Cardiovascular Flashcards
Describe what an ECG is
ECG: Electrocardiogram - A recording of the electrical activity flowing through the heart - Crucial bed-side investigation and first-line for patients with chest pain, palpitations or syncope
Describe cardiac conduction through the heart and corresponding waves on ECG
Impulse starts at the SAN, spreads through the atria causing atrial depolarisation and contraction (P wave) AP reaches AVN, where impulse is delayed for 0.1s (allowing for ventricular filling). This travels down septum through the Bundle of His to the apex then up the Purkinji fibres to the ventricular myocardium causing ventricular depolarisation and contraction (QRS complex) Ventricular cells then repolarise (T wave)
Describe the waves and intervals of a normal ECG (and examples of abnormalities)
P wave: atrial depolarisation (atrial muscle smaller than ventricular muscle therefore smaller electrical charge). This is viewed mostly in lead II (rhythm strip).
PR interval: the time taken for the electrical impulse to spread from SAN through atrial muscle to AVN and into ventricular muscle. Usually 120-200ms (3-5 small sq), prolonged with 1st degree heart blocks
QRS complex: ventricular depolarisation, usually 120ms
ST segment: looking to see if elevated/depressed suggesting ischaemia
Q wave: septal depolarisation (only seen in V5,6,lead I,aVL)
QT interval: ventricular depolarisation and repolarisation i.e. ventricular systole. This varies with HR and is prolonged with electrolyte imbalances and amiodarone. Prolonged QT could lead to ventricular tachycardia
T wave: repolarisation
What are the 12 leads that form an ECG?
Chest leads: V1-V6 (transverse plane, giving detail about R wave progression and transition zone)
Limb and augmented leads: leads I, II, III, aVL, aVR (coronal plane, giving detail about cardiac axis)
How do you determine right or left axis deviation on ECG and give examples of abnormalities?
In general:
Right axis deviation: leads I and II have QRS returning to each other e.g. right sides hypertrophy (e.g. pulmonary embolism), conduction issue, dysfunction of LHS (e.g. MI)
Left axis deviation: leads I and II have QRS leaving each other e.g. LHS hypertrophy, dysfunction of RHS (e.g. MI) can have a look at other leads too
What does a Q wave represent and which lead leads of an ECG is it normally present in?
Represents septal depolarisation
V5, V6, leads I and aVL (left lateral aspect of the heart)
What pathology would explain transitional zone shifts in an ECG?
Seen in transverse chest leads. Shift right would suggest left sided MI (scar tissue) or right-sided hypertrophy (thicker muscle) Vice verse in left
List a systematic approach to interpreting an ECG
- Patient details and previous ECGs
- Rate
- Rhythm
- Cardiac axis
- Conduction intervals
- QRS complexes
- ST segment and T waves
What does the width of the QRS complex tell you?
If the depolarisation has originated in the ventricles or atria Narrow (<3 small squares/120ms): Supraventricular origin (SAN, atrial muscle, AVN) Broad (>3 small sq): Ventricular origin (because ventricles have a slower intrinsic rate)
What is atrial flutter and how is it identified on ECG?
A re-entrant rhythm forms within atrial tissue usually due to atrial tissue damage e.g. ischaemia. Very fast rates of atrial depolarisation and contraction are produced.
‘Flutter’ rather than full contractions - sawtooth appearance
AVN can’t rely every depolarisation onto ventricles, therefore may see a ratio of P waves to QRS complexes e.g. 2 to 1
- P waves present, narrow and regular QRS complexes, T waves usually hidden within sawtooth appearance of P waves
- Flutter waves seen best in leads II, III, aVF (inferior view)
What is ventricular tachycardia and how is it identified on ECG?
The impulse originates in the ventricles and generates very fast paces (~250bpm). Impulse usually generated from a single focal lesion in v. myocardium
- Absent P waves: no atrial contraction
- Broad, monomorphic QRS: contraction originates in ventricles
- Fast rate
- If it lasts >3 beats: sustained period of ventricular tachycardia
Why is ventricular tachycardia dangerous, and what symptoms may be observed?
- It compromises ventricular diastole, therefore reduces ventricular filling
- This leads to reduced cardiac output
- Could lead to cardiac arrest depending on severity of reduced cardiac output
- Patients are usually very symptomatic: chest pain, dizziness, syncope, SOB
What is aetiology and pathogenesis of ventricular tachycardia?
Either:
- Damage to ventricular myocytes causing a re-enterant circuit to form. Myocytes then conduct at different rates
OR
- Damage to ventricular pacemaker cells, altering their firing rates. They fire at higher rates than the SAN and therefore take dominance. Causes: electrolyte imbalance, medication, ilicit drugs
What is Torsades de Pointes? Give an example of what causes it and why it is dangerous
- A polymorphic type of ventricular tachycardia
- Multiple focal lesions generating the impulses
- Fast rate
- Looks like a twisting motion
- Broad, polymorphic QRS complexes
- No P waves
Cause: severe hypoxia
Danger: can degenerate into ventricular fibrillation
What is atrial fibrillation and how is it identified on ECG?
- Small, disorganised electrical activity therefore no atrial contraction (quivering)
- No P waves
- Irregularly irregular QRS complexes (narrow): varying strengths of impulses reach AVN which will only sometimes result in conduction through AVN
- Fibrillating base line
Lack of atrial contraction means loss of ‘kick’ for ventricular filling
What is the aetiology of atrial fibrillation?
- Risk factors put stress onto atrial muscle, leading to tissue heterogeneity
RFs: ischaemic heart disease, HTN, valvular heart disease, hyperthyroidism
Tissue heterogeneity: cells develop different properties, some conducting faster and some slower
What is ventricular fibrillation and how is it identified on ECG?
- Disorganised electrical activity in the ventricles i.e. unco-ordinated muscle fibre contractions. There are no ventricular contractions (fibrillating ventricular tissue) therefore no cardiac output
- No P waves
- No QRS complexes
- No T-waves
I.e. completely disorganised ECG
Why is ventricular fibrillation dangerous?
- V. fibrillation results in compromised ventricular filling and no contractions
- Therefore, there is no cardiac output leading to cardiac arrest
- Patient would have no impulse and be unconscious
Map out tachycardias in a flow chart
Tachycardia (>100bpm) → broad or narrow
Broad QRS = Ventricular tachycardia (1. Ventricular tachycardia (& Torsades de Pointes) 2. Ventricular fibrillation
Narrow QRS = Supraventricular tachycardia (SVT), common locations: SAN, atrial muscle, AVN → regular or irregular
Irregular QRS: atrial fibrillation
Regular: 1. Sinus tachy 2. Atrial tachy 3. Atrial flutter 4. AVNRT 5. AVRT (4&5: AV junctional tachycardias)
What are AV junctional tachycardias?
Aka SVT (supraventricular tachycardia)
- Anatomically SVT means above ventricles
- Clinically SVT means AV junctional tachycardias
Supraventricular tachycardias (SVT) occur as a result of re-entry circuits formed between the atria and ventricles
- AVNRT (atrioventricular nodal re-entrant tachy)
- AVRT
What are the types of SVT (supraventricular tachycardias)?
AVRT - a physical accessory pathway between atria and ventricles, allowing pre-excitation of ventricles. Impulse is generated as a result of a re-entrant circuit and precipitated by pre-mature ventricular or atrial beats. Wolf Parkinson White (WPW) Pattern: presence of the Bundle of Kent that acts as an accessory pathway. WPW Syndrome: WPW presence facilitating tachycardia
AVNRT - more common and consists of a functinal re-entrant circuit forming at the AVN
How are SVTs identified on ECGs?
