Cardiology Flashcards

1
Q

MI infarction suspected

A

Ischeami results in myocardial necrosis

Myocardial necrosis releases proteins (troponins, myoglobin, creatine kinase, etc.)

Ischaemic symptoms
• Development of pathological Q waves on the ECG
• ECG changes indicative of ischaemia (ST segment elevation or depression)
• Coronary artery intervention, for example coronary angioplasty-

( coronary angioplasty/ percatenous transluminal coronary angioplasty ( PTCA)using a balloon to stretch open a narrowed artery.
Nowadays a stent is used and is left there permanently to improve blood flow.

Combination of stent + coronary angioplasty is percatenous coronary intervention (PCI)

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2
Q

Features that indicate increased chance of Acute myocardial infarction ?

A

Described as a pressure

Associated with nausea

Associated with diaphoresis

Radiation to either or both arms

Worse than previous angina

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3
Q

Features that indicate decreased likelihood/ chance of Acute myocardial infarction ?

A

Described as sharp

Described as positional

Reproducible with palpation

Inframammary location

Not associated with exertion

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4
Q

What are the classic presenting symptoms of ACS.

ACS - acute coronary symptoms

A

ACS - a group of conditions which result in ischaemia ( reduced blood flow to heart e.g myocardial infarction . Even none of MI - still very dangerous as associated with increased risk of heart attack.

Heavy, aching or tight

Centre or left side of chest

Not related to respiration or movement

May radiate to one or both arms, neck or jaw

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5
Q

What ECG changes are indicative of myocardial ischaemia that may progress to AMI

A

T wave inversion and ST segment depression may progress to AMI

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6
Q

What is infective endocarditis ?

A
Infection of :
0 endocardial surface of heart incuding:
- Valvular structures
- Chordae tendineae 
- sites of septal defects 
- or mural endocardium ( lining of heart chamber walls) 

SIGNS/ SYMPTOMS

  • Fever / chills (most common)
  • Cardiac murmurs

Non specific symptoms present :

0 Night sweats
0 Malaise
0 Fatigue
0 Anorexia
0 Weight loss
0 myalgias
  • Weakness (systemic emboli should be suspected in pl with asymmetric weakness consistent with stroke)
  • Arthralgias
  • Headache
  • SOB

Uncommon signs

  • Splinter Haemorrhages
    (found on nails of hand & feet - longitudinal, red-brown haemorrhage under a nail and looks like a wood splinter)
  • Osler nodes - (Osler’s nodes are painful, red, raised lesions found on the hands and feet.)
  • Janeway lesions - (Haemorrhagic, macular, painless plaques with a predilection for the palms and soles.)

Oslers , janeway - are skin manifestations of endocarditis.

Roth spots - Haemorrhages in the retina - oval , pale lesions.

Cutaneous infarcts
(if want more info look on BMJ)

RISK FACTORS

  • Hx of IE
  • artifical prosthetic heart valve
  • some types of Congenital heart types
    (including surgically corrected - prosethic materials)
  • Post heart transplant —-> may develop cardiac valvulopathy (increased risk of IE)
  • IV Drug use.

weaker

  • Intravascular Catheters or Implanted electronic devices
  • Mitral valve prolaspe wirh regurgitation
  • ## Hypertrophic cardiomyopathy
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7
Q

Diagnosis of IE ?

A
Blood cultures ( 3 sets from different venepuncture sites at 30 min interval before starting antibiotic therapy) 
* if SEPSIS SUSPECTED DO NOT WAIT TO START ANTIBIOTIC THERAPY. 
  • Echocardiogram - Transthoracic Echo done ——————–> if it does not show vegetations but IE still suspected transesophageal is done.

(First are the main ones used to diagnose - DUKE criteria)

  • FBC - anaemia , leukocytosis
  • CRP - elevated
  • ECG
  • Serum U & E , glucose
  • LFTS (normal or elevated)
  • Urinalysis - blood in urine may indicate septic emboli ( complication of IE)
  • Active sediment in urinalysis - means blood found.

CAN CONSIDER:

  • Rheuamtoid factors (positive result is a minor criteria for diagnosis of endocarditis ) - some places use ANA , anti - CCP etc.
  • complement levels ( e.g C3 , C4 ETC)
  • ESR - elevated
  • MRI
  • CT
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8
Q

What is the Duke Criteria ?

  • just for knowlegde (dont have to memorise)
A

The Duke criteria are a set of clinical criteria set forward for the diagnosis of infective endocarditis

For diagnosis the requirement is:

0 2 major and 1 minor criteria or
0 1 major and 3 minor criteria or
0 5 minor criteria

For adequate diagnostic sensitivity, transoesophageal echocardiography is the preferred modality used in patients designated “high-risk” or those in whom transthoracic echocardiography would likely be difficult. Examples of high-risk patients are those with 3:

past medical history of endocarditis
congenital heart disease
physical exam significant for:
signs of heart failure
a new heart murmur
stigmata of infective endocarditis
history of prosthetic heart valve implantation

Major criteria

0 positive blood cultures for infective endocarditis
0 typical microorganism for infective endocarditis from 2 separate blood cultures :

  • Viridans streptococci, Streptococcus bovis, and HACEK group

or

  • community-acquired Staphylococcus aureus or enterococci in the absence of a primary focus

or

persistently positive blood cultures, defined as recovery of a microorganism consistent with infective endocarditis from:

2 blood cultures drawn 12 hours apart or all of 3 or most of 4 or more separate blood cultures, with first and last drawn at least 1 hour apart.

