 3
A
Usually none
May get a headache
May get Transient Ischaemic attacks -> mini strokes with full neurological return in 24hrs
25
investigations for hypertension 3
Of the blood -> urinalysis, serum biochemistry, serum lipids
ECG
Occasionally renal ultrasounds, renal angiography, hormone estimations
26
treatment for hypertension 3
Aim of treatment to get blood pressure < 120/90mmHg
Modify risk factors -> weight loss, exercise
Single daily dose drug (single to improve compliance but can add more to control)
27
remember for hypertension
Monitoring is important as treatment need changes over time, review at least annually when stable
Monitor blood biochemistry effects of drugs Na/K changes and dehydration
28
what are the two processes that cause acute coronary syndromes?
blood vessel narrowing - ischaemia
blood vessel occlusion - infarction
29
what is ischaemia?
inadequate oxygen delivery for tissue needs
30
how does blood vessel narrowing cause acute coronary syndromes?
causing ischaemia (inadequate oxygen delivery for tissue needs)
Causes cramp in affected muscle/tissue felt as pain
No damage at first but if goes on for many years it can damage the muscle in particular the heart leading to heart failure
31
how does blood vessel occlusion cause acute coronary syndromes?Myocardial infarction and stroke (CVA)
Tissue death due to no oxygen delivery which causes severe pain and loss of function of tissue
32
name 2 consequences of ischaemia
angina
peripheral vascular disease
33
name 2 consequences of infarction
Myocardial infarction and stroke (CVA)
34
what is coronary artery disease?
- Plaque builds up in the arteries of the heart reducing blood flow to the muscles of the heart
35
coronary artery disease tends to happen where?
? blood flow causes ? to the interior surface of the ? allowing the accumulation of ? within the surface which forms ? ?. Their size ? gradually narrowing the ? and ? the blood flow. Limiting ? delivery to the ?
areas of stress to the artery
turbulent
damage
artery
fat
atherosclerotic plaques
increases
vessel
decreasing
oxygen
tissues
36
in coronary artery disease
if the oxygen requirements of the tissue increase what happens?
the patient will not be able to match it with increased blood flow
37
why do more cardiac problems happen at faster heart rates?
the time for diastole decreases compromising the cardiac blood flow as blood only flows through the arteries when the valve is shut
38
Acute ischaemic events affecting the heart have 3 main forms what are they?
atherosclerosis
atherosclerosis with blood clot
spasm
39
how long does ischaemia last for it to cause permanent damage?
>20mins
40
what causes stable angina?
Plaque forms reducing blood flow.
41
when does pain develop in stable angina?
Pain develops during exercise.
42
what is the ECG in stable angina?
normal
43
what are troponins?
chemical released when cardiac tissue death occurs
44
what are the troponin levels in stable angina?
normal
45
what causes unstable angina?
Plaque ruptures and thrombus forms around it causing partial occlusion of the vessel.
46
when does pain develop in unstable angina?
Pain can happen at any time .
47
what is the ECG of unstable angina?
48
what are the troponin levels in unstable angina?
normal
49
what does NSTEMI stand for?
non st segment elevation myocardial infarction
50
what happens in NSTEMI?
Plaque ruptures and thrombus forms around it causing partial occlusion to the vessel.
Causing injury and infarct to the subendocardial myocardium
51
what is the ECG in NSTEMI?
52
what are the troponin levels in NSTEMI?
elevated as cardiac tissue death
53
what does STEMI stand for?
ST segment elevation myocardial infarction
54
what happens in STEMI?
Blood clot completely occludes vessel. No blood flow or O2
Transmural injury and infarct to the myocardium
55
what is the ECG in STEMI?
56
what are the troponin levels in STEMI?
elevated
57
learn the differences
58
define angina pectoris
tightness in the chest
59
what is angina pectoris caused by?
reversible ischaemia of heart muscle - narrowing of one or more coronary arteries
60
what is the difference in pain between unstable and stable angina?