- Fast rate (200-300bpm)
- Narrow QRS complex
- Hidden P waves (hidden in QRS)
Describe the divisions of bradycardia, and what defines bradycardia?
Bradycardia = <60bpm
Sinus bradycardia: could be a normal variant or iatrogenic (e.g. digoxin)
Problems with conduction: escape beats or heart block (i.e. AV conduction issues)
- Escape beats: SAN fails to depolarise therefore other pacemaker cells (atrial, AVN, nodal) take over (usually those with fastest intrinsic rate) - these are protective mechanisms. Can be a whole stretch or single beat
- Heart block: 1st/2nd/3rd degree heart block
What is the class, action and indication of digoxin?
Class: cardiac glycoside
Action:
- Increases vagal parasympathetic activity and inhibits the Na/K pump, causing Na build-up intracellularly. To reduce intracellular Na, more Ca is brought into the cell by Na/Ca exchangers.
Ca build-up is responsible for increased force of contraction and reduced rate of conduction through AVN
Indications: HF and AF (Atrial Fibrillation)
What is the class, action and indication of amiodarone?
Class: anti-arrhythmic
Indication: supraventricular/ventricular arrythmias
Action: blocks cardiac K channels, prolonging repolarisation of the cardiac AP. It restores normal sinum rhythm and slows conduction at the AVN.
DASPITE for 1st degree heart block
D/P: A problem AV conduction i.e. the impulse travelling from SAN, through atria to AVN, then to ventricular muscle. However, impulse from SAN eventually initiates depolarisation and contraction
A: Secondary to ischaemia/fibrosis, electrolyte imbalance, medications
S: usually none
I: ECG: constant prolonged PR interval (>200ms) i.e. all the same length, still 1 P : 1 QRS
T: Identify and rectify cause
Describe 2nd degree heart block and its divisions
D: Conduction issue between ventricles and ventricles i.e. AV conduction issue. Can be split into Mobitz Type I and Mobitz Type II, Type II being more severe.
Mobitz Type I
P: Some impulse reaches the ventricles but is continually prolonged until the impulse is blocked completely. When the SAN fails to conduct an e. impulse to the ventricles, either the SAN fires again or ventricles contract (ventricular escape beat)
Pattern: prolonging, dropping, reset
S: none, light-headed, dizzy, syncope
I: ECG - PR interval continually prolongs until there’s a skipped beat, then another P wave or broad QRS
Mobitz Type II:
P: Intermittent dropped beats occuring randomly or in a pattern (e.g. 2:1 heart block). I.e. the impulse from the atria is constant but doesn’t always conduct to ventricles
S: fatigue, dyspnoea, chest pain, syncope
I: fixed PR interval but sometimes there’s a dropped QRS
DASPITE for 3rd degree heart block
D/P: Signal between atria and ventricles is blocked completely, therefore the atria and ventricles are acting independantly of one another. Activity isn’t synchronised, therefore they return to their intrinsic rates (A: 60, V: 40)
S: syncope, confusion, dyspnoea, severe chest pain
I: ECG - regular PP interval, P waves are not related to QRS complexes, PR interval random, broad QRS
What are the causes of a broad QRS and how do you differentiate them?
Causes:
- Depolarisation originating from the ventricles
- Bundle branch block
How to differentiate: Presence of P wave
- P wave present with regular PR interval: BBB
- No P wave: depolarisation from ventricles
What are the causes of left and right bundle branch block?
LBBB: always indication of left-sided heart disease due to fibrosis e.g. acute - ischaemia, MI; chronic - HTN, coronary artery disease, cardiomyopathies
- LBBB can contribute to HF
RBBB: can be normal variant or can indicate right-sided heart disease
Describe the ECG pattern with left and right BBB
LBBB: WilliaM
- W in V1, M in V6 (best seen in V6)
RBBB: MarroW
- M in V1, W in V6 (best seen in V1)
Diagnosis:
- Bundle branch QRS pattern in V1/V6 and broad QRS (depolarisation and repolarisation of both ventricles takes longer)
Explain stable angina and it’s ECG
Atherosclerotic plaque forms causing ischaemia. Chest pain due to ischaemia only occurs with increased demand i.e. exercise: supply-demand mismatch
- Ischaemia due to increased demand
- Ischaemia of subendocardial tissue
- ECG: ST depression during exercise
Explain unstable angina and it’s ECG
- The atherosclerotic plaque (as seen in stable angina) ruptures and a thrombus forms, causing partial occlusion
- Ischaemia due to poor supply
- Ischaemia in transmural tissue
- Chest pain/Sypmtoms at rest
- ECG: ST depression and T wave inversion
Explain NSTEMI and it’s ECG
- The plaque has ruptured and a thrombus has formed causing partial occlusion. This results in injury and infarct to subendocardial tissue
- Infarct to subchondrial tissue
- ECG: ST depression and T wave inversion
Explain STEMI and it’s ECG
- Characterised by complete occlusion of the blood vessel lumen, resulting in transmural damage and infarct to myocardium
- Infarct to transmural tissue
- ECG: ST elevation, T wave inversion, hyper-acute T waves, pathological Q-wave
ST depression and T-wave inversion are seen in an ECG of a patient with chest pain. What is the differential diagnosis and what investigation do you do next?
ST depression and T wave inversion are seen with unstable angina and an NSTEMI
Troponin levels would differentiate the two - elevated troponin in NSTEMI
In an ECG, what lead correlate to what coronary arteries?
V1 and V2 (septal): left anterior descending (LAD) artery
V3 and V4 (anterior): left anterior descending (LAD) artery
V5, V6, lead I and aVL (lateral): left circumflex artery
lead II, III and avF (interior): right coronary artery and posterior descending artery (PDA)
How do you determine ST depression?
Context: stable angina during exercise, unstable angina at rest and NSTEMI
Determine ST elevation: need to look at the J point (junction between QTS complex and ST segment)
- Use PR interval as reference point to determine the isoelectric line, and if the J point goes >0.5mm (1/2 small sq) below isoelectric line, it is ST depression
What are the causes of ST depression?
Primary (abnormal repolarisation):
- Ischaemia (unstable angina, stable angina (during exercise), NSTEMI)
- Hypokalaemia (would be accompanied by flattened T wave)
- Digoxin
Secondary causes (abnormal depolarisation causing abnormal repolarisation):
- LBBB (prolongs depolarisation)
Wolf Parkinson White Pattern (Pre-excitation)
What is the STEMI criteria in an ECG?
- J point moves up by >1mm (1 small sq)
- In at least 2 contiguous leads e.g. V3 and V4
- If V2 and V3: elevation needs to be >2mm*
How do you determine between acute (ongoing) ischaemia or post-ischaemia?
In acute/ongoing ischaemia: T waves are inverted in combination with ST deviation (usually depression)
Post ischaemia: After an ischaemic event, T waves can remain and remain longer than ST changes. I.e. T-wave inversion without ST deviation
What is a good prognostic factor post-MI?
Normalisation of inverted T-waves
What is the definition of heart failure?
Failure of the heart to pump blood and oxygen at a rate sufficient to meet the metabolic requirements of the tissues, resulting in fatigue, breathlessness and fluid retention. It’s caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure
- Characterised by typical haemodynamic changes: systemic vasoconstriction and neurohumoral activation
What is the aetiology for heart failure?
