Passmedicine Notes With Key Points Passmedicine

Passmedicine Notes With Key Points Passmedicine
download
https://ebookbell.com/product/passmedicine-notes-with-key-points-
passmedicine-56153512
Explore and download more ebooks at ebookbell.com

Here are some recommended products that we believe you will be
interested in. You can click the link to download.
Passmedicine Qbank All Subjects Passmedicine
https://ebookbell.com/product/passmedicine-qbank-all-subjects-
passmedicine-51722980
Hematology Mrcp I Passmedicine 2024 Passmedicine
https://ebookbell.com/product/hematology-mrcp-i-
passmedicine-2024-passmedicine-58435850
Mrcp I Rheumatology Passmedicine 2024 Passmedicine
https://ebookbell.com/product/mrcp-i-rheumatology-
passmedicine-2024-passmedicine-58454354
Mrcp I Passmedicine Passmedicine
https://ebookbell.com/product/mrcp-i-passmedicine-
passmedicine-58459720

Mrcp I Passmedicine Qbank Passmedicine
https://ebookbell.com/product/mrcp-i-passmedicine-qbank-
passmedicine-58485462
Passmedicine Mrcp Ii Hematology Mcqs Passmedicine
https://ebookbell.com/product/passmedicine-mrcp-ii-hematology-mcqs-
passmedicine-91092356
Passmedicine Mrcp Ii Endocrinology Mcqs No Cover Passmedicine
https://ebookbell.com/product/passmedicine-mrcp-ii-endocrinology-mcqs-
no-cover-passmedicine-91094770
Passmedicine Mrcp Ii Ecg Practicepdf Passmedicine
https://ebookbell.com/product/passmedicine-mrcp-ii-ecg-practicepdf-
passmedicine-232329992
Cardiology Mrcp Passmedicine Part I Passmedicine
https://ebookbell.com/product/cardiology-mrcp-passmedicine-part-i-
passmedicine-232928602

P
a
s
s
m
e
d
i
c
i
n
e

N
o
t
e
s

W
i
t
h

k
e
y

P
o
i
n
t
s

U
p
l
o
a
d
e
d

B
y

M
e
d
b
o
o
k
s
v
n
.
o
r
gUploaded by medbooksvn.org

Cardiology
Acute coronary syndrome: a very basic introduction
Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of
ischaemic heart disease.
Itcovers a number of presentations, including
ST elevation myocardial infarction (STEMI)
non-ST elevation myocardial infarction (NSTEMI)
unstable angina
Before we go into more detail into these presentations it's useful to take a step back and consider
how such conditions develop.
ACS generally develops in patients who have ischaemic heart disease, either known or previously
undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and
coronary artery disease. It describes the gradually build up of fatty plaques within the walls of the
coronary arteries. This leads to two main problems:
1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium
at times of increased demand. This results in angina, i.e. chest pain due to insufficient
oxygen reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the
endothelium may rupture leading to sudden occlusion of the artery. This can result in no
blood/oxygen reaching the area of myocardium.
Remember that there are a large number of factors which can increase the chance of a patient
developing ischaemic heart disease:
Unmodifiable risk factors Modifiable risk factors
Increasing age
Male gender
Family history
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity
Pathophysiology
Ischaemic heart disease is a complex process which develops over a number of years. A number of
changes can be seen:Uploaded by medbooksvn.org

initial endothelial dysfunction is triggered by a number of factors such as smoking,
hypertension and hyperglycaemia
this results in a number of changes to the endothelium including pro-inflammatory, pro-
oxidant, proliferative and reduced nitric oxide bioavailability
fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
monocytes migrate from the blood and differentiate into macrophages. These macrophages
then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages
die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in
formation of a fibrous capsule covering the fatty plaque.
Diagramshowing the progression of atherosclerosis in the coronary arteries with associated complications on the
right
Slide showing a markedly narrowed coronary artery secondary to atherosclerosis. Stained with Masson's trichrome.Uploaded by medbooksvn.org

Complications ofatherosclerosis
Once a plaque has formed a number of complications can develop:
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause
reduced blood flow and hence oxygen to the myocardium, particularly at times of increased
demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This
may result in a myocardial infarction
Ruptured coronary artery plaque resulting in thrombosis and associatedmyocardial infarction.
Pathological specimen showing infarction of the anteroseptal and lateral wall of the left ventricle. There is a
background of biventricular myocardial hypertrophy.Uploaded by medbooksvn.org

Symptoms and signs
The classic and most common feature of ACSis chest pain.
typically central/left-sided
may radiate to the jaw or the left arm
often described as 'heavy' or constricting, 'like an elephant on my chest'
it should be noted however in real clinical practice patients present with a wide variety of
types of chest pain and patients/doctors may confuse ischaemic pain for other causes such
as dyspepsia
certain patients e.g. diabetics/elderly may not experience any chest pain
Other symptoms in ACS include
dyspnoea
sweating
nausea and vomiting
Patients presenting with ACS often have very few physical signs to ellicit:
pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly
altered e.g. tachycardia
if complications of the ACS have developed e.g. cardiac failure then clearly there may a
number of findings
the patient may appear pale and clammy
Investigations
The two most important investigations when assessing a patient with chest pain are:
ECG
cardiac markers e.g. troponin
ECG showing a ST elevation myocardial infarction (STEMI). Note by how looking at which leads are affected (in this
case II, III and aVF) we are able to tell which coronary arteries are blocked (the right coronary artery in this case). A
blockage of the left anterior descending (LAD) artery would cause elevation of V1-V4, what is often termed an
'anterior' myocardial infarction.Uploaded by medbooksvn.org

ECG showing a non-ST elevation myocardial infarction (NSTEMI). On the ECG there is deep ST depression in I-III,
aVF, and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high
mortality because it signifies severe ischemia usually of LAD or left main stem.
The table below shows a simplified correlation between ECG changes andcoronary territories:
ECG changes Coronary artery
Anterior V1-V4 Left anterior descending
Inferior II, III, aVF Right coronary
Lateral I, V5-6 Left circumflex
Diagram showing the correlation between ECG changes and coronary territories inacute coronary syndromeUploaded by medbooksvn.org

Management
Once a diagnosis of ACS has been made there are a number of elements to treatment:
prevent worsening of presentation (i.e. further occlusion of coronary vessel)
revascularise (i.e. 'unblock') the vessel if occluded (patients presenting with a STEMI)
treat pain
A commonly taught mnemonic for the treatment of ACS is MONA:
Morphine
Oxygen
Nitrates
Aspirin
Whilst useful it should be rememberthat not all patients require oxygen therapy. British Thoracic
Society guidelines are now widely adopted and oxygen should only be given if the oxygen
saturations are < 94%.
For patients who've had aSTEMI(i.e. one of the coronary arteries has become occluded) the priority
of management is to reopen, or revascularise, the blocked vessel.
a second antiplatelet drug should be given in addition to aspirin. Options include clopidogrel,
prasugrel and ticagrelor
for many years the treatment of choice was thrombolysis. This involved the intravenous
administration of a thrombolytic or 'clot-busting' drug to breakdown the thrombus blocking the
coronary artery
since the early 2000's thrombolysis has been superseded by percutaneous coronary
intervention (PCI). In this procedure the blocked arteries are opened up using a balloon
(angioplasty) following which a stent may be deployed to prevent the artery occluding again
in the future. This is done via a catheter inserted into either the radial or femoral artery
If a patient presents with anNSTEMIthen a risk stratification too (such as GRACE) is used to decide
upon further management. If a patient is considered high-risk or is clinically unstable then coronary
angiography will be performed during the admission. Lowerrisk patients may have a coronary
angiogram at a later date.
Secondary prevention
Patients who've had an ACS require lifelong drug therapy to help reduce the risk of a further event.
Standard therapy comprises the following as a minimum:
aspirin
a secondantiplatelet if appropriate (e.g. clopidogrel)
a beta-blocker
an ACE inhibitor
a statinUploaded by medbooksvn.org

Further images
The following images show the progress of coronary artery atherosclerosis:
Normal coronary artery with blood in the lumen.
Slightlystenosed coronary arteryUploaded by medbooksvn.org

Moderately stenosed coronary artery, beetween 50-75%
Severely stenosed coronary artery
Recanalised old atherothrombotic occlusion of a coronary artery. Numerous small neolumina recanalising the
organisedoccluding thrombus (indicated with arrows)Uploaded by medbooksvn.org

Acute coronary syndrome: management of NSTEMI
NICE produced guidelines in 2013 on theSecondary prevention in primary and secondary care for
patients following a myocardial infarction management of unstableangina and non-ST elevation
myocardial infarction (NSTEMI). These superceded the 2010 guidelines which advocated a risk-
based approach to management which determined whether drugs such as clopidogrel were given.
All patients should receive
aspirin 300mg
nitrates or morphine to relieve chest pain if required
Whilst it is common that non-hypoxic patients receive oxygen therapy there is little evidence to
support this approach. The 2008 British Thoracic Society oxygen therapy guidelines advise not
giving oxygen unless the patient is hypoxic.
Antithrombintreatment. Fondaparinux should be offered to patients who are not at a high risk of
bleeding and who are not having angiography within the next 24 hours. If angiography is likely within
24 hours or a patientscreatinine is > 265 µmol/l unfractionated heparin should be given.
Clopidogrel300mg should be given to all patients and continued for 12 months.
Intravenousglycoprotein IIb/IIIa receptor antagonists(eptifibatide or tirofiban) should be given to
patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-
month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of
hospital admission.
Coronary angiographyshould be considered within 96 hours of first admission
to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be
performed as soon as possible in patients who are clinically unstable.
The table below summaries the mechanism of action of drugs commonly used in the management of
acute coronary syndrome:
Medication Mechanism of action
Aspirin Antiplatelet-inhibits the production of thromboxane A2
ClopidogrelAntiplatelet-inhibits ADP binding to its platelet receptor
Enoxaparin Activates antithrombin III, which in turn potentiates the
inhibition of coagulation factors Xa
FondaparinuxActivates antithrombin III, which in turn potentiates the
inhibition of coagulation factors Xa
BivalirudinReversible direct thrombin inhibitorUploaded by medbooksvn.org