Stable angina -> pain only on exercise, gradual deterioration
Unstable angina -> pain at rest and exercise
61
what are the symptoms of angina pectoris (PCO)?
crushing chest pain can have radiation to arm, back, jaw
62
what are the signs (clinical findings) of angina pectoris? 2
often none
hyperdynamic circulation - mismatch between oxygen delivery and requirement
63
hyperdynamic circulation (mismatch between oxygen delivery and requirement) causes
?: ? carrying capacity of the blood is ? so the ability of the patient to cope with a ? of the coronary artery is also ?. Restoring the patients ? to normal can reduce ? problems.
?: ? the demand for oxygen by the tissues as it increases the ? ?. Treating the hyperthyroidism will solve the ?
?: body loses more ? than it takes in -> decrease in blood ?
anaemia
oxygen
reduced
narrowing
reduced
haemoglobin
angina
hyperthyroidism
increases
metabolic rate
angina
hypovolaemia:
fluid
volume
64
what is angiography?
Using a dye to look at the patency of the arteries
65
what is ecocardiography?
Ultrasound to look at the function of the heart valves and ventricles
66
what do isotope studies do?
Looks at the proportion of blood ejected from the left ventricle shows how much residual function is present
67
what 2 things do you have to do to treat angina pectoris?
Reduce oxygen demands of the heart
Increase oxygen delivery to the tissues
68
when treating angina pectoris what do you have to do to reduce the oxygen demands of the heart? 3
reduce afterload (blood pressure)
reduce preload (venous filling pressure)
correct mechanical issues (valves/septal defects)
69
when treating angina pectoris how can you increase oxygen delivery to tissues? 2
Angioplasty -> dilate blocked, narrowed vessels
CABG coronary artery bypass grafting -> creates a new route for blood to flow around blocked/narrowed arteries
70
what non-drug therapies are used to treat angina pecoris?
Explanation of illness to understand what triggers it so they can manage it by living within limitations
Modify risk factors : smoking cessation, exercise, diet
71
drug therapies for angina pectoris
Reduce MI risk Aspirin -> reduce chance of platelets adhering to atherosclerotic plaque
Reduce hypertension (afterload) -> diuretics, Ca channel antagonists, ACE inhibitors, B blockers
Reduce ? -> dilate coronary vessels through ?
Emergency treatment -> ? ? to reduce preload, short shelf life
aspirin
platelets
hypertension (afterload)
preload (venous filling pressure)
nitrates
GTN spray
72
what is CABG?
(bypas) -> can only be carried out once, lasts 10yrs, major surgery (mortality)
Veins grafted from the leg and attached to the aorta as a new blood supply to bypass the obstruction
It is only possible if the blockage is close to the origin of the artery
73
what is angioplasty?
dilate blocked, narrowed vessels
lower risk (percutaneous intervention) and benefit, risk of vessel rupture during procedure, need antiplatelet therapy
74
what is peripheral vascular disease?
angina of the tissues - usually lower limbs (like angina but doesn’t affect cardiac tissue ).
75
what are the symptoms of peripheral vascular disease?
claudication pain in limb on exercise
76
peripheral vascular disease has an MI risk as ? is a ? disease so if they have it in there peripheral vessels they also have it in the ? vessels
atherosclerosis
systemic
cardiac
77
what are the outcomes of peripheral vascular disease? 3
Limitation of function
poor wound healing
May lead to tissue necrosis and gangrene
78
how does ischaemia lead to infarction?
Embolization: piece of atherosclerotic plaque breaks off and blocks a smaller vessel downstream. Lack of blood flow to that area will cause tissue death if it persists for more than 20 minutes
79
Infarction is an issue with the heart but also affects the ? and ?
limbs
brain
80
Stroke: Happens through ? artery ? which allows ? clots and other clots to ? up the carotid artery and into the ? causing ? in the short term and eventually ? of the brain tissue in the obstructed area
carotid
atherosclerosis
platelet
embolise
brain
ischaemia
infarction
81
define myocardial infarction
Blockage of a coronary artery without collateral blood supply. Therefore all the tissue distal to the blockage will suffer necrosis
82
how is tissue loss from necrosis reduced when treating mi? 2
by opening blood flow to ischaemic tissue
- Thrombolysis: using drugs to absorb the blood clot which is causing the blockage
- Angioplasty
By bypassing the obstruction
- CABG, fem/pop bypass
83
how are further episodes of MI prevented?
