Cardio fifth yr Flashcards
What is pericarditis + its causes?
Condition referring to inflammation of pericardial sac - lasting for less than 4-6 weeks
Aetiology = viral infections (Coxsackie), TB, uraemia, post MI (early - fibrinous pericarditis, late - autoimmune pericarditis (Dresslers)), radiotherapy, CTD (SLE, RA), hypothyroidism, malignancy (lung/breast), trauma
Features of pericarditis?
Chest pain - can be pleuritic, relieved by sitting forwards
Non-productive cough
Dyspnoea
Flu-like Sx
Pericardial rub
Ix and Tx for pericarditis?
ECG - global/widespread, saddle-shaped ST elevation, PR depression
Transthoracic ECHO
Bloods - inflammatory markers, troponin (30% of pt’s may have elevated troponin - indicates possible myopericarditis)
Outpatient, unless fever >39 or elevated troponin then inpatient
Treat underlying cause
Strenuous physical activity avoided until Sx resolution
Combination of NSAIDs and colchicine are first line with acute idiopathic or viral pericarditis - until Sx resolution and normalitistion of inflammatory markers, followed by tapering of dose
RFs for infective endocarditis?
previous episode of endocarditis
previously normal valves - MV most commonly affected
rheumatic valve disease
prostethic valves
congenital heart defects
IVDUs - typically causing tricuspid lesion
recent piercings
Causes of infective endocarditis?
Staph aureus - most common cause - particularly common in acute presentation and IVDUs
Strep viridian’s - most common in developing countries, linked with poor dental hygiene
Staph epidermidis - colonise indwelling lines, most common following prosthetic valve surgery, 2 months post-op spectrum of organisms returns to normal
Strep bovis - associated with colorectal cancer
Non-infective - SLE, malignancy (marantic endocarditis)
Culture negative causes - prior ABx therapy, Coxiella burnetti, Bartonella, Brucella, HACEK (haemophilis, actinobacillus, cardiobacterium, eikenella, kingella)
Poor prognostic factors for infective endocarditis?
Staphylococcus aureus infection
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels
What is infective endocarditis?
condition where the inner lining of the heart (the endocardium) becomes inflamed secondary to an infection.
M>F (2:1)
higher in multimorbid pt’s, elderly, internal cardiac devices, IVDU
mostly left-sided
divided into native or prosthetic valve
Pathophysiology of infective endocarditis?
Transient bacteraemia
Damage to valvular tissue - aggregation of platelets and fibrin
Formation of vegetations - pathogens bind to platelet-fibrin matrix and proliferate causing vegetation
Vegetations can embolism causing further complications. Emboli from left side > cerebral infarcts or cerebral abscess. Right side - mycotic aneurysms, pulmonary infarcts, pulmonary abscesses
Deposition of immune complexes (type 3 hypersensitivity reaction) in skin, kidneys, eyes
Sx of infective endocarditis?
Hx - systemic infection (fever, malaise, night sweats, anorexia), anaemia (fatigue, breathlessness)
O/E
fever, tachycardia
new or changing heart murmur
splinter haemorrhages
oslers nodes (tender in fingers)
Janeway lesions (painless on palms)
Roth spots - retinal haemorrhages, pale in centre
clubbing - late sign
mild splenomegaly
bi-basal lung crepitation
clinical features from emboli (e.g., weakness from stroke)
Ix for infective endocarditis?
Vitals
ECG - exclude AV block as may be seen in aortic root abscesses which is a rare complication of IE
urine dipstick - microscopic haematuria
blood cultures - 3 sets taken 30 mins apart
FBC - exclude anaemia, check WCC to check infection
CRP/ESR - inflammatory markers
U&E - baseline if starting on nephrotoxic ABx such as gentamicin
TTE - identify vegettions
TOE - more detail than TTE
CXR - part of infection screen if Dx unclear, or if HF suspected
CT - if root abscess present
Modified Duke criteria for infective endocarditis?
Infective endocarditis diagnosed if
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria
Pathological criteria - Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria - positive blood cultures (2 positive BC’s showing typical organisms consistent with IE), evidence of endocardial involvement (positive ECHO, new valvular regurgitation)
Minor criteria - predisposing heart condition or IVDU, microbiological evidence doesn’t meet major criteria, fever >38, vascular phenomena (major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura), immunological phenomena (glomerulonephritis, Osler’s nodes, Roth spots)
Management of infective endocarditis?