  • evidence of endocardial involvement
    positive echocardiogram for infective endocarditis
  • oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets

or

  • on implanted material in the absence of an alternative anatomical explanation
  • abscess
  • new partial dehiscence of prosthetic valve - new valvular regurgitation

MINOR CRITERIA

  • predisposing heart condition
  • intravenous drug use
  • fever: 38°C
  • vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway lesions
- immunologic phenomena: 
glomerulonephritis
Osler nodes
Roth spots
rheumatoid factor
  • microbiologic evidence: positive blood culture but not meeting major criterion as noted previously or serologic evidence of active infection with organism consistent with infective endocarditis
  • echocardiography findings consistent with infective endocarditis but not meeting major criterion as noted previously

Capsule version of Duke criteria

Major diagnostic criteria include more than one positive blood culture (typical organism in 2 separate cultures or presistently positive blood cultures), or positive echocardiogram findings of vegetation, abscess or abscess prosthetic valve.
Minor criteria include:

predisposition (cardiac lesion, IV drug abuse);

fever over 38 °C;

vascular signs, e.g. mycotic emboli, Janeway lesions (painless palmar/plantar macules);

immunological signs e.g. Oslers nodes (painful swelling fingers/toes), positive RhF, glomerulonephritis

microbiological evidence not fitting major criteria.

Diagnosis is made on 2 major, 1 major/3minor or >5 minor criteria.

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9
Q

Treatment of IE ?

A

Suspected IE

1ST LINE

  • Supportive care (ABC) + Empirical brooad spectrum antibiotics

Consider surgery :

  • Acute heart failure - emergency surgery or cardiogenic shock despite medical therapy.

(Give IV diuretics to manage pulmonary oedema before surgery)

CONFIRMED IE - targeted antibiotic therapy

consider surgery - Indications for surgery include:[7]

Heart failure: for example, aortic or mitral valve (prosthetic or native) endocarditis with severe acute regurgitation, obstruction or fistula causing persistent pulmonary oedema or cardiogenic shock despite medical therapy
Uncontrolled infection such as:
Abscess, false aneurysm, fistula, or enlarging vegetation
Prosthetic valve endocarditis caused by staphylococci or non-HACEK gram-negative bacteria
Fungal or multidrug-resistant organism endocarditis
Prevention of embolism: for example, aortic or mitral valve (prosthetic or native) endocarditis with persistent vegetations >10 mm after one or more embolic episodes despite appropriate antibiotic therapy.

ONGOING - high risk of IE

1ST LINE

Advice + antibiotic prophylaxis.

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10
Q

What heart valve is most affected by IV drug users ?

A

Tricuspid

Injection into venous circulation will impact tricupsid valve most ( valve after right atrium - where venous blood enters from IVC )

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11
Q

Complications of IE ?

A

Septic emboli ——————> Infarction ( heart block etc) OR TIA

  • Acute kidney injury
  • Heart failure
  • Veterbral osteomylelitis .
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12
Q

Some causes of bradycardia?

A
  • Hypothermia
  • Hypothyroidism
  • Aerobic training (athletes)
  • Myocardial infarction
  • (not sure about this - nothing is support capsule info) Legionnaire’s disease / Legionalla pneumonia (Lung infection caused inhalation of aerolised bacteria e.g from air condition or hot tubs , contaminated drinking water , taps / showers that havent been use often etc
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13
Q

What is pericarditis ?

A

Pericarditis - Inflammation of the pericardium.

Acute - if less than 4-6 weeks.

Can be :

  • Dry (Fibrinous)

or

  • Effusive - with purulent , serous , Haemorrhagic exudate.

CHARACTERISTICS

Traid of main symptoms :

  1. Sharp , pleuritic (on breathing) - can also be stabbing or aching.
    (*sharp , severe , retrosternal (behind breast bone , sternum) worst with inspiration , supine (lying down ) )- sitting down or leaning forward makes it better)
  2. Pericardial rub (TYPICAL OF PERICARDITIS)
    (grating , to - and fro sound produced by friction of the heart against the inflammed pericardium) - can be heard loudest at expiration
  • if large pericardial effusion present - pericardial rub may be absent as pericardium is seperated so cannot rub against each other.
  • Pleural rub vs pericardial rub - ask patient to hold breath , pericardial rub stilll heard & occurs at every heart beat.
    3. Serial electrocardiographic changes.

RISK FACTORS

  • Male
  • Age - 20 -50 years
  • Transmural Myocardial infarction
  • transmural - involves full thickness of myocardium.
  • Cardiac surgery
  • Neoplasm
  • Recent histoy of viral or bacterial infections
  • ureamia or dialysis
    (ureamia - uric acid in blood / if dialysis is not working -
    metabollic toxins are accumulating in blood due to kidney failure and irritating pericardium)
  • systemic autoimmune disease e.g Rh Athritis , SLE.

WEAK

  • pericardial injury ( can occur weeks - months after)
  • mediastinal radiation.

COMPLICATIONS

Cardiac Tamponade
- Constrictive Pericarditis —————–> prevents ventricular filling ————————> Heart failure.

  • pain can mimic Myocardial ischemia / infarction
    (usually describe more as pressure - like , heavy squeezing pain vs sharp & pleurituc

or pulmonary embolism - need to be careful of PE because its treatemnt of anticooagulation can be life threatening in pericardtitis - cause bleeding into pericardial space ————> Cardiac tamponade.

