CARDIOLOGY Flashcards
How is heart failure classified?
Left or right sided
Congestive
Systolic: insufficient contraction (reduced ejection fraction v. Diastolic insufficient relaxation therefore insufficient filling (preserved ejection fraction)
Acute v chronic
What are the causes of left heart failure?
Ventricular inflow obstruction (blood can’t flow into ventricles)
Diastolic dysfunction (not enough blood flows in)
Reduced ventricular contractility (doesn’t contract as well)
Ventricular volume overload
(too much blood flows in)
Ventricular outflow obstruction
(blood can’t flow out)
What causes ventricular inflow obstruction? (blood can’t flow into ventricles)
The atrial-ventricular valves not functioning:
Mentral valve or Tricuspid valve stenosis
What causes diastolic dysfunction? (heart doesn’t fill enough)
Constrictive pericarditis
Cardiac tamponade
Arrhythmias
What causes reduced ventricular contractility?
MI
CAD
Dilated cardiomyopathy
What causes ventricular volume overload? (too much blood flows in)
Mitral regurgitation
VSD and ASD
Increased metabolic demand for blood
What causes ventricular outflow obstruction? (Blood can’t flow out)
Aortic stenosis
Pulmonary stenosis
Pulmonary hypertension
What are the causes of right heart failure?
Left heart failure
Right sided infarct
Congenital heart defect
Pulmonary hypertension and chronic lung disease (e.g. in COPD)
What are the symptoms of left heart failure?
Pulmonary (L=lungs) blood backs up in the lungs as it can’t enter the heart, pressure increases and fluid is forced out of the capillaries under pressure causing:
Cyanosis
Tachypnoea
Paroxysmal nocturnal dyspnoea that wakes patient
Bibasal crepitation
Cardiac symptoms are down to the causes
Murmurs
Laterally displaced apex beat
What are the symptoms of right heart failure?
Blood backs up trying to get into the right heart forcing fluid out of the capillaries under pressure resulting in: Ascites Peripheral pitting oedema Tender hepatomegaly Parasternal heave Riased JVP
What is preload?
Volume of blood in the ventricles at the end of diastole = End Diastolic Volume a
This is measured by the pressure it exerts on the ventricle walls
Essentially a measure of the patient’s volume status
Low pre-load = low volume e.g. in shock, hypotension and tamponade
High pre-load = high volume e.g. in heart failure and bradycardia
What is afterload?
Pressure the ventricles exert to open the pulmonary/aortic valves which must be greater than the pressure greater by the peripheral vessels (TPR)
After-load is high in: Hypertension (the TPR is higher so more pressure is needed), aortic stenosis (greater pressure is needed to open the valve) and SNS stimulation as that causes increased TPR to redirect blood to needed structures
After-load is low in: Hypotension and sepsis (due to vasodilation)
What is Starling’s law?
The more the heart muscle stretches the harder it contracts (to a point)
In heart failure this point is lower
How does heart failure self-perpetuate?
Heart failure leads to reduced C.O which leads to reduced BP which activated the RAASystem.
This retains Sodium and Water which increases preload and causes vasoconstriction which increases afterload.
Increased BP increases cardiac work which increases sympathetic activation which leads to increased cardiac contractility
The heart is forced to work harder and thus is damaged and myocytes are lost, this results in worsening of the heart failure
What are is the NYHA classification for heart failure?
I - no limitations
II - slight limitation
III - marked limitation
IV - symptoms at rest and no physical activity without discomfort
What are the signs of heart failure on CXR?
Alveolar oedema: 'bat wings' kerley B lines (interstitial oedema) Cardiomegaly (s3+4 heart sounds) Dilatation of apex arteries (blood Diverted to upper lobe) pleural Effusion
What is BNP?
Brain Naturitic Peptide is produced by the LV myocardium in response to strain
> 400 pg/ml
- LV Hypertrophy
- Ischaemia
- Tachycardia
- RV overload
- Hypoxaemia-P.E
Also by: sepsis, GFR <60, COPD, Diabetes, >70 y/o, Cirrhosis
< 100 pg/ml
- Obesity
- Diuretics
- Aldosterone antagonists
- ACEi/A2RB
- B blockers
How is heart failure treated?