Acute coronary syndrome: prognostic factors
The 2006 Global Registry of Acute Coronary Events (GRACE) study has been used to derive
regression models to predict death in hospital and death after discharge in patients with acute
coronary syndrome
Poor prognostic factors
age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class*
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segmentdeviation
*Killip class-system used to stratify risk post myocardial infarction
Killip classFeatures 30 day mortality
I No clinical signs heart failure6%
II Lung crackles, S3 17%
III Frank pulmonary oedema 38%
IV Cardiogenic shock 81%Uploaded by medbooksvn.org

Acutepericarditis
Pericarditis is one of the differentials of any patient presenting with chest pain.
Features
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia
Causes
viral infections (Coxsackie)
tuberculosis
uraemia (causes 'fibrinous' pericarditis)
trauma
post-myocardial infarction, Dressler's syndrome
connective tissue disease
hypothyroidism
ECG changes
widespread'saddle-shaped' ST elevation
PR depression: most specific ECG marker for pericarditis
© Image used on license fromDr Smith, University of Minnesota
ECG showing pericarditis. Note thewidespread nature of the ST elevation and the PR depressionUploaded by medbooksvn.org

Adult advanced life support
The following is based on the 2015 Resus Council guidelines. Please see the link for more details,
below is only a very brief summary of key points.
Major pointsinclude:
ratio of chest compressions to ventilation is 30:2
chest compressions are now continued while a defibrillator is charged
during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have
restarted after the third shock and thenevery 3-5 minutes (during alternate cycles of CPR).
atropine is no longer recommended for routine use in asystole or pulseless electrical activity
(PEA).
a single shock for VF/pulseless VT followed by 2 minutes of CPR, rather than a series of 3
shocks followed by 1 minute of CPR
if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then
the 2015 guidelines recommend 'up to three quick successive (stacked) shocks', rather than
1 shock followed by CPR
asystole/pulseless-electrical activity should be treated with 2 minutes of CPR prior to
reassessment of the rhythm
delivery of drugs via a tracheal tube is no longer recommended
following successful resuscitation oxygen should be titrated to achieve saturations of 94-
98%. Thisis to address the potential harm caused by hyperoxaemia
Angina pectoris: drug management
The management of stable angina comprises lifestyle changes, medication, percutaneous coronary
intervention and surgery. NICE produced guidelines in 2011 covering themanagement of stable
angina
Medication
all patients should receive aspirin and a statin in the absence of any contraindication
sublingual glyceryl trinitrate to abort angina attacks
NICE recommend using either a beta-blocker or a calicum channel blockerfirst-line based on
'comorbidities, contraindications and the person's preference'
if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or
diltiazem should be used. If used in combination with a beta-blocker then use along-acting
dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that
beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart
block)
if there is a poor response to initial treatment then medication should be increased to the
maximum tolerated dose (e.g. for atenolol 100mg od)
if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel
blocker and vice versa
if a patient is on monotherapy and cannot toleratethe addition of a calcium channel blocker
or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine,
nicorandil or ranolazine
if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third
drug whilst a patient is awaiting assessment for PCI or CABGUploaded by medbooksvn.org

Nitrate tolerance
many patients who take nitrates develop tolerance and experience reduced efficacy
the BNF advises that patients who develop tolerance should take the second dose of
isosorbidemononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate
levels to fall for 4 hours and maintains effectiveness
this effect is not seen in patients who take modified release isosorbide mononitrate
Ivabradine
a new class of anti-anginal drug which works by reducing the heart rate
acts on the If('funny') ion current which is highly expressed in the sinoatrial node, reducing
cardiac pacemaker activity
adverse effects: visual effects, particular luminous phenomena, are common. Headache.
Bradycardia, due to the mechanism of action, may also be seen
there is no evidence currently of superiority over existing treatments of stable angina
Angiotensin II receptor blockers
Angiotensin II receptor blockers are generally used in situationswhere patients have not tolerated an
ACE inhibitor, usually due to the development of a cough.
Examples
candesartan
losartan
irbesartan
Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-
effects include hypotension and hyperkalaemia.
Mechanism
block effects of angiotensin II at the AT1 receptor
Evidence base
shown to reduce progression of renal disease in patients with diabetic nephropathy
evidence base that losartan reduces CVA and IHD mortality in hypertensive patientsUploaded by medbooksvn.org

Angiotensin-converting enzyme inhibitors
Angiotensin-converting enzyme (ACE) inhibitors are now the established first-line treatment in
younger patients with hypertension and are also extensively used to treat heart failure. They are
known to be less effective in treating hypertensive Afro-Caribbean patients. ACE inhibitors are also
used to treat diabetic nephropathy and have a role in secondary prevention of ischaemic heart
disease.
Mechanism of action:
inhibit the conversion angiotensinI to angiotensin II
Side-effects:
cough: occurs in around 15% of patients and may occur up to a year after starting treatment.
Thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
Cautions and contraindications
pregnancy and breastfeeding-avoid
renovascular disease-significant renal impairment may occur in patients who have
undiagnosed bilateral renal artery stenosis
aortic stenosis-may result in hypotension
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)-
significantly increases the risk of hypotension
hereditary of idiopathic angioedema
Monitoring
urea and electrolytes should be checked before treatment is initiated and after increasing the
dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors.
Acceptable changes are an increase in serum creatinine, up to 30%* from baseline and an
increase in potassium up to 5.5 mmol/l*.
*Renal Association UK, Clinical KnowledgeSummaries quote 50% which seems rather high. SIGN
advise that the fall in eGFR should be less than 20%. The NICE CKD guidelines suggest that a
decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptableUploaded by medbooksvn.org

Flow chart showing the management of hypertensionas per current NICE guideliness
Antiplatelets: summary of latest guidance
The table below summarises the most recent guidelines regarding antiplatelets:
Diagnosis 1st line 2nd line
NSTEMI Aspirin (lifelong) & clopidogrel or
ticagrelor (12 months)
If aspirin contraindicated,
clopidogrel (lifelong)
STEMI Aspirin (lifelong) & clopidogrel or
ticagrelor (1m if no/bare stent, 12 m if
drug-eluting stent)
If aspirin contraindicated,
clopidogrel(lifelong)
TIA* Clopidogrel (lifelong) Aspirin (lifelong) &
dipyridamole (lifelong)
Ischaemic
stroke
Clopidogrel (lifelong) Aspirin (lifelong) &
dipyridamole (lifelong)
Peripheral
arterial disease
Clopidogrel (lifelong) Asprin (lifelong)
*the guidelines for TIA are based on the 2012 Royal College of Physicians National clinical guideline
for stroke. These guidelines corrected the anomaly where patients who've had a stroke were given
clopidogrel, but those who'd suffered a TIA were given aspirin + dipyridamole.Uploaded by medbooksvn.org

Aortic dissection
Stanford classification
type A-ascending aorta, 2/3 of cases
type B-descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification
type I-originates in ascending aorta, propagates to atleast the aortic arch and possibly
beyond it distally
type II-originates in and is confined to the ascending aorta
type III-originates in descending aorta, rarely extends proximally but will extend distally
Associations
hypertension
trauma
bicuspid aortic valve
collagens: Marfan's syndrome, Ehlers-Danlos syndrome
Turner's and Noonan's syndrome
pregnancy
syphilis
Complications of backward tear
aortic incompetence/regurgitation
MI: inferior pattern often seen due to right coronary involvement
Complications of forward tear
unequal arm pulses and BP
stroke
renal failure
Stanford type A / DeBakey type IUploaded by medbooksvn.org

Stanford type A / DeBakey type II
Stanford type B / DeBakey type IIIUploaded by medbooksvn.org

Aortic dissection: management
Stanford classification
type A-ascending aorta, 2/3 of cases
type B-descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification
type I-originates in ascending aorta, propagates to at least the aortic arch and possibly
beyond it distally
type II-originates in and is confined to the ascending aorta
type III-originates in descending aorta, rarely extends proximally but will extend distally
Type A
surgical management, but blood pressure should be controlled to a target systolic of 100-120
mmHg whilst awaiting intervention
Type B*
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression
*endovascular repair of type B aortic dissection may have a role in the futureUploaded by medbooksvn.org

An intraluminal tear has formed a 'flap' thatcan be clearly seen in the ascending aorta. This is a Stanford type A
dissection
Stanford type B dissection, seen in the descending aortaUploaded by medbooksvn.org

Aortic regurgitation
Features
early diastolic murmur
collapsing pulse
wide pulse pressure
mid-diastolicAustin-Flint murmur in severe AR-due to partial closure of the anterior mitral
valve cusps caused by the regurgitation streams
Causes (due to valve disease)
rheumatic fever
infective endocarditis
connective tissue diseases e.g. RA/SLE
bicuspid aorticvalve
Causes (due to aortic root disease)
aortic dissection
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan's, Ehler-Danlos syndromeUploaded by medbooksvn.org

Aortic stenosis
Features of severe aortic stenosis
narrow pulse pressure
slow risingpulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure
Causes of aortic stenosis
degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in youngerpatients < 65 years)
William's syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM
Management
if asymptomatic then observe the patient is general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient> 40 mmHg and with features such as left ventricular
systolic dysfunction then consider surgery
balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve
replacementUploaded by medbooksvn.org