- Coronary heart disease (MI)
- HTN
- Idiopathic
- Toxins (alcohol, chemotherapy)
- Less common: valve disease, infection, congenital heart disease
Describe the main types of heart failure?
HF-REF (systolic HF with reduced ejection fraction)
- Systolic function of the heart is reduced
- Usually younger and males
- Coronary aetiology
HF-PEF (diastolic HP with preserved ejection fraction)
- Diastolic function of the heart is failing
- Usually older and female
- Hypertensive aetiology
Chronic (congestive)
- HF present for a long time
- May have been acute or become acute
Acute (Decompensated)
- When patient is admitted to hospital and deteriorated in some way
- Worsening of chronic or new onset
What is the pathophysiology for heart failure?
- left ventricular systolic dysfunction (LVSD) develops which is perceived as a reduction in circulating volume and pressure due to reduced cardiac output
- Body then initiates own natural mechanisms to increase pressure via neurohumoral activation: Activation of the sympathetic NS (vasoconstriction), RAAS (fluid retention), vasopressin (antidiuretic) and release of atrial natriuetic peptides (ANP released as a counter-regulatory system for RAAS i.e. renin release). I.e. net effect of arterial and venous vasoconstriction and increased blood volume
- -* These are compensatory mechanisms to maintain BP and CO. However they eventually lead to further problems by putting more pressure on the heart: further systemic vasoconstriction, Na and water retention leading to progressive cardiac dysfunction and congestion (oedema)
- Fluid retention manifests as peripheral and pulmonary oedema and SOB
Explain how the renin-angiotensin-aldosterone system works
Reduced BP reduced renal perfusion resulting in reduced urine output and fluid retention. Fluid retention and sympathetic activation in the kidneys activates renin release, activating RAAS. This increases aldosterone release and AVP/ADH that contributes to renal water and Na retention
What are the signs and symptoms of heart failure?
Symptoms:
- Dyspnoea: orthopnoea (lying flat) and paroxysmal noctural dyspnoea (PND) (pul. oedema)
- Cough
- Shortness of breath (pul. oedema)
- Fatigue and exercise intolerance
- Ankle swelling (peripheral oedema)
Signs:
- Peripheral oedema (ankles, legs, sacrum)
- Elevated JVP
- 3rd heart sound
- Displaced apex heart (cardiomegaly)
- Pulmonary oedema (lung crepatations)
- Pleural effusion
How can you measure how functionally limited a patient with heart failure is?
NY Heart Association (NYHA) Functional Classification
Class I: no symptoms or limitations in ordinary physical activity e.g. shortness of breath when walking
Class II: mild symptoms i.e. mild SOB and/or angina and slight limitation during ordrinary activity
Class III: marked limitation in activity due to symptoms, even in less-than-ordinary activity e.g. walking 20-100m. Comfortable only at rest
Class IV: severe limitations, experiences symptoms even when at rest. Mostly bedbound patients
What investigations are needed for a patient with suspected heart failure/how do you diagnose HF?
Diagnosis:
Signs and symptoms → Examination → Natriuretic peptides → ECG and echocardiogram
Investigations:
- Blood chemistry (U&Es, Cr, urea, LFT)
- Haematology (Hb)
- Natriuretic peptides (BNP): if low, definitely not HF
- ECG
- CXR (exlcude lung pathology and look for pulmonary oedema)
- Echocardiogram (chamber size, systolic/diastolic function, valves): can diagnose systolic dysfunction
Show the treatment ladder (steps) for heart failure
Step 1: Beta-blocker (bisoprolol) and ACE inhibitor (ramipril) (or ARB if intolerant to ACE inhibtior)
Step 2 (ongoing symptoms i.e. NYHA II-IV): Add Mineralocorticoid Receptor Antagonist (MRA)
Step 3 (ongoing symptoms i.e. NYHA II-IV): Sacubitril/Valsartan (Stop ACE/ARB but continue beta-blocker and MRA)
Step 4 (ongoing symptoms): Implanted Cardioverted Defibrillator (ICD) or Cardiac Resynchronisation Therapy (CRT) pacemakers and ivabradine. Digoxin can also be added.
What is the class, indication and action of bisoprolol?
Class: cardioselective beta-blocker
Indications: HTN, AF, angina and mild/moderate heart failure
Action:
- Cardioselective B-1-adrenoreceptor antagonist i.e. blocks B-1 adrenoreceptor in cardiac and renal tissue
- Inhibits sympathetic activation of their vasculature (i.e. blocks vasoconstriction)
- Blocks SAN reducing HR and blocks myocardium receptors to depress cardiac contractility
- Renal tissue: blocking B-1 adrenoreceptors inhibits renin release therefore depressing vasoconstrictive effects of RAAS
What is the class, indication and action of ramipril?
Class: ACE-inhibitor
Indication: HTN, stable heart failure, nephropathy
Action: inhibits ACE which converts angiotensin I to angiotensin II (a more potent systemic vasoconstrictor). This inhibits aldosterone release from adrenal cortex
- I.e. reduces renal sodium and fluid retention, thereby reducing blood volume
What is a mineralocorticoid receptor antagonist (MRA)?
It’s an aldosterone antigonist i.e. blocks the final part of the RAAS pathway, used primarily to treat chronic heart failure
- Must stop ACE inhibitor/ARB
What is the action of Sacubitril-Valsartan?
Valsartan
- Angiotensin-receptor blocker (ARB)
- Blocks angiotensin II binding to angiotensin receptors
Sacubitril
- Neprilysin inhibitor
- Neprilysin breaks down natriuretic peptides which are released in response to stretch of the heart (vol overload) and they cause diuresis
- Inhibiting breakdown of NPs allows diuresis and augment’s body’s natural mechanism of dealing with heart failure
- Also causes vasodilation
What substance causes the classical ACE-inhibitor cough?
Bradykinin
How do you choose between implanted cardioverted defib (ICD) and cardiac resynchronisatin therapy (CRT) pacemakers?
ICD:
- Detects abnormal heart rhythms e.g. ventricular tachycardia and applies a shock wave to return to sinus rhythm. Dilated hearts (as seen in HF) are more likely to fibrillate
- Used when the QRS is narrow and in younger patients
CRT:
- Conventional pacemaker that keeps the left and right ventricles in sync
- Used when the QRS is broad
What is the assessment for someone who presents with acute heart failure?
Look for presence of congestion:
- E.g. pulmonary oedema, peripheral oedema, raised JVP, orthopnoea, PND, ascites
- Yes: Wet = need diuresis
- No: Dry
Look for adequate peripheral perfusion:
- Poor peripheral perfusion: cold sweaty extremities, oliguria, narrow pulse pressure, dizziness
- Poor: Cold, Good: Warm
Most patients present as warm-wet: BP okay but need diuresis
How does heart failure lead to pulmonary oedema?
- The heart is enlarged and cannot pump efficiently
- This causes congestion of blood which backs up into pulmonary veins
- Pressure inside pulmonary veins increases
- Fluid is pushed into the interstitial spaces and then alveoli
What are the first, early and late signs of heart failure identified on CXR?
First sign: cardiomegaly and upper lobe venous diversion (redistribution of pulmonary vessels)
Early signs/Early pulmonary oedema: Kerley B lines, peribronchial cuffing (interstitial oedema)
Late signs/Late pulmonary oedema: perihilar consolidation/ ‘cotton wool’ appearance (aveolar oedema) and blunted coscophrenic angles (pleural effusion)
What are pleural effusions and what are the two divisions?
