Cardiology Flashcards
CVD risk factors (modifiable) (9)
Obesity
Hypertension
Smoking
Sedentary lifestyle
High LDL cholesterol
Poor diet
Alcohol drinking
Cocaine use
Uncontrolled DM
CVD risk factors (non-modifiable) (7)
Age
Male gender
Ethnicity (South Asian, African, Caribbean)
Family history
Menopause
Genetic predisposition (hyperlipidaemia)
Socioeconomic status
Normal blood pressure ranges and hypertension staging
90/60 - 120-80
Prehypertension - 120/80 +
Stage 1: 140/90 +
Stage 2: 160/100 +
Stage 3 >180/120
Describe the 3 characteristic features of typical stable angina
- Central crushing chest pain that can radiate to jaw, shoulders or left arm
- Caused by exertion
- Is relieved by GTN spray or rest
Can also be caused by heavy meals, cold weather, strong emotion.
Other causes of an angina exacerbation
heavy meals, cold weather, strong emotion.
Give some primary preventions of cardiovascular disease
QRISK3 score (10 year risk calculator of MI or stroke)
Patients with CKD or T1DM taking statins
Checking lipids, LFTs, BP regularly
Pathophysiology of stable angina
Usually caused by atherosclerosis, narrowing of coronary arteries (>70% stenosis) causes reduced blood flow to heart, which is unable to meet the metabolic demands of the muscle on exertion (myocardial ischaemia). This usually subsides with rest.
Pathogenesis of atherosclerotic plaque formation
- High LDL causes them to deposit and oxidise in tunica intima, activating endothelial cells which present leukocyte adhesion molecules.
- Leukocytes move into intima and attract monocytes (macrophages/T helper cells)
- Macrophages take up oxidised LDL and form foam cells, which release IGF-1 causing smooth muscle to migrate to intima from media.
- Smooth muscle proliferation forms fibrous cap.
- As foam cells die they release lipid content, growth factors and cytokines, growing plaque.
- Plaque either occludes vessel or ruptures, triggering platelet aggregation and clotting.
Signs/symptoms of stable angina
- Central crushing chest pain which may or may not radiate to left arm, neck and jaw. (<5 mins long)
- Pain is provoked by exertion or stress
- Pain is relieved by rest/nitrates
May cause sweating, dyspnoea, fatigue, palpitations and syncope
Investigations for stable angina
- 12 lead ECG: Normal (may show ST depression, ruling out NSTEMI/STEMI)
- CT coronary angiography (GOLD) to highlight stenosis
- FBC, TFT, LFT, HbA1C to rule out causative pathologies
Management of stable angina
- Acute relief of symptoms: sublingual GTN spray
- Lifestyle changes (lose weight, exercise, lipid/diabetes/HTN management)
- Long term treatment: Beta blocker e.g. propanolol (CI: Asthma) or CCB e.g. amlodipine (CI: Heart failure) (must be non rate limiting so doesnt cause bradycardia)
Then dual therapy if needed - Long term prevention may be added: 3As (Aspirin, atorvastatin, ACEi (Ramipril))
If pharmacologically unsuccessful, what surgical options are available to treat angina? With pros and cons
- Percutaneous coronary intervention (PCI) - Balloon stent opens vessel. (less invasive, but higher risk of stenosis)
- Coronary artery bypass graft (CABG) - chest opened along sternum, taking graft vein from patient’s leg and sewing onto artery to bypass stenosis. (better outcomes, more invasive/greater risks. Leaves midline sternotomy scar)
What 3 conditions make up Acute Coronary Syndrome
- Unstable angina
- NSTEMI
- STEMI
Occlusion, infarction, ECG, troponin features in ACS conditions
- Unstable Angina: Partial occlusion, no infarction (just ischaemia), ECG usually normal (can show ST depression/T wave inversion), troponin normal
- NSTEMI: Major occlusion, subendothelial infarction, ST depression/T wave inversion/Pathological Q waves, troponin elevated
- STEMI: Total occlusion, transmural infarction, ST elevation/T wave inversion/New LBBB, troponin elevated
ACS signs/symptoms
Central crushing chest pain that may or may not radiate to left arm and neck. Symptoms continue at rest and last >~20 mins
- Dyspnoea, sweating, nausea, palpitations, anxiety (impending sense of doom in MI)
Investigations in ACS
- ECG - see ECG changes cards (if ST elevation or new bundle branch block, STEMI)
- CT coronary angiography - assess occlusion/stenosis
- Troponin T - raised in STEMI, NSTEMI (no ST elevation but troponin = NSTEMI)
What are troponins, give alternative causes of raised troponin
Cardiac muscle proteins. Released from cardiac muscle in severe ischaemia/infarction.
Alternative causes of raised troponin:
- Chronic renal failure
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
Other imaging warranted in cases of MI
Chest X ray - check for pulmonary oedema
Echocardiogram - assess heart damage
Treatment of NSTEMI or unstable angina
1 - Acute management: MONAC (AB)
M - Morphine
O - Oxygen (if saturation falls below 94%)
N - Nitrates (GTN spray)
A - Aspirin (dual antiplatelet with C)
C - Clopidogrel (P2Y12 inhibitor) or ticagrelor
(A)- anticoagulant (LMWH) may be needed
(B) - Beta blocker may be needed
2 - Risk stratification:
GRACE Score conducted to calculate 6 month risk of repeat MI or mortality.
If risk is medium or high (>3%), or patient unstable, conduct PCI (percutaneous coronary intervention)
STEMI treatment
1 - Acute management: MONAC (AB)
2 - Surgical intervention needed!
- <12 hours since symptom onset and PCI available within 2 hours: PCI. If not, thrombolysis with alteplase, with anticoagulant such as unfractioned heparin. Aspirin/ticagrelor may also be given
Coronary angiography and ECG to assess success of treatment
Complications of MI
DREAD
D - Dressler’s syndrome
R - Rupture of heart septum or papillary muscles
E(fgh) - Heart Failure
A - Arrhythmia/Aneurysm
D - Death
Mitral regurgitation
Cardiac arrest
Secondary prevention of CVD
Pharmacological: 4A
- Aspirin (+- clopidogrel)
- Atenolol (Beta blocker)
- Atorvastatin
- ACEi (Ramipril)
Lifestyle:
- Exercise
- Diet change (Mediterranean best)
- Smoking cessation
- reduced alcohol intake
- Diabetes/HTN control
- Cardiac rehabilitation
Side effects of statins
- Myopathy (creatine kinase must be checked if any muscle pain/weakness)
- Type 2 diabetes
- Haemorrhagic stroke
Aspirin MoA
Antiplatelet: COX-1 inhibition - preventing synthesis of thromboxane A2
Clopidogrel/ticagrelor MoA
Antiplatelet: P2Y12 receptor inhibitor (inhibit binding of ADP to P2Y12 receptor)
LMWH MoA
Antiplatelet: glycoprotein IIb/IIIa receptor antagonist
What are GRACE score variables
GRACE score calculates 6 month risk of repeat MI or death using:
- Age
- Heart rate
- Creatinine
- Cardiac arrest at admission
- ST segment deviation
- Abnormal cardiac enzymes
- Killip class symptoms (JV distention, Pulmonary oedema, Cardiogenic shock)
Give the types of angina
Angina: Myocardial ischaemia leading to central chest pain or tightness
- Stable (pectoris): Induced by effort, resolved by rest
- Unstable (crescendo): Occurs at rest, increases in intensity
- Decubitus: Precipitated by lying flat
- Prinzmetals (variant): caused by coronary artery spasm
Define prinzmetal angina with investigations and treatments with 2 contraindicated medications
- Angina due to coronary artery spasm (can occur even in normal healthy arteries)
- Pain occurs at rest
- ECG shows ST elevation during pain which resolves as pain subsides
- CCB + long-acting nitrates
- Beta blockers and aspirin contraindicated; can cause increased spasm or aggravate pain respectively
Define Dressler’s syndrome with symptoms and treatment
- Occurs between 2-10 weeks after an MI. Myocardial damage causes autoimmunity against heart, causing pericarditis.