Arrhythmogenic right ventricular cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy (ARVC, also known as arrhythmogenic right
ventricular dysplasia or ARVD) is a form of inherited cardiovascular disease which may present with
syncope or sudden cardiac death. It is generally regarded asthe second most common cause of
sudden cardiac death in the young after hypertrophic cardiomyopathy.
Pathophysiology
inherited in an autosomal dominant pattern with variable expression
the right ventricular myocardium is replaced by fatty and fibrofattytissue
around 50% of patients have a mutation of one of the several genes which encode
components of desmosome
Presentation
palpitations
syncope
sudden cardiac death
Investigation
ECG abnormalities in V1-3, typically T wave inversion. An epsilon waveis found in about
50% of those with ARV-this is best described as a terminal notch in the QRS complex
echo changes are often subtle in the early stages but may show an enlarged, hypokinetic
right ventricle with a thin free wall
magnetic resonance imagingis useful to show fibrofatty tissue
Management
drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator
Naxos disease
an autosomal recessive variant of ARVC
a triad of ARVC, palmoplantar keratosis, and woolly hairUploaded by medbooksvn.org

Atrial fibrillation: a very basic introduction
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. It is very common, being
present in around 5% of patients over aged 70-75 yearsand 10% of patients aged 80-85 years.
Whilst uncontrolled atrial fibrillation can result in symptomatic palpitations and inefficient cardiac
function probably the most important aspect of managing patients with AF is reducing the increased
risk of stroke whichis present in these patients.
Types of atrial fibrillation
AF may beclassified as either first detected episode, paroxysmal, persistent or permanent.
first detected episode (irrespective of whether it is symptomatic or self-terminating)
recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF
terminate spontaneously then the termparoxysmal AFis used. Such episodes last less
than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the
termpersistent AFis used. Such episodes usually last greater than 7 days
inpermanent AFthere is continuous atrial fibrillation which cannot be cardioverted or if
attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and
anticoagulation if appropriate
Symptoms and signs
Symptoms
palpitations
dyspnoea
chest pain
Signs
an irregularly irregular pulse
Investigations
An ECG is essential to make the diagnosis as other conditions can give an irregular pulse, such as
ventricular ectopics or sinus arrhythmia.
Management
There are two key parts of managing patients with AF:
1. Rate/rhythm control
2. Reducing stroke risk
Rate vs. rhythm control
There are two main strategies employed in dealing with the arrhythmia element of atrialfibrillation:Uploaded by medbooksvn.org

rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative
effects on cardiac function
rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is
termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical
shocks (electrical cardioversion) may be used for this purpose
For many years the predominant approach was to try and maintain a patient in sinus rhythm. This
approach changed in the early 2000's and now the majority of patients are managed with a rate
control strategy. NICE advocate using a rate control strategy except in a number of specific
situations such as coexistent heart failure, first onset AF or where there is an obvious reversible
cause.
Rate control
Abeta-blockeror arate-limiting calcium channel blocker(e.g. diltiazem) is used first-line to
control the rate in AF.
If onedrug does not control the rate adequately NICE recommend combination therapy with any 2 of
the following:
a betablocker
diltiazem
digoxin
Rhythm control
As mentioned above there are a subgroup of patients for whom a rhythm control strategy should be
triedfirst. Other patients may have had a rate control strategy initially but switch to rhythm control if
symptoms/heart rate fails to settle.
When considering cardioversion it is very important to remember that the moment a patient switches
from AF to sinusrhythm presents the highest risk for embolism leading to stroke. Imagine the
thrombus formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored.
For this reason patients must either of had a short duration of symptoms (lessthan 48 hours) or be
anticoagulated for a period of time prior to attempting cardioversion.
Reducing stroke risk
Some patients with AF are at a very low risk of stroke whilst others are at a very significant risk.
Clinicians use risk stratifying tools such as theCHA2DS2-VAScscore to determine the most
appropriate anticoagulation strategy.Uploaded by medbooksvn.org

Risk factor Points
CCongestive heart failure 1
HHypertension (or treated hypertension) 1
A2Age >= 75 years 2
Age 65-74 years 1
DDiabetes 1
S2PriorStroke or TIA 2
VVascular disease (including ischaemic heart disease and
peripheral arterial disease)
1
SSex (female) 1
The table below shows a suggested anticoagulation strategy based on the score:
ScoreAnticoagulation
0 No treatment
1 Males:Consider anticoagulation
Females: No treatment (this is because their score of 1 is only
reached due to their gender)
2 or
more
Offer anticoagulation
NICE recommend that we offer patients a choice of anticoagulation, including warfarin and the novel
oralanticoagulants (NOACs).Uploaded by medbooksvn.org

Atrial fibrillation: anticoagulation
NICE updated their guidelines on the management of atrial fibrillation (AF) in 2014. They suggest
using theCHA2DS2-VAScscore to determine the most appropriate anticoagulation strategy. This
scoring system superceded the CHADS2score.
Risk factor Points
CCongestive heart failure 1
HHypertension (or treated hypertension) 1
A2Age >= 75 years 2
Age 65-74 years 1
DDiabetes 1
S2Prior Stroke or TIA 2
VVascular disease (including ischaemic heart disease and peripheral
arterial disease)
1
SSex (female) 1Uploaded by medbooksvn.org

The table below shows a suggested anticoagulation strategy based on the score:
Score Anticoagulation
0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due
to their gender)
2 or
more
Offer anticoagulation
NICE recommend that we offer patients a choice of anticoagulation, includingwarfarin and the novel
oral anticoagulants (NOACs). There are complicated rules surrounding which NOAC is licensed for
which risk factor-these can be found in the NICE guidelines. Aspirin is no longer recommended for
reducing stroke risk in patients withAF
Doctors have always thought carefully about the risk/benefit profile of starting someone on warfarin.
A history of falls, old age, alcohol excess and a history of previous bleeding are common things that
make us consider whether warfarinisation is inthe best interests of the patient. NICE now
recommend we formalise this risk assessment using the HASBLED scoring system.Uploaded by medbooksvn.org

Risk factor Points
HHypertension, uncontrolled, systolic BP > 160 mmHg1
AAbnormal renal function (dialysis or creatinine >200)
Or
Abnormal liver function (cirrhosis, bilirubin > 2 times
normal, ALT/AST/ALP > 3 times normal
1 for any renal
abnormalities
1 for any liver
abnormalities
SStroke, history of 1
BBleeding, history of bleeding or tendency to bleed1
LLabile INRs(unstable/high INRs, time in therapeutic
range < 60%)
1
EElderly (> 65 years) 1
DDrugs Predisposing to Bleeding (Antiplatelet agents,
NSAIDs)
Or
Alcohol Use (>8 drinks/week)
1 for drugs
1 for alcohol
There are no formal rules on how we act on the HAS-BLED score although a score of >= 3 indicates
a 'high risk' of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease
>2 g/L, and/or transfusion.Uploaded by medbooksvn.org

Atrial fibrillation: cardioversion
There are two scenarios where cardioversion may be used in atrial fibrillation:
electrical cardioversion as an emergency if the patient is haemodynamically unstable
electrical or pharmacological cardioversion as an elective procedure where arhythm control
strategy is preferred.
The notes below refer to cardioversion being used in the elective scenario for rhythm control. The
wording of the 2014 NICE guidelines is as follows:
offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours,
and start rate control if it is more than 48 hours or is uncertain
Onset < 48 hours
If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised.
Patients who have risk factors for ischaemicstroke should be put on lifelong oral anticoagulation.
Otherwise, patients may be cardioverted using either:
electrical-'DC cardioversion'
pharmacology-amiodarone if structural heart disease, flecainide or amiodarone in those
without structural heartdisease
Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further
anticoagulation is unnecessary
Onset > 48 hours
If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least
3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE)
to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and
cardioverted immediately.
NICE recommend electrical cardioversion in this scenario, rather than pharmacological.
If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is
recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion
Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this
time decisions about anticoagulation should be taken on an individual basis depending on the risk of
recurrenceUploaded by medbooksvn.org

Atrial fibrillation: classification
An attempt was made in the joint American Heart Association (AHA), American College of
Cardiology (ACC) and European Society of Cardiology (ESC) 2012 guidelines to simplify and clarify
the classification of atrial fibrillation (AF).
It is recommended that AFbe classified into 3 patterns:
first detected episode (irrespective of whether it is symptomatic or self-terminating)
recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF
terminate spontaneously then the termparoxysmal AFisused. Such episodes last less
than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the
termpersistent AFis used. Such episodes usually last greater than 7 days
inpermanent AFthere is continuous atrial fibrillation which cannot be cardioverted or if
attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and
anticoagulation if appropriate
Atrial fibrillation: pharmacological cardioversion
The Royal College of Physicians and NICE publishedguidelines on the management of atrial
fibrillation (AF) in 2006. The following is also based on the joint American Heart Association (AHA),
American College of Cardiology (ACC) and European Society of Cardiology (ESC) 2012 guidelines
Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation
amiodarone
flecainide (if no structural heart disease)
others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone
Less effective agents
beta-blockers (including sotalol)
calcium channel blockers
digoxin
disopyramide
procainamide
Atrial fibrillation: post-stroke
NICE issued guidelines on atrial fibrillation (AF) in 2006. They included advice on the management
of patients with AF who develop a stroke or transient-ischaemic attack (TIA).
Recommendations include:
following a stroke or TIA warfarin should be given as the anticoagulant of choice.
Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities
in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be
commenced after 2 weeks. If imaging shows a very large cerebral infarction then the
initiation of anticoagulation should be delayedUploaded by medbooksvn.org

