Chest Pain Flashcards
1
Q
What is the angle of Louis? Where is it? What is its clinical significance
A
sternal angle
between t4-t5
marks the point at which the costal cartilages of the second rib articulate with the sternum. This is particularly useful when counting ribs to identify landmarks as rib one is often impalpable.
2
Q
What systems can cause chest pain
A
cvs
respiratory
msk
gastro
3
Q
What is pleuritic chest pain
A
chest pain on inspiration
4
Q
Pathologies to think about in chest pain (CVS) important
A
MI
Aortic dissection
pericarditis
angina (stable and unstable)
5
Q
Pathologies to think about in chest pain (resp) important
A
PE
Pneumothorax
6
Q
Pathologies to think about in chest pain (msk) important
A
costochondritis
muscle strain / pull
7
Q
pathologies to think about in chest pain (gastro) important
A
peptic ulcer
indigestion
GERD
8
Q
athletes ecg
A
can be abnormal but benign - Can have t wave inversions and st elevations
9
Q
how to calculate hr in ecg
A
look at rhythm strip (lead II)
divide the number of large boxes (5 mm or 0.2 seconds) between two successive QRS complexes into 300.
10
Q
typical evolution of the ECG changes seen in an ST-elevation myocardial infarction, starting with hyper-acute T-waves and ending with pathological Q-waves
A
Normal hyper acute t waves ST segment elevation improvement with ST elevation with repurfusion T wave inversion pathological q waves
11
Q
typical ECG changes in stable angina
A
usually normal between attacks. During an attack there may be a transient ST segment depression, symmetrical T wave inversion or tall, pointed, upright T wave may appear. If the angina is provoked by exertion, an exercise stress ECG should be performed.
12
Q
typical ECG changes in ACS (acute coronary syndrome)
A
Although the ECG may be completely normal in a patient with myocardial ischemia and evolving infarction, classic ECG changes occur in STEMI. 14 Within minutes, there is J-point elevation, and tall, peaked, “hyperacute” T waves develop; ST-segment elevation and reciprocal-lead ST-segment depression also occur.1
13
Q
ECG changes in first degree heart block
A
here is delay, without interruption, in conduction from atria to ventricles
‘Marked’ first degree heart block is present if PR interval > 300ms
14
Q
ECG changes second degree heart block Mobitz type II
A
A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval
(PR intervals are consistent but some P waves do not conduct) - you get a normal looking P and QRS and then a random p sometimes without a QRS
15
Q
ECG changes second degree heart block Mobitz type I
A
increasing delay of AV nodal conduction until a P wave fails to conduct through the AV node. This is seen as progressive PR interval prolongation with each beat until a P wave is not conducted. There is an irregular R-R interval.
16
Q
ECG findings in atrial fibrillation
A
Irregularly irregular rhythm
No P waves
Absence of an isoelectric baseline
Variable ventricular rate
QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm)
Fibrillatory waves may mimic P waves leading to misdiagnosis
17
Q
ECG changes suggestive of PE (including S1 Q3 T3)
A
A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain
18
Q
Normal BP
A
120/80
19
Q
pre hypertension bp
A
systolic: 120–139 mm Hg diastolic: 80–89 mm Hg
20
Q
hypertension bp
A
systolic: 140 mm Hg or higher diastolic: 90 mm Hg or higher
21
Q
hypotension bp
A
systolic blood pressure to less than 90 mm Hg or mean arterial pressure of less than 65 mm Hg. It may be relative to a decrease in diastolic blood pressure to less than 40 mm Hg.
22
Q
define accelerated hypertension
A
defined as a recent significant increase over baseline BP that is associated with target organ damage. This is usually seen as vascular damage on funduscopic examination, such as flame-shaped hemorrhages or soft exudates, but without papilledema.
23
Q
retinal changes in accelerated hypertension
A
retinal vascular damage caused by hypertension. Signs usually develop late in the disease. Funduscopic examination shows arteriolar constriction, arteriovenous nicking, vascular wall changes, flame-shaped hemorrhages, cotton-wool spots, yellow hard exudates, and optic disk edema.