- Pleuritic chest pain and pericardial rub on auscultation. May have fever and recurrent infection
- Treatment with NSAID or steroids
Define pericarditis
Inflammation of the pericardium of the heart
Causes of pericarditis (bacterial and viral)
Bacterial: TB, pneumonia, rheumatic fever
Viral: Coxsackie, EBV, HIV, CMV (most common)
MI (Dressler’s)
Signs/symptoms of pericarditis
Signs
- Pericardial rub on auscultation on left sternal edge as patient leans forward (Squeaky to and fro sound)
- Chest pain that is sharp, central and pleuritic, that is exacerbated by lying flat or inspiration, and is relieved by sitting forwards.
Symptoms: May present with symptoms of effusion or cardiac tamponade (more detail on individual cards)
PE: Dyspnoea, raised JVP, peripheral oedema, tachycardia, tachypnoea
Cardiac tamponade: Beck’s triad, pulsus paradoxus, coughing
Investigations for pericarditis
ECG - PeRicardiTiS
- Widespread saddle shaped ST elevation
- PR depression, followed by T wave flattening and eventual inversion
Chest X ray: “Water-bottle heart” (cardiomegalic) may indicate pericardial effusion
Auscultation: Pericardial rub when patient leans forwards (left sternal edge)
Management of pericarditis
Analgesia e.g. ibuprofen, and/or colchicine
Treat underlying cause (E.g. antibiotics if Bacterial)
Complications of pericarditis
Pericardial effusion
Cardiac tamponade
Myocarditis
Constrictive pericarditis
If pericarditis persists for weeks/months, what is it called?
Constrictive (chronic) pericarditis
Caused by fibrosis of serous pericardium, forming an inelastic shell around the heart, making it difficult for the ventricles to contract
Signs in constrictive pericarditis
Kussmaul’s sign - raised JVP with inspiration
Pulsus paradoxus - Drop in BP during inspiration greater than 10mmHg
Imaging of constrictive pericarditis
CXR: Small heart with pericardial calcification
Echocardiogram: Thick calcified pericardium
Definition of pericardial effusion
Accumulation of fluid in pericardial sac usually secondary to pericarditis (same causes)
Signs/symptoms of pericardial effusion
Ewart’s sign: Large effusion compressing lower left lobe, causes bronchial breathing at left base
- Dyspnoea, raised JVP, peripheral oedema, tachycardia, tachypnoea
Investigations in pericardial effusion
ECG: Low QRS complex voltage
CXR: Enlarged, globular heart
GOLD: Transthoracic Echocardiogram: echo-free zone around heart, heart “dancing” in fluid
Pericardiocentesis may diagnose cause (bacterial culture/ ZN stain) and is possible treatment (cardiac tamponade)
Define cardiac tamponade
Severe pericardial effusion, raising intrapericardial pressure enough to impair ventricular filling
Signs/symptoms of cardiac tamponade
- BECKS TRIAD
- Hypotension
- Distended jugular veins (+- raised JVP)
- Muffled S1 and S2 heart sounds - Pulsus paradoxus (BP drops more than 10mmHg on inspiration)
Tachycardia
Investigations in cardiac tamponade
Same as pericardial effusion
Echocardiogram diagnostic
Urgent pericardiocentesis to determine cause (bacterial culture, ZN stain, viral serology)
Management and complications of cardiac tamponade
Emergency pericardiocentesis and drainage
Complications:
Cardiac arrest
Constrictive pericarditis
What is Becks triad
Suggests cardiac tamponade
- Hypotension
- Distended jugular veins (+- raised JVP)
- Muffled S1,S2 heart sounds
What 2 symptoms strongly suggest endocarditis
Fever + new murmur
Definition of and risk factors for infective endocarditis. Which valves are most affected
Infection of the endocardium usually affecting valves (native or prosthetic)
Mitral valve most affected, tricuspid most in IV drug use
- Poor oral hygiene (viridians streptococci)
- Elderly male
- Rheumatic heart disease
- Regurgitative valve
- Prosthetic valves
- IV drug use
Pathophysiology of infective endocarditis
- Abnormal/damaged endocardium causes platelet deposition (nonbacterial thrombotic endocarditis)
- Bacteria added (infective endocarditis) which use adhesins to adhere to platelets and each other, causing vegetations.
- These can detach and deposit elsewhere (septic emboli)
- Causes regurgitation in valve
Causes of infective endocarditis
Usually bacterial, can be fungal
Viridians streptococci
Staph Aureus
Staph epidermidis
Strep bovis (colon cancer)
Rare gram negative (HACEK group)
- Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
SLE, malignancy
Main hand signs of Infective Endocarditis (4)
Splinter Haemorrhages (under nails)
Janeway lesions (painless plaques on palms/soles)
Osler’s nodes (Painful nodules on fingers/toes)
Clubbing
(Roth’s spots are the other main sign, white centred retinal haemorrhages!)
Signs/symptoms of infective endocarditis
Symptoms:
Fever, rigors, night sweats, weight loss, splenomegaly
Signs
Splinter haemorrhages, janeway lesions, osler’s nodes, roth’s spots, clubbing, petechiae (haemorrhage under skin), septic emboli
What is the scoring system for infective endocarditis
Modified Duke’s criteria.
2 major criteria. 1 major, 3 minor. 5 minor.
Major:
- Positive blood cultures from 2 separate cultures drawn >12 hours apart. OR all of 3 or majority of 4+ positive cultures with over an hour between first and last.
- Echocardiogram evidence of endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)
Minor:
- Predisposition (cardiac lesion, IV drug use)
- Fever >38C
- vascular/immunological signs (janeway lesions, conjunctival petechiae, septic embolism/ glomerulonephritis, osler nodes, roth spots, rheumatoid factor)
- Positive culture that doesnt meet major
- Positive echocardiogram that doesnt meet major
Major Dukes Criteria
- Positive blood cultures from 2 separate cultures drawn >12 hours apart. OR all of 3 or majority of 4+ positive cultures with over an hour between first and last.
- Echocardiogram evidence of endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)
Minor Dukes Criteria
- Predisposition (cardiac lesion, IV drug use)
- Fever >38C
- vascular/immunological signs (janeway lesions, conjunctival petechiae, septic embolism/ glomerulonephritis, osler nodes, roth spots, rheumatoid factor)
- Positive culture that doesnt meet major
- Positive echocardiogram that doesnt meet major
Investigations in Infective Endocarditis
Use Modified Duke’s Criteria!
