Cardiology Flashcards
(560 cards)
1
Q
What is pericarditis?
A
inflammation of the pericardium which is the protective covering of the heart
2
Q
What are the two layers of the pericardium?
A
outer fibrous and inner serous
3
Q
What are the causes of pericarditis?
A
idiopathic, virus e.g. Coxsackie B or echovirus, trauma, post MI, TB, fungal, malignant, uraemic from accumulating toxins, pericardial effusion
4
Q
What are the 3 types of pericarditis?
A
acute and relapsing
pericardial effusion and cardiac tamponade
constrictive pericarditis
5
Q
What is the pain like in pericarditis?
A
sharp central pleuritic chest pain, can spread to neck or shoulders
6
Q
What exacerbates the pain in pericarditis?
A
movement, coughing, breathing, lying down
7
Q
What is pericarditis relieved by?
A
sitting up and leaning forward
8
Q
What other symptoms are associated with pericarditis?
A
fever, chills, dyspnoea, pericardial friction rub, cardiac tamponade
9
Q
What is a pericarditis friction rub?
A
a cardiac rub or leathery sound that is heard on examination
10
Q
What does an ECG show in pericarditis?
A
ST elevation
PR depression
IN ALL LEADS BUT aVR WHICH WILL BE OPPOSITE
(different to MI elevation which is limited to infarcted area)
11
Q
What will a CXR show in pericarditis?
A
cardiomegaly
12
Q
What will an ECHO show in pericarditis?
A
may show effusion
13
Q
What will a CT and MRI show is pericarditis?
A
inflamed pericardium
14
Q
What is the treatment of pericarditis?
A
NSAIDs
aspirin if recent MI
colchicine (before steroids to reduce recurrence)
corticosteroids if resistant or immune cause
15
Q
How common is relapsing in pericarditis?
A
20% of acute cases relapse
16
Q
What is a pericardial effusion?
A
a collection of fluid with space of the serous pericardial which accompanies acute
17
Q
What does pericardial effusion cause?
A
cardiac tamponade, poor ventricular filling and reduced cardiac output, pericarditis
18
Q
What is the treatment of pericardial effusion?
A
pericardial drainage
19
Q
What are the symptoms of pericardial effusion?
A
soft distant, dysponea
20
Q
What happens in chronic pericarditis?
A
the subepicardial layers of myocardium may undergo fibrosis, atrophy and calcification causing a rigid pericardium
21
Q
What will a CXR show in chronic pericarditis?
A
small heart with pericardial calcification
22
Q
What will an ECG show in chronic pericarditis?
A
low QRS, flattened T wave
23
Q
What will an ECHO show in chronic pericarditis?
A
thickened calcification pericardium, small ventricle cavities with thickened walls
24
Q
Why would you do an endomyocardial biopsy in chronic pericarditis?
A
to distinguish it from restrictive myopathy
25
What is the treatment of chronic pericarditis?
complete resection
pericardectomy if no TB
if TB, antiTB drugs then pericardectomy
26
What is a true aneurysm?
Where all the layers of the vessel dilate together
27
What is the difference between a fusiform and berry (saccular) aneurysm?
A fusiform is symmetrical in its dilation but a berry is asymmetrical
28
What causes an asymmetrical aneurysm?
one side of the blood vessel has had a higher pressure, or one side of the wall was weaker?
29
What are the two types of true aneurysm?
fusiform and saccular
30
What is a false aneurysm?
caused by a hole in vessel causing it to leak forming a pool due to the surrounding tissue keeping it in place so it looks like an aneursym
31
How big does a vessel have to be to be classed as an aneurysm?
1.5-2x the size of the original vessel
32
Where do arterial aneurysms most commonly occur?
in the aorta
33
What percentage of aortic aneurysms are in the abdominal?
60%
34
Why are most arterial aneurysms in the abdominal?
Due to there being less collagen
35
What does Laplaces law mean in aneurysms?
That as the diameter of the blood vessel gets bigger, the pressure gets bigger, it is a positive feedback loop
36
What can cause blood vessel walls to weaken?
high blood pressure
37
What are risk factors of aneurysm?
male, age, smokers, obese, alcohol, high bp
38
How can hypertension affect arterial muscle wall?
Can cause atrophy of the smooth muscle, weakening its wall
39
What are vasa vosorum?
the blood vessels that supply the outer muscle in the abdominal aorta?
40
What happens to the vasa vosorum in hypertension and how does that lead to aneurysms?
they undergo arteriosclerosis, causing their lumen to narrow so they have ischaemia, causing the muscle of the aorta to atrophy and weaken
41
How does syphilis cause an aneurysm?
causes inflammation of the vasa vasorum so the lumen narrows, restricting blood supply to the thoracic aorta causing atrophy
42
What is a mycotic aneurysm?
Where an embolic infection elsewhere in the body can travel in the blood and get stuck in intracranial, visceral or peripheral arteries (also a complication of infective endocarditis)
43
What common bacteria cause embolic mycotic aneurysm?
bacteroides fragilis, pseudomas aeurginosa, all salmonella
44
Why can some genetic disorders cause aneurysm?
because they can affect the connective tissue:fibrillin and collagen
45
What genetic disroders can cause aneurysm?
Marfan sydrome and ehlers danlos
46
How can Marfan syndrome cause an aneurysm?
impaired elastic properties in fibrillin so weakened blood vessels
47
How can Ehlers Danlos syndrome cause an aneurysm?
disrupted ability to make collagen proteins causing weakened vessel walls
48
What are two main complications of an aneurysm?
They can rupture or put pressure on another organ
49
What does rupture of an aneurysm cause?
Decreased blood flow to that tissue, causing ischaemia
50
What is a complication of a thoracic aneurysm if it is just above the aorta?
Can lead to aortic insufficiency when the aortic valve cannot close, so blood flows back into the ventricle, this also puts pressure on the left recurrent laryngeal nerve from the stretch aorta, leading to a high pitch cough
51
What happens if a aneurysm in the brain ruptures?
Bleeds into the subarachnoid space, increasing pressure on brain tissue and causing irritation on meninges, so causes a severe headache and unable to flex neck forward
52
How can an aneurysm cause a blood clot?
It can pull the blood over into the extra lumen space, so is not moving along and clots, which can lead to tissue ischemia and an embolism.
53
What are the signs of AAA?
severe pain in left flank, pulsating mass with heartbeat in that area, hypotension
54
What are the symptoms of a thoracic aortic aneurysm?
usually no symptoms, severe back and abdominal pain
55
When should you do surgery for an aneurysm?
if diameter is >5.5cm, it is expanding >1cm a year and if it is symptomatic
56
What is the treatment for an aneurysm?
stop smoking, control hypertension, lipid lowering medication, US surveillance
57
What is an aortic dissection?
part of the tunica intima of the aorta is teared off causing a tear so blood leaks between the tunica intima and tunica media separating the two layers, causes an increased diameter of the blood vessel and blood collects there
58
What is the difference between a false and true lumen in an aortic dissection?
a false lumen is the new lumen made betweeen the tunica intima and the tunica media, the true lumen is the original lumen
59
What is the cause of an aortic dissection?
chronic hypertenion from stress, increased blood volume, or coarctation (narrowing) of the aorta, weakened aortic wall, decreased blood flow to vasa vasroum, aneurysms
60
Where does the aortic dissection usually occur?
In the first 10cm of the aorta
61
What complications can an aortic dissection lead to'?
blood can back up into pericardial space causing pericardial tamponade, could bleed into a mediastinum causing death, could continue to disect until renal artery, reducing blood flow to kidneys
62
What are the symptoms of an aortic dissection?
sudden, severe, chest pain that feels like tearing, radiates to back and down arms
63
What is the treatment of an aortic dissection?
antihypertensive drugs, IV BB, vasodialators, surgery, stents
64
What is a type A aortic dissection?
involves the aortic arch and aortic valve, proximal to the left subclavian artery origin - DeBakey type 1 and 2
65
What is a type B aortic aneurysm?
involves descending thoracic aorta, distal to the left subclavian artery origin - DeBakey type 3
66
What is cardiac tamponade?
compression of the heart leading to acute cardiac failure following bleeding into the pericardial space
67
What is atherosclerosis?
hardening and narrowing of the arteries due to plaque leading to thrombus formation
68
What is arteriosclerosis?
hardening of arteries
69
What are risk factors for atherosclerosis?
age, smoking, cholesterol, obesity, hypertension, diabetes
70
Where is atherosclerosis commonly seen?
in peripheral and coronary arteries
71
Whats the distribution of atherosclerosis like along the artery?
it is focal
72
What are the symptoms of atherosclerosis in the coronary arteries?
vomiting, anxiety, angina, coughing, feeling faint
73
What is a complication of atherosclerosis in coronary arteries?
leads to reduced blood and oxygen flow to the heart muscles, causing ischemia, and a heart attack
74
What symptoms of atherosclerosis in the carotid cause?
weakness dysphea, headache, facial numbness, paralysis, leading to stroke
75
What is peripheral vascular disease?
reduced blood flow to other parts of the body, not the brain
76
What symptoms does atherosclerosis in the renal arteries cause?
reduced appetite, smaller hands and feet, increased renin release and increased blood pressure
77
What happens when a atherosclerotic plaque ruptures?