ACEi* (Ramipril) + B-Blocker* (start low, go slow) (Bisoprolol, Carvedilol, Nebrilol)
Aldosterone Antagonist* (Spironolactone)/ A2RB (Candestartan, Losartan)/ Hydralazine + Nitrate* (Isosorbide mononitrate) which are Vasodilators
Cardiac resynchronisation therapy (pacing) or a Cardiac Glycoside (Digoxin) especially in AF
Diuretics can be used if in fluid overload (Furosemide or Spiron)
Flu and pneumococcal vaccine
*shown to improve mortality
What is Acute Coronary Syndrome?
Acute presentation of ischaemic heart disease (CAD): Reduced blood flow to the heart muscle due to vessel disease
STEMI
NSTEMI
Unstable angina
What are the risk factors for ACS?
Modifiable:
- Obesity and physical inactivity
- Hypertension
- Hypercholesterolaemia
- Smoking
- DM
- Alcohol excess
Unmodifiable:
- Age
- Male sex
- Genetic
- Ethnicity
What are the signs and symptoms of ACS?
Crushing, central chest pain radiating up neck and down left arm *diabetics and the elderly may not have chest pain Dyspnoea Palpitations Sweating Nausea and vomiting Syncope
Pale and clammy
Often normal pulse (sometimes tachy), BP and O2 stats
What cardiac enzymes are measured?
Troponin (T or I) is the most sensitive and begins to raise from 3-12 hours after onset of pain with a peak at 24-48 hours and decline over 5-10 days
CK-MB rises after 3-12 of pain onset and returns to baseline 48-72 hours
LDH
Myoglobin levels rise within 1-4 hours which is sensitive but not specific to ACS
How are MIs localised on ECG?
Inferior- II, III, avF-RCA**branchsupplies AVN so can cause complete heart block Septal- V1+V2-LAD Anterior- V3+V4-LAD Lateral- I, aVL, V5+V6-lCfx Posterior- Tall R in V1+V2-lCfx+ RCA
Tall T wave ST elevation (**in aVR is highly suggestive of 3 vessel or Left main stem disease) T wave inversion Pathological Q (40ms wide >2mm deep) **New LBBB in context of chest pain
How is ACS managed initially?
Morphine O2 (if <94%) Nitrates (Glycerol trinitrate) sublignusally Aspirin 300mg Pasugrel (clopidogrel or ticagrelor)
How are STEMIs managed?
Purcutaneous Coronary intervention angioplasty +/- stent within 2 hours via radial or femoral catheter
Can drive 1 week after angioplasty and 4 weeks without one
Then: Statin Lifelong Aspirin + 1 mo of clopidogrel (lifelong if aspirin contraindicated) or tricagrelor ACEi Beta Blocker to reduce heart rate
What is thrombolysis?
When PCI is not available for STEMI
(Also in stroke and PE)
Convert plasminogen to plasmin which degrades fibrin and breaks up clots
e.g. Alteplase
Tenecteplase
Streptokinase
When is thrombolysis contraindicated?
Can cause a bleed so…
- Active bleeding
- Recent haemorrhage
- Recent trauma/surgery
- Coagulation/bleeding disorders
- Stroke < 3months
- Intercranial neoplasm
- recent head injury
- Aortic dissection
- Severe HTN
- Pregnancy
How are NSTEMIs managed?
Antithrombin treatment:
FONDAPURINUX (Enoxaparin)If no risk of bleeding and no angiography in 24 hours
UNFRACTIONATED HEPARIN if angiography in 24 hours or high creatinine
Lifelong aspirin + 300mg of clipidogrel for 12 months
IV glycoprotein IIb/IIa receptor antagonists EPTIFIBATIDE or TIROFIBAN if high risk of CVS events + angiography within 96 hours
What is Angina?
MI caused by atheroma brought on by exertion and relieved by rest
What are the 4 types of Angina?
Stable: caused by exertion, relieved at rest
Unstable: increased frequency or severity on minimal exertion
Decubitus: precipitated by lying flat
Variant: prinzmetal’s- coronary artery spasm
What precipitates angina?
4 Es Exercise Eating Emotion Exposure to cold
How is Angina managed?