- When there is fluid present in the potential space between parietal and visceral layers of the pleura
- The fluid can be an exudate or transudate
What is the difference between transudate and exudate pleural effusions?
Transudate
- Caused by factors altering hydrostatic pressure, pleural permeability and oncotic pressure e.g. cirrhosis, nephrotic syndrome, pulmonary embolism, congestive heart failure
- Low in protein and LDH
Exudates
- Caused by changes to local factors that influence formation and absorption of plerual fluid e.g. malignancy, infection, trauma
- Light’s criteria for exudate: any of protein levels >30g/l, LDH >200lU, pH <7.1 suggests exudate
- High protein and LDH
What is the stepwise management for hypertension?
W/ diabetes or <55
- 1st line: Ramipril (ACEi) or angiotension II receptor blocker (ARB)
- 2nd line: calcium channel blocker or thiazide-like diuretic
If Black-African or African-Carribean family origin or >55years:
- 1st line: calcium-channel blocker
- 2nd line: ramipril or ARB or thiazide-like diuretic
Step 3 for everyone:
- Ramipril/ARB + calcium channel blocker + thiazide-like diuretic
HTN is said to be resistant if it cannot be controlled with step 3
Step 4 (for resistant hypertension)
- Spironolactone if serum K <4.5mmol/l
- Alpha/Beta-blocker if serum K >4.5
What is the class, indication and action of verapamil?
Class: rate-limiting calcium channel blocker
Indication: supraventricular arrhythmias, angina treatment and hypertension
Action:
- Prevent cellular Ca entry by blocking calcium channels
- myocardial and smooth muscle contractility depressed and cardiac contractility is reduced
- dilate coronary blood vessels and reduce afterload
- antidysrythmic action due to prolonged atrioventricular node conduction - depresses heart rate
What is the class, indication and action of amlodipine?
Class: non-rate limiting calcium channel blocker
Indication: hypertension and angina treatment
Action:
- prevents cellular Ca entry due to blocking calcium channels
- myocardial and smooth muscle contractility is depressed
- coronary blood vessels dilate to reduce afterload
Why may verapamil be chosen over amlodipine?
- Verapamil has a antidysrythemic effect
- Amilodipine has more side effects eg. palpitations, ankle oedema, abdominal pain
What is the class, action and indication of ramipril?
Class: angiotensin converting enzyme inhibitor (ACE inhibitor)
Indication:
- HTN, heart failure, nephropathy, prevention of CV events in high risk patients
Action:
- Inhibits angiotensin converting enzyme (ACE) which converts angiotensin I to angiotensin II (a more potent systemic vasoconstrictor)
- This subsequently inhibits aldosterone release from adrenal cortex, depressing renal sodium and fluid retention, thereby reducing blood volume
What is the main side effect of ramipril?
Dry cough
What is the class, indication and action of bendroflumethazide
Class: thiazide diuretic
Indication: HTN or oedema of cardiac/renal/hepatic/iatrogenic origin
Action:
- Inhibits the Na/Cl transporter at the DCT and collecting duct
- Inc. Na, Cl and water excretion
Name a thiazide diuretic
Bendroflumethazide
What is the class, indication and action of furosemide
Class: loop diuretic
Indication: HTN, hyperkalaemia, HF, liver cirrhosis, nephrotic syndrome
Action:
- Na/Cl/K symporter antagonists
- Act on thick ascending loop of Henle
- Inc. secretion of K, Na, Cl and water
What are the stages of congestive heart failure and how do they present on CXR?
Stage 1: Mild
- Redistribution
- Pulmonary capillary wedge pressure (PCWP): 13-18mmHg
- CXR: upper lobe venous divertion and cardiomegaly
Stage 2: Moderate (Interstitial Oedema)
- PCWP: 18-25mmHg
- CXR: Kerly B lines, peribronchial cuffing, hazy contours of vessels, thickened interlobular fissures
Stage 3: Severe (Alveolar oedema)
- PCWP: >25mmHg
- CXR: perihilar consolidation, air bronchogram, cotton-wool appearance, pleural effusion (blurred coscophrenic angles)
Define pleural effusion
- what are the two types and how are they distinguished
= fluid within the potential space between the visceral and parietal layers of the pleura
Divided into transudate and exudate
Consistent with exudate:
- Protein levels >30g/l
- LDH >200IU
- pH <7.1
In chronic HF: usually bilateral
Define a myocardial infarction
Any elevation in troponin in clinical setting conistent with myocardial ischaemia
NB isolated troponin elevation doesn’t equal MI, needs taken into consideration with other investigations
What is the biggest risk factor for a myocardial infarction?
A history of coronary artery disease or a previous MI
List 4 symptoms and 4 signs of a myocardial infarction
Symptoms:
- pleuritic chest pain (characterised by sudden and intense shart, stabbing pain)
- back pain
- jaw pain
- indigestion
- excessive sweating, clammy (due to autonomic activation)
- SOB (ischaemia and reduced output)
- None/silent MI (diabetes, dementia)
- death
Signs
- Tachycardia (sympathetic NS activation)
- Distressed/Agitated patient
- Heart failure (crackles on auscultation/raised JVP)
- Cardiogenic shock (hypertensive, cold, delirium): when the body suddenly can’t pump enough blood to meet body demands
- arrhythmia
- none
Describe myocardial infarctions, types 1,2 and 3
Type 1: spontaneous MI due to a primary coronary event
- Acute coronary artery plaque rupture and formation of thrombus leading to ischaemia and slcrosis
- Problem = coronary artery
Type 2: increased oxygen demand or decreased oxygen supply
- Degree of MI due to lack of oxygen
- Fixed atherosclerosis
- Eg. HF, sepsis, arrhythmia, anaemia, HTN, hypotension
- Problem = NOT the coronary artery
Type 3: Sudden cardiac death
What investigations must be done if a MI is suspected?
ECG: ST segment depression
Bloods: troponin (biomarker of myocyte necrosis)
CXR and echocardiogram: evidence of acute HF / LV systolic dysfunction
- Echo useful for global assessment of LV function
Coronary angiogram: can see narrowings/blockage of coronary arteries
List 3 non-coronary causes of elevated troponin
Causes of T2MI
- Acute congestive HF
- tachy-arrhythmias
- pulmonary embolism
- sepsis
- apical ballooning syndrome
- anything stressing the heart eg. critically unwell patient
Chronic troponin elevation (not an MI)
- Renal failure (troponin cleared from blood via kidneys)
- Chronic HF
- infiltrative cardiomyopathies eg. haemochromatosis, amyloidosis
Define pleuritic chest pain
Sudden and intense sharp/stabbing/burning pain in the chest when inhaling and exhaling
How is chest pain classified for risk of a MI?
HEART score
- History, ECG, Age, Risk factors, initial Troponin
How is acute coronary syndrome classified and what are the classifications?