24
Q
Complications of hypertension (serious)
A
stroke
retinopathy (damage to retina vasculature)
MI
Aortic dissection
abdominal aortic dissection
left ventricular hypertrophy and nephropathy
25
recognise Left ventricular hypertrophy on ECG
Voltage Criteria
Limb Leads
R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
S wave in aVR > 14 mm
Precordial Leads
R wave in V4, V5 or V6 > 26 mm
R wave in V5 or V6 plus S wave in V1 > 35 mm
Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria
Increased R wave peak time > 50 ms in leads V5 or V6
ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
26
aortic dissection symptoms
Sudden severe chest or upper back pain, often described as a tearing or ripping sensation, that spreads to the neck or down the back.
Sudden severe stomach pain.
Loss of consciousness.
Shortness of breath.
27
abdominal aortic aneurysm rupture symptoms
sudden, severe pain in the tummy or lower back. dizziness. sweaty, pale and clammy skin.
28
physiology of left coronary blood flow
left coronary artery (LCA) arises from the left posterior aortic sinus and quickly bifurcates into the left circumflex artery (LCX) and left anterior descending artery (LAD), which supply blood to the left atrium and left ventricle
29
physiology of right coronary blood flow
right coronary artery (RCA), arising from the anterior aortic sinus, supplies blood to the right atrium, right ventricle, sinoatrial node, atrioventricular (AV) node, and select portions of the left ventricle.
30
define atherosclerosis
thickening or hardening of the arteries. It is caused by a buildup of plaque in the inner lining of an artery. Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin. As it builds up in the arteries, the artery walls become thickened and stiff.
31
four stages of atherosclerosis
1) endothelial tissue injury: damage can occur from smoking, diabetes, abnormal level of cholesterol and other lipid, and force (hypertension)
2) Lipoprotein deposition: lipoprotein molecules can gain entry where they are then modified by oxidation (via free radicals or oxidizing enzymes) or glycation (in diabetes). This modified lipoprotein, or LDL, is inflammatory and able to be ingested by macrophages, creating “foam cells” and causing a “fatty streak” in the arterial wall.
3) inflammatory reaction: The modified LDL is antigenic and attracts inflammatory cells into the arterial wall. Also, after endothelial injury, inflammatory mediators are released further, increasing leukocyte recruitment.
4) smooth muscle cell cap formation: Smooth muscle cells migrate to the surface of the plaque, creating a “fibrous cap.” When this cap is thick, the plaque is stable; however, thin capped atherosclerotic plaques are thought to be more prone to rupture or erosion, causing thrombosis.
32
concept of ischaemic heart disease
term given to heart problems caused by narrowed heart arteries. When arteries are narrowed, less blood and oxygen reaches the heart muscle. This is also called coronary artery disease and coronary heart disease.
33
Compare and contrast stable angina with acute coronary syndromes.
Stable angina is a chest discomfort due to myocardial ischemia that is predictably reproducible at a certain level of exertion or emotional stress. The spectrum of ACS includes unstable angina (UA), non–ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI).
Stable angina - brought on by exertion
ACS - more blockage - brought on by anything!
34
invasive and un-invasive treatments for MI
These aims can be achieved medically using intravenous (i.v.) thrombolysis or invasively either with intracoronary (i.c.) thrombolysis, percutaneous transluminal coronary angioplasty (PTCA), or bypass surgery.
35
what is thrombolysis
also called fibrinolytic therapy, is the breakdown of blood clots formed in blood vessels, using medication. It is used in ST elevation myocardial infarction, stroke, and in cases of severe venous thromboembolism.
the “clot-busting” drug will be delivered through a peripheral intravenous (IV) line, usually through a visible vein in your arm.
36
Potential complications of MI
```
arrhythmias
ventricular wall aneurysm
ventricular wall rupture
mitral valve prolapse
Dressler’s syndrome
thromboembolic complications.
```
37
what is Dressler's syndrome
is a type of inflammation of the sac surrounding the heart (pericarditis). Dressler syndrome is believed to be an immune system response after damage to heart tissue or to the sac surrounding the heart (pericardium)
38
what percentage of people are right coronary artery dominant ?co-dominant? left posterior descending?