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14
Q

Diagnosis of Pericarditis ?

A

ECG -
Changes seen -
0 Global upwardly concave ST-segment (J-point) elevations with PR-segment depressions in most leads
0 J-point depression and PR elevation in leads aVR and V1.

  • Serum Troponin - elevation (indicates pericarditis myopericarditis (myocardial involvement) (or other aetiologies e.g ACS)

0 Echocardiograpgy - do for all those suspected - if Cardiac Tamponade (do urgently at bedside) - normal does exclude diagnosis.

0 Pericardiocentesis - done if :

Cardiac tamponade (urgently needed)

  • Suspected purulent pericarditis

or large / symptomatic pericardial effusion

or High suspicion of neoplastic pericarditis

  • can send fluid for analysis (bacteria , fungi , autoimmune , TB causes)
  • CRP
  • Serum U & E - elevated urea indicates ureamic pericarditis
  • FBC
  • LFTs - elevated with liver congestation occuring developing cardiac tamponade.
  • CXR

CONSIDER

  • Blood cultures
    (if purulent P suspected or signs of sepsis) - infective cause.
  • autoimmune screen - if autoimmune P suspected
  • Viral screen - if viral cause of pericarditis suspected .
  • Creatine Kinase (suggest myocardial injury)
  • ESR
  • Chest CT , or cardiac MRI - if complicated P suspected or atypical presented.
  • pericardial biopsy ( rarely done - Cardiac MRI prefered)
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15
Q

Treatment of Pericarditis ?

Idopathic or viral

and criteria for admission to hospital.

A

SUSPECTED PERICARDITIS

1ST LINE
- Triage & consider hospital admission

Admit to hospital if :

Any of the following high-risk features

  • High fever (i.e., >38°C [>100.4°F])
  • Subacute course (i.e., symptoms over several days without a clear-cut acute onset)
  • Evidence of a large pericardial effusion
  • Cardiac tamponade
  • Failure to respond within 7 days to a non-steroidal anti-inflammatory drug

Minor risk factors (based on expert opinion and literature review)

  • Pericarditis associated with myocarditis (myopericarditis; associated with a rise in troponin)
  • Immunosuppression
  • Trauma
  • Oral anticoagulant therapy.

if none of the high risk features of clinical features that suggest an underlying aeitology that requires inpatient management———————————————> STart empirical anti-inflammatories and arrange 1 week follow up.

Consider Pericardiocentesis - if cardiac tamponade suspected.

ACUTE

Idiopathic or viral (non-purulent)

1ST LINE

0 high dose NSAIDS
(Aspirin or Ibu)
(* aspirin prefered for those recovering from and, other NSAIDS can adversely affect healing & associated with increased risk of cardiac events. )

+ PPI (omeprazole)

+ Colchicine (for 3 months )(Crucial to prevent recurrance)

+ Exercise restriction
(avoid strenous actvitity unitl symptoms resolve & CRP normalised.

Consider -

Corticosteriods - (PRED oral) if NSAIDS , Colchicine is contrainidcated & infectious cause is excluded ( do not use in viral P as there is a risk of re - activation of viral infection & inflammation)
also if there is a indication for use e.g. presence of autoimmune condition - Colchicine is used in combination with steriods in this situation) - IMPORTANT.

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16
Q

Treatment of pericarditis ?

not idiopathic of viral (non - purulent)

A

Not idiopathic - means that there is a known cause of the pericarditis so treat underlying cause.

1ST LINE

  • Treat underlying cause

+ NSAIDS (Aspirin or Ibu) + PPI

+ Colchicine (unless TB pericarditis )

+ Excercise restriction

Consider : Corticosteriod.

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17
Q

Treatment of Pululent Pericarditis ?

A

1ST LINE

  • IV empirical antibiotic therapy
    ( then tailor antibitiocs after results of blood cultures etc.)

+ Specialist management e.g Pericardiocentesis or surgical pericardial intervention

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18
Q

Treatment of Recurrent pericarditis ?

A

1ST LINE

NSAIDS + PPI + Colchicine (not TB P) + excercise restriction + treatment of underlying cause

Consider :

Corticosteriods

  • IV Immunosuppressant
    (Azathiopine , anakinra , normal immunoglobulin human) - only started by rheumatologist

Pericardectomy - if persistent & symptomatic or not improving or declining &
TB P with recurrent effusions and evidence of constrictive physiology despite therapy.

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19
Q

Colchicine - side feffects & cautions

A

Before starting - do a baseline FBC - as it can cause bone myelosupression & neutropenia.

Warn the patient that colchicine may cause gastrointestinal side effects such as diarrhoea. Consider reducing the dose if the patient is unable to tolerate the drug at full initial dose

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20
Q

Causes / types of Pericarditis ?

A
  • Tuberculosis (a common cause in the developing world)
  • Secondary immune processes (e.g., rheumatic fever, post-cardiotomy syndrome,
    &
    *post-myocardial infarction syndrome (POST - MI) - IMPORTANT ( Dressler’s syndrome (autoimmune reaction to damaged cardiac tissue))
  • Metabolic disorders (e.g., uraemia, myxoedema), radiotherapy
  • Cardiac surgery
  • Percutaneous cardiac interventions
  • Systemic autoimmune disorders (e.g., rheumatoid arthritis, systemic sclerosis, reactive arthritis, familial Mediterranean fever, systemic vasculitides, inflammatory bowel disease)
  • Bacterial/fungal/parasitic infections
    (some of these are purulent - produce Pus)
    (ex - influenza , mumps , Coxackie B , varicella)
  • Viral
  • Trauma
  • Certain drugs (e.g., hydralazine, antineoplastic drugs, clozapine, tumour necrosis factor-alpha inhibitors, phenytoin)[1]
  • Neoplasms.
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21
Q

Pericarditis pain vs myocardial ischaemia / infarction pain?

