Cardiology Flashcards
What is heart failure?
A syndrome where cardiac output is not sufficient to meet the body’s requirements
What is systolic failure? What causes it (top 3)
Inability of the ventricle to contract normally, reduced CO, ejection fraction typically <40%
Causes: IHD, MI, cardiomyopathy (hypertension)
What is diastolic failure? What causes it (5)
Inability of the ventricle to relax and fill normally, increased filling pressure. Typical ejection fraction >50%.
Causes include ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity
What are the symptoms of left ventricular failure?
Dyspnoea, poor exercise tolerance, fatigue, orthopnea, PND, nocturnal cough (+/- pink frothy sputum), wheeze, nocturia, cold peripheries, weigh loss.
What are the symptoms of right heart failure ?
Peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis
NY classification of heart failure
I: no undue breath,Essenes
II: Breathlessness during ADLs, not limiting
III: breathlessness during ADLs, limiting
IV: breathlessness at rest
Chest x-ray findings in heart failure (5)
Alveolar Oedema (bat wing appearance)
kerley B lines (interstitial oedema, also known as septal lines)
Cardiomegally (>50% cardiothoracic ratio)
Dilated prominent upper lobe vessels (diversion due to oedema)
Effusions (blunted costophrenic angle and cardiac border)
How should you investigate suspected heart failure?
BNP and ECG. If either abnormal echocardiogram. If abnormal ever to cardiology.
Management of heart failure (not specific drugs, 5 things)
1) treat cause e.g. valvular heart disease, arrhythmia.
2)treat exacerbating factors e.g. anaemia,infection
3 )lifestyle modification e.g smoking cessation, alcohol reduction, reduced salt diet, healthy eating, weight loss.
4)avoid exacerbating factors e.g. NSAIDS and negative inotropes e,g, verapamil
5) annual flu vaccine and one off pneumococcal vaccine
Pharmacological management of heart failure. (3 core things + 2 to add on)
Reduce workload of heart.
1) diuretics - furosemide or bumetanide
2) ACEi or ARB
3) beta blocker e.g. bisoprolol. Start low and go slow.
4) spironolactone if renal function allows and potassium >3.4 or arrhythmia or digoxin therapy. Use if other diuretics not achieving adequate symptom control or if LVSD in post MI patients
5) digoxin considered in all who have LVSD who are still symptomatic with above management.
Palliative care considerations for heart failure patients (5)
1) treat and prevent comorbid conditions e.g. flu vaccine
2) good nutrition, allow alcohol
3) involve GP - discuss prognosis
4) treat symptoms - consider opiates for pain and dyspnoea
5) be realistic about prognosis
Hypertension management (not drugs)
If >135/85 in clinic, monitor, lifestyle advice
If >140/90 in clinic, home recordings
If at home >135/85 then stage 1 hypertension.
No comorbid disease or over 80- monitor
Comorbid disease and under 80- drug treatment
If in clinic >150/95 drug treatment
Pharmacological management of hypertension
A=ACEi
C= CA2+ blocker
D= thiazide diuretic
if <55yrs or diabetic = A
if >=55yrs or Afro-Caribbean =C
Then A and C
Then A and C and D
Then consider adding spironolactone or increasing D, if not tolerated add an alpha or beta blocker
If doesn’t tolerate ACEi use ARB
What is the cardiac output of an average male at rest
5L/min
Leads I and aVL on an ECG refer to which territory and which artery is likely to supply this area?
Septal or lateral - circumflex artery
Leads II, III and aVF on an ECG refer to which territory and which artery is likely to supply this area?
Inferior - RCA or Circumflex
Leads V1 to V4 on an ECG refer to which territory and which artery is likely to supply this area?
Anteroseptal - LAD
Leads V1 to V6 (+/- aVL) on an ECG refer to which territory and which artery is likely to supply this area?
Anteriorlateral - LAD
What ECG change would make you suspicious of a posterior myocardial infarction? What should you do to confirm your suspicions?
ST depression in V1 to V3, there may also be reciprocal change in aVR
Repeat ECG with leads V7, V8 and V9 which are placed on the back, below the left scapula. You would expect to see moderate ST elevation in these leads.
Where does the ductus arteriosus run, what is it’s purpose and what does it become after birth?
Between the pulmonary artery and the aorta. Allows most of the semi-oxygenated blood to bypass the foetuses lungs which are fluid filled and therefore at high pressure.
It becomes the ligamentum arteriosus
What is the foremen ovale, and what does it become?
The foremen ovale is a hole in the interatrial septum providing a shunt for oxygenated blood between the right and left atrium, allowing it to bypass the non-functioning lungs.
After birth the foramen closes forming the fossa ovalis
What is the ductus venousus purpose and what does it become?
The ductus venous provides a shunt from the umbilical vein to the IVC, preventing the liver from using most of the the oxygenated blood from the placenta.