Forms a thrombus and a clot
78
What are LDLs?
low density lipoproteins
79
What does a CXR show in an MI?
cardiomegaly, pulmonary oedema, widening of mediastinum
80
What does a large amount of circulating LDLs cause?
they can deposit in the tunica intima and oxidase to activate endothelial cells causing endothelial dysfunction so they express receptors for WBCs
81
What does the accumulation of WBC to damaged endothelial cells lead to?
This allows monocytes and T helper cells to move into the tunica intima part of the vessel, to become macro-phages which take up the LDLs to become foam cells
82
What are foam cells?
macrophages, bound to LDLs, causing fatty streaks
83
What does the formation of foam cells cause?
promote migration of smooth muscle cells from tunica media into tunica intima and causes smooth muscle cell proliferation to increase collagen synthesis, so the plaque hardens
84
Once collagen is formed in the plaque, foam cells die, what does this cause?
causes the foam cells to release their LDL contents, causing plaque growth and increased pressure and release DNA which attracts neutrophils causing inflammation, also release proinflammatory cytokines, so plaque grows
85
What does growth of the plaque cause?
plaque rupture and thrombus formation from blood coagulation
86
How are LDLs oxidised in the tunica intima layer?
dysfunctional endothelial cells release ROS mediated proteases to oxidise them so that the LDL is trapped in the intima
87
What happens to monocytes when they move into the tunica initima?
they become macrophages
88
What happens to T cells in the tunica intima of an artherosclerotic plaque?
bind to adhesion molecules and form IFN-y which activates more WBCs and leucocytes to increase inflammation and cause the plaque to grow
89
What is ischemic heart disease?
coronary artery disease caused by poor or no blood flow to the heart tissue
90
What causes ischemic heart disease?
myocardial necrosis caused by an atherosclerotic plaque rupture causing an occlusion of a coronary artery causing a mycardial infarction
91
What is angina?
a temporary loss of blood supply to heart causing an mismatch of 02 supply and demand causing chest pain, due to impaired blood flow, increased distal resistance or reduced 02 carrying capacity
92
What are the main 2 types of angina?
stable, unstable
93
What is stable angina?
The plaque is a fixed size, so pain is only caused by exertion and relieved by rest
94
What is unstable angina?
Is caused by a haemodynamically unstable plaque causing thrombosis so pain still occurs at rest
95
What are risk factors for ischemic heart disease?
smoking, age, diabetes, hyperlipidaemia, obesity, genetic factors, oral contraceptive pill
96
What are the symptoms of a myocardial infarction?
nausea, sweating, palpatations, breathless, crushing chest pain for more than 20 mins, increase JVP, increased pulse, pallor, anxiety
97
What are the two types of infarction?
transmural and subendocardial
98
What can a venous blockage cause?
oedema
99
What are the 3 types of myocardial infarction?
ST elevation (STEMI), non ST elevation (NSTEMI) and unstable angina
100
Which of the 3 MIs is a retrospective diagnosis?
NSTEMI - made after troponin results
101
What does an ECG show in an MI?
either ST elevation or depression
inverted t waves
can be a Q wave present retrospectively
102
What is troponin?
a protein complex which regulates actin:myosin contraction
103
When is troponin used?
It is a sensitive marker for cardiac injury , but may not represent permanent damage
104
When does troponin appear positive?
in acute coronary syndrome, gram negative sepsis, pulonary embolism and myocarditis
105
What is a transmural infarct and how does this show on an ECG?
affects all of the myocardial wall - leading to ST elevation and Q wave
106
What is a subendocardial infarct and how does this appear on an ECG?
necrosis of a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles
ST depression
107
What methods can be used for MI treatment?
stop smoking, reduce alcohol, educate, exercise, morphine, oxygen, nitrates, anticoagulants, BBs, ACE-I, aspirin, statins, PCI, LMW heparin, clopidrogrel, GPIIb/IIIa antagonist
108
What are the complications of an MI?
cardiogenic shock, cardic arrhythmia, pericarditis, emoboli, aneurysm formation, rupture of ventricle, dresslers syndrome, rupture of free wall, papillary muscle rupture
109
What does alpha granule secretion cause?
coagulation and inflammation
110
What does dense granule secretion cause?
platelet aggregation
111
How does clopidrogrel treat MI?
it inhibits ADP dependent activation of GPIIb/IIIa complex. Requires hepatic cytochrome p450 enzymes to irreversibly bind to P2Y12 receptors on platelet membranes - used as dual platelet therapy with aspirin
112
How does percutaneous coronoary intervention treat MI?
uses a stent implantation, which is highly effective, placed in with a coronary angiography, need full dose of anticoagulation and high dose heparin
113
What is a risk of using PCI and how do you prevent this?
restenosis, prevent with toxol or slrolimus, drug eluting stents
114
How does GPIIb/IIIa anatgonist treat MI?
used with aspirin of P2Y12 inhibitors to cover P2Y12 delay e.g. Tirofiban, Abciximab
115
How does aspirin work?
causes irreversible inactivation of cyclo oxygenase 1 causing platelet aggregation inhibition also reduces PG synthesis
116
What factors can exacerbate angina?
the cold, exercise, heavy meals, increased demand (hypertension, hyperthyroidism), reduced supply (anaemia, hypoxaemia, hypothermia)
117
What are the symptoms of angina?
chest pain, breathlessness, oedema, palpitations, syncope, 4th heart sound
118
Who is most likely to get angina?
older men
119
what investigations should you do for angina?
ecg, ct scan, coronary calcium score, coronary angiography, thallium scan, cardiac catheter, myoview scan, exercise testing
120
What is ohms law and what does this mean in terms of pressure?
V=IR meaning change in pressure = QR
121
What is Poisuelles law and what does this mean?
change in P=8uLQ/pier4
meaning that nothing in the vessel is really affected until 70% of the diameter of stenosis is reached and then there is a rapid decline.
122
What is decubitus angina and how does it appear on an ECG?
caused by lying down, ST depression
123
What is a prinzmetal angina and how does it appear on an ECG?
caused by coronary artery spasm, ST elevation
124
What is the treatment of angina?
modify risk factors, nitrates, aspirin, Ca blockers, BBs, statins, PCI, coronary bypass, K channel activator, opiates
125
How is nitrates given for treatment and how does it work?
isosorbide mononitrate GTN spray causes vascular dilation to decrease preload / afterload and decrease BP
126
What are the side effects of nitrates?
headache and hypotension
127
What is a side effect of aspirin?
gastric ulceration
128
What is a side effect of Ca blockers?
ankle oedema and flushing
129
How to statins treat angina?
HMG coA reduce inhibitor, reduces cholesterol and is a lipid lowering therapy
130
What is heart failure?
the inability of cardiac output to meet the physiological demands of the body
131
What are the symptoms of heart failure?
exertional dyspnoea, orthopnoea, fatiguem tachycardia, hypotension, pleural effusion, s3 gallop, neck vein dialation
132
What are the complications of heart failure?
renal failure, valve dysfunction, stroke, death
133
What causes left ventricular heart failure?
coronary artery syndrome, hypertension, aortic/mitral valve disease and myocardial disease
134
What causes right ventricular heart failure?
left sided heart failure, tricuspid/pulmonary valve disease and pulmonary vascular disease
135
What is a consequence of right sided heart failure?
blood can be backed up into the liver and abdomen causing congestion, leading to hepatomegaly and ascites
136
What is a consequence of left sided heart failure?
blood can accumulate in the pulmonary veins, causing fluid accumulation in the lungs leading to SOB and oedema
137
What is congestive heart failure caused by?
a mix of left and right heart failure
138
What is LVSD?
heart failure due to left ventricle systolic dysfunction
139
What is HFPEF?