risk factor management and aspirin
84
if a patient is having an MI what do u give?
analgesics, aspirin, reassurance,
85
what basic life support may be required if a patient has a mi?
cardiac arrest due to an arrythmia from altered electrical conduction in the heart tissues
86
bls for cardiac arrrest?
approach with caution
verbal and pain stimulus
call for help
head tilt chin lift
assess breathing 10s
no breathing = cardiac arrest
call 999
30 chest compressions
2 rescue breaths
87
hospital treatment for MI is dependant on time from onset of symptoms
<3hrs angioplasty and stenting
<6hrs thrombolysis if suitable
Drug treatment to reduce tissue damage
88
signs and symptoms of mi
Pain, nausea, pale, sweaty, feel like going to die
89
what are the outcomes of mi?
Death or functional limitation from reduced cardiac muscle action
90
how is MI diagnosed?
STEMI st segment elevation MI, NSTEMI non-st segment elevation MI
§ Note: even after a few weeks the ECG isn't normal as has a q wave
troponin level elevation
91
long term management of mi?
Risk modification
Aspirin, b blocker, ACE inhibitor
92
define valve stenosis
narrowed valves
93
define valve incompetence
valve not closing properly
94
which valves are most likely to have problems? why?
mitral valve and aortic valve due to higher pressure (left heart)
95
heart valve disease is common in the elderly and those with down syndrome
96
causes of heart valve disease 4
Congenital abnormality
○ Valve doesn’t work effectively, patient often has symptoms of heart failure and need a replacement of the valve
Myocardial infarction -> papillary muscle rupture
Rheumatic fever -> immunological reaction to streptococci which can cause damage to the heart valve -> rheumatic heart disease can also lead to infective endocarditis
Dilation of the aortic root which pulls the cusps apart so they can't close fully -> caused by syphilis or aneurysm formation
97
how is valve disease investigated?
- Ultrasound scan
Doppler ultrasound colours the blood based on if it is flowing in or out of the heart
98
why are valve replacements done before heart failure?
as it will not fully reverse any heart failure previous to treatment
99
what risk is there with valve replacements?
endocarditis risk so may consider antibiotic prophylaxis
100
101
list 3 dental implications of valve replacements
Anticoagulants
Endocarditis prevention
○ OHI, prevent oral diseases and remove causes of oral sepsis
Consult with patients medical team
102
Infective endocarditis is ? and ? of the ? (inside heart). Bacteria enter (mouth), go into the circulation and settle onto previously ? areas of heart tissue. The bacteria colonise a ? and multiply to cause ? and ? of the infection, leading to ? formation -> thickenings and areas of damage to the valves
infection
inflammation
myocardium
damaged
thrombus
damage
spread
vegetation
103
what is the main bacteria for infective endocarditis?
oral streptococci so it impacts dental care (bacteraemia).
104
where is infective endocarditis usually found?
on the valves
105
patients at risk of infective endocarditis 4
Other cardiac disease
Intracardiac device
○ Not angioplasty, stent, CABG, implanted pacemaker or defibrillator
Prosthetic valve
Past endocarditis
106
is diagnosis of infective endocarditis difficult?
yes
there is no single test that is reliable
Have to take blood cultures over several days to see if bacteria are present in the blood stream coming from the infection in the heart
107
effects of infective endocarditis 3
Prolonged antibiotic treatment
Cardiac valve damage that may require replacement which is risky
Risk of death from disease or its complications
108
which dental procedures increase risk of infective endocarditis?
any that involve manipulation of the dento-gingival junction
109
what should a dentist do for patients at risk of infective endocarditis?
Identify them -> medical history covering risk conditions
Prevention of oral disease and excellent oral hygiene -> keep bacteria low
110
remember
Nice Guidelines: antibiotic prophylaxis should not be routinely be given to a patient with infective endocarditis
Special consideration: prosthetic valve, previous infective endocarditis, congenital heart disease
111
congenital heart defects/disease is often undetected and asymptomatic but suspect they have them if have other congenital body defects
Can detect them through what?
doppler ultrasound -> shows blood flow and its direction. easy and non-invasive.