- Blood cultures: 3 sets, different sites, at least an hour apart, when fever is highest
- TRANSOESOPHAGEAL echocardiogram: mobile, valvular vegetations if >2mm
Others:
FBC - normochromic, normocytic anaemia
ESR/CRP - high
CXR - Cardiomegaly
ECG - Long PR
Urinalysis
Treatment of Infective Endocarditis
Empirical: Amoxicillin if native, Vancomycin, Gentamicin, Rifampicin if prosthetic
Staph native: Flucloxacillin (1st), vancomycin + rifampicin (2nd)
Staph prosthetic: Flucloxacillin, Gentamicin, Rifampicin
Strep: benzylpenicillin (+gentamicin if prosthetic)
HACEK: Amoxicillin (+gentamicin if prosthetic)
Surgery to remove infected tissue and replace valve if severe sepsis, heart failure, perivalvular abscess
Complications of Endocarditis
Valve regurgitation, rupture or fistula
Septic embolisation
Congestive heart failure
Hypertension staging - hospital vs ambulatory
Stage - Clinical Reading - Ambulatory Reading
1 - >140/90 - >135/85
2 - >160/100 - >150/95
3 - >180/120
Define the white coat effect
A discrepancy of >20/10mmHg between the clinical reading and average daytime ABPM, usually due to the stress of being in hospital
What are the types of hypertension
Primary (essential) - No underlying or known cause
Secondary - known cause
What factors could contribute to essential hypertension
- Genetic susceptibility
- Excessive sympathetic nervous system activity
- High salt intake
- Na+/K+ membrane trnasport abnormalities
- RAAS abnormalities
Give examples of secondary hypertension
Renal:
- CKD
- Glomerulonephritis
- Renal artery stenosis
Endocrine:
- Primary hyperaldosteronism
- Cushing’s syndrome
- Phaeochromocytoma
- Hyperthyroidism
- Acromegaly
Pregnancy (pre-eclampsia)
Describe malignant hypertension
BP >180/120mmHg
Includes signs of retinal haemorrhage and/or papilloedema
Requires emergency treatment
Who should be offered antihypertensive treatment
Stage 1 - Those with:
- Target organ damage
- Established CVD
- Diabetes
- Renal disease
- 10 year CVD risk of >20%
Anyone at Stage 2 or higher
HTN screening every 5 years, more often if borderline. Every year in T2DM
Hypertension treatment
<55 or with T2DM
1) ACEi (ARB if ACEi not tolerated)
2) ACEi + CCB or Thiazide like diuretic
> 55 or Black African/Caribbean
1) CCB
2) CCB + ACEi or Thiazide like diuretic
3) ACEi + CCB + Thiazide like diuretic
4) (3) + alpha or beta blocker or K+ sparing diuretic if K+ <4.5mmol/L
Complications of HTN
Atherosclerosis!!!
4 Cs
Coronary artery disease
Cerebrovascular event
CVD
CKD
Hypertensive retinopathy
ECG in atrial flutter
Sawtooth-like F waves (p wave after p wave)
Give normal pathway of electrical signals in heart
SAN > Atria > AVN > Bundles of His > Purkinje fibres > L/R bundle >Ventricles
Give the types of tachycardia and bradycardia
Bradycardia
- Bundle branch blocks (LBBB,RBBB)
- Heart blocks (1°, 2° (Mobitz 1,2), 3°(complete)
- Sinus bradycardia
Tachycardia
Supraventricular
- AF (Fibrillation and Flutter)
- AVRT (WPW), AVNRT
Ventricular
- Ventricular ectopic
- Prolonged QT syndrome
- Torsades de Pointes
Define sinus tachycardia
Heart rate >100bpm but normal sinus rhythm
Pathophysiology of bundle branch blocks
Blocked side gets impulses late, meaning ventricles do not contract together.
Left bundle branch block causes abnormal Q waves (as left responsible for initial ventricular activation)
Causes and sign on auscultation of RBBB and LBBB
RBBB:
- PE, cor pulmonale, IHD, Atrial/ventricular septal defect
- Wide physiological splitting of S2 heart sound
LBBB:
- IHD, HTN, Cardiomyopathy, fibrosis
- Reverse splitting of S2 heart sound
ECG of RBBB and LBBB
RBBB - MaRRoW
- QRS looks like an M in V1 and V2, looks like an W in V4-V6
- Tall late R wave V1, Slurred S wave V6
LBBB - WiLLiaM
- QRS looks like W in V1 and V2, looks like an M in V4-V6
- Deep S wave in V1, tall late R wave in V6
What are the 4 cardiac arrest rhythms?
VT VF PE A
(Shockable)
- Ventricular tachycardia
- Ventricular fibrillation
(Non-shockable)
- Pulseless electrical activity
- Asystole
Risk factors for Bradycardia
Increasing age (>70)
Hypothyroidism
Hyper/hypo kalaemia, calcaemia
Drugs (Beta blockers, non dihydropyridine CCB, adenosine)
Infections (Typhoid, diptheria)
Pathophysiology of bradycardia/AV blocks
Bradycardia (<50bpm) usually due to sinus node or AV node conduction dysfunction
Types of AV blocks
- 1st degree: Delayed conduction through AV node, every A impulse still causes V contraction. (PR >0.2s)
- Mobitz type 1/Wenckebach: Atrial impulse becomes weaker until it doesn’t trigger Ventricular (PR increases until QRS complex drops) then resets
- Mobitz type 2: Disease of His-Purkinje system causes intermittent failure of AV conduction, causing missing QRS. Usually a set ratio of p waves to QRS. E.g. 2:1 ratio, after every 2nd p wave there is a QRS drop (QRs drop, no PR change)
- Third degree: Complete heart block. No relationship between QRS and P waves
Signs/symptoms of AV Blocks
Signs:
- Cushings triad for raised intracranial pressure: Bradycardia, hypertension, apnoea (temporary cessation of breathing)
- JVP: Cannon A waves (complete heart block, due to atrial contraction against closed tricuspid)
Symptoms:
Bradycardia, Dizziness, Fatigue, Dyspnoea, Syncope
Management of bradycardia/ AV blocks
If unstable Atropine 500mcg
Then pacemaker can be installed
What are the types of supraventricular tachycardia?
AF AF AVRT(WPWS) AVNRT
Caused by electrical signals reentering atria from ventricles
Atrial Fibrillation
Atrial Flutter
AVRT (Wolff-Parkinson White Syndrome)
AVNRT
Define and give risk factors for Atrial fibrillation
Most common arrhythmia. SAN causes uncoordinated, rapid, irregular atrial contraction.
Increasing age
DM
Rheumatic Fever
Obesity
Excessive alcohol
Hyperthyroid
HTN/Cornary artery disease
Congestive heart failure
Thyroxine/beta agonist usage
Causes of Atrial fibrillation
PIRATES
P - PE/COPD
I - IHD and Heart failure
R - Rheumatic heart disease, any valve disease
A - Anaemia, alcohol, age
T - hyperThyroidism
E - electrolytes - Hypo/hyperkalaemia, hypomagnesemia
S - Sepsis/sleep apnoea
Signs/symptoms of atrial fibrillation, as well as course of disease
Signs: Irregularly irregular pulse
Hypotension
ECG changes (other card)
Symptoms: fatigue, palpitations, dyspnoea, syncope, chest pain
Course:
Paroxysmal: Self limiting <7 days
Persistent: recurrent, >7 days
Permanent: Continuous, refractory to treatment
Investigations in atrial fibrillation
Including risk score for 1 year risk of stroke after AF and major bleeding risk for patients with AF on anticoagulants
1) ECG
- Irregularly irregular rhythm
- Absent P waves
- QRS complex <120ms
- Absent isoelectric baseline
- Fibrillatory waves
Also check TFT, electrolytes, CXR, Transthoracic echocardiogram, troponin T
Check CHA2DS2-VASc and ORBIT/HASBLED score
Complications of atrial fibrillation
Ischaemic Stroke
Syncope
MI
Heart failure
Mesenteric ischaemia
What is CHA2DS2-VASc score?