A

Chest pain caused by myocardial ischaemia/infarction (rather than pericarditis) typically:

  • Is described as pressure-like, heavy, and squeezing, rather than sharp and pleuritic
  • Does not with vary with respiration or positional changes
    Is not associated with a pericardial friction rub (unless there is associated pericarditis)
  • Lasts minutes to hours, rather than hours to days
  • Is associated with other key features such as nausea and vomiting, marked sweating, or breathlessness (or particularly a combination of these), or risk factors for cardiovascular disease.
22
Q

What is Hypertropic Cardiomyopathy ?

A

Genetic disorder (autosomal dominant) causes:

Left ventricular hypertrophy with no identifiable cause.

  • MOST COMMON GENETIC HEART DISEASE - AND MOST FREQUENT CAUSE OF SUDDEN CARDIAC DEATH IN YOUNG PEOPLE.

CHARACTERISTICS

  • many people will have no symptoms at the time of diagnosis - will be diagnosed following a rountine examination or family screening of an affected family member.
  • Systolic ejection murmur
  • left ventricular lift
  • double apical impulse or double carotid pulsation.
  • history of syncope or pre - syncope (feeling of about to pass out)
    (Syncope with exertion or without a prodrome (signs before the start of major disease)is particularly concerning and may be due to either outflow tract obstruction or a ventricular arrhythmia)

If symptomatic

  • dyspnoea
  • angina
  • chest pain
    *(Chest pain with exertion is particularly concerning and may be due to :
    0 massive hypertrophy with impaired coronary perfusion
    0 outflow tract obstruction
    0 myocardial bridging (tunnelling of coronary arteries into heart muscle).
    Atherosclerotic coronary artery disease should also be considered in the adult with exertional chest pain.)
  • palpitations ( sign of possible arrhythmias)
  • irregular irregular pulse - sign of atrial arrhythmias.
  • systolic murmur (enlarged septum can interfere with novement of mitral valve )

RISK FACTORS

  • Male
  • Age - 30 to 50 years
  • Fhx of HCM or sudden cardiac death - autosomal dominant
23
Q

Diagnosis of HCM?

A

ECG -
LVH -

  • Most common ECG changes can show Giant T wave inversion ( Large negative T waves ) or ST depression.
  • Prominent Q waves in leads 2 M 3 , AVF , V5 & 6
  • LVH - QRS complexes in Midprecordial leads (V1-V4) are tallest.
  • Some patients ca have a normal ECG.

CXR - can be normal or pathological in HCM.

Changes seen :
0 Cardiomegaly
0 Left atrial enlargement

  • Echo cardiogram -(used to for familial screening for sudden cardiac death with patients diagnosed with HCM.
    (possible results - enlarged IV septum , etc.)

Consider :

0 Exercise ECG
(used to assess risk for HCM patients )

0 Holter monitoring ( portable ECG device over 24 - 72 hours )
( those with Ventricular arrythmias risk of sudden cardiac death)

0 Nuclear Imaging exercise test- uses a small amount of radioactive material (tracer) show blood flow while you are at rest and during activity, showing areas with poor blood flow or damage in your heart.
( done in those with excertional CP , Ventricular tachycardia on Holter monitoring)

0 CT coronary arteriography -
( done evaluate atherosclerotic disease who have excretional chest pain or ischemia on nuclear testing)

0 Cardiac catheterisation ( patients with excertional chest pain , ischemia , increased risk of Coronary Artery D )

0 Cardiac MRI - if poor visualisation by echocardiogram in suspected HCM patients.

24
Q

Treatment of HCM?

A

Asymptomatic

AT RISK OF SUDDEN CARDIAC DEATH

1ST TIME

  • implantable cardio - defibrillator (ICD) + restriction from from high - intensity athletics.

NOT AR RISJ OF SCD

  • Observation

Symptomatic

Left ventricular outflow obstruction - preserved systolic function

1ST LINE
(negative inotropic & chronotrophic agents )

Atenolol , propranolol , metoprolol , nadolol ( Beta blockers)

( Add disopyramide to a Beta blocker or CAB if obstruction is persistent severe & symptomatic despite therapy) - monitor QT interval.

secondary options ( Verapamil , Diltiazem - Calcium channel blockers)
(AVOID IF PATIENT HAS PRONOUCED OBSRUCTION)

ADJUNCT - ICD implantation - if found to be at risk of SCD at any point

ADJUNCT - control of arrhythmias
- Amidarone ( help prevent recurrences of atrial Fibrillation)

  • (beta blockers and verapamil, Diltiazem(non -dihydropyridine CAB) - Can be used in chronic atrial fib)
  • Pacemarker permanent - with HCM patients with symptomatic sinus node dysfunction or V Block , AF , VA)

2ND LINE - refactory to therapy

MYECTOMY (removal of part of septal wall)

or Alcohol septal ablation (ADULTS ONLY) - (alcohol injected through a tube & and destroys some of the thickened. muscle)

or DUAL CHAMBER PACEMACKER - if patient does not want other options.

ADJUNCT - same as first line.