Becomes the ligamentum venosum, which separates the caudate lobe of the liver
Give two examples of acyanotic congenital heart defects
Atrial septal defect
Ventricular septal defect
Give two examples of cyanotic congenital heart defects
Tetralogy of fallot
Transposition of the great arteries
What defects are present in tetralogy of fallot?
Which direction is the shunt?
Ventricular septal defect
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy
Produces right to left shunt, therefore some degree of cyanosis. Severity depends on level of pulmonary stenosis (and therefore amount of blood shunted)
What autonomic receptors are found in the heart?
Beta 1 adrenoreceptors - increase rate and contractility
M2 muscarinic ACh receptor - decrease rate
What is starling’s law?
The stroke volume of the heart increases if there is an increased volume of blood in the heart (i.e. a greater preload will result in greater contractility)
How do you calculate cardiac output?
CO= stroke volume * heart rate
What is preload?
The end diastolic pressure -the volume at which the ventricles are stretched the most.
What is afterload?
The tension within the left ventricle during systole -depends on arterial or pulmonary pressures
Describe Stable angina
- transient ischaemia which is relived when O2 demand decreases
- brief episodes of chest pain on breathlessness brought on by exertion or emotion and relieved by rest
- resting ECG normal, ST depression on stress test, troponin normal
Describe unstable angina
- ischaemia even at rest
- ST depression at rest
- no raised troponin as no necrosis
Describe an NSTEMI
ST depression or T wave changes pm ECG
Raised troponins
Some infarction but not full thickness
Describe STEMI
ST segment elevation on ECG with reciprocal changes
Troponins raised
Full thickeners infarction
When is troponin I most raised? How long will it remain raised? When would you look at creatinine kinase?
Troponin I reaches its peak level 24hours post infarction
It remains raised for approximately 1 week
CK may be used if there is a second episode of chest pain within 2 days of a confirmed MI
NYHA scale of dyspnoea in heart failure… go!
I - no symptoms or limitation
II - mild symptoms and slight limitation during ordinary activity
III - marked limitation on activity due to symptoms e.g. walking short distances. Only comfortable at rest.
IV - severe limitation, symptoms at rest, bed bound.
Causes of heart failure
Ischaemic heart disease Valvular disease Hypertension Arrhythmia Hypertrophic cardiomyopathy
What general advice would you give to someone with heart failure?
Regular, low level exercise, such as brisk walking
Have a low salt diet
STOP SMOKING
Education about the disease and it’s progression
Vaccination
Define cardiogenic shock
The inability of the heart to eject enough blood e.g. following myocardial infarction
What is a third heart sound and what can cause it?
Due to a stiff or dilated ventricle suddenly reaching its elastic potential which decelerates the incoming blood. “Lub…dub de”
Normal in under 30s and children
Causes include HF, MI, cardiomyopathy, hypertension
What is a fourth hear sound and what does it mean?
Low pitched sound of atrial contraction into a non-compliant or hypertrophied ventricle. “Le lub…dub”
Always abnormal
Heart failure, MI, cardiomyopathy, hypertension
What is the grading system for murmurs?
1- very faint
2- soft
3- heard easily
4- loud, with palpable thrill
5- very loud, with thrill. Heard with stethoscope partly off the chest
6- very loud, with thrill. Heard with stethoscope completely off the chest
What ECG changes in left ventricular hypertrophy?
S waves in V1 + r waves in V5/V6 = greater than 3.5 big squares
ECG changes 1st degree heart block
Constant but prolonged PR interval
Second degree heart block mowbitz 1 ECG changes
Progressively lengthening PR interval until a QRS is dropped
What are the ECG changes in mowbitz II 2nd Degree heart block
Occasional Failure of the AV node to conduct atrial depolarisations to the ventricle. May occur in a fixed pattern I.e. 2:1 or 3:1
What ECG changes in third degree heart block?
No relationship between the p waves and the qrs
What ecg changes are suggestive of right ventricular hypertrophy?
Right axis deviation
Narrow QRS
Dominant R waves in V1 ( 7mm or taller)
Dominant S waves in V6 (7mm or deeper)
ECG changes in LBBB
Wide QRS
W in V1, M in V6
(WiLLiaM)
What ECG changes in RBBB?
Wide QRS
M in lead V1, W in lead V6
(MaRRoW)
Heart failure changes on CXR (abcde)
Air space shadowing Kerley B lines Cardiomegaly Diversion of blood to upper lobes Effusions - pleural
Class I antiarrythmics
Action
Sodium Channel Blockers (N -1 line)
Ia - quinidine - ventricular dysrhythmias, atrial fibrillation
Ib - lidocaine - VT & VF
Ic - flecainide - paroxysmal AF, recurrent tachycardias incl. WPW
Class II antiarhytmics
Action, example
Beta Blockers (two lines for B) Bisoprolol, atenolol, propanol
Class III antiarhythmics
Action, example, use
K+ channel Blockers (3 lines to draw a K)
Amiodarone - end SVT in acute incl. WPW
Class IV antiarrythmics
Action, example
Calcium channel blocker, verapamil or diltiazem
These are both examples of non-dihydropyridines which act centrally on the heart
Adenosine
What is it?