What results give low medium and high score
Calculates 1 year risk of stroke in atrial fibrillation patients
CHADS VASc
Congestive heart failure
Hypertension
Age>75 (2pts)
Diabetes Mellitus
Stroke/TIA/Thromboembolism (2pts)
Vascular disease (PAD, MI, Aortic plaque)
Age 65-74
Sex category (female)
0 low
1 moderate
2+ high - oral anticoagulant required
What is the ORBIT score?
Calculates major bleeding risk for patients with AF on anticoagulants (similar to HASBLED, replaced in 2021!)
Low Hb (+2)
Age >74
Bleeding history (+2)
eGFR <60
Treatment with antiplatelet agents
Management of AF
Rate control and rhythm control
If unstable: emergency electrical synchronised DC cardioversion
- Rate control first: Beta blocker (atenolol) or rate limiting CCB (Verapamil). Dual if refractory
- Rhythm control: Amiodarone or electrical cardioversion if persistent (with amiodarone 4 weeks before and 12 months after)
- Anticoagulation (DOAC or vitamin K) if CHADSVASC>2
Atrial flutter definition/ pathophysiology
Continuous atrial depolarisation caused by a re-entrant rhythm, where electrical signal recirculates in self perpetuating loop. Atrial contraction goes up to 300bpm. Ventricular contraction every 2 cycles (2:1 AV block)
ECG: Diagnostic, Sawtooth-like F waves (p wave after p wave)
Causes of atrial flutter
CHD, obesity, COPD, pericarditis, Cardiomyopathy, Heart failure
Treatment of atrial flutter
Treatment:
If unstable: electrical synchronised DC cardioversion
- Rate control: 1 Beta blocker (atenolol) or rate limiting CCB (Verapamil). Dual if refractory
- Rhythm control: Amiodarone or electrical cardioversion
ECG in AVRT/AVNRT
Short PR
Slurred delta wave
Wide QRS
AVRT/AVNRT (Wolff Parkinson White) pathophysiology
Congenital accessory conduction pathway (bundle of kent) between atria and ventricles
(In AVNRT re-entrant pathway through AV node)
Type A - +ve delta wave in V1
Type B - -ve delta wave in V1
Treatment: Amiodarone and ablation (surgical removal) of accessory pathway
Indications for pacemakers
Symptomatic bradycardia, unresponsive to atropine
AV Blocks
Suppression of tachycardia, unresponsive to drugs
AVRT/NRT treatment
Amiodarone and ablation (surgical removal) of accessory pathway
Define ventricular ectopic tachycardia with ECG
Premature ventricular beats caused by ectopic electrical discharges
ECG shows random abnormal QRS on background of normal ECG
Define long QT syndrome with common causes (3)
Long QT = prolonged repolarisation of muscle cells in heart after a contraction. QT >430 males, >450 females
- Romano-Ward syndrome: Aut Dom inheritance of 1 copy of KCNQ1 gene, causing long QT without deafness
- Jervell-Lange-Nielsen syndrome: Aut Rec. inheritance of two copies of variant gene, causes deafness and long QT
- Can also be caused by drugs that block potassium channels (amiodarone, tricyclic antidepressants, erythromycin also hypokalaemia/calcaemia, myocarditis)
Types of Long QT syndrome
LQT1 - mutation in KCNQ1, causing exertional syncope
LQT2 - mutation in KCNH2, causing syncope in emotional stress
LQT3 - Syncope at night/rest
Treatment of Long QT and main 2 complications
Beta blocker (propanolol) and implantable cardioverter-defibrillator
- Torsade de pointes (depolarisation without proper repolarisation. Fixed with magnesium infusion)
- Cardiac arrest
Define heart failure
Cardiac output inadequate for body’s metabolic demands
How does left heart failure cause right heart failure
Left side of heart is unable to pump efficiently, causing blood to back up into pulmonary veins and arteries. This increases pulmonary blood pressure. This pressure is then transmitted back towards the right ventricle.
The dilation of the right ventricle stretches the AV valve, causing a regurgitation into the right atrium during systole. This causes right atrium dilation, which puts further pressure on the right ventricle causing it’s hypertrophy. Eventually neither work efficiently causing right heart failure. RHF causes an increase in blood backing up into general circulation
How does right heart failure cause its cardinal symptoms
Jugular vein distension - Increased pressure in right atrium is transmitted back to the jugular veins
Hepatomegaly - Increased pressure of the hepatic veins, which usually directly drain into the inferior vena cava
Peripheral pitting oedema - Increased pressure in the systemic venous circulation, forcing fluid out of the blood into surrounding tissues
Systolic vs diastolic heart failure. Causes and pathophysiology
Systolic:
Caused by: IHD, MI, Cardiomyopathy.
Inability of ventricle to contract normally, reducing cardiac output. Ejection fraction is REDUCED (<40%)
Diastolic:
Caused by: Constrictive pericarditis, cardiac tamponade, HTN, restrictive cardiomyopathy.
Inability of ventricles to relax and fill with blood properly. Ejection fraction PRESERVED (>50%)
Signs and symptoms of left heart failure
Signs
- Tachypnoea, tachycardia
- Cool peripheries
- Peripheral cyanosis
- Pink frothy sputum/crackles on auscultation
- Wheeze
- Third heart sound
- Displaced apex beat
Symptoms:
- Dyspnoea, Orthopnoea (SOB when lying flat), Paroxysmal nocturnal dyspnoea (SOB at night)
- Fatigue and weakness
- Weight loss
Signs and symptoms of right heart failure
(usually due to pathology involving lungs/pulmonary vessels e.g. pulmonary stenosis)
Signs (due to backing up of fluid):
- Raised JVP
- Peripheral pitting oedema (thighs, sacrum, abdomen)
- Hepatosplenomegaly
- Ascites
- Facial engorgement
- Pulsing in face/neck (tricuspid regurgitation)
Symptoms:
- Fatigue/weakness
- Swelling in legs/distended abdomen
- Nausea/anxiety
- Nose bleed
What is congestive heart failure
When both left and right heart failure occur together
How might a heart failure patient present on examination?
- Increased resp rate
- Reduced O2 saturation
- Tachycardia
- Hypotension
- Dyspnoea
- Oedema in legs
Auscultation:
- 3rd heart sound/ displaced apex beat
- Bilateral basal crackles (that sound wet)
How does left heart failure cause pulmonary oedema, and how does this lead to right sided heart failure
LV unable to move blood out into body, causing backlog.
This increases blood stuck in LA, pulmonary veins and lungs. They leak fluid as a result and are unable to reabsorb it. This causes pulmonary oedema; lung tissues and alveoli become full of interstitial fluid, interfering with gas exchange, leading to SOB and other symptoms.