Atrial fibrillation: rate controland maintenance of sinus
rhythm
The Royal College of Physicians and NICE published guidelines on the management of atrial
fibrillation (AF) in 2006. The following is also based on the joint American Heart Association (AHA),
American College of Cardiology(ACC) and European Society of Cardiology (ESC) 2012 guidelines
Agents used to control rate in patients with atrial fibrillation
beta-blockers
calcium channel blockers
digoxin (not considered first-line anymore as they are less effective at controlling theheart
rate during exercise. However, they are the preferred choice if the patient has coexistent
heart failure)
Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation
sotalol
amiodarone
flecainide
others (less commonly usedin UK): disopyramide, dofetilide, procainamide, propafenone,
quinidine
The table below indicates some of the factors which may be considered when considering either a
rate control or rhythm control strategy
Factors favouring rate
control Factors favouringrhythm control
Older than 65 years
History of ischaemic heart
disease
Younger than 65 years
Symptomatic
First presentation
Lone AF or AF secondary to a corrected
precipitant (e.g. Alcohol)
Congestive heart failureUploaded by medbooksvn.org

Atrial flutter
Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial
depolarisation waves.
ECG findings
'sawtooth' appearance
as the underlying atrial rate is often around 300/min the ventricular or heart rate isdependent
on the degree of AV block. For example if there is 2:1 block the ventricular rate will be
150/min
flutter waves may be visible following carotid sinus massage or adenosine
Management
is similar to that of atrial fibrillation although medicationmay be less effective
atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
Atrial myxoma
Overview
75% occur in left atrium
morecommon in females
Features
systemic: dyspnoea, fatigue, weight loss, fever, clubbing
emboli
atrial fibrillation
mid-diastolic murmur, 'tumour plop'
echo: pedunculated heterogeneous mass typically attached to the fossa ovalisregion of the
interatrial septumUploaded by medbooksvn.org

Atrioventricular block
In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria
and ventricles. There are three types:
First degree heart block
PR interval > 0.2 seconds
Second degree heart block
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped
beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS
complex
Third degree (complete)heart block
there is no association between the P waves and QRS complexesUploaded by medbooksvn.org

Beta-blockers
Beta-blockers are an important class of drug used mainly in the management of cardiovascular
disorders.
Indications
angina
post-myocardial infarction
heartfailure: beta-blockers were previously avoided in heart failure but there is now strong
evidence that certain beta-blockers improve both symptoms and mortality
arrhythmias: beta-blockers have now replaced digoxin as the rate-control drug of choice in
atrial fibrillation
hypertension: the role of beta-blockers has diminished in recent years due to a lack of
evidence in terms of reducing stroke and myocardial infarction.
thyrotoxicosis
migraine prophylaxis
anxiety
Examples
atenolol
propranolol: one of thefirst beta-blockers to be developed. Lipid soluble therefore crosses
the blood-brain barrier
Side-effects
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
Contraindications
uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardiaUploaded by medbooksvn.org

Bicuspid aortic valve
Overview
occurs in 1-2% of the population
usually asymptomatic in childhood
the majority eventually develop aortic stenosis or regurgitation
associated with a leftdominant coronary circulation (the posterior descending artery arises
from the circumflex instead of the right coronary artery) and Turner's syndrome
around 5% of patients also have coarctation of the aorta
Complications
aortic stenosis/regurgitation asabove
higher risk for aortic dissection and aneurysm formation of the ascending aorta
Bivalirudin
Bivalirudin is a reversible direct thrombin inhibitor used as an anticoagulant in the management of
acute coronary syndrome.
Broad complex tachycardia
Features suggesting VT rather than SVT with aberrant conduction
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 msUploaded by medbooksvn.org

Brugada syndrome
Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden
cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of
1:5,000-10,000. Brugadasyndrome is more common in Asians.
Pathophysiology
a large number of variants exist
around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the
myocardial sodium ion channel protein
ECG changes
convex ST segment elevation > 2mm in> 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
changes may be more apparent following flecainide
ECG showing Brugada pattern, most marked in V1, which has an incomplete RBBB, a downslopingST segment and
an inverted T wave
Management
implantable cardioverter-defibrillator
Buerger's disease
Buerger's disease (also known as thromboangiitis obliterans) is a small and medium vessel
vasculitis that is strongly associated with smoking.
Features
extremity ischaemia: intermittent claudication, ischaemic ulcers etc
superficial thrombophlebitis
Raynaud's phenomenonUploaded by medbooksvn.org

Cardiac catherisation and oxygen saturation levels
Questions regarding cardiac catherisationand oxygen saturation levels can seem daunting at first
but a few simple rules combined with logical deduction can usual produce the answer.
Let's start with the basics:
deoxygenated blood returns to the right side of the heart via the superior vena cava (SVC)
and inferior vena cava (IVC). It has an oxygen saturation level of around70%. The right
atrium (RA), right ventricle (RV) and pulmonary artery (PA) normally have oxygen saturation
levels of around 70%
the lungs oxygenate the blood to a level of around98-100%. The left atrium (LA), left
ventricle (LV) and aorta should all therefore have oxygen saturation levels of 98-100%
The table below shows theoxygen saturationsthat would be expected in different scenarios:
Diagnosis & notes RARVPALA LV Aorta
Normal 70%70%70%100%100%100%
Atrial septal defect (ASD)
The oxygenated blood in the LA
mixes with the deoxygenated
blood in the RA, resulting in
intermediate levels of
oxygenation from the RA
onwards
85%85%85%100%100%100%
Ventricularseptal defect (VSD)
The oxygenated blood in the LV
mixes with the deoxygenated
blood in the RV, resulting in
intermediate levels of
oxygenation from the RV
onwards. The RA blood remains
deoxygenated
70%85%85%100%100%100%Uploaded by medbooksvn.org

Diagnosis & notes RARVPALA LV Aorta
Patent ductus arteriosus(PDA)
Remember, a PDA connects the
higher pressure aorta with the
lower pressure PA. This results in
only the PDA having
intermediate oxygenation levels
70%70%85%100%100%100%
VSD with Eisenmenger's 70%70%70%100%85%85%
PDA with Eisenmenger's 70%70%70%100%100%85%
ASD with Eisenmenger's 70%70%70%85%85%85%Uploaded by medbooksvn.org

Cardiac enzymes and protein markers
Interpretation of the various cardiac enzymes has now largely been supercededby the introduction
of troponin T and I. Questions still however commonly appear in exams.
Key points for the exam
myoglobin is the first to rise
CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T
remains elevated for up to 10 days)
Begins to risePeak value Returns to normal
Myoglobin 1-2 hours 6-8 hours 1-2 days
CK-MB 2-6 hours 16-20 hours2-3 days
CK 4-8 hours 16-24 hours3-4 days
Trop T 4-6 hours 12-24 hours7-10 days
AST 12-24 hours 36-48 hours3-4days
LDH 24-48 hours 72 hours 8-10 daysUploaded by medbooksvn.org

Cardiac tamponade
Features
dyspnoea
raised JVP, with an absent Y descent-this is due to the limited right ventricular filling
tachycardia
hypotension
muffled heart sounds
pulsus paradoxus
Kussmaul'ssign (much debate about this)
ECG: electrical alternans
The key differences between constrictive pericarditis and cardiac tamponade are summarised in the
table below:
Cardiac
tamponade Constrictive pericarditis
JVP Absent Y descentX + Y present
Pulsus paradoxus Present Absent
Kussmaul's sign Rare Present
Characteristic
features
Pericardial calcification on
CXR
A commonly used mnemonic to remember the absent Y descent in cardiac tamponade is
TAMponade = TAMpaXUploaded by medbooksvn.org

Cardiomyopathies: key points
The old classification of dilated, restricted and hypertrophic cardiomyopathy has been largely
abandoned due to the high degree of overlap. The latest classification of cardiomyopathy by the
WHO and American Heart Association reflect this.
The tables below shows a very limited set of exam related facts for the various cardiomyopathies:
Primary cardiomyopathies-predominately involving the heart
Genetic-both conditions listed below are autosomal dominant. An implantable cardioverter-
defibrillator is often inserted to reduce the incidence of sudden cardiac death.
Type of
cardiomyopathy Selected points
Hypertrophic
obstructive
cardiomyopathy
Leading cause of sudden cardiac death in young
athletes
Usually due to a mutation in the gene encoding β-
myosinheavy chain protein
Common cause of sudden death
Echo findings include MR, systolic anterior motion
(SAM) of the anterior mitral valve and asymmetric
septal hypertrophy
Arrhythmogenic right
ventricular dysplasia
Right ventricular myocardium is replaced byfatty and
fibrofatty tissue
Around 50% of patients have a mutation of one of the
several genes which encode components of
desmosome
ECG abnormalities in V1-3, typically T wave
inversion. An epsilon wave is found in about 50% of
those with ARV-this is best described as a terminal
notch in the QRS complex
Mixed-rather confusingly most of the causes of dilated and restrictive cardiomyopathy are now
listed separately in the 'secondary' causes. This category servers as a reminder that many patients
willhave a genetic predisposition to cardiomyopathy which is then triggered by the secondary
process, hence the 'mixed' categoryUploaded by medbooksvn.org

Type of cardiomyopathy Selected causes/points
Dilated cardiomyopathy Classic causes include
alcohol
Coxsackie B virus
wet beri beri
doxorubicin
Restrictive cardiomyopathy Classic causes include
amyloidosis
post-radiotherapy
Loeffler's endocarditis
Acquired
Type of
cardiomyopathy Selected points
Peripartum
cardiomyopathy
Typical develops between last month of pregnancy and
5months post-partum
More common in older women, greater parity and
multiple gestations
Takotsubo
cardiomyopathy
'Stress'-induced cardiomyopathy e.g. patient just found
out family member dies then develops chest pain and
features of heart failure
Transient,apical ballooning of the myocardium
Treatment is supportive
Secondary cardiomyopathies-pathological myocardial involvement as part of a generalized
systemic disorderUploaded by medbooksvn.org