ADJUNCT - Coronary artery unroofing - if myocardial brigding is causing ischemia by compression.
(MB common in HCM - Coronary ateries tunnel through heart muscle instead of resting on top)

Non onstructive with preserved systolic function

  • same as obstruction one but without surgery options. ( except for potential myocardial brigding surgery unroofing)

End stage heart failure with systolic dysfunction

1ST LINE

Beta blocker + ACE / ARB + consider ICD + high intensity athletic restriction

ADJUNCT - Diuretic (if evidence of Fluid retention)

ADJUCNT - Aldosterone antagonists (spiralactalone - 1st , eplernone - 2nd) for moderate - severe HF

ADJUNCT - management of arrythmias

ADJUCNT - CA unroofing.

AdJUNCT - refactory to all medical therapy - referral to transplant.

25
Q

Cautions- Digoxin ?

A

Digoxin levels need monitoring. Toxicity may occur especially if there is renal dysfunction, hypokalaemia, hypomagnesaemia, or hypothyroidism.

26
Q

Most common mechanism of sudden death in HCM ?

A

Arrhythmias

due to increased risk of ischemia in subendocardial region (btw endocardium & myocardium ) —-> getting further away from blood supply on hear t surface.

27
Q

What is mitral regurgitation ?

A

Condition where mitral valve does not close properly letting blood flow backwards.

CAUSES

0 Mechanical failure in mitral valve appartus ( anterior & posterior leaflets , chordae tendineae , paillary muscles etc)
ex - mitral valve proplaspe

-Rupture of mitral valve support structures

  • Infection of mitral valve appartus
  • Rheumatic heart disease (untreated strep infection)
  • Endocarditis (infection of valves)
  • Trauma
  • Autoimmune - RA etc.
  • MI or CAD
  • Cadiomyopathy
  • Medicines
  • Metabollic , congential , degenerative causes.

SIGNS/SYMPTOMS

0 Dyspnoea on excretion
0 Decreased excercise tolerance
0 Lower extremity oedema
0 Holosystolic murmur - Blowing murmur ( whooshing , blowing sound ) at the apex which radiates to axilla.
0 fatigue
0 Displaced point of maximal impulse - where pulse can best felt on chest wall ( found at the same place as Apex beat) - INDICATES SEVERE & CHRONIC MR.

RISK FACTORS

  • Mitral valve proplaspe
  • Hx of Rheumatic heart disease
  • Infective endocarditis
  • Hx of cardiac trauma
  • Hx of MI
  • Hx of Congenital heart disease
  • HCM
  • Hx of ischeamic heart disease
  • Left ventricular systolic dysfunction
  • anoretic / doperamingeric drugs
    (ergotamine , perolide , cabergoline)
28
Q

Diagnosis of Mitral regurgatation?

A

Transthoraic echo (determine if valve dysfunction present & severity)

ECG - may underlying arrhythmia or prior infaraction

29
Q

Treatment of Mr?

A

Acute

1ST LINE - emergency surgery

Annuloplasty - procedure tighten annulus (fibrous ring connected to leaftlets)

or

Mechanical valve (artifical made of metal etc) & anticoagulation

or

Bioprothesis - aftifical valve made from organic material (dont need anticoagulation)

ADJUNCT - Pre - operative diuretics ( furosemide (most common) , indapamide - to reduced afterload & stablise patient if needed.

ADJUNCT - if hypotension with severe acute MR - Intra-aortic ballon counterpulsation

ONGOING - asymptomatic chronic MR

left ventricular ejection fraction larger than 60 % & end diastolic diameter < 45mm

1ST LINE

ACE inhibitors (lisinopril , enalapril, captopril) etc. )

+ Beta - blockers

If more than less than 60 % & more than 45mm -

1ST LINE- Surgery

same as earlier surgeries for emgency + one other option - Valvuloplasty

Symptomatic chronic MR

Left VEF > 30 % or more

1ST LINE
Surgery + ACE + Beta + pre-operative diuretics.

Left VEF > 30 % or less

ACE + Beta + pre-operative diuretics.

ADJUNCT - Intra-aortic balloon counterpulsation.

30
Q

What is mitral stenosis ?

A

Narrowing of mitral valve orifice.

CAUSES
- Rheumatic Vasculitis - linked to rheumatic fever complication of scarlet fever ( infection - Strept B) - causes fusion of commissures and thickening of valve leaflets .

COMPLICATIONS - Pulmonary hypertension , right sided heart failure
- decreased filling of left Ventricle ———–> left atrium pressure increases .

SIGNS / SYMPTOMS

  • Dyspnoea
  • Othropnoea
  • snap on opening of valve on auscultation (valve is stiff)
  • Diastolic murmur (low pitch rumbling sound)
  • loud first heart sound (S1)

Indicates that pulmonary hypertension and/or Right Ventricular failure present:

  • neck vein distension ( Jugular vein distension)
  • Loud P2 (P2 - sound of pulmonary valve closing )
  • 2 heart sounds - S1 & S2 (P2 is a component of S2 with A1 (aortic valve closure)
    (s1 = t1 (tricuspid) , m2 (mitral)
  • might see flushed cheeks 9 prominent reddish cheeks.

RISK FACTORS

  • Hx of rheumatic fever
  • Hx of strept B infection
  • Age - 40 to 50 yrs
  • Female

Weak

Mitral stenosis rare complication of SLE related valvular disease.

31
Q

Diagnosis of MS?