Pulmonary HTN puts pressure on right ventricle, meaning it isn’t able to pump as much blood, causing right sided heart failure.
Signs of heart failure that suggest an underlying cause
Chest pain - ACS
Fever - Sepsis
Palpitations - Arrhythmia
Investigations in Heart failure
BNP (Brain Natriuretic Peptide) blood test
- Released from stressed ventricles in response to increased mechanical stress
- (NOT specific, also released in tachycardia, sepsis, PE, renal impairment, COPD)
CXR (ABCDE)
- Alveolar Oedmea, Kerley B lines (interstitial oedema), Cardiomegaly, Dilated upper lobe vessels, Pleural effusion
ECG will show wide QRS and may help diagnose causation
Echocardiography is KEY. Measures Ejection fraction, ventricular function, valvular abnormalities
Scoring system for heart failure functional limitations
New York Heart Association classifications of heart failure
I (Mild) - No limitation on physical activity. Ordinary physical activity doesnt cause fatigue/palpitations/dyspnoea
II (Mild) - Slight limitation n physical activity. Comfortable at rest; dyspnoea on ordinary activity
III (Moderate) - Less than ordinary activity causes dyspnoea, which is limiting. Rest is fine.
IIII (Severe) - Symptoms present at rest, all activity causes discomfort
Criteria for congestive cardiac failure
Framingham criteria (2 major, 1 major 2 minor)
Major - PNDyspnoea, Crepitations, JV distention, Pulmonary oedema, S3 gallop, Cardiomegaly, weight loss
Minor - Bilateral ankle oedema, nocturnal cough, dyspnoea on exertion, tachycardia, hepatomegaly, pleural effusion
3 cardinal non specific signs in heart failure
SOB AS FAT
Dyspnoea, Ankle Swelling, Fatigue
Pathophysiology of ischaemic, HTN, LV hypertrophy and dilated cardiomyopathy heart failure, and what HF do these cause?
Cause systolic failure
- Ischaemic: Myocytes start to die, reducing ability of contraction
- HTN: Arterial pressure increase in systemic circulation means it is harder for LV to pump blood into hypertensive circulation
- LV hypertrophy: increased muscle mass requires increased oxygen supply, more likely muscles will die
- Dilated cardiomyopathy: Heart chambers dilate, become thinner, weaker contractions.
Acute management of heart failure
Pour SOD
Pour away fluids (Stop fluids)
Sit up
Oxygen
Diuretics
GTN may be needed
Management of chronic heart failure
ABAS
ACEi (ramipril)
Beta blocker (propanolol)
Aldosterone antagonist (spironolactone)
SGLT2i - empagliflozin
1) ACEi + beta blocker
2) Add spironolactone and SGLT2i if Ejection fraction not controlled with ACEi and BB
What should be kept in mind when prescribing for heart failure? (reg ACEi)
ACEi contraindicated in Heart valve disease
ARB (candesartan) can be used instead of ACEi
Aldosterone antagonists added if ejection fraction not controlled with ACEi and BB
Define abdominal aortic aneurysm
Dilatation in the aorta of >50%, or 3cm. Caused by increased stress to vessel wall which weakens it and eventually causes an outpouching of the vessel.
Where do abdominal aortic aneurysms occur most commonly, and why?
Occur below level of renal arteries (infrarenal aneurysm). Due to the abdominal aorta below this level lacking vasa vasorum in its adventitial layer, which deliver nutrients to the aorta, making it susceptible to ischaemia.
Thickening of the intima also makes it harder for oxygen to diffuse into the tunica media
How does atherosclerosis contribute to aneurysm formation?
Atherosclerosis is the most important AAA risk factor
Chronic inflammation causes release of matrix proteinases which degrade extracellular matrix in tunica media, weakening the aortic wall
2 main differentials for AAA
Pseudoaneurysm (ie false aneurysm, does not involve all 3 layers of vessel wall, [E.G. AORTIC DISSECTION] when bleeding into one or 2 vessel layers causes bulging in those layers, resembling an aneurysm)
Inflammatory AAA (younger patients, occurs with smoking, atherosclerosis, vasculitis, presents similarly but with fever.)
Most common causes for AAA
Atheroma
Trauma
Inflammation
Connective tissue disorder (Ehrling-Danlos, Marfans)
True vs False aneurysm
True - Stress to vessel wall causes weakening of wall, leading to the occurrence of an outpouching and dilation. Affects all 3 layers
False (Pseudoaneurysm e.g. Aortic dissection) - Defect in vessel wall leads to bleeding into a layer or 2 (Extravascular haematoma). Causes a pulsatile haematoma
Risk factors for AAA
Increasing age
Male
Smoking
ATHEROSCLEROSIS!!
Hypertension/lipidaemia
Connective tissue disorders (Marfans, Ehlers Danlos)
Diabetes is protective!
Signs/symptoms of AAA
Mostly asymptomatic until it is about to rupture imminent or occurred (emergency)
Signs
- Pulsatile abdominal mass
- Sudden abdominal pain that radiates to flank
If ruptured:
- Grey turner’s signs: Flank bruising caused by retroperitoneal haemorrhage
- Cullen’s sign - Peri-umbilical bruising
What imaging is diagnostic for AAA
(X ray, CT, MRI, CT Angiography, Ultrasound)? + other investigations
Abdominal ultrasound
Group and save and crossmatch needed if ruptured to ensure blood for transfusion
Worth doing FBC, U&E, CT angiogram, CRP/ESR to find cause
Screening and associated management for AAA
Abdominal ultrasound for over 65s
<3cm - Discharge
3-4.4cm - Annual surveillance
4.5-5.4 cm - 3 monthly surveillance
>5.5cm - refer to surgery (Open or Endovascular Aortic Repair (EVAR) or AAA graft surgery if ruptured)
In general, reduce risk factors (lifestyle), underlying cause treatment (Steroids for inflammatory)
Complications of AAA
- Aneurysm rupture: Medical emergency with poor prognosis, IMMEDIATE SURGERY
- Thromboembolism: Thrombus more likely in dilated aneurysm
- Aortovenous fistula formation
- Ureteric obstruction
Aortic dissection definition + pathophysiology
Tear in tunica intima of aorta causes high pressure blood to tunnel into tear, causing pooling between intima and media. This eventually increases diameter of aorta, causing false aneurysm.
Risk factors for aortic dissection
Similar to RF for AAA
HTN
Smoking
Atherosclerosis
Connective tissue disorders (Ehlers-Danos, Marfans)
Trauma
Pregnancy
Family history!
Signs/symptoms of aortic dissection and Marfans and Ehlers Danlos
Sudden onset tearing/ripping chest pain that radiates to back.
Signs:
- Weak downstream pulses
- Differences in BP of both arms
- Diastolic murmur due to aortic regurgitation
- Hypertension
- Tachycardia, hypotension as progresses
Marfans: Tall, Arachnodactyly, Hypermobile joints, Narrow face
Ehlers-Danos: Translucent skin, Easy bruising, hypermobile small joints
Classification of Aortic dissection
Stanford classification
(2/3) Type A: Dissection involves ascending aorta. Aortic arch and Descending aorta may be involved. Proximal to left subclavian artery
(1/3) Type B: Dissection doesnt involve ascending aorta. Only descending, thoracic, abdominal aorta. Distal to left subclavian artery.