Three classifications based on ECG presentation and release of troponin
- STEMI (ST elevation myocardial infarction)
- Classical ECG - NSTEMI
- Evidence of MI (elevated troponin) but no ST elevation - Unstable angina
Define an unstable angina
- Explain the relationship between pathology and investigation changes
= An acute coronary event without a rise in troponin
- Heart is under strain and patient presents with symptoms of ischaemia but not sufficient ischaemia to result in myocardial damage
ie. clinical presentation of MI and ECG changes OR tight narrowing on coronary angiography but no troponin release
Define atherosclerosis
Deposition of lipids in the coronary artery wall which builds up over time leading to risk of rupture of the plaque and development of an acute coronary thrombous
Describe the progression of an atherosclerosis
Lipid deposition in the coronary artery wall
- Initially, there is Glagovian remodelling ie. compensatory expansion/dilatation of the coronary artery to maintain lumen diameter. This allows the body to maintain blood flow to myocytes
- This is the case for minimal and moderate CAD
- Over time the artery cannot expand anymore and the atherosclerotic plaque impinges on the coronary lumen reducing lumen diameter (narrowing)
- This is called advanced CAD and presents with stable angina
A patient presents with ischaemic discomfort and diagnosed with acute coronary syndrome
- Describe the pathway from here to reach a diagnosis
- ECG:
- ST elevation: STEMI
- No ST elevation: look at troponin - Troponin:
- Elevated: NSTEMI
- Normal: unstable angina
Describe the evolutions of the ECG in an acute STEMI
As MI progresses and level of myocyte necrosis increases, can see sequential changes in the ECG
A: normal ECG
B: Elevation of the J-point, subtle ST elevation, hyper-acute T waves (tenting of T waves)
C: marked elevation of the J-point and ST elevation
D: abnormal repolarisation of ventricles (T wave inversion)
E and F: following an MI, ECG never returns to normal as pathological Q waves persist
ST elevation in leads V1-4
ST depression in leads II, III and aVF
What artery is most likely to be blocked?
left anterior descending
Subtle ST elevation in leads I and AVL
ST depression in leads II, III and aVF
Which coronary artery is most likely to be blocked?
left circumflex artery
ST elevation in leads II, III and aVF
ST depression in leads I and aVL
What artery is likely to be blocked?
right coronary artery and left circumflex
Which arteries supply the posterior wall of the heart?
How would a blockage of these arteries be detected on ECG?
Arterial supply: left cirucmflex and right coronary artery
- No ECG leads directly look at the posterior heart wall
- Anterior leads are directly opposite and will see the opposite of any current generates at the posterior wall
ie. posterior ST elevation = anterior ST depression - often associated with inferior or lateral ST elevation
Outline the immediate management following a STEMI
- Airways, Breathing, Circulation, Disability (ABCD)
- Ambulance with defibrillator
- Unfractioned heparin 5000UI IV: alleviates pain and relaxes the patient
- Morphine 5-10mg IV
- Anti-emetics
- Clopidogrel: to break down the thrombus
What is the indication and action of heparin
Indication:
- treatment and prophylaxis of thromboembolic event diseases, including induction of Vit K antagonists
- renal dialysis
- acute coronary syndrome treatment
Action:
- Enhances the activity of antithrombin III
- Antithrombin III inhibits thrombin
- Heparin also inhibits other coagulation factors
- Produces an anticoagulation effect
What is the class, indication and action of clopidogrel?
Class: anti-platelet drug
Indication:
- Secondary prevention of thrombotic events
Action:
- irreversibly blocks the ADP-receptor on the platelet cell membrane
- this inhibits the formation of GPIIb/IIIa complexes, needed for platelet aggregation
- Decreased thrombus formation
What is primary percutaneous coronary intervention (PPCI) and list 3 advantages for treatment of a STEMI?
aka. coronary angioplasty
- Use of a catheter to place a stent in the blocked coronary artery
Advantages:
- improved survival
- reduced strokes
- reduces change of further MI and angina
- Speeds up recovery
- Shortens the time spent in hospital
What is the longer-term management for an acute MI
Monitor in Coronary care unit for complications
- Aspirin, cloidogrel, LMWH
Drugs for secondary prevention:
- ACEi
- Beta blockers
- Statins
Echocardiogram for LV function and cardiac structure
Cardiac rehabilitation
If LVSD at >9 months, consider primary prevention ICD
Describe 3 complications of acute myocardial infarction
Arrhythmias
- ventricular tachycardia / ventricular fibrillation
- atrial fibrillation : can lead to HF/LVSD
Heart failure
Cardiogenic shock
Myocardial rupture
Psychological: anxeity/depression
Define atrial fibrillation
- It’s the commonest sustained cardiac arrhythmia
= An arrhythmia caused by abnormal electrical discharges that generate choatically throughout the atria, causing the heart to beat irregularly and fast
List 3 conditions pre-disposing to atrial fibrillation
- HTN
- Symptomatic HF (NYHA II-IV) including tachycardiomyopathy
- Valvular heart disease
- atrial septal defect and other congenital heart defects
- coronary artery disease
- obesity
- diabetes mellitus
- COPD and sleep apnoea
- Chronic renal disease
What is the major complication of atrial fibrillation?
Stroke
(5-fold increase in risk)
List 3 risk factors for stroke and thrombo-embolism in non-valvular atrial fibrillation
CHA2DS2VASc
Cardiac failure
Hypertension
Age >75 (2 points)
Diabetes
previous Stroke (2 points)
Vascular heart disease
Age 65-74
Sex (female)
Max score: 9
Score >2: high risk of developing stroke therefore put on a DOAC
List 3 presentations of atrial fibrillation
- May be asymptomatic
- palpatition
- dyspnoea
- rarely: chest pain, syncope
- may present with complications eg. stroke
What essential investigations are needed for the diagnosis of atrial fibrillation
- ECG
(May need prolonged ambulatory ECG recordings to detect paroxysmal AF ie. intermittent, starting and stopping)
- Progresses from paroxysmal to persistent (requires intervention) to permanent*
- Echocardiogram
- TFTs
- LFTs
What would be the ECG results with atrial fibrillation?
- Rate: irregularly irregular
- QRS: irregular, narrow
- No P wave before each QRS
- chaotic atrial activity
What are 3 objectives of treatment for atrial fibrillation?
- Stroke prevention
- Symptom relief
- Optimum management of associated CV disease
- Rate control
+/- correction of sinus rhythm disturbance
How is rate control managed in atrial fibrillation
Target: <100/min
- If still symptomatic, aim for HR <80/min
Patients without HF: start on beta-blocker (bisoprolol) or rate-limiting Ca antagonist (Verapamil)
- Don’t use amlodipine as it increases HR
- Don’t use BB and verapamil together as it will slow HR too much
- 2nd line: Digoxin
Patients with HF: follow heart failure guidelines
What is the class, indication and action of digoxin?
Class: cardiac glycoside
Indication:
- Heart failure
- Rate control for atrial fibrillation
Action:
- inc. vagal parasympathetic activity and inhibits the Na/K pump, causing a build up of Na intracellularly
- In an effort to remove Na, more Ca is brought into the cell by action of Na/Ca exchangers
- the build-up of Ca intracellularly is responsible for increased force of contraction and reduced rate of conduction through the AV node
What pharmacological management is used for prevention of stroke in AF?
Warfarin
- Vitamin K antagonist
- very effective and reduces risk of stroke by 2/3
- Very narrow therapeutic window therefore needs constant monitoring
- High INR (>4): high bleeding risk esp. intracranially
- Low INR (<2): high risk of stroke
- Used for those with mechanical heart valves/severe mitral stenosis/severe AF
New Oral Anticoagulants (NOAC/DOAC)
- Apixaban: direct factor Xa inhibitor
- Dabigatran: direct thrombin (IIa) inhibitor
- Rivaroxaban: direct factor Xa inhibitor
- less need for monitoring that warfarin and less side effects
In what situations would warfarin be chosen over NOACs for stroke prevention in atrial fibrillation?