A

ECG
may show :
- atrial F , Left atrial enlargement , right ventricular hypertrophy,
CXR
may show ;
Kerley B lines (septal lines) - indicates intersitial oedema (look whenever HF OR Pulmonary oedema
Echocardiogram

  • trans-thoracic echocardiography - CONFIRMS DIAGNOSIS.
32
Q

Treatment of MS?

A

Asymptomatic

progressive asymptomatic disease - valve area > 1.5m2)

1ST LINE - NO THERAPY

Severe asymptomatic disease - valve area - <1.5m2
)

1ST LINE - No therapy

ADJUNCT - ballon valvatomy ( valvuloplasty) - widens narrowed valve (inflate balloon etc.)
(CAN BE DONE IN ASYMPTOMATIC PL IF VALVE AREA < 1.0M2 OR PULMONARY HYPERTENSION PRESENT)

symptomatic -valve area <1.5 m2)

1ST LINE - Diuretic - (furosemide , bumetanide) + Balloon valvotomy ( valve score less than 9 or Valve replacement or repair ( valve score above 9)

Valve score - the lower the score the better condition the valve.

  • Beta - blocker (atenolol0)or ivabradine
    (if normal sinus rhythm which gets worse with exercise )

PREGNANT

1ST LINE - Diuretic

ADJUNCT - Ballloon valvotomy - if symptoms worsen & HF threatens life of mother or child.

33
Q

NSAIDS & Heart failure ?

A

NSAIDS have cardiovascular effects - should not be used.

34
Q

What is DVT ?

A

Deep vein thrombosis - Blood clot development in a major vein in leg , thigh , pelvis or abdomen, arm.

MOST COMMONLY IN LEG

Not usually life threatening but is dangerous because can cause Pulmonary embolism (Can be fatal)

SIGNS/ SYMPTOMS

  • Calf swelling
  • swelling of entire leg (uncommon)
  • localised pain along venous system * assessed by tapping gently along Deep venous system from groin to adductor canal to popliteal fossa).
  • asymmetric oedema
  • Dilated superfical veins over foot and leg (not varicose veins)

Phlegmasia cerulea dolens
(Phlegmasia - inflammation cerulean - dark blue, dolens (painful)
- massive DVT massive - swelling can obstruct not only venous outflow but arterial inflow, leading to this due to ischaemia.
*leg is usually blue and painful. - LIFE THREATENING - LEADS TO LIMB LOSS .

note - Phlegmasia Alba dolens ( swelling of leg due to extensive DVT & early compromise of aterial supply - MILK LEG (usually affects pregnant women)

RISK FACTORS

  • Major surgery within the 3 months proceeding - ( damage to venous system , immbolisation , inflammation etc)
  • medical hospitalisation eithin preceeding 2 months (Immbolisation , IV catheters etc)
  • Active cancer
  • Previous venous thromboembolic event ( DVT or PE)
  • Recent fracture (commonly require surgery , immobilisation) or trauma
  • Increasing age
  • Pregnancy and post natal period
  • paralysis of lower limbs
  • Factor V Leiden mutation ( type of clotting factor )
  • Protein C or S , antithrombin deficiency
  • prothrombin gene mutation
  • Anti- phospholipid syndrome
  • Drugs -
    0 oestrogen containg contraceptives (especially in presence of thrombophilla & smoking & obesity)
    0 Tamoxifen & raloxifen (specially in presence of thrombophillic condition e.g factor V oLeiden.
    )
    0 Eryhropoietin in cancer therapy
    0 Adalimumab
    0 androgen deprivation therapies (prostate cancer)
    0 Testerone replacement therapy
    0 NSAIDS
35
Q

Treatment of DVT?

Initiation - phase therapy - no bleeding
& treatment phase & extended treatment phase ?

look at BMJ to really understand reasons for choice of anticoagulants

A

If interim anticoagulation needed (if wait for d- dimer test or proximal duplex ultrasound is longer than 4 hours ):

1ST LINE

Apixaban or rivaroban

secondary

LMWH (low molecular heparin) ( 5 days) then dabigatran or edoxaban.

or LWMH with Vitamin K.
(for at least 5 days)

PROXIMAL DVT OF LEG - NON -PREGNANT

1ST LINE - anticoagulation

(DOACs - Direct oral anticoagulnats - dabigatran, rivaroxaban, apixaban, or edoxaban ) ————————> if not possible wafarin —————————————> if not possible LMWH. )

Fondaparinux ( can be used but normally reserved for pl with heparin-induced thrombocytopenia.)

IV unfractioniated heparin (UFH) - used if increased risk of bleeding (recent surgery , peptic ulcertaion etc)

PLUS - Physical activity ,

Gradient stocking s - not useful in all (can trail in pl with acute / chronic symptoms of DVT )

Acute isolated Distal DVT of leg - non pregnant

1ST LINE

  • Serial imaging of deep veins for 2 weeks
  • Anti coagulation only given if thrombus propagates ( increases /move towards heart ?? - dont’t know )

PREGNANT

1ST LINE

LMWH or Subcantaneous UFH
(enoxaparin or dalteparin (1st) , heparin (2nd)

( DOACs - not used in pregnancy or other anticoags apart from heparin)

TREATMENT PHASE THERAPY

1ST LINE

  • maintain anticoagulation
    (minimum of 3 months - can be longer if needed)

(all above sections and lines of treatment have: + physical activity , adjunct - gradient stockings (special condition))

EXTENDED - BEYOND 3 MONTHS - maintains same anticoagulants

if post - natal (planning to breast feed - LMWH or Sub UFH)

if Not post- natal but not breastfeeding - Can use any antcoagulant

RECURRENT VTE

  • further investigation.
36
Q

Diagnosis of DVT?