IV ABx for 2 weeks before switching to oral. Tx for at least 6 weeks in prosthetic valve, 2-6 weeks for native valve.
start of the antibiotic course is taken from the first day a negative set of blood cultures is obtained
choice of antibiotic regimen depends on multiple factors including previous antibiotic use, the type of valve affected (native vs prosthetic), the microorganism involved and the antibiotic sensitivity of the particular organism
initial blind - native (amoxicillin and consider low-dose gentamicin), pen allergic, MRSA or severe sepsis (vancomycin + low dose gentamicin), prosthetic valve (vancomycin, rifampicin, + low dose gentamicin)
Native caused by staph - flucloxacillin
Caused by streptococci - benzylpenicillin
Indications for surgery:
severe valvular incompetence
aortic abscess (^ PR interval)
infections resistant to ABx/fungal infectons
cardiac failure refractory to standard medical Tx
recurrent emboli after ABx Tx
Complications of infective endocarditis?
Localised = valve destruction, HF, arrhythmias and conduction disorders, MI, pericarditis, aortic root abscess
Systemic = emboli, immune complex deposition, septicaemia, death
Management of stable angina?
Lifestyle changes - smoking cessation, cut down alcohol intake, dietary modification, exercise, target BMI <25
Medication - all pt’s receive aspirin and a statin if no CI. Sublingual GTN to abort angina attacks. Beta-blocker or calcium-channel blocker first-line depending on comorbidities, CI’s and pt preference.
if Ca-channel blocker as mono therapy should be rate-limiting - so verapamil or diltiazem. If in combination with beta-blocker then longer-acting dihydropyridine (amlodipine, nifedipine).
If poor response to initial Tx, then increase to maximum tolerated dose.
If not tolerated, add BB or CCB depending on which mono therapy
If can’t tolerate addition of CCB or BB, consider: long-acting nitrate, ivabradine, nicorandil, ranolazine
if pt taking both BB and CCB, then only add third drug whilst awaiting PCI or CABG
if using nitrate - asymmetric dosing interval to minimise nitrate tolerance
Procedure/surgical intervention - PCI with coronary angioplasty (catheter, ballon dilatation, stent)
CABG - if severe stenosis, midline sternotomy scar, graft vein (usually great saphenous vein) and bypass stenosis,
What is angina?
Constricting chest pain, due to increased demand of the heart (during exertion) but there is insufficient supply of blood to meet demand
due to narrowing of coronary arteries reducing blood flow to myocardium
stable as on exertion and relieved by rest or GTN
NICE define anginal pain as the following:
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by 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
Ix for stable angina?
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography - gold standard
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) - MPS with sPECT, stress ECHO
3rd line: invasive coronary angiography
Baseline Ix:
examination - heart sounds, signs of HF, BMI
BP
ECG
FBC - check for anaemia
U&Es - prior to starting ACEi and other meds
LFTS - prior to statins
Lipid profile
TFTs - thyrotoxicosis can exacerbate angina
HbA1c and fasting glucose
MOA of nitrates?
release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
Side effects of nitrates?
hypotension
tachycardia
headaches
flushing
nitrate tolerance - asymmetric dosing
Why are beta-blockers not used concurrently with non-dihydropyridine calcium channel blockers such as verapamil?
risk of complete heart block
What is heart failure?
defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body
usually result of structural or functional heart disease, but the term is also sometimes used more broadly e.g. high-output heart failure
How is heart failure classified?
By ejection fraction - can have normal or abnormal LVEF. Reduced LVEF is typically defined as < 35 to 40%. So HF-rEF or HF-pEF. HF-rEF patients typically have systolic dysfunction (impaired myocardial contraction during systole - ineffective pumping), whereas HF-pEF patients have diastolic dysfunction (impaired ventricular filling during diastole - ineffective filling)
By time - acute or chronic. Most urgent Sx are usually due to LVF causing pulmonary oedema.
By left/right - HF-rEF and HF-pEF typically develop left-sided heart failure - due to increase LV afterload (HTN or aortic stenosis) or increase LV preload (AR resulting in back flow to LV)
Right-sided heart failure is caused by either increased right ventricular afterload (e.g. pulmonary hypertension) or increased right ventricular preload (e.g. tricuspid regurgitation).
High-output HF - ituation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body. Causes = anaemia, AVM, Paget’s, pregnancy, thyrotoxicosis, thiamine deficiency
Systolic vs diastolic dysfunction in heart failure?
Systolic:
Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias
Diastolic:
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis
Sx of heart failure?