Heart failure due to preserved ejection fraction, diastolic failure
140
At what age are you most likely to get heart failure?
60-90years
141
What detects myocyte size?
brain natireutic peptide (BNP) shows how much they have stretched
142
What is the treatment of heart failure?
smoking cessation, weight loss, healthy diet, exercise, loop diuretics (e.g. furosemide which inhibits Na/K/2cl transporter), heart transplant, neurohumoral blockade inhibiting RAAS and SNS, ACE-I, BBs, aldosterone antagonist, ARBs (candersartan), hydralazine/nitrate combination, digoxin (direct inotropic effect to increase force of heart contraction)
143
What is the classification called for heart failure?
The New York Association Diagnosis
144
What are the 4 stages of the NYAD?
1- no limitation of physical activity (asymptomatic)
2- slight limitation (mild)
3- marked limitation (symptomatic)
4- inability to carry out physical activity
145
What does a CXR show in heart failure? (ABCDE)
```
alveolar oedema
kerley B lines
cardiomegaly
dilated upper lobe vessels
pleural effusion
```
146
What tests should you do in heart failure?
CXR, ECG, ECHO
147
Would the pre load and after load decrease or increase in heart failure?
increase
148
What is cardiomyopathy?
primary heart muscle disease, mainly genetic (autosomal dominant)
149
What are the 3 main types of cardiomyopathy?
dilated, hypertrophic and restrictive (arrhythmogenic)
150
What is dilated cardiomyopathy?
When less blood is pumped from the heart because ventricles are enlarged and weakened
151
What mutation causes dilated cardiomyopathy?
mutation in the genes of the cytoskeleton proteins
152
What can dilated cardiomyopathy lead to?
systolic heart failure with decrease ejection fraction, causing breathlessness and fatigue and conduction defect thromboembolism
153
What causes dilated cardiomyopathy?
left ventricular nonconpaction, myocarditis, toxins, autoimmune, endocrine and neuromuscular
154
How does a dilated cardiomyopathy appear?
dilated ventricles with thin walls
155
What is the treatment of dilated cardiomyopathy?
cardiac reconstruction and as you would for heart failure
156
What is hypertrophic cardiomyopathy?
Less blood pumped from the heart due to the ventricles not being able to relax
157
What mutation causes hypertrophic cardiomyopathy?
mutations of genes encoding sarcomeric proteins leading to disorganization of the cardio myocytes e.g. B myosin heavy chain MYH7 or myosin binding C MYBPC3
158
What can hypertrophic cardiomyopathy lead to?
diastolic heart failure, angina, dyspnoea, palpatations, syncope, chest pain,
159
How does a hypertrophic cardiomyopathy appear?
thick ventricle wall and thick interventriculer septum and small ventricles so ventricles cannot fill properly with blood
160
What is the most common cause of cardiac death in young people?
hypertrophic cardiomyopathy
161
How does hypertrophic cardiomyopathy appear on an ECG?
abnormal, with ventricular arrhythmia
162
What does a troponin T mutation cause?
death
163
What is a primary restrictive disease?
decreased volume of both ventricles and impaired ventricular and impaired ventricular filling
164
What is sudden arrhythmic death syndrome?
an inherited condition in young people
165
What is the appearance in restrictive cardiomyopathy?
Left ventricle maintains normal dimensions but left atrial hypertrophy and dilation and right ventricular hypertrophy due to back flow from left atria.
166
What is the mutation seen in restrictive cardiomyopathy?
mutations of the genes encoding desmosome proteins
167
What some restrictive cardiomyopathy cause?
arrhythmia
168
What is naxos disease?
fibrous fatty replacement of RV causing small hands and feet and woolly hair
169
What is an ion channelopathy?
a mutation in ion channels e.g. K, Cl, Na
170
What does an ion channelopathy cause?
inherited arrhythmia
171
What is the structure like in ion channelopathy?
normal
172
How is an ion channelopathy diagnosed?
on ECG
173
What does the ECG show in ion channelopathy?
long QT
short QT
Brugade and CPVT
174
What is CPVT?
abnormal heat of adrenergic drive arrhythmia problem
175
Who are the target groups for a cardiomyopathy screening?
close relative and athletes to allow early identification
176
What is the treatment of cardiomyopathy?
ICD, BBs, statins, vascular surgery, low sodium diet to remove backed up fluid, diuretics, ACE-1, digoxin, pacemaker
177
what are the symptoms of ion channelopathy?
recurrent syncope
178
What causes peripheral vascular disease?
atherosclerosis in the peripheral arteries, blocking blood flow
179
What can peripheral vascular disease lead to?
MI or losing a leg
180
Where does acute peripheral vascular disease affect?
Parts furthest way from the heart, e.g. the lower limbs
181
What are the symptoms of peripheral vascular disease? (6Ps)
pain, pallor, perishing cold, pulseless, paraesthesia, paralysis
182
What causes acute peripheral vascular disease?
embolic disease from thrombus or arrhythmia or thrombotic disease from arthertosclerosis
183
What is the treatment of acute peripheral vascular disease?
LMW heparin, treat underlying cause, long term warfarin in MI or AF
184
What complications can acute peripheral vascular disease lead to?
embolism, stenosis, occlusion, aneurysm, progression, haemorrhage, plaque rupture, overlying thrombosis
185
What are the risk factors for chronic peripheral vascular disease?
smoking, diabetes, hypochloesterolaemia, hypertension,
186
What are the symptoms of chronic peripheral vascular disease?
cold and dry lower limbs, poor peripheral pulses, ulceration, dark discoloration of toes
187
What does an ABPI show in intermittent claudication?
0.5-0.9
188
What does an ABPI show in critical ischemia?
189
What does an ABPI show in heavily calcified arteries?
falsely elevated
190
What is the treatment for chronic peripheral vascular disease?
manage risk factors, revascularisation if critical, low dose aspirin, exercise, control diabetes
191
What are the four stages in chronic peripheral vascular disease?
asymptomatic, intermittent claudication, rest pain/nocturnal pain, necrosis/ulceration
192
What does intermittent claudication mean in chronic peripheral vascular disease?
calf pain on exertion but relieved on rest
193
What is nocturnal pain so bad in chronic peripheral vascular disease?
means severe unremitting pain in the foot, preventing sleep and poor blood supply even at rest so definitely no blood reserve for increased demand
194
What is circulatory shock?
when the CV system has inadequate organ perfusion for aerobic cellular respiration
195
What causes circulatory shock?
low BP, low systolic, MAP
196
How is MAP calculated?
MAP = CO x systemic vascular resistance
197
What is CO calculated?
CO = SV x HR
198
What are the 3 main types of shock?
hypovolemic (non hemorrhagic and hemorrhagic),
199
How can you get non hemorrhagic hypovolemic shock?
from loss of fluid volume from high dehydration, vomiting, diarrhea etc
200
How can you get hemorrhagic hypovolemic shock?
Through blood vessels bleeding so that volume of blood decreases, decreasing EDV, SV, CO and BP
201
What happens to hormones when CO is decreased?
Catecholamines like adrenaline and noradrenaline, ADH and angiotensin II are released to cause vasoconstriction of blood vessels to increase resistance to blood flow and increase HR to increase CO.
202
What is MVO2?
The amount of O2 bound to Hb in the blood entering the right ventricle (so the amount of O2 left over not used)
203
What happens to MVO2 in hypovolemic shock?
It decreases due to less blood volume and less O2
204
What symptoms are seen in hypovolemic shock?
pale, cold, sweaty, vascoconstricted skin, weak rapid pulse, low pulse pressure, low urine output, confusion, weakness, collapse, coma, tachycardia, dehydration, skin turgor
205
What is cardiogenic shock?
The heart can't pump enough blood to tissue e.g. secondary to MI and ischemia, due to reduced muscle cells, leading to weaker contractions so decreased in SV and BP
206
What happens if there is an obstruction to the heart so it cannot fill properly e.g. fluid in chest, stab wound ?