What is it used for.
Antiarrythmic - unclassified
Rapid reversion to sinus rhythm of SVT including WPW
Don’t use in broad complex irregular tachycardias as could be preexcited AF because could cause VT
Beta blockers
Examples
Action
Indications
Bisoprolol, atenolol, propranolol.
Negatively inotrophic (contractility) and chronotophic (rate)
Indicated for ischaemic heart disease, dysrhythmias such as AF and is a third line option for hypertension.
Beta Blockers
Side effects
Contraindications
Vagal- GI disturbance, bradycardia, fatigue, cold peripheries, sexual dysfunction, exacerbation of Raynaud’s or intermittent claudication, bronchospasm.
Contraindications - brittle asthma, marked bradycardia, heart block, peripheral vascular disease
Calcium channel Blockers
Two types - examples and uses
Non-dyhydropyridines - verapamil and diltiazem - act on myocardium - used in SVTs but should be cautioned in Heart failure
(especially in combination with beta blockers) can be used for hypertension
Dihydropyridines - act on arteries more than myocardium. E.g. amlodipine, felodipine,nifedipine 1st line for hypertension in over 55s and afrocarribeans of any age. Prevent angina.
Side effects of calcium channel blocker
Non-dihydropyridines - CONSTIPATION, nausea, flushing, headache, dizziness, fatigue
Dihydropyridines - abdo pain, nausea, palpitations, flushing, oedema, headache, dizziness, fatigue
Contraindications for calcium channel blockers
Non-dihydropyridines - Heart failure, 2nd or 3rd Degree heart block, cardiogenic shock
Dihydropyridines - unstable angina, significant atherosclerosis
Nitrates
Examples
Indications
Isosorbide mononitrate - oral
GTN spray
Stable angina (prevention and treatment) unstable angina, acute heart failure, chronic heart failure.
ECG Changes in posterior MI and which artery is most likely effected
Tall R waves in V1 and V2
usually left circumflex, can be right coronary
CHADSVASc
Risk of thromboembolic disease in AF patients - used to inform anticoagulation decisions Congestive HF Hypertension Age >75 =2, 65-74=1 Diabetes Previous stroke or TIA =2 Vascular disease = IHD or PVD Sex= female
What is a third heart sound?
What causes it? (5)
‘lub dub DE’
blood rushing into ventricle during early diastole or a stiff or dilated ventricle suddenly reaches its limit and the incoming blood decelerates.
Causes: Normal in under 30s Heart failure myocardial infarction cardiomyopathy hypertension
What is a fourth heart sound?
What causes it? (4)
“LE lub dub”
atrial contraction into a non-compliant or hypertrophied ventricle.
low pitched
Causes: ALWAYS ABNORMAL Heart failure MI cardiomyopathy ( + hypertrophic) hypertension
Mitral Stenosis How best heard? What does it sound like? Causes (2) Effects
LUB De Derrr
Loud S1, Opening snap ‘De’ followed by rumbling mid-diastolic murmur.
Best heard with bell over apex with patient lying on left side.
Causes - calcification in old age or rheumatic fever.
Effects - raised LA pressure, pulmonary hypertension, eventually RHF.
ECG and CXR Changes in Mitral Stenosis
AF, Pifid P waves, RHF - right axis deviation and tall R waves in leads V1 and V2.
Mitral Regurgitation How best heard? What does it sound like? Causes (5) Effects
pan systolic murmur at the apex which radiates to the axilla
‘burrrrr’
Prolapsed mitral valve, rheumatic mitral regurgitation, papillary muscle rupture, cardiomyopathy, connective tissue disorder.
left atrial and left ventricular enlargement - LHF
ECG and CXR Changes in Mitral regurgitation
bifid P wave, Left axis deviation due to LVH
CXR - cardiomegally
Aortic Stenosis How best heard? What does it sound like? Causes (3) Effects
Ejection systolic, radiates to the carotid
Lub-whoshhh Dub
Bicuspid aortic valve (under 65), age related calcification, rheumatic fever.
Left heart failure
ECG and CXR Changes in aortic stenosis
Left ventricular strain - ST segment depression and T wave inversion in left ventricular leads - chest leads
prominent, dilated aorta on CXR
Aortic Regurgitation How best heard? What does it sound like? Causes (5) Effects
High pitched, early diastolic murmur - best heard at left sternal edge, 4th intercostal space, with the patient leaning forwards.