RCA - 70%
co - 20%
left - 10%
39
atherosclerotic constitutional risk factors
age
gender (earlier age and greater frequency in males compared to females)
genetics
40
atherosclerotic modifiable risk factors
hypertension (> risk of IHD by 60%)
hyperlipidaemia/hypercholesteramia
smoking
diabetes
41
describe stable angina (likely symptoms)
```
pain over sternum radiating to left shoulder/ arm, jaw, tongue, teeth
pain duration from seconds to hours
sharp, sticking, stabbing, knifelike
obstruction >60-70%
relieved by rest
ECG normal or ST segment depression
no cardiac biomarkers (troponin, CRP)
```
42
What is a CABG
coronary artery bypass graft
43
what are lipids
organic biomolecules which are soluble in non-polar solvents and much less soluble in water
they themselves are non-polar
44
major lipids in the plasma are
fatty acids
TAG - triacylglyerols/triglycerides
cholesterol
phospholipids
45
discuss triaclyglycerols
form of storage of energy (more efficient than glycogen)
formed in liver and adipose tissue
metabolism of them is regulated via triglyceride lipase
46
discuss cholesterol (few facts)
is a component of membranes
bile acids - synthesised in the liver and stored in gallbladder
involved in vitamin d synthesis
involved in steroid synthesis (aldosterone, cortisol and sex hormones)
47
what is HMG CoA reductase
stage in cholesterol synthesis where statins come in
| statin is the enzyme inhibitor to stop the synthesis of cholesterol
48
what do lipoproteins consist of
consist of a non-polar core and a surface layer of phospholipids, cholesterol and apolipoproteins
49
what do apolipoproteins do
let body work out which lipoproteins are which
50
are chylomicrons TAG rich or cholesterol rich
TAG rich
51
are LDL TAG rich or cholesterol rich
cholesterol rich
52
5 lipoproteins
```
chlymicrons
VLDL
IDL
LDL
HDL
```
53
chylomicrons description
major transport of dietary fat (exogenous)
90% TAG
TAG removed from them by lipoprotein lipase
also transports cholesterol and fat-soluble vitamins
54
How does the body get rid of chlyomicrons
by the liver
55
VLDL description
-very low density lipoprotein
principal transport form of endogenous TAG
formed in the liver
TAG removed by LPL, similar to chylomicrons - making IDL (intermediate density lipoprotein)
more TAG removed with hepatic TAG lipase to form LDL
56
LDL description
-low density lipoprotein
formed from VLDL via IDL
10% TAG 50% cholesterol
binds to LDL receptors on cell membranes, then are broken down releasing cholesterol
uptake of LDL in the arterial wall contributes to atherosclerosis
LDL = bad cholesterol
57
HDL description
high density lipoprotein
synthesised in liver (and gut) - initially as nascent hdl (disc shaped)
carry cholesterol from adipose tissue to the liver and to tissues for steroid hormone synthesis
HDL = good cholesterol, want high proportion of this on blood tests
58
3 lipid disorders
familial hypercholesterolaemia
type III hyperlipidaemia
hypertriglyceridaemia
59
describe familial hypercholesterolaemia
| gene? raised what? mutations affecting what?
autosomal dominant
raised cholesterol - usually TAG level is normal
several mutations affecting the LDL receptor pathway
genetic testing is available in UK
60
signs of familial hypercholesterolaemia
```
tendon xanthomata (swelling of knuckles, knees or achilles tendon)
xanthelasmata (small clumps of cholesterol near inner corner of eye)
corneal arcus ( pale white ring around iris)
```
61
define pathgnomonic
(of a sign or symptom) specifically characteristic or indicative of a particular disease or condition.
62
management of familial hypercholesterolaemia
refer to lipid clinic
cascade testing (to identify relatives with it)
start high intensity statin treatment
include diet and lifestyle advice
63
describe type III hyperlipoproteinaemia
| gene, polymorphism of? what are increased? signs? treatment?