112
what is finger clubbing?
swelling of the terminal digits of the hands and changes of the nail bed angle to the finger.
113
what medical issues is finger clubbing seen in? 4
Cardiac disease
Lung disease
Inflammatory bowel disease
Liver cirrhosis
114
what is cyanosis?
Lack of oxygenated haemoglobin / increase in deoxygenated haemoglobin in the blood
115
how much deoxygenated haemoglobin in the blood is considered cyanosis?
5g/dl or more of deoxygenated haemoglobin in the blood
116
central cyanosis is mostly caused by what?
congenital heart disease causing Poor oxygenation of the blood or oxygenated and deoxygenated blood mixing
117
what are the signs of central cyanosis?
warm tissues being blue e.g. tongue
118
peripheral cyanosis is caused by
cold extremeties or vascular spasm
causing slow circulation taking more oxygen out of the haemoglobin in cold tissues
119
what are the signs of peripheral cyanosis?
Cold peripheral tissues look blue e.g. hands
120
which septal defects are the most common?
atrial
121
what happens in atrial septal defects?
oxygenated blood from left atrium leaks into right atrium
122
are atrial septal defects usually cyanotic?
no as no deoxygenated blood is going to the left side and to rest of body
123
how do atrial septal defects lead to heart failure?
due to increase strain on the heart
On an x-ray shows a bulge in the left side of the heart due to increased workload
124
125
what happens in ventricular septal defects?
Blood flows from left to right ventricle and pulmonary artery due to higher pressure in left side.
126
how is ventricular septal defects an increased endocarditis risk?
more turbulent flow as the volume of blood in the right ventricle and circulating into the lungs is higher
127
are ventricular septal defects usually cyanotic?
non-cyanotic as no deoxygenated blood is going to the left side and to res of body
128
treatment for septal defects 2
Some shrink naturally (atrial defects often require no intervention)
'Patch' repair -> open heart surgery where mesh is place on either side of the defect by arterial access
129
what is coarctation of the aorta?
Narrowing of the aorta just after the left carotid artery has exited, restricts blood flow to the left arm and lower limbs.
Blood pressure would differ taken on the right vs left arm, the left arm would have considerably lower blood pressure
130
what is patent ductus arteriosus?
The ductus fails to close so the pulmonary artery and aorta are connected.
131
is there cyanosis in patent ductus arteriosus?
No cyanosis as oxygenated blood flows into the pulmonary artery due to higher pressure in aorta
132
how can patent ductus arteriosus lead to heart failure and endocarditis risk?
due to turbulent blood flow
133
define heart failure
output of the heart is incapable of meeting the oxygen demands of the tissues
134
what are the 2 situations where heart failure can occur?
Low output failure - most common
High output failure
135
in heart failure what is low output failure?
Pump is failing and not strong enough to force liquid around the body
136
what causes low output heart failure?
Most commonly due to heart muscle disease, pressure overload, volume overload
Also due to
- Arrhythmias -> Atrial contractile signal not transferred to the ventricle so they continue at a rate independent to the atria
- Drugs e.g. corticosteroids and anticancer drugs can affect heart muscle
137
in heart failure what is high output failure?
Demands of the body have exceeded the capacity of the pump
138
what is high output heart failure due to?
Due to anaemia, thyrotoxicosis etc.
139
is left or right heart failure more common? why?
Left heart failure is more common than right because the left side does the most work.
140
what is congestive heart failure
Left heart failure often leads to right as increased blood volume into the lungs causes the right side to have to work harder which then starts to fail -> congestive heart failure
141
what are the 2 mechanisms of heart failure?
systolic dysfunction (pumping)
diastolic dysfunction (filling)
142
mechanisms of heart failure
in systolic dysfunction what happens during diastole and systole?
diastole: enlarged ventricles fill with blood
systole: ventricles pump out less blood than normal
143
mechanisms of heart failure
systolic dysfunction is due to what?