- Lifestyle changes
- Statin
- Aspirin
- B-B or CCB then combine (but not Verapapamil with BBlocker)
- Nitrates
Symptoms: spray subligually every 1/2 hour
Prophylaxis: Regualr oral nitrate e.g. isosorbide mononitrate (can develop tolerence so take every 8 hours not 12 hours in standard release) - Ivabradine
- PCI or CABG
What are the ECG changes that indicate thrombolysis or PCI?
ST elevation >2mm in 2 or more consecutibe anterior leads (V1-V6)
or
ST elevation > 1mm in >1 consecutive inferior leads (II, III, aVF, aVL)
or
New LBBB
What is coarctation of the aorta?
Stenosis in the aortic arch distal to the left subclavian artery
Hypertension proximally (upper limbs):
- Dizziness
- Headache
- Neuro symptoms
Hypotension distally (lower limbs) - Caudication
Collateral arteries between the pre-coarctation and post-coarctation aorta (e.g. intercostal and internal mammary arteries) enlarge and communicate between the aortic segments proximal and distal to the coarctation.
Enlarged intercostal arteries notch the inferior margins of te ribs detectable on XRAY.
What is an Atrial Myxoma?
Benign tumour of the heart
75% are in the left atrium
Surgery is curative
What are the features of Atrial Myxoma?
Mid diastolic murmur with ‘tumour plop’ in early diastole
Systemic: - Dypnoea - Fatigue - Weight loss - Fever - Clubbing Embolic (e.g. TIA) Atrial Fibrillation
What is an Atrial Myxoma?
Benign tumour of the heart
75% are in the left atrium
Surgery is curative
What are the features of Atrial Myxoma?
Mid diastolic murmur with ‘tumour plop’ in early diastole
Systemic: - Dypnoea - Fatigue - Weight loss - Fever - Clubbing Embolic (e.g. TIA) Atrial Fibrillation
What is Pulsus Paradoxus?
Systemic blood pressure falls by >10mmHg during INSPIRATION so the pulse is faint or absent when breathing in
CARDIAC TAMPONADE
Severe Asthma
What presents with Slow Rising/ Plateu pulse?
Prominant in carotids and brachials
AORTIC STENOSIS
LVF
What presents with Collapsing Pulse?
Waterhammer-Corrigan’s
Lift arn up vertically-hold muscular forarm, should feel tapping over muscles
AORTIC REGURGITATION
PDA
Hyperkinetic
e.g. exercise, fever, thyrotoxic, pregnancy
What presents with Pulsus Alternans?
Regular alternation of the arterial pulse
SEVERE LVF
What presents with Bisferiens Pulse?
Double pulse x2 systolic beats
MIXED AORTIC VALVE DISEASE
What presents with a Jerky Pulse?
HOCM
Where is Right Ventricular hypertrophy detected?
4th intercostal space in left parasternal area (right ventricular heave)
What is Transfusion Haemosiderosis?
Deposition of iron in heart (and endocrine organs) can lead to heart failure
What is Cardiomyopathy?
Muscle becomes hard and thick and is sometimes replaced by scar tissue
What are the Primary Cardiomyopathies?
Predominantly affect the heart
Genetic:
A.D
- Hypertrophic Obstructive (HOCM)
- Arrhythmic Right Ventricular Dysplasia (ARVD)
Mixed Cardiomyopathies:
Genetic predispositon to cardiomyopathy which is triggered by a secondary process
- Dilated Cardiomyopathy
- Restrictive Cardiomyopathy
Acquired Cardiomyopathies:
- Peripartum
- Takotsubo
What is Hypertrophic Obstruction Cardiomyopathy?
Defects in the genes encoding for CONTRACTILE PROTEINS - B-myosin heavy chain - myosin-binding C protein - cardiac troponin T 1/500
What are the features of Hypertrophic Obstruction Cardiomyopathy?
Asymptomatic but: - Dyspnoea - Angina - Syncope - Sudden death Arrhythmias -> ventricular Heart failure: preserved ejection fraction
Jerky pulse Large 'a' waves on JVP Double apex beat Ejection systolic murmur: increased during valsalva manouver and decreased when squatting 4th heart sound
What are the features of Hypertrophic Obstruction Cardiomyopathy on ECG?