- Mechanical heart valves
- moderate/severe mitral stenosis
- severe atrial fibrillation
List 3 situations in which patients with AF would be referred for specialist assessment
List 3 options available for these patients
Situations:
- Symptomatic patients with good rate control
- Young (<60years)
- Inadeuqate rate control despite beta blocker or rate-limiting Ca antagonist (verapamil) and digoxin
- Structural heart disease on echo
- AF and co-existing HF
Options: Rhythm control
- Arrhythmic drugs
- Catheter ablation
- direct current cardioversion
What antiarrhythmic drugs are used for rhythm control with atrial fibrillation
Class 1: Na channel blcokers
Class 3: K channel blockers, prolong action potential duration / QT interval
- Amiodarone: prolongs repolarisation of cardiac AP, slows conduction at the AVN and restores normal sinus rhythm. Contains iodine which could affect the thyroid and cause hyper/hypothyroidism
Multichannel blockers
What is the aim of catheter ablation and list 2 situations which it could be used
- the application of extreme heat/cold to form tiny scars at certain points to damage heart muscle and disrupt the erratic electrical signals
Used for:
- Highly symptomatic paroxysmal AF resistent to one or more anti-arrhythmic drugs and little/no co-morbidity
- Symptomatic AF, symptomatic HF and LVSD with left ventricular ejection fraction of 24-35%
- Highly symptomatic patients with little/no co-morbidity
Define infective endocarditis
Infection of the endocardium and formation of a vegetation resulting in damage to the cusp of valves
What are the common sites for infective endocarditis
- mitral valve
- aortic valve
- tricuspid valve (most common site in IVDUs)
- Pulmonary valve
What is the vegetation in infective endocarditis made of?
- fibrin mesh
- WBCs
- RBC debris
- Platelets
Define and describe quorum sensing
= the ability to detect and respond to cell population density by gene regulation
- A mechanism by which bacteria regulate gene expression in accordance with population density through use of signal molecules
- Allows bacteria populations to communicate and co-ordinate group behaviour
Eg. can restrict the expression of specific genes to high cell densities which the resulting phenotypes would be the most beneficial
What are the main causative organisms of infective endocarditis?
Bacterial Gram +ve:
- Staphylococci: s. aureus (meticillin sensitive (MSSA) and meticillin resistant (MRSA))
- Strephococci: strep. viridans and enterococci
Bacterial Gram -ve:
- HACEK organisms
- Enterobacteriaceae aka coliforms (E. Coli)
Fungal IE:
- Candida albicans
What are the most common causative organisms in native valve endocarditis (NVE), endocarditis in IVDUs and prosthetic valve endocarditis (PVE)?
NVE: streptococcus species
- Strep viridans then enterococci
Endocarditis in IVDU: staphylococcus
- S. aureus
- Higher incidence of Gram -ve infections and fungal BE in IVDU that NVE
PVE: staphylococci
- CoNS more common than S. aureus
What are the classifications of infective endocarditis
- Native Valve Endocarditis (NVE)
- Endocarditis in IVDU
- Prosthetic Valve Endocarditis (PVE)
List 2 risk factors for native valve endocarditis (NVE)?
RFs:
- undelrying valve abnormalities: aortic stenosis and mitral valve prolapse (MVP)
- no identifiable RFs in 30%
List 3 aetiologies of aortic stenosis
- Incidence inc. with age
- Age-related calcification (50%)
- calcification of congenitally abnormal valve (30-40%)
- rheumatic fever (10%)
What is the commonest valve involved in endocarditis in IVDUs and why?
- Tricuspid valve endocarditis more common than aortic or mitral
- Underlying valve is normal in most patients: repeated bouts of IE in an IVDU will lead to gradual inc. in structural abnormalities of the valve
inc. tendency to involve right-sided valves due to: - inc. bacterial loads in these patients
- direct physiologic effects of injected drugs
- deficient immune response caused by IV drug abuse
What is the relevance of the causative organism in infective endocarditis?
Strepococcal bacterial endocarditis (esp viridans) usually present more indolently therefore termed ‘subacute’
S. aureus, Gram -ve and funal endocarditis all present acutely, causing rapid valve destruction
What are the two clinical syndromes of infective endocarditis?
- Acute
- toxic presentation
- progressive valve destruction and metastatic infection developing in days-weeks (septic emboli dissociating from the vegetation to other body parts)
- mostly caused by S. aureus - Subacute
- more common and mild toxicity
- indolent presentation over weeks-months in an insidious manner
- rarely leads to metastatic infection
- Mostly Strep. viridans and enterococcus
List 3 clinical features that correspond to
- early manifestations
- embolic events
- long-term effects
of infective endocarditis
Early manifestations:
- Incubation period: 2 weeks
- Fever and murmur = IE until proven otherwise
- Fever is the most common sign but may be absent in the elderly/immunosuppressed
- Fatigue and malaise
Embolic events:
- Small emboli: splinter haemorrhages, petechiae, haematuria
- Large emboli: cerebrovascular accident, renal infarction, stroke
- Right sided endocarditis often presents with septic pulmonary emboli (results in pleuritic chest pain and classical CXR appearance)
Long-term effects:
- Immunological reaction: splenomegaly, nephritis, vasculitis lesions of skin and eye, clubbing, Osler’s nodes
- Tissue damage: valve destruction, valve abscess
A patient presents to the ward with pleuritic chest pain and a murmur
- CXR shows multiple emboli
- History indicates patient is an Iv drug user
What do you suspect?
Right-sided (usually tricuspid) infective endocarditis
What are the most important investigations to order if suspecting infective endocarditis?
Microbiology (blood cultures)
imaging (echocardiograph)
Duke’s criteria
What is the process involved for assessing blood cultures for IE?
In what situations would you think IE?
- In IE there is constant bacteraemia therefore don’t wait for fever to appear
- need 3 sets of blood cultures with 10ml blood per bottle
- needs carried out before abx treatment initiated
- aseptic technique
When to thick IE?
- all patients with s.aureus bacteraemia
- IVDU with any positive blood cultures (any organism could get into the bloodstream and cause IE due to nature of injecting)
- All patients with prosthetic valves and positive blood cultures
What are the two methods for echocardiograph imaging for diagnosing infective enodcarditis
Transthoracic (TTE)
- Non-invasive with transducer placed at front of chest
- 50% sensitivity: if -ve cannot rule out IE
- If negative and high clinical suspicion remains, a TOE is indicated
Transoesophageal (TOE)
- invasive with transducer placed in oesophagus
- 85% sensitivity and better at detecting smaller vegetations
What is Duke’s criteria used to diagnose and how does it do this?
Used to diagnose definite/possible IE
Can split findings into major and minor criteria
Definite IE: 2maj, 1maj and 3min or 5min criteria
Major:
- Typical organism in 2 separate blood cultures
- Positive echocardiograph or new valve regurgitation
Minor:
- Predisposition (heart condition or IVDU)
- fever >38
- vascular phenomena eg. septic emboli
- immunological phenomena eg. Osler’s nodes
- positive blood cultures that don’t meet maj criteria
What is the medical treatment for infective endocarditis?