This fluid physically constricts the heart from expanding and contracting so reduces SV (obstructive shock)
207
What is distributive shock?
A leakiness of blood vessels with lots of vasodilation, reducing resistance to blood flow and decreased blood pressure.
208
What is the most common type of distributive shock?
Septic shock
209
What is sepsis?
a systemic inflammatory response associated with an infection
210
What is septic shock?
sepsis with persistent hypo-tension, unresponsive fluid resuscitation causing vasodilation from inflammatory cytokines, causing warmth
211
Which shock is considered a warm shock not a cold shock?
septic
212
What kind of pathogen normally causes septic shock?
gram negative endotoxins
213
How do endotoxins causes septic shock?
they damage endothelial cells, causing them to release vasodilators like NO, and they activate the complement pathway to stimulate histamine release, activate macro-phages and pro inflammatory cytokines, this then damages the endothelial cells, increasing their vascular permeability, making the blood vessels leaky. Also produce tissue factor to increase clotting, which reduces perfusion and low vascular resistance so the blood returns to the heart with a high MVO2
214
Which shock increases MVO2?
septic
215
What is anaphylactic shock?
a type 1 hypersensitivity allergic reaction causing low BP
216
What is neruogenic shock?
When the nervous system is damaged causing low BP
217
What are the 3 types of distributive shock?
septic, anaphylactic, neurogenic
218
How does an anaphylactic allergic reaction cause shock?
releases histamine and vasoactive mediators without involving antibodies causing haemodynamic collapse, leading to capillary leak, wheeze, cyanosis, oedema, breathlessness, skin, mucosal uritcana and erythema
219
What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 1 haemorrhagic shock?
15% blood loss, pulse 30ml/hr, slightly anxious
220
What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 2 haemorrhagic shock?
15-30% blood loss, pulse >100bpm, normal BP, reduced PP, 20-30RR, urine output 20-30ml/hr, mild anxious
221
What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 3 haemorrhagic shock?
30-40% blood loss, pulse >120bpm, decreased PP and BP, 30-40RR, urine output 5-15ml/hr, confused
222
What is the treatment of shock?
ensure adequate O2, fluids, maintain organ perfusion, treat cause with specific therapy, ABC, ECG, antibiotics, fluid bolus, low dose steroids
223
What is a complication of shock?
ARDS
224
What is ARDS?
acute respiratory distress syndrome
225
What is ARDS caused by?
direct lung injury or secondary to severe systemic illness
226
What happens in ARDS when there is lung damage?
releases inflammatory mediators causing increased capillary permeability, non cardiogenic pulmonary oedeme and multiorgan
227
What are some extrapulmonary causes of ARDS?
shock, septicaemia, multiple transfusion, drug reaction, head injury
228
What are some pulmonary cuases of ARDS?
pneumonia, gastric aspiration, smoke inhalation, chemical pneumonitis, near drowning
229
What are the symptoms of ARDS?
cyanosis, tachypnoea, tachycardia, peripheral vasodilation
230
What is the diagnostic criteria of ARDS?
bilateral fine inspiratory crackles, pulmonary capillary wedge pressure
231
what is the treatment of ARDS?
ITU, supportive therapy, treat underlying cause, mechanical ventilation, circulatory support to maintain CO, invasive haemodynamic monitoring, sepsis organism identification, broad spectrum antibiotics, nutritional support, high fat and antioxidant formulants
232
What is the mortality of ARDS?
50-70%, based on age and cause and no. of organisms
233
What are the 3 stages of lung injury in ARDS?
exudative stage, proliferative phase, fibrotic phase
234
Why does shock reduce urine output?
reduced BP, reduces GFR
235
What is valvulitis and what is its most common cause?
inflammation of the valve, mainly cause by rheumatic heart disease
236
What is rheumatic heart disease?
Permanent damage to the heart muscle, mainly caused by rheumatic fever
237
What is rheumatic fever?
an inflammatory disease in children and young adults due to a group A streptococcus infection causing and autoimmune reaction
238
What causes rheumatic fever?
group A streptococcus infection, leading to pharyngitis causing rheumatic fever and rheumatic heart disease
239
How long after a group A streptococcus infection does rheumatic fever occur?
2-3 weeks
240
How common is rheumatic fever?
incidence has decreased due to improved sanitation, a change or virulence of the organism and the use of antibiotics
241
What are the clinical features of rheumatic fever?
fever, joint pains, loss of appetite, changing heart murmurs, mitral and aortic regurgitation, heart failure, chest pain, pericardial effusion, polyarthritis, erythema marginatum and small non tender subcutaneous nodules over the tendons and bony prominences, Sydenhams chorea
242
What will investigations show in rhuematic fever?
leucocytosis, raised ESR, high antistreptolysin O titre, and antiDNAase B
243
What is the diagnosis criteria for Rheumatic fever called?
Duckett Jones criteria
244
What is the treatment of rheumatic fever?
bed rest, high dose aspirin, penicillin to eradicate streptococcol infections, NSAIDs
245
At what age are you most likely to get rheumatic fever?
5-15 years
246
What is a normal cholesterol value?
5
247
What is familia hypercholestrolaemia?
gene abnormality so unable to uptake cholesterol so have a high cholesterol of 10
248
What does LVNC look like?
sponge like appearance of LV
249
What is the difference between a cardiac amyloid and an amyloidosis cardiomyopathy?
cardiac amyloid is related to the heart and amyloidosis is part of a systemic disorder
250
What is a sarcoid?
a chronic granulomatous disease with numerous granulomas of non caseating giant cell type, can produce widespread fibrosis and compensatory hypertrophy, produce a restrictive cardiomyopathy
251
How many types of glycogen storage disease are there?
4
252
What is mucopolysaccharosis?
where excess glycosaminoglycans are deposited in cells (Hurler syndrome)
253
In who is endomyocardial disease commonly seen?
African settings as a temperature region disorder
254
How does endomyocardial disease present?
endomyocardial fibrosis, high grade eosinophilia, rash and progressive endocarditis, cardiac failure
255
What are the ventricles like in endomyocardial disease?
stiff and poor compliant, there is grey/white layer of fibrous tissue extending onto the endocardial surfaces of ventricular cavities
256
What is myocarditis?
reflects inflammation of the myocardium, associated with muscle cell necrosis and degeneration
257
What are the potential causes of myocarditis?
virus, bacteria, metazoa, fungi, protazoa, rickettsia, hypersensitivity/immune related, radiation, sarcoid, uraemia
258
How does myocarditis appear macroscopically?
dilated
259
What happens in the cell in acute myocarditis?
lymphocyte infiltration cutting through the myocardium and destroying muscle fibres, healed by patchy fibrosis
260
What are the symptoms of myocarditis?
palpatations, latitude, upper resp tract infection, chest pain, breathlessness
261
What is giant cell myocarditis?
area of muscle cell death due to macrophage giant cells
262
What percentage of births have a cardiac deficit?
1%
263
What percentage of those with a cardiac deficit at birth have a poor prognosis?
20-25%
264
At how many weeks is the foetal echo?
18-22 weeks
265
What causes a congenital heart defect?
maternal alcohol, drugs, radiation and disease, or chromosome or genetic abnormalities
266
What is the most common congenital heart defect?
Tetrology of Fallot
267
What are the 4 main features of Tetrology of Fallot?
ventricular septal defect, overiding aorta, pulmonary stenosis and right ventricular hpertrophy
268
What is a ventricular septal defect?
A hole between the two ventricles
269
What does a ventricular septal defect lead to?
causes an abnormal blood flow of deoxygenated blood into the left ventricle, can limit blood flow to the lungs leading to pulmonary stenosis.
270
What investigations are used to detect a ventricular spetal defect?
ECG, ECHO, CXR
271
Why does a ventricular septal defect affect aorta size?
Causes increased blood flow through the left side of the heart, so aortic valve is enlarged to override the VSD so blood still enters the systemic system
272
How does a VSD affect right ventricular size?
The RV wall thickens and hypertrophies due to outflow obstruction
273
What is VSD blood shunting?
where oxygenated and deoxygenated blood becomes mixed leading to decreased oxygen in systemic system
274
How do patients with Tetrology of Fallot and VSD appear?