- LV hypertrophy
- Progressive T wave inversion
- Deep Q waves
- AF occasionally
What are the features of Hypertrophic Obstruction Cardiomyopathy on ECHO?
MR SAM ASH
MR - Mitral Regurgitation
SAM - Systolic Anterior Motion of Anterior
ASH - Asymmetrical Septal Hypertrophy
What is Arrhythmic Right Ventricular Dysplasia?
RV myocardium replaced by fatty and fibrofatty tissue
~50% have a desmosome gene mutation
What are the features of Arrhythmic Right Ventricular Dysplasia on ECG?
ECG: V1-V3
- T wave inversion
- Epsilon wave - terminal notch in QRS
What is Dilated Cardiomyopathy?
Dilated heart leads to systolic (with or without diastolic) dysfunction leads to enlarged heart with or without thickening
1/3 have genetic predisposition
no congenital, ischaemic or valve disease
What are the features of Dilated Cardiomyopathy?
Reduced ejection fraction
Arrhythmias
Emboli
Mitral Regurgitation
What is Restrictive Cardiomyopathy?
Walls of heart are rigid (not thickened) - restricted from stretching and filling
What are the features of Restrictive Cardiomyopathy?
Tiredness Leg swelling Shortness of Breath Chest pain Fainting
What are the Complications of Restrictive Cardiomyopathy?
Heart failure
Valve disease
Irregular heart beat
What is Loeffer Endocarditis?
Restrictive cardiomyopathy affects the endocardium
WBC proliferation - specifically eosiniphils
What is Peripartum cardiomyopathy?
Last month of pregnancy until 5 months post-partum
Older women, greater parity and multiple gestation
What is Takotsubo?
‘Stress-induced’ e.g. traumatic events leading to chest pain (can mimic Anterior MI) and heart failure which is temporary
Transient, apical ballooning of the myocardium
Supportive treatment
What are the Secondary Cardiomyopathies?
pathological myocardial involvement due to a generalised systemic disorder
e.g.
Amyloidosis SLE Haemachromatosis Sarcoidosis Myotonic dystrophy DM Thyrotoxicosis Acromegaly Alcohol Thiamine-VitB1-Wet Beri Beri Coxsackie B Chagas
What are the Early Diastolic Murmurs?
Aortic Stenosis Pulmonary Stenosis HOCM (loudest standing and during vagal, quietist squatting) ASD Fallot's
What are the Pan Systolic Murmurs?
Mitral Regurgitation
Tricuspid regurgitaton
VSD ‘harsh’
What are the Late Systolic Murmurs?
Mitral Valve Prolapse
Coarctation of the Aorta
What are the Early Diastolic Murmurs?
Aortic Regurgitation
Pulmonary Regurgitiation
Graham-Steel
What are the Pan Diastolic Murmurs?
Mitral Stenosis (L lateral) Austin-Flint
What is a Graham-Steel Murmur?
Mitral Stenosis + Pulmonary HTN + Pulmonary Regurgitation
Mitral stenosis causes pulmonary HTN causes Pulmonary regurg
When is S3 heard?
Ventricle filling
Normal in young and women <50
Pathological causes:
- LVF e.g. in dilated cardiomyopathy
- Contstrictive pericarditis - pericardial knock
- Mitral Regurgitation
When is S4 heard?
Atrial contraction against a stiff ventricle
- HOCM (double apicle impusle due to palpable S4)
- Aortic Stenosis
- HTN
What are the features of an Aortic Stenosis murmur?
Best heard RSE and radiate to carotids and apex on EXPIRATION
Syncope
Angina
Dyspnoea (exertional)
Associated with:
- Slow rising pulse
- Narrow pulse pressure
- Heaving apex beat
- Soft or absent S2
- May have LVF w/ S3
What are the causes of an Aortic Stenosis murmur?
- Senile calcification
- Congenital bicuspid valve e.g. in Turner’s
- Rheumatic
- HOCM
What is the differentiating feature of an Aortic Sclerosis murmur?
Doesn’t radiate
What are the features of an Aortic Regurgitation murmur?
Early diastolic
RSE or LSE sitting forward
- Fatigue
- SOB
- Syncope
- Exertional Dyspnoea
- Orthopnea
- Paroxysmal Nocturnal Dyspnoea
Associated with:
- Collapsing pulse
- Wide pulse pressure
- Displaced apex
- Quinke’s sign: pulsation in nails
- Corrigan’s sign visible carotid pulsation
What are the causes of an Aortic Regurgitation murmur?