Antimicrobial therapy
- Aim to use cidal agents over static agents
- Choice dependent on organism
Duration of therapy:
- NVE: 4 weeks
- PVE: 6 weeks
Usually IV therapy for during
- Short course IV abx followed by oral abx may be used for IVDU patients who refuse to be hospitalised
Organism:
- Strep: benzylpenicillin +/- Gentamicin
- Enterococcus: amoxicillin or vancomycin +/- Gentamicin
MSSA: flucloxacillin +/- Gentamicin
MRSA: vancomycin +/- gentamicin
CoNS: vancomycin +/- gentamicin
What are the 3 indications for surgical intervention in infective endocarditis?
Heart failure
Uncontrolled infection
- Locally uncontrolled infection including abscess, false aneurysm, enlarging vegetation
- Persisting fever + positive blood cultures 7-10 days
- infection caused by multi-drug resistant organisms
Prevention of embolism
- Large vegetations following an embolic episode
Define systemic hypertension
Persistent elevation in arterial blood pressure >140/90mmHg
- a blood pressure level that increases the vascular risk in patients sufficient to require intervention
List 3 conditions that hypertension is considered a risk factor for
- Coronary artery disease eg. MI
- Cerebrovascular disease eg. stroke
- Peripheral vascular disease
- Heart Failure
What are the grades of hypertension?
Grade 1:
- Systolic BP 140-159 +/or diastolic BP 90-99
Grade 2:
- S BP 160-179 +/or D BP 100-109
Grade 3:
S BP >180 +/or D BP >110
What are the two classifications of hypertension?
Primary hypertension: no identifiable cause, 90-95% of cases
Secondary hypertension: there is usually a cause, rare
List 3 modifiable and 3 non-modifiable RFs for primary hypertension
Non-modifiable:
- Age
- Gender
- Ethnicity
- Genetics
Modifiable:
- Diet
- Physical activity
- Obesity
- Alcohol in excess
- Stress
List 5 causes of secondary hypertension
At what age does it usually present
Usually presents in patients <40
Causes:
Endocrine - hyperaldosteronism, pheochromocytoma, thyroid disorders, Cushing’s syndrome
Vascular - co-arctation of the aorta
Renal - renal artery stenosis, renal parenchymal disease
Drug - NSAIDs, herbal remedies, cocaine, exogenous steroid use
Other - obstructive sleep apnoea
How is hypertension diagnosed?
Clinical presentation:
- generally asymptomatic, discovered incidentally
- may present with headache and visual disturbances
NOT made on a single elevated BP reading:
GP:
- 2 readings 5 minutes apart then repeat in a few weeks
24hr ambulatory BP monitoring:
- portable device with BP taken hourly throughout the day and 2 hourly overnight
- prevents ‘white-coat’ BP
Home BP monitoring
- 2 readings twice a day taken for 4-7 days
- patient does it themselves
Why is it important to treat hypertension?
Uncontrolled HTN affects specific organ groups leading to end organ damage
Reduce incidence of..
CV Disease: Stroke, MI, HF
Renal failure
Hypertensive retinopathies
Once diagnosis of hypertension is made, what are the next steps?
- Confirm diagnosis with out-of-office BP monitoring
- Assess CV risk
- Determine presence of end-organ damage or associated complication eg. CKD, PVD, CVA
- Assess presence of secondary hypertension (if there is a cause for the hypertension)
Eg.
- Renin and aldosterone: ? primary aldosteronism
- 24hr catecholamines: ? pheochromosytoma
- Echo: ? HF
- Renal ultrasound: ? Renal failure
What are the mainstays for treating hypertension?
What blood pressure is aimed for with treatment?
- Lifestyle measures
- Pharmacological management
- Device based management eg. renal denervation, baroceptor stimulation
Aim: <140/90mmHg
List 4 lifestyle modifications recommended in hypertension
- exercise
- weight loss
- reduce sodium intake
- reduce alcohol intake
- smoking cessation
Outline the pharmacological pathway for treating hypertension
HTN with diabetes or <55:
- 1st line: ACEi (ramipril)/ARB
- 2nd line: add rate-limiting Ca channel blocker (Verapamil) or thiazide-like diuretic
HTN if >55 or black-african or aftrican-carribean
- 1st line: rate-limiting Ca channel blocker (Verapamil)
- 2nd line: ACEi/ARB or thiazide-like diuretic
3rd line for all: ACEi/ARB + Ca channel antagonist + thiazide-like diuretic
Outline the foetal circulation
- in-utero oxygenation via the maternal placenta
- pulmonary circulation is minimal and at high resistance (lungs aren’t fully formed)
- oxygenated blood returns to the right atrium via the IVC
- it then bypasses the right ventricle and pulmonary artery via the foramen ovale directly to the left atrium: path of least resistance
- a minority will pass into the right ventricle and through the pulmonary vein but will then pass through the ductus arteriosus into the aorta to bypass the lungs
Outline the morphology of the heart chambers
Heart chambers are characterised by their morphology rather than their position
Right atrium:
- sinoatrial node
- broad appendage
Left atrium:
- narrow, long appendage
Right ventricle:
- trabeculated endocardium
- insertion of chordae to intravascular septum
- moderator band
Left ventricle:
- smooth endocardium
- ellipsoid cavity
- 2 papillary muscles
Outline where the valves sit in the heart
Atrioventricular valve always follows the ventricle
- Tricuspid valve always with the right ventricle (even if supplied by the left atrium)
- Bicuspid/Mitral valve always with with left ventricle
Aortic and pulmonary valves say with their relevant artery and can be connected to the wrong ventricle
List 3 acyanotic and 3 cyanotic congenital heart diseases
Acyanotic (don’t impact patient’s sats)
Left-to-right shunts:
- ventricular septal defect (LSD)
- persistent ductus arteriosus
- atrial septal defect (ASD)
Outflow obstruction:
- pulmonary stenosis
- aortic stenosis
- coarctation of the aorta
Cyanotic:
- Tetralogy of fallot
- Transposition of the great vessels
- complete atrioventricular septal defect
Outline the types of atrial septal defect
Different types depending on the location:
- Secundum ASD: hole between the atria
- Primum ASD: occurs close to the atrioventricular valve so can distort the valve, causing it to become regurgitant
- The hole can extend down into the ventricle and cause a VSD: partial atrioventricular septal defect (partial AVSD)
Describe the pathophysiology of a secundum ASD
= a hole between the atria
- Blood will always take the path of least resistance and will flow from high to low pressure
- Therefore blood shunts from left to right when in isolation
- The r. ventricle receives blood from the right atrium and the additional volume from the left atria = right heart volume loading
- R. ventricle then dilates to accomodate for the extra volume
- If this continues, the right ventricle won’t be able to pump efficiently and lead to RV failure
List 2 complications could arise from an atrial septal defect
- right ventricular failure
- tricuspid regurgitation
- atrial arrhythmias
- pulmonary hypertension
How are atrial septal defects managed?
- Surgically with a sternotomy or through the groin with a transcatheter device if small enough
What is coarctation of the aorta?
Outline it’s pathophysiology
= narrowing of the aorta, typically located at the insertion point of the ductus arteriosus
- acyanotic
- the narrowing means the l. ventricle has to generate a higher pressure to force blood out, leading to LV hypertrophy
- could lead to LV failure if not treated
- blood will find a path of least resistance to reach the descending aorta and will develop collateral arteries
- highly variable in severity
- will cause discrepancies in limb BPs
List 2 common associations with coarctation of the aorta
- bicuspid aortic valve
- upper body hypertension
- berry aneurysms
What is the management for coarctation of the aorta?