Investigations for aortic dissection
CXR - Widened mediastinum
Transoesophageal echocardiogram
GOLD - CT Angiography (U+E conducted before this)
Cross match needed before transfusion
Treatment of aortic dissection
Blood transfusion if blood loss
Opioid analgesia if in pain
1 - Beta blocker
- Vasodilator (Sodium nitroprusside)
2- Urgent Surgery (Thoracic endovascular aortic repair (TEVAR))
Complications of aortic dissection
- Aortic rupture (emergency, death without surgery)
- Aortic regurgitation!
- Renal failure (if blood continues to tunnel till it reaches renal arteries, pressuring those arteries, reducing flow to kidneys)
- Pericardial tamponade
- MI
- Stroke
Define PAD with pathophysiology
Peripheral Arterial Disease
Arterial obstruction, usually due to atherosclerosis and thrombosis, causing ischaemia of lower limbs. Ischaemic muscles release adenosine causing pain.
3 main patterns;
- Intermittent claudication
- Critical limb ischaemia
- Acute limb-threatening ischaemia
Signs/symptoms of PAD
6P’s
Pulseless
Paralysis
Pale
Perishingly cold
Pain
Paraesthesia
Usually due to acute limb ischaemia together but some present in PAD
Other signs:
- Ulcers
- Pale, shiny, taut atrophic skin
- Hair loss
Classification of PAD
Fontaine classification
1 - Asymptomatic - Low ABPI/lack of pulses
2 - Intermittent claudication - Aching/burning on exertion, after walking:
- 2a: >200m, 2b: <200m. Pain never present at rest
3 - Critical limb ischaemia - Rest pain, “dangling over edge of bed for pain relief”. Risk of limb loss
4 - Tissue loss (Ulceration/Gangrene)
Site of claudication with associated site of disease
- Unilateral buttock
- Unilateral thigh
- Unilateral calf
- Foot
Unilateral buttock - Common iliac
Unilateral thigh - Common femoral or iliac
Unilateral calf - Popliteal or Superficial Femoral
Foot - Peritoneal or tibial
What is the Buerger’s test?
Test for PAD
Raise patient’s legs 45 degrees. Pallor after 1-2 mins suggests PAD.
Next, have them sit over the edge of a bed with their legs hanging.
In PAD patient, legs will go blue (as ischaemic tissue deoxygenates blood) and then dark red (reactive hyperaemia due to post-hypoxic vasodilation)
What is Leriche syndrome
PAD causes occlusion of aortoiliac artery
Patient presents with triad of
- Bilateral buttock and thigh claudication
- Absent or decreased femoral pulses
- Erectile dysfunction
Investigations in PAD
Ankle-brachial pressure index: systolic BP recorded in both arms, posterior tibial, dorsalis pedis and peroneal arteries.
- >1.4 - Abnormally calcified vessels
- 1.2-0.9 - Normal
- 0.9-0.5 - Intermittent claudication
- <0.5 - Critical limb ischaemia
- Absence of pulse in lower extremities suggests acute limb ischaemia
Duplex ultrasound - First line imaging. CT angiography can be done after
Management of PAD
- Exercise first line, control risk factors (clopidogrel as prophylaxis)
- Vasodilator: naftidrofuryl oxalate
- Surgical interventions if exercise doesnt work. Percutaneous Transluminal Angioplasty or Atherectomy.
- Amputation if severe
Acute limb ischaemia AKA Acute limb-threatening ischaemia definition and main cause
- Sudden decrease in perfusion due to arterial occlusion, resulting in severe ischaemia. MEDICAL EMERGENCY.
- Caused by thrombosis/embolism (AF, recent MI causing mural thrombus, valvular vegetation)
Signs/symptoms of Acute limb ischaemia and management
Pale
Pulseless
Paralysis
Paraesthesia
Pain
Perishingly cold
Initially - IV unfractioned heparin
Then: (depends on Rutherford criteria)
1 - Thrombolysis
2 - Thrombolysis or percutaneous thromboembolectomy
3 - Amputation
Complications of PAD
Progression to critical limb ischaemia
Ulceration/gangrene
Infection/poor tissue healing
Rhabdomyolysis
Permanent limb pain/weakness
Define DVT
Formation of a blood clot in the deep veins of leg/pelvis (as opposed to superficial arteries in PAD)
Risk factors/causes of DVT
Increasing age
Smoking
Pregnancy
SLE
Thrombophilias
Immobility (long haul travel, hospitalisation, bed bound)
Synthetic Oestrogen (combined oral contraceptive pill)
Leg fracture
What is Virchows triad
Triad for thrombosis
1) Hypercoagulability
- Increased platelet adhesion and clotting tendency (pregnancy, obesity, chemotherapy, antiphospholipid syndrome, malignancy)
2) Venous stasis
- Stasis disrupts laminar flow, increasing risk of thrombus formation
3) Endothelial damage
- Damage disrupts anticoagulant secretion by endothelial cells (Smoking, trauma, surgery, inflammation)
Signs/symptoms of DVT
- Pitting Oedema
- Red, tender, swollen calf
- Distended superficial veins
- Mild fever
What is the Wells score
Predicts DVT
Highly sensitive but not very specific
DVT likely 2 points
DVT unlikely 1 point or less
Some point factors include:
- pitting oedema
- active cancer
- Distended superficial veins
- calf swelling
- previous DVT
- localised tenderness
- recent bedriddenness
If alternative diagnosis equally likely take 2 from points
If DVT unlikely (<1), conduct D Dimer, if positive ultrasound
If DVT likely, do both D dimer and ultrasound
What is a possible cause of recurrent venous thromboembolism
Antiphospholipid syndrome (or other thrombophilias)
What should a patient be started on if at risk of VTE whilst in hospital?
LMWH (enoxaparin) is go to prophylaxis for VTE
Investigations in DVT
Wells score guides investigations
<=1- Perform D dimer
If positive, do duplex ultrasound
>=2 - Duplex ultrasound of leg, perform D dimer and offer interim anticoagulation
Interim coagulation always offered if results cant be obtained within 4 hours.
Management of DVT
Initial: If no renal impairment: Offer apixaban (factor Xa inhibtor)
If renal impairment: LWMH, or unfractioned heparin
If cancer, DOAC
Preventative advice for DVT
- Wear compression stockings
- Frequent calf exercises
- Prophylactic anticoagulation (LMWH) in patients with recent surgery/long immobilisation
Define Pulmonary Embolism
Sudden onset pleuritic chest pain caused by embolus (most commonly by DVT) lodging in pulmonary vasculature.
Embolus travels through circulation, into right atrium then out of right ventricle into lungs. Blockage leads to ischaemia/infarction of lung tissue. Causes V/Q mismatch severe enough to collapse alveoli
Signs/symptoms of Pulmonary embolism
Hypoxia (+- cyanosis)
Tachypnoea, tachycardia
Hypotension
Crackles
Pleuritic chest pain, dyspnoea, cough +- haemoptysis, fever, fatigue
Investigations for thrombophilias
Antiphospholipid antibodies
Thrombophilia screen (Especially indicated in unprovoked DVT/PE)
Scoring system for pulmonary embolism
Well’s Two-Level PE score
<4, low probability
4+, high probability
Contra indication for compression stockings
PAD
Investigations for Pulmonary embolism
D dimer and CT pulmonary angiography 1st and GOLD!