Bluish appearance
275
How does the heart appear in Tetrology of Fallot?
boot shaped
276
What happens to the blood flow in Eisenmegers?
there is decreased blood flow through the lungs, damaging the pulmonary vasculature, and resistance to blood flow in lungs increases, RV pressure increases, shunts from right to left causing blue appearance
277
What are the clinical signs in a small VSD?
asymptomatic, normal heart rate and size, loud systolic murmur
278
What are the clinical signs in a large VSD?
breathless, poor feeding, failure to thrive so must fix in infancy, small baby, increase RR, big heart, tachycardia, murmurs
279
What does a VSD lead to?
pulmonary hypertension and Eisenmengers complex
280
How do you treat Tetrology of Fallot and what could this lead to in adults?
surgical repair before 2y/o , good prognosis, but some adults then develop pulmonary regurgitation so must redo the surgery to relieve ventricular outflow tract
281
What is an atrial septal defect?
an abnormal connection between the two atria
282
Where is the usual place to get an atrial septal defect?
in the ostium secundum
283
What is an atrial septal defect which is closer from the bottom, and in who in this normally seen?
ostium prinium
| Downs syndrome
284
What is an atrial septal defect which comes from the top?
Sinus venosus
285
What the clinical signs in an atrial septal defect?
asymptomatic, paradoxical embolus, pulmonary flow murmur, fix split second heart sound, large pulmonary arteries and big heart
286
what causes a second heart sound in an atrial septal defect?
delayed closure of the pulmonary vein as more blood has to get out form right to left shunt
287
What does an CXR in an atrial septal defect?
big pulmonary arteries and big heart
288
What is the treatment of atrial septal defect?
surgical or percutaenous key hole to close the hole
289
What causes the shunt in atrial septal defect?
higher pressure in left atrium so shunts to right so more blood flows through the lungs
290
Do patients appear blue in atrial septal defect?
no, due to no decreased blood flow through the lungs
291
What are the symptoms of a large defect in an atrial septal defect?
SOB on exertion, increased chest infections, right heart dilation
292
What are the symptoms of a small atrial septal defect?
no dilations so no symptoms
293
What is the ductus arteriosus?
persistent communication between the proximal left pulmonary artery and the descending aorta
294
What happens to the ductus artiosus at birth?
will close due to increase in o2 from breathing and due to prostagladin production decreases
295
What would the ductus arterious remain open at birth?
a premature birth causing undeveloped lungs, increased sensitivity to prostagladins, large amount of prostagladins, mother infected with Rubella
296
What can you hear in a patent ductus arteriosus?
the sound of the blood flowing back in the pulmonary artery
297
What clinical features are seen in a patent ductus arteriosus?
widening pulse pressure (difference between systolic and diastolic pressure)
298
What is the treatment of a patent ductus arteriosus?
PG inhibitors, local anaesthetic, venous approach with AV loop, idomethacin, surgery or percutaneous, NSAIDs, coil occlusion
299
What can a patent ductus arteriosus lead to?
pulmonary hypertension, enlarged heart
300
What is a risk in small patent ductus arteriosus?
endocarditis
301
What are the symptoms in a large patent ductus arteriosus?
breathless, poor feeding, failure to thrive
302
What is an atrioventricular septal defect?
hole in the centre of the heart, so 1 big valve instead of 2 separate AV valves
303
In who is an atrioventricular septal defect common in?
Downs syndrome
304
When does a partial atrioventricular septal defect present?
in late adulthood
305
When does a complete atrioventricular septal defect present?
as a neonate
306
How does a complete atrioventricular septal defect present?
breathless neonate, poor feeding and poor weight gain,
307
What is the foramen ovale?
the septum and hole between the two atrias in the foetus
308
What happens in the patent foramen ovale?
when the forman ovale doesn't close after birth
309
Where is the patent foramen ovale usually occur?
in the osteum secundum
310
What is a paradoxical emboli?
an emboli that can get lodged in the hole in the heart and cause a CNS infarction
311
What can a patent foramen ovale lead to if not treated?
arrhythmias, pulmonary hypertension, right ventricle hypertrophy, cardiac failure, infective endocarditis risk
312
What is complete transportation of the great arteries?
when the aorta breaks off the left ventricle and comes to the right ventricle
313
What do people with complete transportation of the heart also have?
an atrial septal defect to allow communication of blood, to allow blood mixing
314
Who is most likely to get complete transportation of the heart?
males, with diabetes, diabetic mothers, Di George
315
What is the treatment of a complete transportation of the heart?
arterial switch, leading to less than 10% mortality
316
What is endocardial fibroetastosis?
profound dense collagen and elastic tissues deposited on endocardium of LV causing stiffening of the heart and heart failure
317
What causes endocardial fibroetastosis?
genetic, or complication of congenital aortic stenosis and coarction
318
What is dextocardia?
abnormal positioning of visceral organs, associated with organ isomerism
319
What is coarctation of the heart?
narrowing of the aorta at the insertion of the ductus arteriosis causing excessive blood flow being diverted through the carotid and subclavian vessels into the systemic vascular shunts to supply the rest of the body
320
In who is coarctation of the heart most commonly seen?
men are twice as likely , associated with Turner's, Berry aneurysms,
321
In coarctation of the heart is the aorta normally tricuspid of bicuspid?
bicuspid
322
What clinical features are seen in coarctation of the heart?
systemic (right arm) hypertension, bruits (buzzes) over the scapula and back, murmur, poor peripheral pulses, cold legs, headaches, nose bleeds
323
What can coarctation of the heart lead to in the long term?
hypertension, CAD, stroke, re coarctation, aneurysm at site of rupture, infective endocarditis, cerebral haemorrhage,
324
What is the appearance of coarctation of the heart on investigations?
ECHO, CXR, 3 sign and rib notching
325
What is the treatment of coarctation of the heart?
PGE1, surgical correction or balloon angioplasty
326
What are the complications of treatment of coarctation of the heart?
restenosis, dissection of aneurysm
327
What murmur is heard on coarctation of the heart?
systolic murmur in L axilla
328
What murmur is heard in ASD?
wide fixed split S2, systolic ejection at upper left SB
329
What murmur is heard in tetrology of Fallot?
systolic ejection at upper left SB
330
In who is a bicuspid AV seen more in?
males
331
Why is a biscupid AV worse?
has 2 cusps not 3 so does not last as long as can become severely stenotic, become regurgitate, coarct and degenerate
332
What is pulmonary stenosis?
narrrowing of the outflow of right ventricle (can be valvar, subvalvar, supra valvar or branch)
333
what is the treatment of a pulmonary stenosis?
balloon valvuloplasty, open valvotomy, open transannula patch, shunt to bypass the blockage
334
What are the complications in mild pulmonary stenosis?
right ventricular hypertrophy
335
What are the complications in severe pulmonary stenosis?
RV failure, poor pulmonary blood flow, RV hypertrophy, tricuspid regurgitation
336
What is mitral stenosis?
narrowing of the mitral valve of the heart, causing obsturction of LV inflow, preventing proper filling during diastole
337
How does mitral stenosis affect the atria and pulmonary vein?
causes increased pressure in the left atria and the pulmonary vein
338
In who is mitral stenosis most common?
females
339
What is the cause of mitral stenosis?
rheumatic heart disease, calcification of the valave, congenital, rheumatic arthritis, ankylosing spndylitis, SLE, malignant carcinoid
340
What is the main cause of mitral stenosis?
rheumatic heart disease
341
How does rheumatic heart disease cause mitral stenosis?
it is an inflammatory disease caused by streptococcus group A pyogenes, causing inflammation of the valves with fibrinous repair, thickening the mitral valve
342
What are the symptoms of mitral stenosis?
progressive dyspnea, AF palpatations, orthopnea, paraxysaml nocturnal dyspnoea, palpitations, chest pain, hemoptysis, ascites.
343
At what size of the mitral valve is mitral stenosis causing symptoms?
a 2cm2
344
What is the difference in area of the mitral valve in mild, moderate and severe mitral stenosis?
mild = >1.5cm2
moderate = 1-1.5cm2
severe =
345
What signs are seen in mitral stenosis?
malar flush, irregularly irregular pulse, distension of jugular veins, tapping pulse on left side/parasternal impulse due to RV hypertrophy, loud S1, rumbling midiastolic murmur, short S2 indicates more severe
346
What is the pathophysiology behind mitral stenosis?
raised LA pressure, causes LA hypertrophy and dilation, causes referred pressure to lungs, causing pulmonary hypertension, leading to RV pressure overload, RV hypertrophy and right sided heart failure
347
What will invetsigations show in mitral stenosis?