Lub Taaarrr
rheumatic fever, bicuspid valve, infective endocarditis, Marfan’s, tertiary syphilis
LV dilation
Aortic regurge - changes on ECG
ECG - left ventricular hypertrophy
Left axis deviation on ECG
If lead I is positive and lead II is negative - i.e. they are Leaving each other (aVF also negative)
Right axis deviation on ECG
Lead I is negative and lead AVf is positive (I and II are Reaching for each other)
ECG changes in bundle branch block
QRS is broad
up in V1, becoming progressively more negative = RBBB
down in V1, becoming progressively more positive - LBBB
ECG changes in PE
TACHYCARDIA S1, Q3, T3 Large S waves in I Q wave inversion in III T wave inversion in III RAD
Pathophysiology of atherosclerosis formation
Superficial endothelial injury causes:
-increased permeability causes lipoprotein accumulation
- cytokine release causing macrophage recruitment
macrophages phagocytose lipoproteins producing foam cells creating fatty plaque
inflammation causes smooth muscle cell migration and proliferation and collagen production, creating a fibrous cap
pathophysiology of plaque thrombosis
the fibrous cap is ruptured or eroded
platelets adhere and aggregate
platelets release serotonin and thromboxane A2 causing localised thrombosis (which may embolise distally) and vasoconstriction
reduced coronary blood flow causes myocardial ischaemia and later necrosis, causing an increase in serum troponins.
STEMI Management
MONA and PCI or thrombolysis
NSTEMI/Unstable angina management
Morphine nitrates, ACEi, Beta blocker, calcium channel blocker, statin aspirin, clopidogrel LMWH Consider PCI
Causes of acute LHF (5)
MI hypertension aortic stenosis or aortic incompetence mitral incompetence increased demand on heart i.e. shock - sepsis, hypovolaemia
Acute HF Mx (9)
ABCDE Sit upright 100% O2 via non-rebreathe IV access and ECG monitoring Morphine and antiemetic If systolic BP >100 GTN infusion Furosemide - caution if hypotensive CPAP - think ceiling of care address cause
Mx of Tachyarrhythmia with adverse features and what are adverse features
Shock, snycope, MI, HF
A to E, periarrest call, prepare to DC cardiovery
Mx narrow tachyarrhythmia
Regular - SVT so vagal manouvere, adenosine 6mg IV
Irregular - Probable AF - beta blocker if in HF consider digoxin or amiodarone
Mx broad tachyarrhythmia
Regular - VT so amiodarone 300mg over 20-60 mins
if known SVT with BBB then beta blocker
Irregular - ? AF with BBB beta blocker
?Preexcided AF - ?amiodarone
infective organism endocarditis
strep viridans most common
staph aureus in IVDU, central lines
presentation of infective endocarditis
systemic infection - malaise, pyrexia, myalgia, weight loss, fatigue
Cardiac- heart murmur, heart failure, conduction abnormalities
Embolic disease
immune vasculitis - Roth spots, Osler’s nodes, Janeway lesions, clubbing, splinter haemorrhages, glomerulonephritis.
Mx of infective endocarditis
involve micro and cardiology
empirical ABx gentamycin and penicillin IV
presentation of pericarditis
chest pain - sharp, worse on inspiration, central, radiating to left shoulder, eased by sitting forward
+/- dyspnoea and fever
ECG changes in pericarditis
1) saddle shaped ST elevation in most leads
2) days later - ST normalises, T wave flattening
3) T wave then inverts
4) Weeks to months later - ECG normalised.
Ix Pericarditis
Bloods - FBC, U&E, LFT, CRP, CK, Trop I
Virology screen, blood culture
Rheumatology panal
Tuberculin and sputum for acid fast bacilli
Imaging - ECHO for effusion, CT/MRI
Causes of pericarditis (7)
Viral - cocksakie idiopathic tuberculosis bacterial secondary to MI, neoplasm renal failure rheumatological - RA, sarcoid, SLE
Mx of pericarditis
treat cause
supportive care
high dose NSAIDs unless MI
What is rheumatic fever
immunological reaction to a strep infection - usually URTI
Diagnostic criteria for rheumatic fever
Confirmed Strep infection - swab or increasing antibodies 2 major or 1 major + 2 minor Major: erythema marginatum sydenham's chorea polyarthritis carditis and valvulitis subcutaneous nodules Minor: raised CRP/ESR pyrexia arthralgia if no arthritis prolonged PR interval
Ix rheumatic fever
blood culture antistreptolysin titre throat swab ECG Echocardiogram CXR
Mx Rheumatic fever
admit and bed rest
oral aspirin
IM penicillin 1.2mg followed by 10 day course
long term Abx may be required to prevent cardiac damage
BP targets in diabetes
No end-organ damage - 140/80
End organ damage - 130/80