Type of cardiomyopathy Selected causes/points
Infective Coxsackie B virus
Chagasdisease
Infiltrative Amyloidosis
Storage Haemochromatosis
Toxicity Doxorubicin
Alcoholic cardiomyopathy
Inflammatory (granulomatous)Sarcoidosis
Endocrine Diabetes mellitus
Thyrotoxicosis
Acromegaly
Neuromuscular Friedreichs ataxia
Duchenne-Becker muscular dystrophy
Myotonic dystrophy
Nutritional deficiencies Beriberi (thiamine)
Autoimmune Systemic lupus erythematosisUploaded by medbooksvn.org

Catecholaminergic polymorphic ventricular tachycardia
Catecholaminergic polymorphic ventricular tachycardia(CPVT) is a form of inherited cardiac disease
associated with sudden cardiac death. It is inherited in an autosomal dominant fashion and has a
prevalence of around 1:10,000.
Pathophysiology
the most common cause is a defect in the ryanodine receptor (RYR2) which is found in the
myocardial sarcoplasmic reticulum
Features
exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
sudden cardiac death
symptoms generally develop before the age of 20 years
Management
beta-blockers
implantable cardioverter-defibrillator
Centrally acting antihypertensives
Examples of centrally acting antihypertensives include:
methyldopa: used in the management of hypertension during pregnancy
moxonidine: used in the management of essential hypertension when conventional
antihypertensives have failed to control blood pressure
clonidine: the antihypertensive effect is mediated through stimulating alpha-2 adrenoceptors
in the vasomotor centreUploaded by medbooksvn.org

Chest pain: assessment of patients withsuspected cardiac
chest pain
NICE issued guidelines in 2010 on the 'Assessment and diagnosis of recent onset chest pain or
discomfort of suspected cardiac origin'.
Below is a brief summary of the key points. Please see the link for more details.
Patients presenting with acute chest pain
Immediate management of suspected acute coronary syndrome (ACS)
glyceryl trinitrate
aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel)
outside of hospital
do not routinely give oxygen, only give if sats < 94%*
perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG
does not exclude ACS
Referral
current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency
admission
chest pain 12-72 hours ago: refer to hospital the same-day for assessment
chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement
before deciding upon further action
*NICE suggest the following in terms of oxygen therapy:
do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as
soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic
respiratory failure, aiming for SpO2 of 94-98%
people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory
failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.
Patients presenting with stablechest pain
With all due respect to NICE the guidelines for assessment of patients with stable chest pain are
rather complicated. They suggest an approach where the risk of a patient having coronary artery
disease (CAD) is calculated based on their symptoms (whether they have typical angina, atypical
angina or non-anginal chest pain), age, gender and risk factors.Uploaded by medbooksvn.org

NICE define anginal pain as the following:
1. constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
2. precipitatedby physical exertion
3. relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
The risk tables are not reproduced here but can be found by clicking on the link.
If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further
diagnostic testing is required. It should be noted that all men over the age of 70years who have
typical anginal symptoms fall into this category.
For patients with an estimated risk of 10-90% the following investigations are recommended. Note
the absence of the exercise tolerance test:
Estimated likelihood
of CAD Diagnostic testing
61-90% Coronary angiography
30-60% Functional imaging, for example:
myocardial perfusion scan with SPECT
stress echocardiography
first-pass contrast-enhanced magnetic
resonance (MR) perfusion
MR imaging for stress-induced wall motion
abnormalities.
10-29% CT calcium scoringUploaded by medbooksvn.org

Cholestyramine
Cholestyramine is a bile acid sequestrant used in the management of hyperlipidaemia. It decreases
bile acid reabsorption in the small intestine, therefore upregulating the amount of cholesterol that is
converted to bile acid. The main effect it has on the lipid profile is to reduce LDL cholesterol. It is
also occasionally used in Crohn'sdisease for treatment resistant diarrhoea.
Adverse effects
abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides
Chronic kidney disease: anaemia
Patients with chronic kidney disease (CKD) may develop anaemia due to a variety of factors, the
most significant of which is reduced erythropoietin levels. This is usually a normochromic normocytic
anaemia and becomes apparent when the GFR is less than 35 ml/min (other causes of anaemia
should be considered if the GFR is > 60 ml/min). Anaemia in CKD predisposes to the development
of left ventricular hypertrophy-associated with a three fold increase in mortality in renal patients
Causes of anaemia in renal failure
reduced erythropoietin levels-the most significant factor
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due tocapillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
Management
the 2011 NICE guidelines suggest a target haemoglobin of 10-12 g/dl
determination and optimisation of iron status should be carried out prior to the administration
of erythropoiesis-stimulating agents (ESA). Many patients, especially those on
haemodialysis, will require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those 'who are likely to
benefit in terms of quality of lifeand physical function'Uploaded by medbooksvn.org

Coarctation of the aorta
Coarctation of the aorta describes a congenital narrowing of the descending aorta.
Overview
more common in males (despite association with Turner's syndrome)
Features
infancy: heart failure
adult:hypertension
radio-femoral delay
mid systolic murmur, maximal over back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young
children
Associations
Turner's syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosisUploaded by medbooksvn.org

Complete heart block
Features
syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1
Types of heart block
First degree heart block
PRinterval > 0.2 seconds
Second degree heart block
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped
beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS
complex
Third degree (complete) heart block
there is no association between the P waves and QRS complexes
ECG showing third degree (complete) heart blockUploaded by medbooksvn.org

Random documents with unrelated
content Scribd suggests to you:

LETTER VIII
My dear friend , Your letter raised me for a moment from the
depths of despair; but not hearing from you yesterday or to-day (as I
hoped) I have had a relapse. You say I want to get rid of her. I hope
you are more right in your conjectures about her than in this about
me. Oh no! believe it, I love her as I do my own soul; my very heart is
wedded to her (be she what she may) and I would not hesitate a
moment between her and ‘an angel from Heaven.’ I grant all you say
about my self-tormenting folly: but has it been without cause? Has
she not refused me again and again with a mixture of scorn and
resentment, after going the utmost lengths with a man for whom she
now disclaims all affection; and what security can I have for her
reserve with others, who will not be restrained by feelings of delicacy
towards her, and whom she has probably preferred to me for their
want of it. ‘She can make no more confidences’—these words ring for
ever in my ears, and will be my death-watch. They can have but one
meaning, be sure of it—she always expressed herself with the
exactest propriety. That was one of the things for which I loved her—
shall I live to hate her for it? My poor fond heart, that brooded over
her and the remains of her affections as my only hope of comfort
upon earth, cannot brook this new degradation. Who is there so low
as me? Who is there besides (I ask) after the homage I have paid her
and the caresses she has lavished on me, so vile, so abhorrent to love,
to whom such an indignity could have happened? When I think of
this (and I think of nothing else) it stifles me. I am pent up in
burning, fruitless desires, which can find no vent or object. Am I not
hated, repulsed, derided by her whom alone I love or ever did love? I
cannot stay in any place, and seek in vain for relief from the sense of
her contempt and her ingratitude. I can settle to nothing: what is the
use of all I have done? Is it not that very circumstance (my thinking
beyond my strength, my feeling more than I need about so many
things) that has withered me up, and made me a thing for Love to
shrink from and wonder at? Who could ever feel that peace from the
touch of her dear hand that I have done; and is it not torn from me
for ever? My state is this, that I shall never lie down again at night
nor rise up in the morning in peace, nor ever behold my little boy’s

face with pleasure while I live—unless I am restored to her favour.
Instead of that delicious feeling I had when she was heavenly-kind to
me, and my heart softened and melted in its own tenderness and her
sweetness, I am now inclosed in a dungeon of despair. The sky is
marble to my thoughts; nature is dead around me, as hope is within
me; no object can give me one gleam of satisfaction now, nor the
prospect of it in time to come. I wander by the sea-side; and the
eternal ocean and lasting despair and her face are before me.
Slighted by her, on whom my heart by its last fibre hung, where shall
I turn? I wake with her by my side, not as my sweet bedfellow, but as
the corpse of my love, without a heart in her bosom, cold, insensible,
or struggling from me; and the worm gnaws me, and the sting of
unrequited love, and the canker of a hopeless, endless sorrow. I have
lost the taste of my food by feverish anxiety; and my favourite
beverage, which used to refresh me when I got up, has no moisture in
it. Oh! cold, solitary, sepulchral breakfasts, compared with those
which I promised myself with her; or which I made when she had
been standing an hour by my side, my guardian-angel, my wife, my
sister, my sweet friend, my Eve, my all; and had blest me with her
seraph kisses! Ah! what I suffer at present only shews what I have
enjoyed. But ‘the girl is a good girl, if there is goodness in human
nature.’ I thank you for those words; and I will fall down and worship
you, if you can prove them true: and I would not do much less for
him that proves her a demon. She is one or the other, that’s certain;
but I fear the worst. Do let me know if anything has passed: suspense
is my greatest punishment. I am going into the country to see if I can
work a little in the three weeks I have yet to stay here. Write on the
receipt of this, and believe me ever your unspeakably obliged friend.