AF, LA enlargement, RV hypertrophy, prominent pulmonary arteries, Kerley B lines, TTECHO measure mitral area, cardiac catheterisation
348
What is the treatment of mitral stenosis?
diuretics for fluid overload, rate control and anticoagulants it AF, valvotomy, valve replacement, prophylaxis against IE and rheumatic fever
349
What do you use to confirm the diagnosis in mitral stenosis?
ECHO
350
What is a malar flush?
red cheeks from mitral stenosis due to CO2 retention and vasodilation
351
What is mitral regurgitation?
the backflow of blood from the LV to the LA during systole
352
What are the causes of mitral regurgitation?
infective endocarditis, rheumatic fever, mitral valve prolapse, papillary muscle rupture, myxomatous degeneration, ischemic heart disease, SLE, Marfans syndrome, Ehlers and Danlos syndrome, cariomyopathy
353
What is the pathophysiology behind mitral regurgitation?
regurgitation of blood into the LA causing LA dilation from a small increase in pressure, this causes pulmonary hypertension leading to pulmonary oedema so there is LV hypertrophy to maintain SV, leads to heart failure
354
What are the symptoms of mitral regurgitation?
dysponoea, orthopnoea, fatigue, lethargy, ascites, ankle oedema, palpitations, weight loss (cardiac cachexia)
355
What signs are heard/seen from mitral regurgitation?
deviated apex beat, systolic thrill, harsh pansystolic murmur radiating to axilla, soft S1, prominent 3rd heart sound, AF, pulmonary hypertension, heart failure, IE symptoms,
356
Is it in mitral regurgitation or mitral stenosis that intensity of sound of heart that correlates to the severity?
mitral regurgitation
357
What do investigations show in mitral regurgitation?
LA and LV enlargement, increase in CTR, valve calcification, P mitrale, AF, TOEECHO, colour doppler, cardiac catheterisation, pulmonary oedema, cardiomegaly, see valve structure
358
What is the treatment of mitral regurgitation?
conservative managment, serial ECHO, IE prophylaxis (amoxcillin), control rate and anticoagulants if AF, diuretics , surgery if deteriorating with valve repair/replacement, vasodialators,
359
At what EF would you consider surgery for mitral regurgitation treatment?
if
360
What is mitral valve prolapse?
degeneration of mitral valve so inner fibrosa layer becomes loose and fragmenty with mucopolysaccharide material accumulation
361
What happens in mitral valve prolapse?
valve cusp bows upwards so may not close properly, causing regurgitation
362
What percentage of the female population have mitral valve prolapse?
6% - but not all are symptomatic
363
What sounds are heard in mitral valve prolapse?
S3 sound on ausculation due to the snap of redundant leaflets as it proplapses in to the LA
364
How many valves does the aortic valve have?
3
365
What is aortic stenosis
outflow obstruction during systole, when the valve is 1/4 of the original size
366
Causes of aortic stenosis?
age related calcification, bicuspid aortic valve which causes local destruction and stenosis, degenerative calcification, rheumatic heart disease, dissection, aneurysm and coarctation, Williams, infected vegetations
367
When does congenital aortic stenosis usually occur?
in 30-50yrs
368
When does acquired aortic stenosis usually occur?
in 70-80 years
369
What kind of stenosis is seen in children?
supravalvular stenosis
370
What is the pathophysiology behind an aortic stenosis?
obstructed LV outflow causes an increased LV pressure, with compensatory LV hypertrophy leading to LV myocardium ischemia, angina, arrhythmias and LV failure, resulting in a reduced CO
371
What are the 3 main symptoms seen in aortic stenosis?
syncope, angina and dyspnoea
372
does infection endocarditis usually cause regurgitation or stenosis?
regurgitation
373
What are the sign of an aortic stenosis?
carotid pulse, sinus rhythm, small volume, slow rising
systolic thrill in aortic
apex is sustained
ejection click, soft A2, paradoxically split s2, possible s4
ejection systolic murmur radiating to carotids
Heyders syndrome
374
What will investigations show in aortic stenosis?
Lv hypertrophy, thickened calcified immobile cusps, CXR, TTECHO, cariac catheterisation, MRI, CT
375
What is the treatment of aortic stenosis?
if symptomatic - AV replacement
asymptomatic - regular review and serial echo
dental hygiene, TAVI, control BP, vasodilation meds
376
What is aortic sclerosis?
Valve thickening without outflow obstruction
377
What is the area of a normal aorta?
3-4 cm2
378
What is the area of a mild, moderate and severe aortic stenosis?
mild=>1.5cm2
moderate=1-1.5cm2
severe=
379
What is TAVI??
transcutaenous aortic valve implantation which is a non surgical, minimal invasive catheter up the aorta, passing a balloon acorss the narrow valave to damage the valve and cause regurgitation, then another catheter with a metabllic cage is put above the natural valve
380
When is TAVI preferred over surgery?
for co morbidities, has a good prognosis and is less invasive
381
What is aortic regurgitation?
an incompetence of the aortic valve causing blood to flow back into the left ventricle during diastole
382
What are the acute causes of aortic regurgitation?
cusp rupture, infective endocarditis, connective tissue disease, aortic dissection, perforation secondary to infection, rheumatic fever
383
What are the chronic causes of aortic regurgitation?
connective tissue disease, autoimmune diseases (RA, SLE, takayau arteritis), ankylosing spondylitis, sphylis
384
What is the pathophysiology behind aortic regurgitation?
reflux of blood into LV leads to LV hypertrophy to maintain CO, then leads to reduced diastolic blood pressure causing reduced coronary perfusion, and increased myocardium metabolic demand leading to cardiac ischemia
385
What are the main symptoms of aortic regurgitation?
palpitations, angina, dyspnoea, fatigue, sudden cardiac death
386
What signs are seen in aortic regurgitation?
collapsing or bounding pulse, wide pulse pressure, deviated apex beat, high pitched early diastolic murmur at left sternal edge in 4th intercostal space with patient leaning forward and breath held in expiration
387
What will investigations show in aortic regurgitation?
LV hypertrophy, ECHO, CXR
388
What is the treatment of aortic regurgitation?
treat underlying cause, antibiotics, vasodilators, inotropes, aortic valve replacement, surgery
389
What causes a low pitched mid diastolic murmur with opening snap?
mitral stenosis
390
What causes a harsh pansystolic murmur radiating to axilla?
mitral regurgitation
391
What causes a decrescendo early diastolic murmur?
aortic regurgitation
392
What causes a crescendo-decrescendo ejection systolic murmur that radiates to the carotids?
aortic stenosis
393
What causes a waterhammer pulse and a wide pressure pulse?
aortic regurgitation
394
What causes a slow rising pulse and a narrow pulse pressure?
aortic stenosis
395
What causes a displaced apex beat?
Mitral regurgitation
396
What causes an irregular irregular pulse if in AF?
mitral regurgitation
397
What causes a malar flush with a tapping apex beat , a hoarse voice and an irregularly irregular pulse if in AF?
mitral stenosis
398
What percentage of the world have hypertension?
25%
399
What is stage 1 hypertension?
140-159/90-99mmHg
400
What is classed as pre hypertension?
120-139/80-89mmHG
401
What is a normal BP?
90-119/60-79mmHg
402
What is stage 2 hypertension?
160-179/100-109mmHg
403
What is stage 3 hypertension?
>180/>110mmHg
404
What is isolated systolic hypertension?
When systolic BP is hypertensive but diastolic isnt. and vice versa for isolated diastolic
405
What effect does hypertension have on blood vessels?
causes damage to the endothelial cells, leading to tears, MI, aneuryms etc
406
What percent of hypertension are primary?
90%
407
What are the risk factors for hypertension?
old age, obesity, high salt diets, lack of exercise
408
What causes secondary hypertension?
atherosclerosis, vasculitis, aortic dissections, fibromuscular dysplasia, tumour that secrets aldosterone
409
What happens when BF is lowered to the kidneys?
the kidneys secrete renin so the kidneys can retain more water in the arteries so they are more full, so there is increased hypertension
410
How does fibromuscular dysplasia cause hypertension?
in young women, causing the artery walls to thicken
411
What is classed at benign hypertension?
stage 1 and 2 which causes no immediate symptoms
412
What is classed at malignant hypertension?
stage 3 which can cause organ failure
413
What can untreated hypertension lead to?
eye problems, MI, stroke, renal failure
414
What antihypertenisve drugs are available?