Due to loss of muscle or stiffness of the ventricle wall
144
mechanisms of heart failure
in diastolic dysfunction what happens during diastole and systole?
diastole: stiff ventricles fill with less blood than normal
systole: ventricles pump out blood (may be less than normal)
145
heart failure compensation mechanism
how does the body compensate for heart failure? how is this managed?
by increasing blood volume which makes heart failure worse
management needs to fix the cause and prevent the compensatory mechanisms from making things worse
146
what are the signs of left heart failure?
Affect systolic blood pressure and systemic tissues
Lungs accumulate more blood than normal and have higher blood pressure than expected
147
what are the signs of right heart failure?
Venous pressure increases as systemic veins fill as blood is not taken away and pumped around the body.
This leads to fluid transudate from the blood in the tissues
148
symptoms of heart failure 4
Shortness of breath -> fluid in lung tissues prevent alveoli from transmitting oxygen into the blood, worse if patient lies flat as venous pressure in the lungs rises
Swelling of feet and legs -> fluid moving into tissues from RHF due to gravity
○ Pitting oedema: Severity of heart failure is assessed based on how far up the leg it goes
Swollen or tender abdomen -> liver engorgement and fluid
Cough with frothy sputum from air mixing with liquid in the lungs causing irritation
149
what is the treatment for acute heart failure (emergency)
oxygen, morphine, frusemide
Patient is short of breath and gasping
due to fluid in lungs
High dose diuretic to remove fluid -> frusemide
150
treatment for chronic heart failure
Improve ??
- Hypertension, valve disease, arrhythmias, anaemia, thyroid disease
Reduce ??
Treat the ? where possible
Drugs
Stop negative ? - B blocker -> make heart failure worse
myocardial function
compensation effects
cause
inotropes
151
drugs used to treat heart failure
? -> increase salt and water loss
? -> reduce water and salt retention
? -> reduce venous filling pressure
? -> treat problems with electrical impulses of the heart by improving heart efficiency and control electrical activity
diuretics
ACE inhibitors
nitrates
inotropes
152
name a negative inotrope that can make heart failure worse (medicine)
B-blocker
153
cardiac arrhythmias are issues of what?
heart rate
154
define tachycardia (tachy arrhythmias)
heart rate too fast
155
tachycardia results in impaired ?? by ? the ???. reduced cardiac output leads to ??
cardiac function
reducing
diastolic filling time
heart failure
156
what are the 2 groups of tachyarrhythmias?
atrial tacchyarrhythmias
ventricular tachyarrhythmias
157
describe the qrs complex on an ECG for atrial tachyarrhthymias
narrow
158
describe the qrs complex on an ECG for ventricular tachyarrhythmias
broad as the signal passes through multiple tissues
159
what is atrial fibrillation?
rapid atrial impulses conducted to ventricles -> irregular and high pulse
160
what is ventricular fibrillation?
no organised rhythm or qrs pattern
161
how are tachy arrhythmias treated
beta blockers - can result in postural hypotension
162
define brady arrhythmias
heart rate too slow
163
what are brady arrhythmias caused by?
drug induced or heart block
164
what is heart block?
reduction in conduction through the atrioventricular node which prevents another impulse to travel preventing tachy arrhythmia or atrial fibrillation
165
how is a heart block shown on an ECG?
prolonged pq interval
166
the level of a heart block is classified based on what?
the length of the signal delay. 1 2 or 3, 3 means there is no signal passed to the ventricles so they pulse at their own intrinsic rate
167
what is the treatment for brady arrythmias?
cardiac pacemaker -> takes over if pulse drops below a certain rate
168
in normal sinus rhythm what do parts of an ECG represent:
P wave
qrs complex
t wave
p wave = atrial repolarisation
qrs complex = ventricular depolarisation
t wave = ventricular repolarisation
169
define asystole
no electrical activity
170
this is what asystole looks like on an ECG
171
is asystole treated with a defibrillator? why?
no as defibrillators dont give electrical activity they just coordinate existing electrical activity
172
how is a pt with asystole treated?
adrenaline to try produce electrical activity so a defibrillator can be used
173
is there cardiac output with ventricular fibrillation? why?