TO EDINBURGH
——‘Stony-hearted’ Edinburgh! What art thou to me? The dust of
thy streets mingles with my tears and blinds me. City of palaces, or of
tombs—a quarry, rather than the habitation of men! Art thou like
London, that populous hive, with its sunburnt, well-baked, brick-
built houses—its public edifices, its theatres, its bridges, its squares,
its ladies, and its pomp, its throng of wealth, its outstretched
magnitude, and its mighty heart that never lies still? Thy cold grey
walls reflect back the leaden melancholy of the soul. The square,
hard-edged, unyielding faces of thy inhabitants have no sympathy to
impart. What is it to me that I look along the level line of thy
tenantless streets, and meet perhaps a lawyer like a grasshopper
chirping and skipping, or the daughter of a Highland laird, haughty,
fair, and freckled? Or why should I look down your boasted Prince’s
Street, with the beetle-browed Castle on one side, and the Calton Hill
with its proud monument at the further end, and the ridgy steep of
Salisbury Crag, cut off abruptly by Nature’s boldest hand, and
Arthur’s Seat overlooking all, like a lioness watching her cubs? Or
shall I turn to the far-off Pentland Hills, with Craig-Crook nestling
beneath them, where lives the prince of critics and the king of men?
Or cast my eye unsated over the Frith of Forth, that from my window
of an evening (as I read of Amy and her love) glitters like a broad
golden mirror in the sun, and kisses the winding shores of kingly
Fife? Oh no! But to thee, to thee I turn, North Berwick-Law, with thy
blue cone rising out of summer seas; for thou art the beacon of my
banished thoughts, and dost point my way to her, who is my heart’s
true home. The air is too thin for me, that has not the breath of Love
in it; that is not embalmed by her sighs!
A THOUGHT
I am not mad, but my heart is so; and raves within me, fierce and
untameable, like a panther in its den, and tries to get loose to its lost
mate, and fawn on her hand, and bend lowly at her feet.

ANOTHER
Oh! thou dumb heart, lonely, sad, shut up in the prison-house of
this rude form, that hast never found a fellow but for an instant, and
in very mockery of thy misery, speak, find bleeding words to express
thy thoughts, break thy dungeon-gloom, or die pronouncing thy
Infelice’s name!
ANOTHER
Within my heart is lurking suspicion, and base fear, and shame
and hate; but above all, tyrannous love sits throned, crowned with
her graces, silent and in tears.

LETTER IX
My dear P——, You have been very kind to me in this business;
but I fear even your indulgence for my infirmities is beginning to fail.
To what a state am I reduced, and for what? For fancying a little
artful vixen to be an angel and a saint, because she affected to look
like one, to hide her rank thoughts and deadly purposes. Has she not
murdered me under the mask of the tenderest friendship? And why?
Because I have loved her with unutterable love, and sought to make
her my wife. You say it is my own ‘outrageous conduct’ that has
estranged her: nay, I have been too gentle with her. I ask you first in
candour whether the ambiguity of her behaviour with respect to me,
sitting and fondling a man (circumstanced as I was) sometimes for
half a day together, and then declaring she had no love for him
beyond common regard, and professing never to marry, was not
enough to excite my suspicions, which the different exposures from
the conversations below-stairs were not calculated to allay? I ask you
what you yourself would have felt or done, if loving her as I did, you
had heard what I did, time after time? Did not her mother own to
one of the grossest charges (which I shall not repeat)—and is such
indelicacy to be reconciled with her pretended character (that
character with which I fell in love, and to which I made love) without
supposing her to be the greatest hypocrite in the world? My
unpardonable offence has been that I took her at her word, and was
willing to believe her the precise little puritanical person she set up
for. After exciting her wayward desires by the fondest embraces and
the purest kisses, as if she had been ‘made my wedded wife yestreen,’
or was to become so to-morrow (for that was always my feeling with
respect to her)—I did not proceed to gratify them, or to follow up my
advantage by any action which should declare, ‘I think you a
common adventurer, and will see whether you are so or not!’ Yet any
one but a credulous fool like me would have made the experiment,
with whatever violence to himself, as a matter of life and death; for I
had every reason to distrust appearances. Her conduct has been of a
piece from the beginning. In the midst of her closest and falsest
endearments, she has always (with one or two exceptions)
disclaimed the natural inference to be drawn from them, and made a

verbal reservation, by which she might lead me on in a Fool’s
Paradise, and make me the tool of her levity, her avarice, and her
love of intrigue as long as she liked, and dismiss me whenever it
suited her. This, you see, she has done, because my intentions grew
serious, and if complied with, would deprive her of the pleasures of a
single life! Offer marriage to this ‘tradesman’s daughter, who has as
nice a sense of honour as any one can have;’ and like Lady Bellaston
in Tom Jones, she cuts you immediately in a fit of abhorrence and
alarm. Yet she seemed to be of a different mind formerly, when
struggling from me in the height of our first intimacy, she exclaimed
—‘However I might agree to my own ruin, I never will consent to
bring disgrace upon my family!’ That I should have spared the
traitress after expressions like this, astonishes me when I look back
upon it. Yet if it were all to do over again, I know I should act just the
same part. Such is her power over me! I cannot run the least risk of
offending her—I love her so. When I look in her face, I cannot doubt
her truth! Wretched being that I am! I have thrown away my heart
and soul upon an unfeeling girl; and my life (that might have been so
happy, had she been what I thought her) will soon follow either
voluntarily, or by the force of grief, remorse, and disappointment. I
cannot get rid of the reflection for an instant, nor even seek relief
from its galling pressure. Ah! what a heart she has lost! All the love
and affection of my whole life were centred in her, who alone, I
thought, of all women had found out my true character, and knew
how to value my tenderness. Alas! alas! that this, the only hope, joy,
or comfort I ever had, should turn to a mockery, and hang like an
ugly film over the remainder of my days!—I was at Roslin Castle
yesterday. It lies low in a rude, but sheltered valley, hid from the
vulgar gaze, and powerfully reminds one of the old song. The
straggling fragments of the russet ruins, suspended smiling and
graceful in the air as if they would linger out another century to
please the curious beholder, the green larch-trees trembling between
with the blue sky and white silver clouds, the wild mountain plants
starting out here and there, the date of the year on an old low door-
way, but still more, the beds of flowers in orderly decay, that seem to
have no hand to tend them, but keep up a sort of traditional
remembrance of civilization in former ages, present altogether a
delightful and amiable subject for contemplation. The exquisite
beauty of the scene, with the thought of what I should feel, should I

ever be restored to her, and have to lead her through such places as
my adored, my angel-wife, almost drove me beside myself. For this
picture, this ecstatic vision, what have I of late instead as the image
of the reality? Demoniacal possessions. I see the young witch seated
in another’s lap, twining her serpent arms round him, her eye
glancing and her cheeks on fire—why does not the hideous thought
choke me? Or why do I not go and find out the truth at once? The
moonlight streams over the silver waters: the bark is in the bay that
might waft me to her, almost with a wish. The mountain-breeze sighs
out her name: old ocean with a world of tears murmurs back my
woes! Does not my heart yearn to be with her; and shall I not follow
its bidding? No, I must wait till I am free; and then I will take my
Freedom (a glad prize) and lay it at her feet and tell her my proud
love of her that would not brook a rival in her dishonour, and that
would have her all or none, and gain her or lose myself for ever!—
You see by this letter the way I am in, and I hope you will excuse it
as the picture of a half-disordered mind. The least respite from my
uneasiness (such as I had yesterday) only brings the contrary
reflection back upon me, like a flood; and by letting me see the
happiness I have lost, makes me feel, by contrast, more acutely what
I am doomed to bear.

LETTER X
Dear Friend , Here I am at St. Bees once more, amid the scenes
which I greeted in their barrenness in winter; but which have now
put on their full green attire that shews luxuriant to the eye, but
speaks a tale of sadness to this heart widowed of its last, its dearest,
its only hope! Oh! lovely Bees-Inn! here I composed a volume of law-
cases, here I wrote my enamoured follies to her, thinking her human,
and that ‘all below was not the fiend’s’—here I got two cold, sullen
answers from the little witch, and here I was —— —— and I was
damned. I thought the revisiting the old haunts would have soothed
me for a time, but it only brings back the sense of what I have
suffered for her and of her unkindness the more strongly, till I
cannot endure the recollection. I eye the Heavens in dumb despair,
or vent my sorrows in the desart air. ‘To the winds, to the waves, to
the rocks I complain’—you may suppose with what effect! I fear I
shall be obliged to return. I am tossed about (backwards and
forwards) by my passion, so as to become ridiculous. I can now
understand how it is that mad people never remain in the same place
—they are moving on for ever, from themselves!
Do you know, you would have been delighted with the effect of the
Northern twilight on this romantic country as I rode along last night?
The hills and groves and herds of cattle were seen reposing in the
grey dawn of midnight, as in a moonlight without shadow. The whole
wide canopy of Heaven shed its reflex light upon them, like a pure
crystal mirror. No sharp points, no petty details, no hard contrasts—
every object was seen softened yet distinct, in its simple outline and
natural tones, transparent with an inward light, breathing its own
mild lustre. The landscape altogether was like an airy piece of
mosaic-work, or like one of Poussin’s broad massy landscapes or
Titian’s lovely pastoral scenes. Is it not so, that poets see nature,
veiled to the sight, but revealed to the soul in visionary grace and
grandeur! I confess the sight touched me; and might have removed
all sadness except mine. So (I thought) the light of her celestial face
once shone into my soul, and wrapt me in a heavenly trance. The
sense I have of beauty raises me for a moment above myself, but
depresses me the more afterwards, when I recollect how it is thrown

away in vain admiration, and that it only makes me more susceptible
of pain from the mortifications I meet with. Would I had never seen
her! I might then not indeed have been happy, but at least I might
have passed my life in peace, and have sunk into forgetfulness
without a pang.—The noble scenery in this country mixes with my
passion, and refines, but does not relieve it. I was at Stirling Castle
not long ago. It gave me no pleasure. The declivity seemed to me
abrupt, not sublime; for in truth I did not shrink back from it with
terror. The weather-beaten towers were stiff and formal: the air was
damp and chill: the river winded its dull, slimy way like a snake
along the marshy grounds: and the dim misty tops of Ben Leddi, and
the lovely Highlands (woven fantastically of thin air) mocked my
embraces and tempted my longing eyes like her, the sole queen and
mistress of my thoughts! I never found my contemplations on this
subject so subtilised and at the same time so desponding as on that
occasion. I wept myself almost blind, and I gazed at the broad golden
sun-set through my tears that fell in showers. As I trod the green
mountain turf, oh! how I wished to be laid beneath it—in one grave
with her—that I might sleep with her in that cold bed, my hand in
hers, and my heart for ever still—while worms should taste her sweet
body, that I had never tasted! There was a time when I could bear
solitude; but it is too much for me at present. Now I am no sooner
left to myself than I am lost in infinite space, and look round me in
vain for support or comfort. She was my stay, my hope: without her
hand to cling to, I stagger like an infant on the edge of a precipice.
The universe without her is one wide, hollow abyss, in which my
harassed thoughts can find no resting-place. I must break off here;
for the hysterica passio comes upon me, and threatens to unhinge
my reason.