Acute:
- IE
- Aortic dissection
Chronic:
- CT disorders
- Ank Spon
- RA
- Congenital
- HTN
What are the features of a Mitral Regurgitation murmur?
Best heard in apex and radiates to left axilla Expiration
- Dyspnoea
- Fatigue
- Palpitations
Associated with:
- AF
- Displaced thrusting apex due to volume overload
- Soft S1
- LVF S3
- Pulmonary HTN
What are the causes of a Mitral Regurgitation murmur?
Papillary muscle dysfunction e.g. after an MI Dilated cardiomyopathy Rheumatic Infective Endocarditis Congenital CT
What are the causes of JVP ‘A’ wave changes?
Atrial Contraction
Large in:
Tricuspid Stenosis
Pulmonary Stenosis
Cannon in: contraction against a closed Tricuspid
Complete heart block
VT/Ectopics
Nodal Rhythm
Absent in:
AF
What is the JVP ‘C’ wave?
Closure of the Tricuspid valve
What are the causes of prominant JVP ‘X’ and ‘Y’ wave?
Fall in atrial pressure in ventricular systole
- Constrictive pericarditis
- Restrictive cardiomyopathy
What is the cause of an absent ‘Y’ wave?
Cardiac Tamponade
What is the cause of a giant JVP ‘V’ wave?
Filling of atria when tricuspid valve closed
Tricuspid regurgitation
What are the causes of a raised JVP?
Constrictive pericarditis: Kussmaul’s: paradoxically raised in JVP during inspiration
Left ventricular free wall rupture (with pulsus paradoxus and reduced heart sounds)
Raised non-pulsatile JVP in SVC obstruction
What is Anaphylaxis?
Severe lifethreatening and generalised type 1 IgE mediated hypersensitivity reaction
What are the features of Anaphylaxis?
SERUM TRYPTASE HIGH FOR 12 HOURS
Capillary leak:
- Urticaria
- Erythema
Oedema:
- Larynx
- Lids
- Tongue
- Lips
Cyanosis
Wheeze
Laryngeal obstruction
How is Anaphylaxis managed?
Secure airway, 100% O2
Adrenaline:
500mcg (0.5ml 1:1000) every 5 minutes into the ANTEROLATERAL MIDDLE 1/3 THIGH IM
Hydrocortisone
200mg
CLORPHENAMINE 10mg (continue 4mg/6hours if still itchy)
0.9% Saline 500ml over 5min up to 2 litres
What is Pericardial Effusion and when does it occur?
Accumulation of fluid in the pericardial sack as a result of
Heart Failure
Vascular: Nephrotic syndrome Idiopathic Trauma AI: Dressler's syndrome Met: Uraemia I Neoplasm D
What are the features of Pericardial Effusion?
- Dyspnoea
- Raised JVP
- Bronchial breathing
What are the features on ECHO, CXR and ECG?
Enlarged ‘water-bottle heart’
Echo-free zone surrounding
Low QRS
Pericardiocentesis to determine bacterial cause
What is Cardiac Tamponade and what can cause it?
Accumulation of pericardial fluid causing a rise in intercardial pressure, heart doesn’t fill, cardiac output falls
- Biopsy
- Transeptal rupture
- Warfarin
- Aortic dissection
What are the features of Cardiac Tamponade?
- Dyspnoea
- Tachycardia
- HoTn
- Pulses Paradoxus (abnormally large fall in systolic BP + pulse wave amplitude during INSPIRATION)
ABSENT Y WAVE on JVP
Beck’s triad:
- Low arterial BP
- Distended neck veins
- Muffled heart sounds
What is Acute Pericarditis and what causes it?
Inflammation of the pericardium due to:
- MI
- CT diseases
- Viruses e.g. Coxsackie, HIV, EBV, Flu, Varicella
- Bacteria e.g. TP, Pnuemonia, Rheumatic, Staph and strep
- Fungi
- Drugs
What are the features of Acute Pericarditis?