```
autosomal recessive
polymorphism of APOE2
cholesterol and TAG are increased
signs: palmar xanthomata ( in creases of palms) and eruptive xanthomata on knees and elbows
generally responsive to diets or statins
```
64
causes of primary hypertriglyceridaemia
familial combined hyperlipidaemia
| polygenic hypertriglcyeridaemia
65
causes of secondary hypertriglyceridaemia
uncontrolled diabetes
hypothyroidism
alcohol related liver disease
66
most common side effect of statins
muscle pain
67
what does the drug ezetimibe do
decreases absorption of cholesterol from the gut
not licensed for first line use - but can be used in combination with statins for patients with familial hypercholesteramia
68
describe primary prevention of lipid lowering therapy
lifestyle modification, address other CVS risks
| if risk assessment indicates then start atorvastatin 20mg when >10% risk of developingCVD in 10 years
69
describe secondary prevention of lipid lowering therapy
start atorvastatin 80mg unless lower dose is indicated
| do not delay treatment to manage modifiable risk factors
70
why is myoglobin used as a marker for myocardial necrosis
its released earlier from damaged cells than other cardiac markers allowing for earlier detection of acute MI
71
troponin as a cardiac marker
type of protein found in the heart
only found in the blood when the heart muscle is damaged
indicator of damage but not an indicator of the mechanism to which its damaged
72
potassium effect on heart
keeps heart beating at the right pace
| helps to control electrical signals in the myocardium
73
effects of hypokalaemia and hyperkaleamia on the heart
causes arrhythmias
74
what is myositis
name for a group of rare conditions. The main symptoms are weak, painful or aching muscles. This usually gets worse, slowly over time. You may also trip or fall a lot, and be very tired after walking or standing.
can be caused by statins
75
9 potentially modifiable risk factors for CVD
```
smoking
poor diet
hypercholesteramia
hypertension
insufficient physical activity
obesity
diabetes
stress
excess alcohol consumption
```
76
assessment tool for CVD
QRISK3 - use an online calculator
77
Diagnostic criteria for MI
rise and/or fall in cardiac biomarkers & one of following:
symptoms of ischaemia
new significant ST changes or new LBBB
development of pathological Q wave on ECG
imaging evidence of new loss of viable myocardium
identification of intracoronary thrombus by angiography
78
ECG changes in hyperkalaemia
tented t waves, reduced P wave amplitude
79
causes of hyperkalaemia
acute kidney injury
chronic kidney disease
drugs - (potassium-sparing diuretics, ACE Inhibitors, NSAIDS
mineralocorticoid deficiency (Addison disease)
80
hypokalaemia and the heart
increases the gradient across the cardiac cell membrane -increases the action potential and therefore reducing cardiac excitability
may cause arrhythmia's such as AF
81
ecg changes in hypokalaemia
reduced t waves
st depression
prolonged PR interval
82
causes of hypokalaemia
gastrointestinal loss - vomiting or diarrhoea
endocrine conditions - increased mineralocorticoid activity (conn's disease, Cushing syndrome)
diuretics - non potassium sparing
insulin treatment with no potassium supplementation
83
causes for secondary hypertension
```
chronic kidney disease
renovascular hypertension (renal artery stenosis)
phaeochromocytoma (excess adrenaline)
Conn's syndrome (excess aldosterone)
Cushing syndrome (excess cortisol)
Acromegaly (excess GH)
Coarction of the aorta
pregnancy
```
84
lab investigations for hypertension
```
plasma creatinine
plasma potassium
urinalysis for protein
plasma renin/aldosterone
dexamethasone suppression test
urinary catecholamines
```
85
how does chronic kidney disease cause secondary hypertension
because of fluid retention
86
how does phaeochromocytoma cause secondary hypertension
produces too much adrenaline and noradrenaline
| because of stimulation of cardiac beta adrenoreceptors
87
how does conn's or cushings syndrome cause secondary hypertension
excess aldosterone causes sodium retention
88
6 complications of hypertension
1. stroke
2. heart failure
3. kidney disease
4. eye disease
5. diabetes
6. pre-eclampsia
89
what is considered normal blood pressure?
systolic of 120-129
| diastolic of <80-84
90
what is considered high normal blood pressure?