A

Wells score - determines probability that someone has DVT in those suspected
- Score 2 or above - DVT likely
- Score less than 2 - unlikely
(not used in pregnant women)

D DIMER TEST
( d- dimer is a protein that dissolve in the blood when clot is dissolved)

If Wells score below 2 - do D DIMER TEST
(if this is negative (normal ) exclude DVT)

0 Proximal Duplex ultrasound - if Dimer elevated cotinue to this & for those with well score > 2.
(assess all deep veins in affected area)
- if negative repeated in 5 to 7 days.
(recommended for pregnant women)

0 Whole leg ultrasound - not need to repeat if negative

*either promixal duplex vs whole leg ultrasound can be used.

0 INR & aPPT (activated partial thromboplastin time) - before starting wafarin , IV heparin to check baseline levels

0 Urea & Creatine - some anticaogulants therapies (Heparin, apixaban,dabigatran, edoxaban etc) - need to be adjusted or stopped if renal impairment present.

0 LFTs - some anticoagulants not used in hepatic dysfunction ,

0 FBC - assess bleeding risk

Can consider:

0 Colour flow doppler
0 CT abdomen & pelvis with contrast (more accurate than ultrasound for visceral veings and deep veins of Abdo & pelvis)

0 Thrombophilla screen.
( if considering stopping interim anticoagulants - screen in those who have unprovoked DVT only - checks for anti - phospholipid )

37
Q

What is the wells critera ?

A

use determine the probability of DVT in suspected patient.

The criteria are as follows:

Active cancer (any treatment within past 6 months): 1 point

Calf swelling where affected calf circumference measures >3 cm more than the other calf (measured 10 cm below tibial tuberosity): 1 point

Prominent superficial veins (non-varicose): 1 point

Pitting oedema (confined to symptomatic leg): 1 point

Swelling of entire leg: 1 point

Localised pain along distribution of deep venous system: 1 point

Paralysis, paresis, or recent cast immobilisation of lower extremities: 1 point

Recent bed rest for >3 days or major surgery requiring regional or general anaesthetic within past 12 weeks: 1 point

Previous history of DVT or pulmonary embolism: 1 point

Alternative diagnosis at least as probable: subtract 2 points.

38
Q

Treatment of DVT ?

Initiation phase - active bleeding

A

1ST LINE

IVC filter (small device that stops blood clots from going into the lungs ) + Physical activity

ADJUCNT - gradient stockings (maybe)

39
Q

Treatment of DVT ?

special cases :

Renal impairment
- Hepatic impairment

A

Hepatic - LWMH or UFH overlapped with warafin

Renal - IV or subcantenous UFH followed by warafin.

Cancer - Oral Xa inhibitor (Apixaban , rivaoxaban , edoxaban) or LMWH for at least 6 months.

40
Q

How is Warafin & Heparin monitored

A

Warafin - INR (2 -3 - range ,2.5 - target INR) - normal
(If recurrent DVT /PE OR mechanical heart valve when on warfarin (3-4- range , 3.5 - target INR)

Heparin - aPPT ( activated prothrombin time)

41
Q

What is pulmonary embolism ?

A

Complication of DVT – dislodged thrombi occludes the pulmonary vasculature.

signs/symptoms

0 Dyspnoea - most common
( also includes possible tachypnoea > 20)
0 chest pain (Pleuritic) - localised to one side. normally acute.
* central PE - can present like angina like pain - unikely tho
0 signs of concurrent DVT
0 Hypocaemia (low oxygen sat <94%)
0 cough

RISK FACTORS

  • Active cancer
  • previous or current DVT
  • Recent surgery or hospitalisation
  • pregnancy
    (similar to DVT - havent written all)
42
Q

Diagnosis of PE?

A

0 CTPA - CT pulmonary angiography (for definitive diagnosis)

0 Echocardiogram
- if CTPA not availabe or in Haemodynamically unstable patients.

0 Wells score or geneva score

0 D- Dimer - non pregnant in any patients whose well score suggest unlikely PE but haemodynamically unstable.
(if negative excludes PE - IF WELL SCORE NEGATIVE)

Check baseline levels before starting anticagulant :

FBC

  • U & E
  • INR
  • aPPT
  • PT (prothrombin time)
  • Liver function tests

ECG - not diagnostic - but may exclude other causes or support diagnosis e.g
show right ventricular dysfunction suggest PE (RBBB , R axis deviation etc )
Normal results does not rule out PE.

- CXR - same reason as ECG. - usually normal that does not rule out ECG
may show :
0 atelectasis
0 pleural effusion 
0 elevation of hemidiaphragm 
  • (Pulmonary infarction secondary to PE can be difficult to distinguish from pneumonia on CXR.0
43
Q

Diagnosis of PE?

A

0 CTPA - CT pulmonary angiography (for definitive diagnosis)

0 Echocardiogram
- if CTPA not availabe or in Haemodynamically unstable patients.

(Ventilation perfusion also used in some place if CTPA cannot be used - limited use in sig underlying lung disease , left ventricular failure or HF)

0 Wells score or geneva score
(PE likely’ (Wells score >4) or ‘PE unlikely’ (Wells score ≤4))

0 D- Dimer - non pregnant in any patients whose well score suggest unlikely PE but haemodynamically unstable.
(if negative excludes PE - IF WELL SCORE NEGATIVE)

Wells / geneva score (likely) ——————–> CTPA or alternative —————> if wells score unlikely —————–> D-Dimer ———————> CTPA or alternative

Check baseline levels before starting anticagulant :

FBC

  • U & E
  • INR
  • aPPT
  • PT (prothrombin time)
  • Liver function tests

ECG - not diagnostic - but may exclude other causes or support diagnosis e.g
show right ventricular dysfunction suggest PE (RBBB , R axis deviation etc )
Normal results does not rule out PE.