Left ventricular failure typically results in:
pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles
cardiac wheeze
cardiac cachexia - WL
Right ventricular failure typically results in:
peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly - right hypochondriac pain
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)
What is cardiac output?
stroke volume X HR
stroke volume - volume of blood pumped in 1 beat
What is ejection fraction?
stroke volume / end diastolic volume
normal 55-70%
Causes of HFrEF?
decreased contractility - coronary artery disease, volume overload (valvular disease - MR/AR, and RAAS neurohormonal system) and dilated cardiomyopathy
increased afterload - HTN, aortic stenosis - LV becomes hypertrophied, (increasing O2 demand, decreasing O2 supply)
Causes of HFpEF?
stiff left ventricle
left ventricular hypertrophy - doesn’t stretch, doesn’t fill during diastole
restrictive cardiomyopathy
myocardial fibrosis
pericardial constriction
RFs for HFrEF and HFpEF?
obesity
HTN
DM
renal disease
RFs for HFpEF?
elderly
2:1 F:M
higher co-morbidity burden - HTN, AF, anaemia, COPD
Dx of heart failure?
clinical diagnosis
Hx
O/E - bibasal crackles, peripheral oedema, raised JVP, additional heart sounds (S3 in dilated ventricle, S4 poor LV compliance)
Ix for heart failure?
NTproBNP - released from atria and ventricle during volume expansion and pressure overload - prognostic marker
if high (>2000) - assessment within 2 wks
if raised (400-2000) - assessment within 6 wks
Imaging -
CXR - pulmonary oedema, pleural effusion, upper flow distribution, cardiomegaly
ECHO - valves, volume of chambers, EF
Scoring systems for HF?
Framingham
Boston
Tx of HF?
reduce mortality and manage Sx
loop diuretics don’t reduce mortality - just Sx
First-line - ACEi and BB. One at time. ACEi and BB have no effect on mortality in heart failure with preserved ejection fraction
Second-line - aldosterone antagonist. Can cause hyperkalaemia (as well as ACEi) so monitor K+.
SGLT-2 if HFrEF
Third-line - initiated by specialist - ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
Surgical:
Implantable cardiac defibrillators (if EF <35% due to risk of VT/VF)
Cardiac resynchronisation therapy (if EF <35% and QRS>150 or LBBB, paces left and right ventricle together)
Other treatments
offer annual influenza vaccine
offer one-off pneumococcal vaccine
Classification of HF?
The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure:
NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
Factors affecting BNP levels?
Increased - LVH, ischaemic, tachycardia, RV overload, hypoxia (including PE), GFR <60ml/min, sepsis, COPD, DM, age>70, liver cirrhosis
decreased - obesity, diuretics, ACEi, BB, ARB, aldosterone antagonists
Criteria for ivabradine?
sinus rhythm > 75/min and a left ventricular fraction < 35%
Criteria for sacubitril-valsartan?
criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period
Criteria for digoxin?
strongly indicated if there is coexistent atrial fibrillation
Not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
Criteria for cardiac resynchronisation therapy?
widened QRS (e.g. left bundle branch block) complex on ECG
Effects of BNP?
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
Summary of acute HF?
sudden onset or worsening of the symptoms of heart failure. Thus it may present with or without a background history of pre-existing heart failure
causes T1RF
Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function)
Causes of de novo HF - ischaemia, Viral myopathy, Toxins, Valve dysfunction
Causes of decompensated HF - Acute coronary syndrome, Hypertensive crisis, Acute arrhythmia, Valvular disease
Features of acute HF?
Sx - SOB, reduced exercise tolerance, oedema, fatigue, cough (frothy white/pink sputum)
Signs - cyanosis, tachycardia, elevated JVP, displaced apex beat, bibasal crackles, wheeze, S3
Ix for acute HF?
Blood tests – this is to look for any underlying abnormality such as anaemia, abnormal electrolytes or infection. FBC, U&E, LFTs, CRP/ESR, BNP, TFT, cardiovascular bloods (lipid, HbA1c, glucose)
Chest X-ray – findings include pulmonary venous congestion, interstitial oedema and cardiomegaly
Echocardiogram – this will identify pericardial effusion and cardiac tamponade
B-type natriuretic peptide – raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.
Management of acute HF?