130-139 systolic
| 85-89 diastolic
91
blood pressure reading of hypertension
```
grade 1 (mild): systolic 140-159 and diastolic 90-99
grade 2 (moderate): systolic 160-179 and diastolic 100-109
grade 3 (Severe): >180 systolic and >110 diastolic
```
92
primary hypertension
90-95% of cases - termed "essential" or "idiopathic"
93
secondary hypertension
| some examples of what cause it
about 10% of cases
- renal or renovascular disease
- endocrine disease: phaeochomocytoma (tumour of adrenal medulla), Cushings syndrome (excess cortisol), Conn's syndrome (excess aldosterone), Acromegaly (excess growth hormone), hypo/hyper thyroidism, pregnancy, coarctation of aorta, iatrogenic (contraception/HRT)
Secondary high blood pressure (secondary hypertension) is high blood pressure that's caused by another medical condition
94
does hypertension cause hypertrophy
yes
95
What determines blood pressure
MAP=CO x TPR
| mean arterial pressure = cardiac output x total peripheral resistance
96
what is the physiological role and source of Nitric Oxide (Vascular SM relaxation mediators)
physiological role: paracrine mediator
| source: endothelium
97
what is the physiological role and source of Atrial Natriuretic Peptide (ANP) (Vascular SM relaxation mediators)
physiological role: reduce BP
| source: atrial myocardium, brain
98
what is the physiological role and source of Vasoactive intestinal Peptide (VIP)
(Vascular SM relaxation mediators)
physiological role: digestive secretion and relax smooth muscle
Source: neurons
99
What is the physiological role and source of histamine
| Vascular SM relaxation mediators
physiological role: increase blood flow
| source: mast cells
100
what is the physiological role and source of adrenaline
| Vascular SM relaxation mediators
physiological role: increase flow to skeletal muscle, heart and liver
source: adrenal medulla
101
what is the physiological role and source of Ach (via NO and decreased NA)
(Vascular SM relaxation mediators)
physiological role: erection
| Source: parasympathetic nerves
102
what is the physiological role and source of bradykinin
| Vascular SM relaxation mediators
physiological role: increases local blood flow via NO
| source: tissues
103
what is the physiological role and source of adenosine
| Vascular SM relaxation mediators
physiological role: increases blood flow to match metabolism
| source: hypoxic cells
104
What is the physiological role and source of prostanoids
| Vascular SM relaxation mediators
physiological role: relaxation and/or contraction in various tissues
source: autocrine/paracrine
105
ACD algorithm for drugs for hypertension
Younger than 55years then give A which is ACE inhibitors as first line
over 55yrs or black patients of any age give C (Ca channel blockers) or D (Diuretics) as first line
Second line: give A+C or A+D
Third line: A+C+D
Fourth line: Add either: further diuretic therapy or alpha-blocker or beta-blocker or consider seeking specialist advice
106
Brief description of ACE inhibitors as used for regulation of BP
(including two commonly used ones, and some side effects)
Long term control of BP involves renin angiotensin aldosterone system (RAAS)
angiotensin is a vasoconstrictor
catopril and enalapril are prototypic drugs
Side effects: Rash, hyperkalaemia, taste disturbances, first dose hypotension
(Angiotensin-converting enzyme (ACE) inhibitors are medications that help relax the veins and arteries to lower blood pressure. ACE inhibitors prevent an enzyme in the body from producing angiotensin II, a substance that narrows blood vessels)
107
describe calcium channel blockers in regulating BP
lower BP
prevent calcium from entering cells of heart and arteries
calcium causes heart and arteries to contract more frequently
by blocking calcium, calcium channel blockers allow blood vessels to relax and open
Dihydropyridines - Nifedipine, Amlodipine
108
Side effects of calcium channel blockers in regulating BP
peripheral oedema
| dizziness
109
3 classes of diuretics and some examples and strength
loop agents (examples: furosemide, bumetanide) - powerful.. up to 30% filtered Na
Thiazide (example: hydrochlorothiazide) - mild diuretic effect <10% filtered Na
K sparing (Examples: Amiloride, Spironolactone) - weak diuretics <5% filtered Na
110
Describe thiazides (diuretics) drugs
a drug that increases urine flow
act directly on the kidneys and promote diuresis (urine flow) by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron (functional unit of a kidney)
They decrease sodium reabsorption which increases fluid loss in urine, which in turn decreases extracellular fluid and plasma volume
it reduces cardiac output and lowers blood pressure
111
side effects of thiazide (diuretic) drugs
| and what can it reduce the efficacy of
electrolyte disturbances
decrease glucose tolerance
can reduce efficacy of anticoags and uricosurics -(substances that increase the excretion of uric acid in the urine, thus reducing the concentration of uric acid in blood plasma.)
can increase LDL and cholesterol
112
beta blockers effect on the heart
(also known as beta adrenergic blocking agents)
they reduce blood pressure
block effects of hormone adrenaline
cause heart to beat more slowly and with less force, also help to widen veins and arteries to improve blood flow
113
examples of beta blockers
Bisoprolol
Atenonol
Propranolol
114
When are beta blockers used (or not)
not used to treat ONLY high blood pressure, only used when diuretics haven't worked etc.