- CXR - same reason as ECG. - usually normal that does not rule out ECG
may show :
0 atelectasis
0 pleural effusion 
0 elevation of hemidiaphragm 
  • (Pulmonary infarction secondary to PE can be difficult to distinguish from pneumonia on CXR.

0Lower limb compression venous ultrasound - in suspected DVT patients.

Thrombophilla screening - same as written in DVT

  • if unprovoked PE - could be an undiagnosed cancer - further investigation.
  • if low risk and meets all criteria in PERC rule - PE can be ruled out.
    If low risk but do not meet one of critera should do a D- dimer test.
44
Q

What is PERC rule

A

No further investigation is indicated if a patient meets the PERC rule (a PE can effectively be ruled out). The risk of PE is considered to be lower than the risk of testing.[76]

Request D-dimer testing for any patient in whom the PERC rule fails to rule out a PE (i.e., one or more criteria not fulfilled).[98]

0 Age <50 years
0 Heart rate <100 bpm
0 SaO2 on room air ≥95%
0 No unilateral leg swelling
0 No haemoptysis
0 No recent surgery or trauma (≤4 weeks ago requiring treatment with general anaesthesia)
0 No prior PE or DVT
0 No hormone use (oral contraceptives, hormone replacement, or oestrogenic hormones used in male or female patients).
45
Q

Treatment of PE?

A

PE suspected - haemodynamically unstable and/ or hypoxaemic

1ST LINE
- Respiratory support

  • Fluid resuscitation
    (Give intravenous fluids if SBP is <90 mmHg and the JVP is not elevated)
    & monitor for signs of RIGHT HEART FAILURE
    (bcc leading cause of death in high risk PE patients)

PE confirmed - H unstable

1ST LINE
- Start UFH (Heparin) (stop within 24 hrs ) + Thrombolysis (alteplase , streptokinase, urokinase)——————————————–> switch to alternative anticoagulant after

Consider :
Vasoactive drug (Noradrenaline , dobutamine , adrenaline) if systolic BP remains <90mmHg after thrombolysis or if Thrombolysis not possible. 

0 surgical embolectomy or percutaneous catheter-directed therapy
- problems with thrombolysis or not working.

  • if contraindication thrombolysis (just do everything the same and leave this out)
  • if contraindication to both thrombolysis & anticoagulation

1ST LINE - Vasoactive drug + plus MDT discussion to consider starting surgical embolectomy or percutaneous catheter-directed therapy

46
Q

Treatment of PE?

  • Confirmed PE - haemodynamically stable.
A

1ST LINE

  • anticoagulation + risk assessment
    (to detemie if in patient or outpatient treatment)

UNsuitable for anticoagulation

(ask senior management)
Consider if relative risk - try alternative
if deemed not possibel to use do Venous filter

*(anti- coagulants should be done for at least 3 months )

Recurrent PE despite adequate anticoag therapy

1ST LINE

  • Increase anticoag dose or switch to alternative

Consider : Venous filter

47
Q

Absolute contraindecations to anticoagulants.

A
Active bleeding
Recent intracranial haemorrhage
Recent, planned, or emergent surgery or procedure with high bleeding risk
Platelet count <50,000/uL
Severe bleeding diathesis.
48
Q

What reverse he effects of Wafarin and Heparin?

A

Wafarin - Vitamin K

Heparin - protamine

49
Q

WarafrIn & NSAIDS?

A

should be avoided - beacuse together significantly increase risk of GI bleed - SEVERE INTERACTION

50
Q

Maximum dose of paracetamol for adults?

A

Oral adminstration

4g maximum a day (0.5g - 1 g every 4-6 hrs)

For IV infusion - depends if under 50kg or above.

< 50KG - 60mg /Kg (maximum dose)

> 50kg - 4g a day.
(if risk of hepatoxicity - (3g a day)

51
Q

Warafirin contraindications?

A
  • alcohol
  • amiodarone
  • Amoxicillin (penicillins - drugs in this class.)
  • aspirin
  • carbamazepine ( anti - consulvant)
  • ceftriaxone
    -ciproflaxin
  • citalopram (prams)
  • clarithromycin (mycins)
  • clopidogrel
  • cranberry juice
  • nsaids
  • doxycycline
  • fluorouracil
  • flucanazole (azoles)
  • glucagon
  • indomethacin
  • rifampcin
  • seratraline
    -st johns wort
  • tamifoxen
    Tetracycline
    Trimethoprim

FAB 5 - main ones .

FLUCANZOLE
AMIDARONE
BACTERIALS- TRIMETHOPRIM / SULFAMETHOZAZOLE , METRONIDAZOLE, Rifampin

FLOXACINS , AZOLES, MYCINS

52
Q

In what situations is PE even less specific for PE?

A

When the person has had recent bed rest , surgery or malignancy- these can cause a rise in d dimer
( can also be elevated in heart attack, infection , liver disease ( conditions which result in a reduction in the clearance of fibirin)