Pour away (stop) their IV fluids
Sit up
Oxygen
Diuretics
IV loop diuretics
O2
vasodilators - if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease
if respiratory failure - CPAP
if hypotension/cardiogenic shock - inotropic agents (e.g. dobutamine), vasopressors (e.g. norepinephrine), mechanical circulatory assistance (e.g. intra-aortic balloon counterpulsation or ventricular assist devices)
Stop BB if patient has heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock
IV opiates not recommended - act as vasodilators
MDT approach - GP, cardiologisy, HF specialist nurses, OT, PT, social care
Mechanism of PND?
fluid settling across a large surface area of their lungs as they sleep lying flat. As they stand up the fluid sinks to the lung bases and their upper lungs clear and can be used more effectively.
during sleep the respiratory centre in the brain becomes less responsive so their respiratory rate and effort does not increase in response to reduced oxygen saturation like it normally would when awake. This allows the person to develop more significant pulmonary congestion and hypoxia before waking up and feeling very unwell.
less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed and this worsens reduces the cardiac output.
What are inotropes?
strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.
SE of ACEi?
cough
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
SE of beta blockers?
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
What is atrial fibrillation?
Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly.
This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles. This results in:
Irregularly irregular ventricular contractions
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke
Features of AF?
Asymptomatic
Palpitations
SOB
Syncope (dizziness/fainting)
Symptoms of associated conditions - stroke, sepsis, thyrotoxicosis
Differentials for irregularly irregular pulse?
Atrial fibrillation
Ventricular ectopics
These can be differentiated using an ECG.
Ventricular ectopics disappear when the heart rate gets over a certain threshold. Therefore a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
What is valvular AF?
Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve.
AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.
Most common causes of AF?
Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension
AF findings on ECG?
Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm
Treatment of AF?
There are two principles to treating atrial fibrillation:
Rate or rhythm control
Anticoagulation to prevent stroke
Rate control - The higher the heart rate, the less time is available for the ventricles to fill with blood, reducing the cardiac output. The aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.
NICE guidelines (2014) suggest all patients with AF should have rate control as first line unless:
There is reversible cause for their AF
Their AF is of new onset (within the last 48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled
Then rhythm control used. Return to sinus rhythm. This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.
Options for rate control in AF?
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
Summary of cardioversion in AF?
There are two options for cardioversion:
Pharmacological cardioversion
Electrical cardioversion
Pharmacological Cardioversion:
NICE guidelines (2014) say for pharmacological cardioversion first line is:
Flecanide
Amiodarone (the drug of choice in patients with structural heart disease)
Electrical Cardioversion:
The aim of electrical cardioversion is to rapidly shock the heart back into sinus rhythm. This involves sedation or a general anaesthetic and using a cardiac defibrillator machine to deliver controlled shocks in an attempt to restore sinus rhythm.
Long Term Medical Rhythm Control in AF?
Beta blockers are first line for rhythm control
Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction
What is paroxysmal atrial fibrillation?
when the AF comes and goes in episodes, usually not lasting more than 48 hours.
anti coagulated based on CHADVASc score
may be appropriate for a “pill in the pocket” approach. This is where they take a pill to terminate their atrial fibrillation only when they feel the symptoms of AF starting. To be appropriate for a pill in the pocket approach they need to have infrequent episodes without any underlying structural heart disease. - this uses flecanide
Summary of anticoagulation in AF?
uncontrolled and unorganised movement of the atria leads to blood stagnating in the left atrium, particularly in the atrial appendage. Can lead to thrombus, and if mobilises becomes embolus. Can cause ischaemic stroke.
Anticoagulation based on CHADVASC - reduces risk by 2/3
HASBLED/ORBIT score
Summary of CHA2DS2-VASc
List of RFs. The higher the score the higher the risk of developing a stroke or TIA and the greater the benefit from anticoagulation.
Score:
0: no anticoagulation
1: consider anticoagulation
>1: offer anticoagulation
C – Congestive heart failure
H – Hypertension
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease
A – Age 65-74
S – Sex (female)
Summary of ORBIT tool?
ORBIT tool for assessing a patient’s risk of major bleeding whilst on anticoagulation.
It is scored based on:
Low haemoglobin or haematocrit
Age (75 or above)
Previous bleeding (gastrointestinal or intracranial)
Renal function (GFR less than 60)
Antiplatelet medications
Summary of HASBLED tool?
H – Hypertension
A – Abnormal renal and liver function
S – Stroke
B – Bleeding
L – Labile INRs (whilst on warfarin)
E – Elderly
D – Drugs or alcohol
DOACs vs Warfarin?
DOAC - more expensive, no monitoring, no major interaction problems
Warfarin - cost of monitoring, restrictions for patient,
What is S1?