```
used to prevent, treat or improve symptoms of:
Arrhythmia
Heart failure
Angina
Heart attacks
Migraine
certain types of tremors
```
115
three common side effects of beta blockers
cold feet/hands
weight gain
fatigue
116
how do direct renin inhibitors work
block the enzyme renin from triggering a process that helps regulate blood pressure (the angiotensin-aldosterone system)
so blood vessels relax and widen, making it easier for blood to flow through the vessels
117
Causes of heart failure
volume overload: valve regurgitation
pressure overload: systemic hypertension, outflow obstruction
loss of muscle: post MI, chronic ischaemia, connective tissue diseases, infection, poisons
restricted filling: pericardial diseases, restrictive cardiomyopathy, tachyarrhythmia
Chronic heart failure
118
define pathophysiology
the disordered physiological processes associated with disease or injury
119
pathophysiology of heart failure
```
inadequate tissue perfusion
volume overload
oedema
enlarged ventricles
spherical shape
reduced efficacy
```
120
what does RAP stand for (chest pain case)
right atrial pressure
121
what drugs for HF improve the symptoms
nitrates (acute treatment to quickly reduce RAP - right atrial pressure)
potent diuretics (loop agents to reduce RAP)
ACE inhibitors
Digoxin
(Digoxin is a type of drug called a cardiac glycoside. Their function is to slow your heart rate down and improve the filling of your ventricles (two of the chambers of the heart) with blood. For people with atrial fibrillation, where the heart beats irregularly, a different volume of blood is pumped out each time.)
122
Nitrates and HF
they dilate the blood vessels of the heart to reduce stress on heart
they have a direct relaxant effect on vascular smooth muscle
example: mononitrate, isosorbide dinitrate
123
what is Digitalis drug?
made from plant foxglove that stimulates heart muscle
124
digitalis drug actions
2 up 2 down rule
for heart
increased force
increased excitability
decreased A-V conduction
decreased rate
125
when to use digitalis
indicated when heart failure with atrial flutter/fibrillation
more likely to be given to older sedentary patients
long half life means careful titration of patient does is indicated
126
what are receptor sympathomimetics
agents which in general mimic responses due to stimulation of sympathetic nerves. These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing noradrenaline and adrenaline (mediators of the sympathoadrenal system) levels.
127
what is a pulmonary embolism
thrombus within the pulmonary arterial circulation
usually arises from embolisation of proximal DVT from lower limb through R heart
128
virchows triad
hypercoagulability
endothelial injury
venous stasis
129
what does CTEPH stand for
chronic thromboembolic pulmonary hypertension
130
Describe CTEPH
chronic thromboembolic pulmonary hypertension
chronic breathlessness, hypoxia and right sided heart failure
caused by obstruction of major pulmonary arteries
clots are replaced by fibrous tissue
lifelong anticoags are recommended
131
symptoms of a PE
breathlessness (Dyspnoea)
chest pain ( can be pleuritic or non pleuritic)
haemoptysis
syncope or pre-syncope (loss of consciousness or feeling faint)
fever
unilateral leg swelling (if associated with a DVT)
palpitations
generally low grade fever
132
clinical signs of a PE
tachycardia
tachypnoea
hypotension (its a severe PE as it effects L heart CO)
hypoxia
right heart strain
unremarkable respiratory exam
rarely pleural rub (late and rare feature as part of lung has died)
133
5 aims of clinical assessment and investigations of a PE
1. does the patient have a pe?
2. severity of pe (high, intermediate or low mortality risk)
3. why has patient had a clot (risk factors for VTE or underlying cause)
4. any cautions or contraindications to anticoagulants?
5. other important considerations (suitability for outpatient management)?