ECG also significant (S1Q3T3)
- Large S wave lead 1
- Large Q wave lead 3
- Inverted T wave in lead 3
- Also shows sinus tachycardia
Management of pulmonary embolism
Supportive in hospital (Oxygen, analgesia etc)
Massive PE: Thrombolysis - Alteplase
Non massive:
- Initial: If no renal impairment: Offer apixaban (factor Xa inhibtor)
- If renal impairment: LWMH, or unfractioned heparin
- If cancer, DOAC
Complications of pulmonary embolism
- Cor pulmonale
- Pulmonary infarction
- Respiratory alkalosis
- Embolic stroke
Define rheumatic fever with pathophysiology
Type 2 hypersensitivity reaction; Autoimmune condition caused by antibodies created against Group A beta-haemolytic streptococcus infection (strep pyogenes) (Molecular mimicry)
Rheumatic fever is usually secondary (2-4 weeks) to strep throat (Tonsilitis due to streptococcus)
Rare in West, more common in developing world
Systemic, causes joint pain and carditis.
Repeat exposure can become chronic, leading to fibrosis of valves, causing regurgitations.
What can be found histologically on the hearts of people with rheumatic fever
Aschoff bodies
Scoring system for Rheumatic fever, major and minor signs
Revised Jones criteria - Evidence of recent strep infection + 2 major signs or 1 major 2 minor (JONES-FEAR)
Evidence of recent infection: group A strep antigen test, positive throat culture, strep antibodies
Major: JONES
- Joint arthritis
- Organ inflammation (CARDITIS! + Murmurs)
- Nodules under skin
- Erythema marginatum rash - red raised edges, clear middle
- Sydenham’s chorea - involuntary semi purposeful movements
Minor: FEAR
- Fever
- ECG (prolonged PR)
- Athralgia without arthritis
- Raised CRP/ESR
other Sx
- Pericardial rub
- rash
- joint pain
- SOB
What murmurs does rheumatic fever cause
Acute - Mitral and aortic Regurgitations
Chronic - Mitral stenosis
Management and complications of rheumatic fever
Oral penicillin V for 10 days, NSAIDs
- Rheumatic heart disease - Fibrosis of valves leading to regurgitations (Stenoses possible if chronic)
- Heart failure
- Infective endocarditis/pericarditis
- Atrial fibrillation
Complications of valve disorders
Mitral stenosis - Left atrial hypertrophy
Aortic stenosis - Left ventricular hypertrophy
Mitral regurgitation - Left atrial dilatation
Aortic regurgitation - Left ventricular dilatation
Mitral stenosis pathophysiology
Narrow mitral valve, difficult to push blood into ventricle. Sx occur when mitral bicuspid valve lumen <2cm². Pressure increases until the valve “snaps” open. Backing up of blood can cause right sided heart failure.
Mitral stenosis causes, associated symptoms and valve sounds
- Caused by rheumatic fever and Infective endocarditis
- Malar flush (due to reduced cardiac output causing vasodilation) and atrial fibrillation (strain on heart). May present with Right heart failure signs.
- Loud S1 snap and mid diastolic murmur
Mitral Stenosis investigations
CXR - left atrium enlargement - Double right heart border, splayed trachea, calcified mitral valve
ECG - Atrial fibrillation - p mitrale(tall, long p wave), and tall R waves in V1 if RV hypertrophy
Transthoracic Echocardiogram (GOLD)
Mitral stenosis treatment and complications
Percutaneous mitral valvotomy
Mitral valve replacement
Right sided heart failure
Atrial fibrillation
Thrombus
Stroke
What causes S3 and S4 heart sounds
S3 - rapid ventricular filling. Normal in young (15-40), indicates heart failure in older patients
S4 - Heard before S1. Always abnormal. Indicates a stiff or hypertrophic ventricle causing turbulent flow against a contracting atrium.
Mitral regurgitation pathophysiology
Mitral valve allows blood back into atrium during systolic contraction. Causes congestive heart failure due to reduced ejection fraction and backlog of blood.
Mitral regurgitation causes and valve sounds
- Ischaemic heart disease, rheumatic heart disease, connective tissue disorders (Ehlers Danos, Marfan), Infective endocarditis
- Pansystolic whistling murmur that radiates to axilla with mid systolic click and additional S3 sound
Mitral regurgitation investigations
ECG - p-mitrale may suggest left atrial enlargement, may show AF
CXR - left sided enlargement and pulmonary oedema
Echocardiogram GOLD
Aortic stenosis pathophysiology and causes
Aortic valve doesn’t open as easily, preventing flow out of heart. Causes LV hypertrophy and dilatation.
- Idiopathic age related calcification
- Rheumatic heart disease
- Bicuspid valve
Aortic stenosis signs and symptoms and valve sound
Ejection systolic crescendo-decrescendo murmur radiating to carotids. Ejection click and S4 sound.
Sx
- Slow rising pulse and narrow pulse pressure
- Exertional syncope
Aortic regurgitation pathophysiology and causes
Diastolic leakage of blood from aorta to left ventricle. Causes heart failure
- Connective tissue disorders (Ehlers Danlos/Marfans)
- Idiopathic aging related weakness
Aortic regurgitation signs and valve sounds
Early diastolic murmur, water hammer pulse, soft S1, S2.
OR Austin-Flint murmur: Rumbling murmur at apex (Severe) due to vibration of mitral valve
- Corrigan’s pulse: collapsing pulse due to blood pumping out of ventricles and immediately back in.
- de Musset’s sign: Head bobbing with each beat due to severe bounding (water hammer) pulse
- Quincke’s sign: Pulsation of capillary beds in finger nails
- Traube’s sign: Pistol shot femoral pulse
Define Tetralogy of Fallot with signs/symptoms
Congenital abnormalities cause an increase in deoxygenated blood in circulation. This causes:
- Cyanosis
- Clubbing
- Failure to thrive
- Ejection systolic murmur
Risk factors for Tetralogy of Fallot
- Family congenital heart disease history
- Alcohol consumption during pregnancy
- Diabetic mother
- Down syndrome (trisomy 21)
- Rubella infection
4 congenital abnormalities in Tetralogy of Fallot
VORP - cause right to left cardiac shunt; blood bypasses lungs.
Ventricular Septal Defect - Blood shunts between ventricles. Oxygenated and deox. mix. Deox more into left than ox into right.
Overriding Aorta - Aorta further right than normal. RV sends deox blood into it
RV Hypertrophy - Due to added resistance of LV, ensures deox blood is shunted to left, rather than the other way.
Pulmonary stenosis - RV outflow obstruction makes it harder for deox blood to reach lungs
Explain a Tet spell with the symptoms that come with it
Cyanosis exacerbated when infant demands extra oxygen (crying, feeding etc)
- Reduced oxygen saturation
- Knees to chest “Squatting” position (femoral arteries partially occluded, increasing systemic vascular resistance and reducing shunt)
- Respiratory distress
- Severe cyanosis
- Syncope
Treatment of Tetralogy of Fallot
- Cyanosis managed with prostaglandins (e.g. alprostadil)
- Tet spells managed with oxygen, morphine, sodium bicarbonate, beta blockers, phenylephrine, and squatting position of child
- Surgery is definitive
What does a chest x ray show in Tetralogy of Fallot
Boot shaped heart. Echocardiogram may also be shown
Coarctation of the Aorta definition and pathophysiology
Narrowing of the aortic arch, strongly associated with genetic condition Turner’s syndrome. This causes reduced blood pressure to arties distal to the narrowing, whilst increasing blood pressure on heart and first 3 branches of the aorta.