Central chest pain
- Worse on inspiration
- Worse lying flat
- Better sitting forward
- Pleuritic: central, sharp, stabbing
- Dyspnoea, Tachypnoea
- Hear PERICARDIAL FRICTION RUB
- Fever
- Tachycardia
What are the diagnositic tests for Acute pericarditis?
WIDESPREAD SADDLE ST ELEVATION with PR depression Cardiomegaly if effusion
1/3 have raised troponin
What is Constrictive Pericarditis?
Heart encased in stiff pericardium, cause usually unknown ?TB
What are the features of Constrictive Pericarditis?
- RHF signs: ascites, oedema, hepatosplenomegaly
- Soft apex beat
- Pericardial knock: LOUD S3
KUSSMAUL’S SIGN: Paradoxical rise in the JVP on inspiration or JVP fails to fall
JVP: PROMINENT X+Y
CXR: PERICARDIAL CALCIFICATION
How is Acute Heart Failure managed?
- oxygen
- diuretics (furosemide-higher doses in renal failure)
- opiates (diamorphine)
- vasodilators
- inotropic agents
- CPAP
- ultrafiltration
- mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
What is Bradycardia and how does it present?
HR <60bpm
- Dizziness
- Syncope
- Palpitations
What are the causes of Bradycardia?
SA Node Bradycardia (Sick Sinus Syndrome) due to fibrosis
- SA Arrest
- SA Block (1’, 2’, 3’)
- Tachy-brady syndrome
AV Node block
- 1’, 2’, 3’
RBBB
LBBB
Bi and Trifasicular blocks
What is SA Node Arrest?
SAN fails to depolarise so atria and ventricles don’t depolarise: NO QRS
What is SA Node Block?
Depolarises but not conducted to the atria
1'-no changes 2' - Type I Wenckeback - Type 2 3' absent P ways
What is Tachy-Brady syndrome?
SA Node dysfunction leads to SVT Tachyarrhythmia
Run of tachycardia followed by a run of bradycardia
Tachycardia can either be ESCAPE RHYTHMS or EXISTING TACHY (e.g. AF with SAN remodeling)
What are the causes of AV Node Block?
AI Infective: endocarditis Acute MI: INFERIOR RCA Surgical: after ablation/valve surgery AI: Ankylosing Spondylitis Degenerative: - fibrosis - calcification of nearby valves Drugs: Digoxin, B Blockers, Ca channel blockers, anti-arrhythmics
What is 1’ AV Node block?
Delayed conduction betwen the A+V through or around the AVN
- Asymptomatic (pace if symptomatic)
- P-R >5small squares (0.2s) but at a constant interval
- Narrow QRS - Block within node
- Broad QRS - Block in bundle of HIS
What is 2’ AV Node block?
Partial conduction
Some make it through
MOBITZ TYPE 1 WENKEBACK
P-R lengthens until no WRS Black usually within node
Likely to progress
MOBITZ TYPE 2
No elongation in P-R but QRS dropped occasionally
e.g. every 3rd dropped = 3:1 block
PACE
What is 3’ AV Node block?
Complete heart block Complete dissociation of atrial and ventricular depolarisation No P-QRS relationship Narrow=Node Broad= Bundle of His
PACE
What is BBB?
Slowed conduction through ventricular system and higher
If one bundle is blocked impulse is transmitted to the other ventricle by non-specialised vascular tissue in between
What are the causes of RBBB?
- Ischaemia
- P.E
- Rheumatic heart disease
- Myocarditis
- Congenital heart defects
- Cardiomyopathy
- Cor Pulmonale
What are the features of RBBB?
Wide QRS (>3sq, 0.12s)
Secondary R wave (Ri) in V1 and V2
ST changes are COMMON so hard to comment on ischaemia
SLURRED S in I/V5/V6
MORROW
What are the causes of LBBB?
- Cardiomyopathy
- HTN
- Coronary Artery Disease (acute anterior MI)
What are the features of LBBB?
Wide WRS
R’ in
Absent Q in V5/V6
WILLIAM
What are the fascicular blocks?
Bifasicular block:
- RBBB +R/L HEMIBLOCK
(RBBB +R/L axis deviation)
Trifasicular block:
BIFASICULAR + 1’ HB
What are the hemiblocks?
Anterior MC : Left axis deviation
Posterior: Right axis deviation