134
What scoring system do you use to assess likelihood of PE (think MDCalc)
Wells score for PE
135
Clinical investigations of suspected PE
D -Dimer: VTE very unlikely if wells score is unlikely and negative D-Dimer
Arterial blood gas (if done): may be normal but could also be hypoxia, hypocapnia and respiratory alkalosis
Other blood tests of: FBC, renal, liver, clotting, troponin, CRP and Ca2+
136
PE manifestation on a ECG
S1Q3T3
Deep S wave in lead I ( the first downward deflection of the QRS complex that occurs after the R wave.)
Q wave in lead III
inverted T wave in lead III
137
what scan is usually used to confirm diagnosis of PE
CTPA
| (CT pulmonary angiogram) performed with contrast material
138
CXR to diagnose PE
```
usually shows normal CXR
rarely can show:
-reduced vascularity in peripheral lung
-enlargement of central pulmonary artery
-pleural based area of increased opacity
-wedge shaped infarct
```
139
when would you use VQ SPECT or planar scan to diagnose PE
may be considered if CXR is normal and young patient (esp women of childbearing age) or contraindication to CT (e.g. contrast allergy or severe renal impairment)
140
What to do if suspected PE with wells score of more than 4 points but CTPA negative
DVT suspected so consider proximal leg vein US
| or DVT not suspected so stop any anticoags and think about other diagnoses
141
criteria for haemodynamic instability
- cardiac arrest
- systolic BP <90mmHg
- Vasopressors required to achieve a BP>90mmHg despite an adequate filling status, in combination with end organ hypoperfusion
- systolic BP drop of >40mmHg for >15min, not caused by new onset arrhythmia, hypovolaemia or sepsis
142
What scoring system do you use to assess mortality risk of PE
```
sPESI
-Simplified Pulmonary Embolism Severity Index
-Includes:
Age (<80(0),>80(+1))
history of cancer: no(0), yes (+1)
history of chronic cardiopulmonary disease: no(0), yes(+1)
heart rate bpm: <110(0), >110(+1)
Systolic BP mmHg: >100 (0), <100 (+1)
O2sats: >90%(0), <90%(+1)
```
143
What to do with a patient who has an acute PE, is on anticoagulants but is haemodynamically unstable
reperfusion treatment and haemodyamic support
144
Preferred anticoagulants for PE
rivaroxaban and Apixaban (can be initiated without heparin)
145
When is outpatient management of a PE not suitable
- HR>110, systolic BP <100, requirement for inotropes, critical care, thrombolysis or embolectomy
- SaO2 <94%
- Evidence of R heart dysfunction
- Active bleeding or risk of major bleeding
- On anticoagulants at time of PE
- Severe pain (requiring opiates)
- Other co-morbidities requiring hospital admission
- Chronic kidney disease
146
Talk about anticoagulant dose and duration for a VTE
initial treatment for acute PE: 3-6 months (therapeutic dose)
after that decision is who stays on them long term and who doesn't: balance risk of long term bleeding and recurrence
147
difference between a therapeutic dose and a prophylactic dose
therapeutic: quantity which is required to elicit the desired therapeutic response in the individual in the treatment of disease or ailment.
prophylactic: A preventive measure. The word comes from the Greek for "an advance guard," an apt term for a measure taken to fend off a disease or another unwanted consequence.
148
patient with a provoked PE: how long should you keep them on anticoagulants
3-6 months
149
patient with an unprovoked PE or persistent risks: how long should you keep them on anticoagulants
consider long term
150
How many days before an operation should you stop warfarin
5 days before
151
how many days before an operation should you stop DOACs
2 days before
152
low bleeding risk operation examples
dental extraction
joint injection
cataract surgery
low risk endoscopies
153
medium and high bleeding risk operation examples
medium - most surgery
| high - neurosurgery
154
how does a PE cause RVD (right ventricular dysfunction)
a PE results in a rapid increase in pulmonary vascular resistance which leads to pulmonary hypertension (PH) that only reverses with the lysis of the vascular blockage or the failure of the RV contractile function
155
Investigation and management options of Non Cardiac Chest Pain (NCCP)
careful history and examination
ECG
blood tests including cardiac biomarkers
CXR
156
Causes on non-cardiac chest pain (Generally)
```
Lung pathology
MSK chest pain
Abdominal pathology
systemic inflammatory disorders
medically unexplained chest pain
```
157
structures that would give rise to MSK chest pain
```
skin and subcutaneous tissue
ribs
tendons and ligaments
intercostal muscles
diaphragm
nerves
```
158
characteristics of MSK chest pain
```
worse with movement
reproducibility
chest wall tenderness
pleuritic
little or no physiological compromise
```
159
Causes of MSK chest pain
```
strains and sprains (coughing, vomiting, trauma)
Costochondritis
Tietze Syndrome
Fibromyalgia
Rheumatological disease
```
160
Treatment options for MSK causes of chest pain
anti inflammatories are the main stay of treatment
| advice and reassurance
161
what is costochondritis
inflammation where your ribs join your breastbone. It causes sharp pain in the middle of your chest.