LETTER XI
My dear and good Friend , I am afraid I trouble you with my
querulous epistles, but this is probably the last. To-morrow or the
next day decides my fate with respect to the divorce, when I expect to
be a free man. In vain! Was it not for her and to lay my freedom at
her feet, that I consented to this step which has cost me infinite
perplexity, and now to be discarded for the first pretender that came
in her way! If so, I hardly think I can survive it. You who have been a
favourite with women, do not know what it is to be deprived of one’s
only hope, and to have it turned to shame and disappointment.
There is nothing in the world left that can afford me one drop of
comfort—this I feel more and more. Everything is to me a mockery of
pleasure, like her love. The breeze does not cool me: the blue sky
does not cheer me. I gaze only on her face averted from me—alas! the
only face that ever was turned fondly to me! And why am I thus
treated? Because I wanted her to be mine for ever in love or
friendship, and did not push my gross familiarities as far as I might.
‘Why can you not go on as we have done, and say nothing about the
word, forever?’ Was it not plain from this that she even then
meditated an escape from me to some less sentimental lover? ‘Do
you allow anyone else to do so?’ I said to her once, as I was toying
with her. ‘No, not now!’ was her answer; that is, because there was
nobody else in the house to take freedoms with her. I was very well as
a stopgap, but I was to be nothing more. While the coast was clear, I
had it all my own way: but the instant C—— came, she flung herself
at his head in the most barefaced way, ran breathless up stairs before
him, blushed when his foot was heard, watched for him in the
passage, and was sure to be in close conference with him when he
went down again. It was then my mad proceedings commenced. No
wonder. Had I not reason to be jealous of every appearance of
familiarity with others, knowing how easy she had been with me at
first, and that she only grew shy when I did not take farther liberties?
What has her character to rest upon but her attachment to me, which
she now denies, not modestly, but impudently? Will you yourself say
that if she had all along no particular regard for me, she will not do
as much or more with other more likely men? ‘She has had,’ she says,

‘enough of my conversation,’ so it could not be that! Ah! my friend, it
was not to be supposed I should ever meet even with the outward
demonstrations of regard from any woman but a common trader in
the endearments of love! I have tasted the sweets of the well
practiced illusion, and now feel the bitterness of knowing what a
bliss I am deprived of, and must ever be deprived of. Intolerable
conviction! Yet I might, I believe, have won her by other methods;
but some demon held my hand. How indeed could I offer her the
least insult when I worshipped her very footsteps; and even now pay
her divine honours from my inmost heart, whenever I think of her,
abased and brutalised as I have been by that Circean cup of kisses, of
enchantments, of which I have drunk! I am choked, withered, dried
up with chagrin, remorse, despair, from which I have not a moment’s
respite, day or night. I have always some horrid dream about her,
and wake wondering what is the matter that ‘she is no longer the
same to me as ever?’ I thought at least we should always remain dear
friends, if nothing more—did she not talk of coming to live with me
only the day before I left her in the winter? But ‘she’s gone, I am
abused, and my revenge must be to love her!’—Yet she knows that
one line, one word would save me, the cruel, heartless destroyer! I
see nothing for it but madness, unless Friday brings a change, or
unless she is willing to let me go back. You must know I wrote to her
to that purpose, but it was a very quiet, sober letter, begging pardon,
and professing reform for the future, and all that. What effect it will
have, I know not. I was forced to get out of the way of her answer, till
Friday came.
Ever your’s.

TO S. L.
My dear Miss L——, Evil to them that evil think, is an old saying;
and I have found it a true one. I have ruined myself by my unjust
suspicions of you. Your sweet friendship was the balm of my life; and
I have lost it, I fear for ever, by one fault and folly after another.
What would I give to be restored to the place in your esteem, which,
you assured me, I held only a few months ago! Yet I was not
contented, but did all I could to torment myself and harass you by
endless doubts and jealousy. Can you not forget and forgive the past,
and judge of me by my conduct in future? Can you not take all my
follies in the lump, and say like a good, generous girl, ‘Well, I’ll think
no more of them?’ In a word, may I come back, and try to behave
better? A line to say so would be an additional favour to so many
already received by
Your obliged friend,
And sincere well-wisher.

LETTER XII. TO C. P——
I have no answer from her. I’m mad. I wish you to call on M—— in
confidence, to say I intend to make her an offer of my hand, and that
I will write to her father to that effect the instant I am free, and ask
him whether he thinks it will be to any purpose, and what he would
advise me to do.

UNALTERED LOVE
‘Love is not love that alteration finds:
Oh no! it is an ever-fixed mark,
That looks on tempests and is never shaken.’
Shall I not love her for herself alone, in spite of fickleness and folly?
To love her for her regard to me, is not to love her, but myself. She
has robbed me of herself: shall she also rob me of my love of her? Did
I not live on her smile? Is it less sweet because it is withdrawn from
me? Did I not adore her every grace? Does she bend less
enchantingly, because she has turned from me to another? Is my love
then in the power of fortune, or of her caprice? No, I will have it
lasting as it is pure; and I will make a Goddess of her, and build a
temple to her in my heart, and worship her on indestructible altars,
and raise statues to her: and my homage shall be unblemished as her
unrivalled symmetry of form; and when that fails, the memory of it
shall survive; and my bosom shall be proof to scorn, as her’s has been
to pity; and I will pursue her with an unrelenting love, and sue to be
her slave, and tend her steps without notice and without reward; and
serve her living, and mourn for her when dead. And thus my love will
have shewn itself superior to her hate; and I shall triumph and then
die. This is my idea of the only true and heroic love! Such is mine for
her.

PERFECT LOVE
Perfect love has this advantage in it, that it leaves the possessor of
it nothing farther to desire. There is one object (at least) in which the
soul finds absolute content, for which it seeks to live, or dares to die.
The heart has as it were filled up the moulds of the imagination. The
truth of passion keeps pace with and outvies the extravagance of
mere language. There are no words so fine, no flattery so soft, that
there is not a sentiment beyond them, that it is impossible to express,
at the bottom of the heart where true love is. What idle sounds the
common phrases, adorable creature, angel, divinity, are? What a
proud reflection it is to have a feeling answering to all these, rooted
in the breast, unalterable, unutterable, to which all other feelings are
light and vain! Perfect love reposes on the object of its choice, like
the halcyon on the wave; and the air of heaven is around it.

FROM C. P., ESQ.
London, July 4th, 1822.
I have seen M——! Now, my dear H——, let me entreat and adjure
you to take what I have to tell you, for what it is worth—neither for
less, nor more. In the first place, I have learned nothing decisive
from him. This, as you will at once see, is, as far as it goes, good. I am
either to hear from him, or see him again in a day or two; but I
thought you would like to know what passed inconclusive as it was—
so I write without delay, and in great haste to save a post. I found
him frank, and even friendly in his manner to me, and in his views
respecting you. I think that he is sincerely sorry for your situation;
and he feels that the person who has placed you in that situation is
not much less awkwardly situated herself; and he professes that he
would willingly do what he can for the good of both. But he sees great
difficulties attending the affair—which he frankly professes to
consider as an altogether unfortunate one. With respect to the
marriage, he seems to see the most formidable objections to it, on
both sides; but yet he by no means decidedly says that it cannot, or
that it ought not to take place. These, mind you, are his own feelings
on the subject: but the most important point I learn from him is this,
that he is not prepared to use his influence either way—that the rest
of the family are of the same way of feeling; and that, in fact, the
thing must and does entirely rest with herself. To learn this was, as
you see, gaining a great point.—When I then endeavoured to
ascertain whether he knew anything decisive as to what are her views
on the subject, I found that he did not. He has an opinion on the
subject, and he didn’t scruple to tell me what it was; but he has no
positive knowledge. In short, he believes, from what he learns from
herself (and he had purposely seen her on the subject, in
consequence of my application to him) that she is at present
indisposed to the marriage; but he is not prepared to say positively
that she will not consent to it. Now all this, coming from him in the
most frank and unaffected manner, and without any appearance of
cant, caution, or reserve, I take to be most important as it respects
your views, whatever they may be; and certainly much more

favorable to them (I confess it) than I was prepared to expect,
supposing them to remain as they were. In fact, as I said before, the
affair rests entirely with herself. They are none of them disposed
either to further the marriage, or throw any insurmountable
obstacles in the way of it; and what is more important than all, they
are evidently by no means certain that SHE may not, at some future
period, consent to it; or they would, for her sake as well as their own,
let you know as much flatly, and put an end to the affair at once.
Seeing in how frank and strait-forward a manner he received what
I had to say to him, and replied to it, I proceeded to ask him what
were his views, and what were likely to be her’s (in case she did not
consent) as to whether you should return to live in the house;—but I
added, without waiting for his answer, that if she intended to persist
in treating you as she had done for some time past, it would be worse
than madness for you to think of returning. I added that, in case you
did return, all you would expect from her would be that she would
treat you with civility and kindness—that she would continue to
evince that friendly feeling towards you, that she had done for a great
length of time, &c. To this, he said, he could really give no decisive
reply, but that he should be most happy if, by any intervention of his,
he could conduce to your comfort; but he seemed to think that for
you to return on any express understanding that she should behave
to you in any particular manner, would be to place her in a most
awkward situation. He went somewhat at length into this point, and
talked very reasonably about it; the result, however, was that he
would not throw any obstacles in the way of your return, or of her
treating you as a friend, &c., nor did it appear that he believed she
would refuse to do so. And, finally, we parted on the understanding
that he would see them on the subject, and ascertain what could be
done for the comfort of all parties: though he was of opinion that if
you could make up your mind to break off the acquaintance
altogether, it would be the best plan of all. I am to hear from him
again in a day or two.—Well, what do you say to all this? Can you
turn it to any thing but good—comparative good? If you would know
what I say to it, it is this:—She is still to be won by wise and prudent
conduct on your part; she was always to have been won by such;—
and if she is lost, it has been (not, as you sometimes suppose,
because you have not carried that unwise, may I not say unworthy?
conduct still farther, but) because you gave way to it at all. Of course