ACE-I, angiotensin receptor blockers, B blockers, calcium channel blockers, a-1-adrenoreceptor blockers, centrally acting antihypertensives and direct renin inhibito, diuretics, endothelin antagonists
415
How do alpha-1-antagonists treat hypertension?
prevent function of alpha 1 and alpha 2 receptors in the post synpatic cells like on the smooth muscle e.g.doxazosn blocks binding site of neuroadrenaline so no contraction so lowers blood pressure
416
How do ACE-I treat hypertension?
blocks the conversion of angiotensin 1 to angiotensin 2 in the lung, but by doing this increases bradykinin
417
What is the function of angiotensin 2?
cause aldosterone release to increase salt reabsorption and retention, and causes vascular hypertrophy and hyperplasia and increased peripheral resistance via vasoconstriction
418
Examples of ACE-I?
ramipril, enalapril, trandolapril, lisinopril, inudapril, catotopril
419
How do angiotensin receptor blockers treat hypertension?
Block angiotensin 2 receptors, preventing angiotensin 2 function
420
Side effects of ARBs?
renal failure, first dose hypotension, hyperkalaemia, rash, angiooedema
421
When are ARBs contraindicated?
in renal artery stenosis, concurrent NSAIDs and pregnancy
422
Examples of ARBs?
candesartan, valsartan, telmisartan, eposartan
423
When are ACE-I contraindicated?
renal artery stenosis, concurrent NSAIDs, pregnancy
424
What are the side effects of ACE-I?
due to decreased angiotensin 2 = hypotension, acute renal failure, hyperkalaemia, tetratogenic effects in pregnancy
due to increased angiotensin 1 = cough, rash, anaphylactoid reaction
425
How do Beta Blocks treat hypertension?
block the action of the receptors that cause contraction, and the selectivity is relative non absolute
426
Examples of B1 selective BBs?
metranolol, bisoprol
427
Examples of B2 selective BBs?
propanolol, nadalol, carvedilol
428
Examples of non selective BBs?
atenolol
429
side effects of BBs?
HF, heart block, cold peripheries, fatigue, headaches, sleep disturbance, bradycardia, hypotension, erectile dysfunction
430
When are BBs contraindicated?
unstable HF, heart block, asthma, concurrent verapamil, COPD, pulmonary complications (due to B2 receptors in the lungs that normally cause bronchodialation)
431
When are BBs preferred for hypertension?
good in the young or those who are contraindicated or intolerant to ACE-I
432
How do calcium channel blockers treat hypertension?
inhibit contraction of vascular smooth muscle, myocytes and conduction of the heart leading to a decrease in blood pressure.
433
What are the 3 main types of CCBs and how do each work??
dihydropyridines - vasodialtors
phenylakyamines - negatively chonotrophic and negatively inotropic
benzothiazipines - intermediate heart/vascular effects
434
Examples of CCBs?
amiodipine, nifedipine, diltvazen
435
Examples of dihydropyridine CCBs?
nifedipine, amlodipine
436
Examples of phenylakyamine CCBs?
verapamil
437
Lifestyle change to treat hypertension?
diet, physical exercise, biofeedback, relaxation, meditation, low sodium,
438
When are CCBs the preferred treatment for hypertension?
When over 55 or in Afro Caribbean, they are the 1st stage treatment
439
What is the first stage treatment for hypertension if under 55 or not afro caribbean?
ace-i or arbs
440
What is the treatment for stage 2 hypertension?
ace-1/arb with ccb
441
What is the treatment for stage 3 hypertension?
add a thiazide diuretic to the meds
442
What is the treatment for stage 4 hypertension?
potenially add a spironolactone, or a high dose thiazine diuretic
443
What are the 4 types of diuretics?
thiazides, loop, aldosterone angiotensins or potassium
444
Example of thiazide diuretic?
bendrofluemethiazide
445
Example of loop diuretics?
frusemide
446
Example of potassium diuretic?
spironolactone
447
How do thiazide diuretics treat hypertension?
block sodium reabsorption at the distal convoluted tubule, given at loss dose, decreases potassium
448
Side effects of thiazide diuretics?
renal failure, hypovalemic
449
Contraindications of thiazide diuretics
kidney stones?, pre existing gout
450
How do centrally acting medications treat hypertension?
act directly on the sympathetic nervous system to reduce peripheral reisistance and reduce cardiac output
451
What is malignant hypertension?
fibrinoid necrosis of the vessel with local inflammation and focal smooth muscle proliferation
452
What is Monckeberg medial sclerosis?
degenerative calcification of large and medium sized arteries
453
What is fibromuscular dysplasia?
abnormal architecture for the arteries producing variable lumen narrowing and distal poverty of circulation. Occurs in the renal arteries, producing renal vascular insufficiency and progressive hypertension due to RAAS.
454
What is phaeochromocytoma?
rare tumour of the SNS, that secretes catecholamines, noradrenaline, adrenaline and their metabolites
455
In how man cases of hypertension does phaeochromocytoma occur?
1/1000
456
What is phaechromocytoma called if not in the adrenal medulla?
paragangliomas
457
symptoms of phaechromocytoma?
pallor, palpatations, panic, pain
458
in large phaechromocytoma tumours, what is mainly produced?
noradrenaline
459
What causes phaechromocytoma?
genetics, bilateral adrenal, malignant, extra adrenal
460
What is Conn's syndrome?
cuases 60% of primary hyperaldosterone cases, which causes increased in aldosterone which account for 5-10% of all hypertenisve cases
461
What is Cushings syndrome?
increased cortisol from ACTH
462
What are the main causes of Cushings syndome?
cushings disease (increased ACTH from pituitary), ectopic tumour producing AcTH, adrenal tumour, nodular hyperplasia
463
What are the clinical features of Cushings syndrome?
pigmentation of skin, cushingoid appearance, hypertension
464
What is the treatment of cushings syndrome?
BBs
465
What causes renal artery stenosis?
fibromuscular disease of renal arteries and atherosclerotic renovascular disease
466
what is tachycardia?
fast heart rate >100bpm
467
What is sinus tachycarida?
a raised heart beat which is expected e.g. from exercise - caused by the bodys requirement for more o2
468
What is a premature ventricular contraction?
a single beat originating from the ventricles
469
What is defined as a ventricular tachycardia?
3 beats in a row that are PVC
470
What can ventricular tachycardia lead to?
sudden death
471
symptoms of ventricular tachycardia?
chest pain, fainting, dizziness, shortness of breath
472
What are the two types of ventricular tachycardia?
focal or reentrant
473
What is focal ventricular tachycardia?
part of the ventricle has abnormally fast automaticity rate which is faster than the sino atrial rate so the heartbeat is being driven by the ventricles
474
What is automaticity rate?
the frequency at which a cell sends out a signal
475
What can cause ventricular tachycardia?
medications, illicit drugs, electroylyte imbalance, ischaemia to ventricular muscle
476
What is reentrant ventricular tachycardia?
caused by mismatch of refractory periods and conduction times in cariomyocytes
477
What is a monomorphic ventricular tachycardia?
when all the QRS complexes are the same duration
478
What kind of ventricular tachycardia has a monomorphic pattern?
reentrant or focal if one group of cells is responsible
479
What is a polymorphic ventricular tachycardia?
the shape of the QRS complex changes because the signal is originating from different points in the venticles
480
When is a polymorphic ventricular tachycardia seen?
in focal ventricular tachycardia when multiple parts are affected e.g. in severe hypoxia
481
What is a complication of ventricular tachycardia?
ventricular fibrillation
482
What is the treatment of ventricular tachycardia?
drug or electrical cardioversion
483
What is electrical cardioversion?
Where it pulse is set to be delievered to the heart on the R wave to avoid it being delievered during a vunerable period in the T wave which could cause fibrillation
484
What is a radiofrequency catheter ablation?