no as no emptying of the ventricles due to muscle spasm
174
how is ventricular fibrillation treated?
with a defibrillator
175
antiplatelet drugs e.g. aspirin reduce the chance of what?
heart attack and stroke in at risk population
176
what are the dental implications of antiplatelet drugs?
prolonging the bleeding time after extraction
177
Oral anticoagulants (e.g. warfarin)
inhibit the ?? and reduce the amount of ? formed and therefore ??
clotting cascade
fibrin
clotting stability
178
what is the dental imact of oral anticoagulants?
increase in post-treatment bleeding a few hours later as no fibrin so unstable clot formation which breaks down after a few hours.
179
warfarin
Inhibits synthesis of ????? (2,7,9,10 and protein ? and protein ?)
Initial ?? as protein C and S ??.
Anticoagulation takes 2-3 days as clotting factors 2,7,9,10 are ? without replacement
so ? is often used initially also given as has instantaneous affect preventing hypercoagulation
vitamin k dependant clotting factors
C
S
hypercoagulation
inhibit clotting
consumed
Heparin
180
pt on warfarin have to be monitored using what test?
IRN ratio of a healthy volunteers prothrombin time (time to convert prothrombin to thrombin) measured against the patient
Aim for INR between 2 and 4
181
remember
Warfarin and dentistry
Local haemostatic measures e.g. fibrinogen activator, suture, or local anaesthetic with vasoconstrictor
Assume all drugs interact with warfarin -> INR test day after prescribing antibiotics, avoid NSAIDs
182
remember
New oral anticoagulants
No significant drug interactions with dentistry
Short half life -> can do extraction just before dose is due when effects of the drug are lowest
183
what do statins do?
inhibit cholesterol synthesis in the liver
184
what are the side effects of statins?
can cause inflammation in the muscles (myositis) with some drug interactions
185
what do B blockers do?
reduce the excitability of the cardiac conduction system reducing the risk of cardiac arrest, ventricular fibrillation and death
186
beta blockers can make heart failure and asthma worse. what dental impact do they have?
more susceptible to lichenoid reactions
187
Diuretics -> antihypertensive (BP) and for heart failure
Increase ? and ? loss reducing ? volume and ??
can lead to ?? so has to be monitored by looking at ? in the blood periodically
salt
water
plasma
cardiac workload
Na/K imbalance
electrolytes
188
what is the dental impact of diuretics?
dry mouth if excessive water loss
189
Nitrates -> Used for emergency treatment or long term prevention of ?
dilates the veins -> reducing the preload to the heart
dilates the coronary arteries -> reducing ?? and cardiac ? requirement
This reduces ? from ischaemia as the ? needs can be better balanced.
dilates ??? supply -> if narrowed coronary arteries, other blood vessels to the tissue will be enhanced
angina
dilates
preload
cardiac workload (afterload)
oxygen
pain
oxygen
collateral coronary artery
190
Calcium channel blockers -> treats ? and ?
They can act on different places for example some act on peripheral blood vessels whilst others act on the heart muscle
Block calcium channels in smooth muscles -> ? and ?
Slow ? of pacing ? in the heart
hypertension
migraines
vasodilation
relaxation
conduction
impulses
191
Angiotensin converting enzyme (ACE) inhibitors do what to things ?
reduce blood pressure and reduce water/salt retention
192
Angiotensin converting enzyme (ACE) inhibitors
Inhibit conversion of ?? to ??
Angiotensin II is a ? and triggers ? dependant resorption of ? and ?
direct ? affect on the arteries and also a reduction in ?? by preventing salt and water reabsorption
angiotensin I
angiotensin II
vasoconstrictor
aldosterone
water
salt
vasodilatory
plasma volume
193
side effects of ACE inhibitors?
hypotension and cough as they cause tissue changes which can irritate
Angiotensin II inhibitors work the same but don’t cause these side effects
194
what is the dental impact of ACE inhibitors? 2
More susceptible to lichenoid reaction
Angio-oedema -> sudden increase in tissue fluid due to inhibition of the complement cascade by the ace enzyme -> rapid swelling of the tongue/lips