I use the terms ‘wise’ and ‘prudent’ with reference to your object.
Whether the pursuit of that object is wise, only yourself can judge. I
say she has all along been to be won, and she still is to be won; and
all that stands in the way of your views at this moment is your past
conduct. They are all of them, every soul, frightened at you; they
have seen enough of you to make them so; and they have doubtless
heard ten times more than they have seen, or than anyone else has
seen. They are all of them, including M—— (and particularly she
herself) frightened out of their wits, as to what might be your
treatment of her if she were your’s; and they dare not trust you—they
will not trust you, at present. I do not say that they will trust you, or
rather that she will, for it all depends on her, when you have gone
through a probation, but I am sure that she will not trust you till you
have. You will, I hope, not be angry with me when I say that she
would be a fool if she did. If she were to accept you at present, and
without knowing more of you, even I should begin to suspect that she
had an unworthy motive for doing it. Let me not forget to mention
what is perhaps as important a point as any, as it regards the
marriage. I of course stated to M—— that when you are free, you are
prepared to make her a formal offer of your hand; but I begged him,
if he was certain that such an offer would be refused, to tell me so
plainly at once, that I might endeavour, in that case, to dissuade you
from subjecting yourself to the pain of such a refusal. He would not
tell me that he was certain. He said his opinion was that she would
not accept your offer, but still he seemed to think that there would be
no harm in making it!—One word more, and a very important one.
He once, and without my referring in the slightest manner to that
part of the subject, spoke of her as a good girl, and likely to make
any man an excellent wife! Do you think if she were a bad girl (and if
she were, he must know her to be so) he would have dared to do this,
under these circumstances?—And once, in speaking of his not being
a fit person to set his face against ‘marrying for love,’ he added ‘I did
so myself, and out of that house; and I have had reason to rejoice at it
ever since.’ And mind (for I anticipate your cursed suspicions) I’m
certain, at least, if manner can entitle one to be certain of any thing,
that he said all this spontaneously, and without any understood
motive; and I’m certain, too, that he knows you to be a person that it
would not do to play any tricks of this kind with. I believe—(and all
this would never have entered my thoughts, but that I know it will

enter your’s) I believe that even if they thought (as you have
sometimes supposed they do) that she needs whitewashing, or
making an honest woman of, you would be the last person they
would think of using for such a purpose, for they know (as well as I
do) that you couldn’t fail to find out the trick in a month, and would
turn her into the street the next moment, though she were twenty
times your wife—and that, as to the consequences of doing so, you
would laugh at them, even if you couldn’t escape from them.—I shall
lose the post if I say more.
Believe me,
Ever truly your friend,
C. P.

LETTER XIII
My dear P——, You have saved my life. If I do not keep friends
with her now, I deserve to be hanged, drawn, and quartered. She is
an angel from Heaven, and you cannot pretend I ever said a word to
the contrary! The little rogue must have liked me from the first, or
she never could have stood all these hurricanes without slipping her
cable. What could she find in me? ‘I have mistook my person all this
while,’ &c. Do you know I saw a picture, the very pattern of her, the
other day, at Dalkeith Palace (Hope finding Fortune in the Sea), just
before this blessed news came, and the resemblance drove me almost
out of my senses. Such delicacy, such fulness, such perfect softness,
such buoyancy, such grace! If it is not the very image of her, I am no
judge.—You have the face to doubt my making the best husband in
the world; you might as well doubt it if I was married to one of the
Houris of Paradise. She is a saint, an angel, a love. If she deceives me
again, she kills me. But I will have such a kiss when I get back, as
shall last me twenty years. May God bless her for not utterly
disowning and destroying me! What an exquisite little creature it is,
and how she holds out to the last in her system of consistent
contradictions! Since I wrote to you about making a formal proposal,
I have had her face constantly before me, looking so like some
faultless marble statue, as cold, as fixed and graceful as ever statue
did; the expression (nothing was ever like that!) seemed to say—‘I
wish I could love you better than I do, but still I will be your’s.’ No,
I’ll never believe again that she will not be mine; for I think she was
made on purpose for me. If there’s anyone else that understands that
turn of her head as I do, I’ll give her up without scruple. I have made
up my mind to this, never to dream of another woman, while she
even thinks it worth her while to refuse to have me. You see I am not
hard to please, after all. Did M—— know of the intimacy that had
subsisted between us? Or did you hint at it? I think it would be a
clencher, if he did. How ought I to behave when I go back? Advise a
fool, who had nearly lost a Goddess by his folly. The thing was, I
could not think it possible she would ever like me. Her taste is
singular, but not the worse for that. I’d rather have her love, or liking
(call it what you will) than empires. I deserve to call her mine; for

nothing else can atone for what I’ve gone through for her. I hope
your next letter will not reverse all, and then I shall be happy till I see
her,—one of the blest when I do see her, if she looks like my own
beautiful love. I may perhaps write a line when I come to my right
wits.—Farewel at present, and thank you a thousand times for what
you have done for your poor friend.
P.S.—I like what M—— said about her sister, much. There are good
people in the world: I begin to see it, and believe it.

LETTER THE LAST
Dear P——, To-morrow is the decisive day that makes me or mars
me. I will let you know the result by a line added to this. Yet what
signifies it, since either way I have little hope there, ‘whence alone
my hope cometh!’ You must know I am strangely in the dumps at
this present writing. My reception with her is doubtful, and my fate is
then certain. The hearing of your happiness has, I own, made me
thoughtful. It is just what I proposed to her to do—to have crossed
the Alps with me, to sail on sunny seas, to bask in Italian skies, to
have visited Vevai and the rocks of Meillerie, and to have repeated to
her on the spot the story of Julia and St. Preux, and to have shewn
her all that my heart had stored up for her—but on my forehead
alone is written—Rejected ! Yet I too could have adored as fervently,
and loved as tenderly as others, had I been permitted. You are going
abroad, you say, happy in making happy. Where shall I be? In the
grave, I hope, or else in her arms. To me, alas! there is no sweetness
out of her sight, and that sweetness has turned to bitterness, I fear;
that gentleness to sullen scorn! Still I hope for the best. If she will but
have me, I’ll make her love me: and I think her not giving a positive
answer looks like it, and also shews that there is no one else. Her
holding out to the last also, I think, proves that she was never to have
been gained but with honour. She’s a strange, almost an inscrutable
girl: but if I once win her consent, I shall kill her with kindness.—Will
you let me have a sight of somebody before you go? I should be most
proud. I was in hopes to have got away by the Steam-boat to-
morrow, but owing to the business not coming on till then, I cannot;
and may not be in town for another week, unless I come by the Mail,
which I am strongly tempted to do. In the latter case I shall be there,
and visible on Saturday evening. Will you look in and see, about eight
o’clock? I wish much to see you and her and J. H. and my little boy
once more; and then, if she is not what she once was to me, I care not
if I die that instant. I will conclude here till to-morrow, as I am
getting into my old melancholy.—
It is all over, and I am my own man, and your’s ever—

PART III

Welcome to our website – the perfect destination for book lovers and
knowledge seekers. We believe that every book holds a new world,
offering opportunities for learning, discovery, and personal growth.
That’s why we are dedicated to bringing you a diverse collection of
books, ranging from classic literature and specialized publications to
self-development guides and children's books.
More than just a book-buying platform, we strive to be a bridge
connecting you with timeless cultural and intellectual values. With an
elegant, user-friendly interface and a smart search system, you can
quickly find the books that best suit your interests. Additionally,
our special promotions and home delivery services help you save time
and fully enjoy the joy of reading.
Join us on a journey of knowledge exploration, passion nurturing, and
personal growth every day!
ebookbell.com

Passmedicine Notes With Key Points Passmedicine

About This Presentation

Slide Content

Tags

Categories

Download

Quick Actions

Statistics

Related Slideshows

Passmedicine Notes With Key Points Passmedicine

About This Presentation

Slide Content

Slide 1

Slide 2

Slide 3

Slide 5

Slide 6

Slide 7

Slide 8

Slide 9

Slide 10

Slide 11

Slide 12

Slide 13

Slide 14

Slide 15

Slide 16

Slide 17

Slide 18

Slide 19

Slide 20

Slide 21

Slide 22

Slide 23

Slide 24

Slide 25

Slide 26

Slide 27

Slide 28

Slide 29

Slide 30

Slide 31

Slide 32

Slide 33

Slide 34

Slide 35

Slide 36

Slide 37

Slide 38

Slide 39

Slide 40

Slide 41

Slide 42

Slide 43

Slide 44

Slide 45

Slide 46

Slide 47

Slide 48

Slide 49

Slide 50

Slide 51

Slide 52

Slide 53

Slide 54

Slide 55

Slide 56

Slide 57

Slide 58

Slide 59

Slide 60

Slide 61

Slide 62

Slide 63

Slide 64

Slide 65

Slide 66

Slide 67

Slide 68

Slide 69

Slide 70

Slide 71

Slide 72

Slide 73

Slide 74

Slide 75

Slide 76

Slide 77

Slide 79