Radio frequency waves are used to heat up and destroy the tissue causing the irregular heartbeat
485
What is an implantable cardioverter defibrillator?
delivers electrical cardioversion
486
What happens in supraventricular tachycardia?
the SA node is overriden by another part of the heart which controls the pulse
487
What kind of heart beat occurs in supraventricular tachycardia?
a fast regular heart beat, constant PR interval, narrow QRS
488
What are the 3 types of supraventricular tachycardia?
atrioventricular nodal reentry, atrial and Wolff Parkinson White syndrome
489
Which is the most commmon supraventricular tachycardia?
Atrioventricular nodal reentry - there is a short circuit in the centre of the heart
490
At what age are you most likely to get Atrioventricular nodal reentry?
20-30years
491
Where does atrial tachycardia arise from?
the atria - no underlying cause
492
What causes Wolff Parkinson syndrome?
congenital abnormality
493
What are the symptoms of Wolff Parkison syndrome?
palpitations, severe dizziness or syncope
494
In which supraventricular tachycardia is there an accessory pathway between atria and ventricles?
the wolff parkinson syndrom
495
What are the symptoms of supraventricular tachycardia?
tachycardia, palpitations, dizziness, breathlessness, chest discomfort, asymptomatic
496
What are the features of atrial fibrillation?
absent p wave, narrow QRS complex, irregular rhythm, varying rate
497
What is the most important kind of atrial fibrillation?
the permanent one which is long standing over a year and not terminated by cardioversion
498
What are the causes of atrial fibrillation?
hypertension, coronoary artery disease, valve disease, hyperthyroidism,
499
What investigations should be done for atrial fibrillation?
ECG, ECHO, CXR, routine bloods
500
what is the treatment of atrial fibrillation?
BB or CCB, electrical cardioversion, rhythm control pharmacology, thromboprophylaxis, digoxin, maintain sinus rhythm with flecainide, amiodarome, sotalol and dronedarone
501
What score can be used for thromboprophylaxis in atrial fibrillation?
CHA2DS2-VASc score
502
What can be used as thromboprophylaxis?
warfarin
503
How many types of heart block are there?
3
504
What is seen in a first degree heart block
a prolonged P-R interval (>200ms)
505
How long is a p wave and pr interval?
120-200ms
506
What are the 2 types of 2nd degree heart block?
Mobitz 1 (Wenckeback) and Mobitz 2
507
What is seen in a Wenckeback heart block?
gradual progressive P-R prolongation before a QRS is dropped
508
What is seen in a Mobitz 2 heart block?
the same P-R interval followed by an absent QRS complex
509
What is seen in a 3rd degree heart block?
There is no association between P wave and QRS complex
510
What are the causes of first degree heart block?
athletes, myocarditis, hypokalaemia, hypomagnesaemia, medications
511
What are the causes of second degree heart block?
athletes, post MI, lyme disease, medications
512
What are the causes of 3rd degree heart block?
complication of heart surgery, coronary heart disease, radiotherapy, injection, hypertension, medications
513
What are the symptoms of first degree heart block?
asymptomatic
514
What are the symptoms in a Wenckebach heart block?
light headedness, dizziness, syncope
515
What are the symptoms in a Mobitz 2 heart block?
chest pain, shortness of breath, tiring on exertion, postural hypotension
516
What are the symptoms of a third degree heart block?
light headedness, dizziness, fainting, fatigue, chest pain, slow heart beat (bradycardia)
517
What is the management of a heart block?
a pacemaker
518
What is an ectopic beat?
an arrhythmia which is not sustained arising from the atira or ventricles, normally benign, symptoms of skipped or missed beats
519
In what pattern do ectopic beats occur?
in couplets/triplets or in bigeminy/trigeminy
520
What type of tachyarrhythmia is associated with a narrow QRS complex?
supraventricular
521
What is the most commmon sustained arrhythmia?
atrial fibrillation
522
What are the two types of atrial fibrillation?
paroxysmal (self terminates) or persistant
523
What are the symptoms of atrial fibrillation?
palpitations, breathlessness, chest pain, fatigue, stroke risk
524
What new types of oral agents are there to treat atrial fibrillation?
Direct Xa inhibitors and Direct thrombin inhibiotrs
525
Examples of direct Xa inhibitors?
Rivaroxaban and apixaban
526
Examples of direct thrombin inhibitors?
Dabigatran
527
What is an atrial flutter?
often coexists with atrial fibrillation, can be paroxysmal or persistent
528
What are the 3 types of narrow complex tachycardias?
atrioventricular nodal reentry, atrioventricular reentry, focal atrial tachycardia
529
In who is atrioventricular nodal reentry tachycarida most common?
females in their 20s
530
What is an accessory pathway?
a congenital remnant muscle strand between the ventricle and the atria, can be manifest or concealed
531
What kind of complex is in atrioventricular reentry tachycardia?
narrow or broad
532
What are the two types of broad complex tachycardias?
ventricular tachycardia or supraventricular tachycardia with bundle branch block or pre excitation
533
Which is more dangerous VT or SVT?
VT so treat this if in doubt and the patient is unstable , if stable, then work it out
534
What causes a diseased ventricle?
MI, cardiomyopathy
535
What is the difference between william and marrow?
left bundle branch block and right bundle branch block
536
What is the diagnosis if atrial activity can be seen or looks less typical looking?
ventricular tachycardia
537
When can a normal heart VT be seen?
younger patients with a structurally normal heart, have a better prognosis
538
What are the typical patterns seen in a normal heart VT?
outflow tract Vt or fascicular VT
539
What is long QT syndrome?
rare condition where delayed repolarization of the heart following a heartbeat increases the risk of torsades de pointes
540
What can trigger long QT syndrome?
stress, sudden noise, strenuous exercise, slow heart rate during sleep
541
What causes long QT syndrome?
delayed flow of potassium ions out the hearts muscle, so each heart beat takes longer to rest itself, can be inherited or drug induced
542
What is the treatment of long QT syndrome?
BBs, pacenaker, ICD, potassium rich foods
543
What is infective endocarditis?
infection of the endocardium involving the heart valves and vegetation of infectious agents, causing holes in the heart valves mainly in the mitral valve
544
what organisms cause infective endocarditis?
```
streptococcus viridans
staphylococcus aureus
staphylococcus epidermidis
diphtheroids
microaerophilic streptococci
haemophilius actinobacillus cardiobacterium eikenella kingela (HACEK)
```
545
What criteria is used for infective endocarditis?
Dukes criteria
546
What is classed as infective endocarditis in the dukes criteria?
2 major, 1 major and 3 minor or 5 minor
547
What are major factors in dukes criteria?
2 separate positive blood cultures
| endocardial involvement
548
What are the minor factors in dukes criteria?
```
fever >38
IV drug user/predisposing heart condition
immunological phenomena
vascular phenomena
echocardiograph findings
```
549
What are the 5 types of infective endocarditis?
```
L native IE
L prosthetic IE
R IE (right is rarely prosthetic)
Device IE
Prosthetic IE
```
550
What investigations should be done for infective endocarditis?
blood cultures - 3 separate cultures from 3 peripheral sites
bloods for anaemia
urinalysis, shoes microscopic haematuria
CXR
ECHO - for vegetations (TOE is better than TTE for looking for vegatations and if the patient is ventilated
ECG
raised ESR, Ig and cryoglobins
551
What symptoms will infective endocarditis show?
fever, roth spots, osler nodes, new murmur, janeway lesions, anemia, nail splinters and haemorrhages, emboli
552
What are janeway lesions?
painless papules on palms and plantars
553
What are osler nodes?
painful nodules on fingers and toes
554
What complications can infective endocarditis lead to?
heart fialure, arrhythmias, abscess formation incardiac muscle, emboli formation, stroke, vision loss, infection spread
555
What are the main sites of vegetations in infective endocarditis??
atrial surface of AV valves
ventricular surfaces of semilunar valves
jet lesion in a shunt including venous or pulmonary side of AV fistula
556
What is non bacterial thrombotic endocarditis?
sterile thrombotic deposit on valves with variable valve dysfunction in patients, neoplastic conditions and degenerative valve disease
557
In who is infective endocarditis more common?
females
558
What is the 10year survival for infective endocarditis?
60-90%
559
What are risk factors for infective endocarditis?
elderly, young IV drug abusers, young with congenital heart disease, prosthetic heart valves, rheumatic heart disease, dental treatment, poor dental hygiene
560
What is the mortality for infective endocarditis?
30-40%