How is Coarctation of the Aorta diagnosed?
In neonates: Weak femoral pulses are first sign. Measuring BP of all 4 limbs will show high BP in limbs supplied before narrowing, low in rest. Systolic murmur may be present.
What key organs are at risk of failure from shock?
Kidney, Lung, Heart, Brain
Define Hypovolaemic shock with signs/symptoms
- Shock due to a low blood volume (Decreased by >20%), can be haemorrhagic or non-haemorrhagic (e.g. dehydration, burns)
- Considered “Cold” shock (cold clammy skin, confusion, tachycardia, narrow pulse pressure)
- Treated with ABCDE and IV Fluids
Define Cardiogenic shock with causes and symptoms
- Shock caused by decreased pumping of blood around body. Causes cold shock due to lack of flow around body.
- Caused by MI, pericardial effusion/cardiac tamponade, arrhythmia, myocarditis, pneumothorax etc.
- Presents with symptoms of heart failure (oedema, JVP increase, S4 sound)
Define septic shock with symptoms and treatment
Uncontrolled bacterial infection
- pyrexia, warm, flushed skin
- Bounding pulse
- Rigors
Treat with broad spectrum antiobiotics
Already ill patient suddenly goes tachycardic, cyanotic, tachypnoic and red. What has happened?
Acute respiratory distress syndrome. Lungs cannot provide body’s vital organs with enough O2
Pathophysiology of acute respiratory distress syndrome
- Alveolar capillary membrane injury
- Causes neutrophil invasion
- Fibroblasts initiate fibrosis
- Lungs scar and go stiff, less ventilation
Consequences of Shock on
Kidney
Lung
Heart
Brain
Kidney - Acute tubular necrosis
Lung - Acute respiratory distress syndrome
Heart - Myocardial ischaemia
Brain - Confusion, Coma, Irritability.
Define neurogenic shock with symptoms and treatment
Due to spinal cord trauma disrupting sympathetic nervous system but not parasympathetic
- Hypotension, BRADYCARDIA, confusion
- IV Atropine
Define hypertrophic cardiomyopathy with causes
LVH causing thick non compliant heart, leading to impaired diastolic filling.
Caused by autosomal dominant mutation of sarcomere proteins (Beta myosin, Troponin T)
Pathophysiology of hypertrophic cardiomyopathy
Walls of heart get thick, heavy and hypercontractile.
- Walls take up more room, less cavity space
- Walls stiff and less compliant cant stretch to fill with blood
- Less blood pumped from heart (Decreased stroke volume)
- Bigger heart requires more oxygen, increased ischaeamia
Auscultation sounds of hypertrophic cardiomyopathy
Definitive investigation and treatment
Ejection systolic murmur (crescendo-decrescendo)
Bifid pulse
S4 sound (think HTCM - 4 letters)
Sudden death may be first sign
- Echocardiogram (ECG will show abnormality too)
- Amiodarone, BB
What do Ventricular Septal defect, Atrial septal defect, Patent ductus arteriosus all cause
Left to right shunt of blood. Causes excess blood in pulmonary system causing pulmonary hypertension. Usually asymptomatic but in severe cases can lead to right heart failure
What is ventricular septal defect and how does it present on examination
Congenital hole in ventricular septal wall allowing blood to shunt from left to right ventricles
Loud, pan systolic harsh murmur with palpable thrill
What is atrial septal defect and how does it present on examination
Congenital hole between atria. Causes blood shunt from left to right.
Ejection systolic murmur.
What is Patent Ductus arteriosus and how does it present on examination
Connection between aorta and pulmonary artery that doesn’t close
Murmur at left sternal edge, thrill at upper left sternal border
Usually treated surgically in first year of life due to infective endocarditis risk
What 2 bacteria are most commonly found in lung abscesses
Staph aureus and strep millieri
What 3 things can you hear on auscultation of a heart failure patient
- Bilateral basal crackles
- S3 sound
- Displaced apex beat
Leads showing change, site of heart and coronary artery affected in ECG
Septal - V1, V2 - Left anterior descending
Anterior - V3, V4 - Left anterior descending
Inferior - II,III, aVF - Right coronary
Lateral- I, aVL, aVR, V5, V6 - Lateral circumflex
What are the criteria for cardiac resynchronisation therapy
- Bundle branch block
- Ejection fraction < 40%
- NYHA classification lll
Define cor pulmonale
Right heart failure that occurs secondary to long standing pulmonary hypertension
What does cor pulmonale show on ecg
P pulmonale - tall, peaked P wave
What rule must be followed when prescribing a beta blocker and CCB
CCB must be dihydropyridine (non rate limiting) to not cause bradycardia
Resuscitation council guidelines on tachycardia treatment
1 - If life threatening/unstable (shock, syncope, MI, Heart failure), Synchronised DC shock up to 3 times. If unsuccessful, amiodarone and go again.
If stable:
2 - If QRS narrow (120ms/0.2s), and regular, give amiodarone. If irregular most likely Afib, rate limit with beta blocker.
2- If QRS normal, valsalva manoeuvres. If unsuccessful, give adenosine (6 then 12 then 18). Then verapamil if still unsuccessful
What is the valsalva maneuvre
Patient breathes out as hard as they can against a closed airway (blocked mouth and nose)
Helps in Supraventricular tachycardia (Normal QRS)
What is a carotid sinus massage and when is it used?
Pressure applied to carotid sinus, slowing down or terminating arrhythmia in AVNRT or SVT.
It is contraindicated if history or risk of stroke/TIA or carotid artery disease
Resuscitation council bradycardia treatment algorithm
Life threatening (syncope, shock, MI, heart failure) - Atropine 500mcg. Can be repeated to max of 3 mg or isoprenaline or adrenaline. If pharmacologically unsuccessful, transvenous pacing
If not life threatening and no recent asystole, mobitz 2 or complete heart block, just observe
Causes of Long QT
Romano-ward syndrome
Jervell-Lange-Nielsen
Hypokalaemia
Hypomagnesaemia
Other obvious heart problems
What is an innocent flow murmur and what are 3 things it can be caused by?
No valvular pathology. Have a “blowing” sound and can appear anywhere.
Usually due to increased flow across aortic and pulmonary valves caused by:
- Anaemia
- Pregnancy
- Thyrotoxicosis
How should a provoked (bed rest, recent surgery etc) PE be anticoagulated?
DOAC (Apixaban) 3 months
How should an unprovoked PE be anticoagulated?
DOAC (Apixaban) 6 months
What are the 4 steps of platelet plug formation?
- Damage to a blood vessel causes exposure of collagen. Von Willebrand Factor (vWF) binds to collagen which acts as a molecular anchor for platelets to join.
- Platelets adhere to the damaged endothelium via vWF. When platelets adhere, they activate and degranulate– their shape changes and they release chemicals that keep the vessel constricted and draw more platelets to the damaged area. This positive feedback loop continues.
- The aggregation of platelets results in the formation of a plug that temporarily seals the break in the vessel wall.
- Following formation of the platelet plug, coagulation is activated to form a fibrin mesh which stabilises the platelet plug.