Closure of AV valves - tricuspid and mitral
Start of systolic contraction of ventricles
What is S2?
Closure of semilunar valves - pulmonary and aortic valves
Once systolic contraction is complete
What is S3?
heard roughly 0.1 seconds after the second heart sound
rapid ventricular filling causing chord tendineae to pull to their full length and then twang like a guitar string
normal in young healthy people - as ventricles allow rapid filling
Older people = indicates heart failure - as ventricles and chord are stiff and weak so reach limit much faster than normal.
What is S4?
Heard before S1
Always abnormal and relatively rare to hear
Stiff or hypertrophic ventricle - turbulent flow from atria contracting against a non-compliant ventricle
What is Erbs point?
Third intercostal space of left sternal border - best area for listening to heart sounds (S1 and S2)
Special manoeuvres to emphasise murmurs?
Patient on left hand side - mitral stenosis
Patient sat up, leaning forward and holding exhalation - aortic regurgitation
How to assess a murmur?
SCRIPT
S – Site: where is the murmur loudest?
C – Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter)
R – Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?
I – Intensity: what grade is the murmur?
1 - Difficult to hear
2 - Quiet
3 - Easy to hear
4 - Easy to hear with a palpable thrill
5 - Can hear with stethoscope barely touching chest
6 - Can hear with stethoscope off the chest
P – Pitch: is it high pitched or low and grumbling? Pitch indicates velocity.
T – Timing: is it systolic or diastolic?
How does valvular heart disease cause hypertrophy/dilatation?
Hypertrophy - thickening both outwards and into the chamber
Dilatation - thinning and expanding - balloon!
Stenosis = pushing against stenotic valve so muscle has to try harder = hypertrophy
MS = left atrial hypertrophy
AS - LV hypertrophy
Regurgitation = leaky valve allows blood to flow back into chamber and hence stretches muscle = dilatation
MR = left atrial dilatation
AR - left ventricular dilatation
Summary of mitral stenosis?
Causes = rheumatic heart disease, infective endocarditis
Mid-diastolic, low pitched “rumbling” - due to low velocity of blood flow
Loud S1 = due to requiring large systolic force to shut, and then shutting suddenly
Associated with:
Malar flush - due to back-pressure of blood into pulmonary system, caused a rise in CO2 and vasodilation
AF - caused by LA struggling to push blood through stenotic valve causing strain, electrical disruption and resulting fibrillation
Summary of mitral regurgitation?
When incompetent mitral valve allows blood to leak back through during systolic contraction of left ventricle
Results in congestive cardiac failure as causes reduced ejection fraction, and backlog of blood waiting to be pumped through left side of the heart
Pan-systolic, high-pitched ‘whistling’ murmur due to high velocity blood flow through the leaky valve. Radiates to left axilla. May hear S3
Causes = idiopathic weakening of valve with age, IHD, IE, rheumatic heart disease, CTD (EDS and Marfan)
Summary of aortic stenosis?
Most common valve disease
Ejection-systolic, high pitched. Crescendo-decresendo - due to speed of blood flow across valve during different parts of systole.
Radiates to carotids
Slow rising pulse and narrow pulse pressure
Exertional syncope
Causes = idiopathic age related calcification, rheumatic heart disease
Summary of aortic regurgitation?
early diastolic, soft murmur
Corrigans pulse (collapsing pulse)
Results in heart failure due to a back pressure of blood waiting to get through the left side of the heart.
Can cause Austin-Flint murmur. Heard at the apex and is an early diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.
Causes = idiopathic aged related weakness, CTD (EDS, Marfan syndrome)
Use of adrenaline in ALS?
1mg ASAP for non-shockable rhythms
In VF/VT - 1mg after 3rd shock
Repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
Use of amiodarone in ALS?
amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered
Further dose of 150mg after 5 shocks
Lidocaine as alternative if amiodarone not available
Reversible causes of cardiac arrest?
H’s
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acideaemia and other metabolic
Hypothermia
T’s
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade
Toxins
Summary of coarctation of the aorta?
Congenital narrowing of descending aorta
More common in males
SX:
HF in infancy
HTN in adult
Radio-femoral delay
Mid systolic murmur
Apical click from aortic valve
Notching of inferior border of ribs
Associations - Turners, biscuspid aortic valve, berry aneurysms, neurofibromatosis
Signs of hypothermia on ECG?
Bradycardia
J wave
First degree heart block
Long QT
Partial and ventricular arrhythmias