often gets better within a few weeks
not sure what causes it: can be from excessive coughing, chest injury or strain due to exercise
162
what is Tietze syndrome
rare, inflammatory disorder characterized by chest pain and swelling of the cartilage of one or more of the upper ribs (costochondral junction), specifically where the ribs attach to the breastbone (sternum). Onset of pain may be gradual or sudden and may spread to affect the arms and/or shoulders.
163
what is fibromyalgia
Fibromyalgia is a condition that causes widespread pain and extreme tiredness.
Symptoms of fibromyalgia vary from person to person. The main symptom is pain all over your body.
There's no cure for fibromyalgia, but treatments like painkillers, talking therapies and exercise programmes may help ease some of your symptoms.
It's not clear what causes fibromyalgia. It can start after a stressful event like an injury, illness or the death of a loved one.
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abdominal pathology causing chest pain
```
peptic ulcer disease
perforated viscus
choelcystitis
pancreatitis
biliary colic
oesophageal spasm
```
165
what is peptic ulcer disease
Peptic ulcers are open sores that develop on the inside lining of your stomach and the upper portion of your small intestine. The most common symptom of a peptic ulcer is stomach pain. Peptic ulcers include: Gastric ulcers that occur on the inside of the stomach.
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Causes of peptic ulcer disease
Helicobacter pylori infection
- secretes urease to create an alkaline environment
- commonest cause of PUD
non-steroidal anti-inflammatory
- protective mucus secretion is stimulated by prostaglandins
- NSAIDs, corticosteroids and aspirin interfere with Prostaglandin synthesis
stress
lifestyle
rare syndromes
167
symptoms of peptic ulcer disease
epigastric pain
-classically upper abdominal and associated with mealtimes
bloating
water brash (when your body makes too much saliva, causing it to mix with your stomach acid and back up into your throat.)
nausea
loss of appetite
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what happens in haemorrhage of a peptic ulcer
haematemesis (vomiting blood)
melaena
syncope
breathlessness
169
what happens in perforation of a peptic ulcer
full-thickness ulceration through the GI wall
- digestive secretions, food and gas leak into abdominal cavity
- chemical and bacterial peritonitis ensues
severe, sharp unremitting abdominal pain
-diaphragmatic pain can cause shoulder/chest pain
managed with emergency surgery
170
what if familial mediterranean fever
inherited disorder of pyrin
-found in granulocytes, mediates inflammatory cytokine release
causes attacks of painful inflammation of various organs
- accompanied by fever
- first attack usually by age 20
171
what kind of body attacks (inflammation?) do you get with familial mediterranean fever
```
classically affects abdomen - peritonitis
joint attacks - synovitis
skin - erysipeloid eruptions
pleuritis
pericarditis
```
172
management of familial mediterranean fever (FMF)
acute attacks
- self-limiting
- treatment is supportive - analgesia, antipyretics(reduces fever), fluids
Prophylaxis
colchicine - reduces attack frequency and amyloid deposition
amyloid (an abnormal protein that is produced in your bone marrow and can be deposited in any tissue or organ. Amyloidosis frequently affects the heart, kidneys, liver, spleen, nervous system and digestive tract. )
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Acute chest syndrome in a sickle crisis
```
vaso-occlusive crisis of the pulmonary vasculature
second most common crisis type
accounts for 25% deaths in sickle cell disease
features include:
-pleuritic chest pain
-dyspnoea
-fever
-cough +/- sputum, haemoptysis
```
174
clues pointing to non-cardiac aetiology on presentation of chest pain
```
pleuritic pain
chest wall tenderness
"non-anginal" chest pain - not related to exertion or onset at rest
little or no effect on anti-anginals
younger age
psychiatric co-morbidities
```