Surgical repair via thoractomy
- The narrowed aorta is cut out, or the narrow area is reconstructed using the subclavian artery
Non-surgical ie. transcatheter
- through the femoral artery, which is fed up to the coarctation, a balloon is passed through and inflated to stretch the narrowed artery
Describe the pathophysiology of transposition of the great arteries (TGA)
The aorta and pulmonary artery switch palces
- Aorta is now attached to the right ventricle and pulmonary artery is attached to the left ventricle
This creates two separate circulation systems
- Systemic circulation: deoxygenated blood returns to RA via inferior and superior vena cava, passed through tricupsid valve into RV, then pumped through aortic valve into the aorta and around the body without being oxygenated
- Pulmonary circulation: oxygenated blood enters LA via pulmonary veins, through mitral valve to LV then through pulmonary valve into pulmonary artery back to the lungs
This causes profound cyanosis therefore is a cyanotic lesion
- the two foetal shunts are the only points at which oxygenated blood can get around the body and therefore critical for a baby with TGA
What is the management for transposition of the great arteries (TGA)?
2 foetal shunts are the only points at which oxy and deoxy blood can mix and therefore crucial for a baby with TGA
- When baby takes it’s first breath, the changes in pressure in the lungs and heart mean the foramen ovale and ductus arteriosus close within a few hours
- Closing of these shunts delayed with prostaglandins to allow time for surgery
Arterial switch procedure
- disconnect aorta and pulmonary artery, swtich them and sew back on
- caution with sewing, ensure not to occlude the aorta which could lead to MI or sudden death
Describe the pathophysiology of tetralogy of fallot
- cyanotic lesion
4 components:
- ventricular septal defect
- right ventricular outflow tract (RVOT) obstruction: often stenosis below the pulmonary valve due to large muscle mass
- Right ventricular hypertrophy
- Overriding aorta: the aortic valve is enlarged and appears to arise from both the left and right ventricles
RVOT obstruction results in restricted flow into the pulmonary arteries with the remainder of flow passing through the VSD into the systemic circulation.
As a result you get mixing of blood and a drop in saturations
Perfusion of the pulmonary circulation is dependent on the ductus arteriosus with flow from aorta to pulmonary circulation
What is the management for tetralogy of fallot?
- Prevent the natural closer of the ductus arteriosus after birth with IV prostaglandins (dependent on this for pulmonary circulation perfusion)
Operative strategy: corrective surgery
- close VSD with a patch
- resection of the RVOT obstruction
- enlargement of the pulmonary artery with a patch
Describe the pathophysiology of a univentricular heart
Presence of only one effective pumping ventricle
Commonest cause: tricuspid atresia (abnormal narrowing)
- Only one functioning ventricle, so foetal circulation is reliant on shunts for mixing of oxygenated and deoxygenated blood
Shunts: patent foramen ovale and patent ductus arteriosus
What is the management for a univentricular heart?
Surgery aiming to create two functional ventricles, if this is not faesible a fontan circulation will be created
Options:
- BT shunt: tube graft placed from an atery (usually left subclavian) to the pulmonary artery
Norwood Operation (aortic stenosis ie. small l. ventricle): right ventricle becomes systemic ventricle. A new aorta is made from part of the pulmonary artery and the original (tiny) aorta is reconstructed to provide blood flow to the body. A small tube graft placed from artery to the lung vessels or from RV to lung vessels for blood flow to the lungs
Fontan: inferior vena cava connected directly to the pulmonary artery
Describe the process of forming a Fontan circulation
The single functional ventricle is used to support the systemic circulation (done by disconnecting the pulmonary artery and valve from the heart)
- the IVC and SVC are directly pumped into the pulmonary arteries bypassing the heart
- Now deoxy blood flows up IVC into pulmonary arteries and it oxygenated at the lungs
- Flows back to left ventricle once oxygenated, passing through mitral valve into single ventricle through the aortic valve into the aorta and thr body
Outline the issue with the fontan circulation
Pulmonary circulation is dependent on high systemic venous pressure and low pulmonary vascular resistance due to absence of RV to actively pump blood into the pulmonary circulation
Anything causing imalance of this could lead to haemodynamic compromise
- Pulmonary embolism: inc. pul vascular resistance
- Arrhythmias: reduce systemic circulation and pressure
- Dehydration: reduces venous pressures
What valves are found in the heart and what are their functions?
Tricuspid and pulmonary valves: RHS
Bicuspid/Mitral and aortic valves: LHS
- The aortic and pulmonary valves = semilunar valves and work based on pressure gradients (when in diastole, pressure in the aorta is greater than the ventricles so valves will with blood and close)
Function:
- control passage of fluid, allowing movement in one direction only
Classify the abnormalities that can be seen with valves
Valve leaflets
- Calcification, thickening, degeneration, infection (can destroy valves), prolapse (valves don’t meet but move backwords)
Apparatus/Annulus (Structures around the valves)
- Annular dilatation: annulus is where the mitral valve leaflets are attached to the wall
- Annular calcification
- Chordae tendinae rupture
Stenosis
- Leads to pressure overload
Regurgitation
- Leads to volume overload
Describe the pathophysiology of rheumatic valve disease
Consequence of acute rheumatic fever
- results from the body’s immune repsonse to a group A strep. infection eg. strep throat or scarlet fever
Cardiac injury is generated by recurrent inflammation and fibrinous repair and scarring
- The valve(s) is chronically scarred, infalmed and neovascularised
- Leads to valve thickening and calcification
What is the most common valvular abnormality?
Aortic stenosis
Describe the pathophysiology of aortic stenosis
Functional narrowing of the aortic valve caused by mechanical stress
- Stress damages the endothelium around the valve over time, leading to fibrosis and calcification (occurs with age)
- Calcification deposits on the aortic valve increases stiffness
- This hardens the valve making it harder to completely open (functional narrowing)
- This causes obstruction to blood flow from LV to systemic circulation
- Increased LV cavity pressure and pressure overload leading to LV hypertrophy
Outline 3 causes of aortic stenosis
Stress over time (with age): leads to thickening and calcification
Rheumatic valve disease: repeated inflammation and repair, leading to fibrosis
Congenital: bicuspid aortic valve and more at risk of mechanical stress
List 3 symptoms and 3 signs seen with aortic stenosis
Symptoms:
- SOB
- Syncope (temp loss of consciousness due to reduced blood flow to the brain)
- Angina/chest pain
- presyncope
- reduced exercise capacity
- can hear murmur themselves
Signs:
- ejection systolic murmur
- soft 2nd heart sound
- narrowed pulse pressure (LV hypertrophy, reduced systolic BP and elevated diastolic BP)
- Heaving apex beat
- If really bad, signs of HF
Describe the pathophysiology of aortic regurgitation
- Leaking of the aortic valve (don’t close properly) causing blood to flow in the opposite direction during ventricular diastole (from aorta to LV)
- Results in volume overload on LV that’s receiving blood from LA and aorta: increased stroke volume
- Increased stroke volume increases systolic pressure and results in LV dilatation
- In diastole: less blood volume in the aorta so diastolic BP falls
- Increased systolic and reduced diastole BP: increased pulses pressures and can lead to head bobbing and pulsating nailbeds
List 2 symptoms and 3 signs of aortic regurgitation
Symptoms:
- SOB
- Reduced exercise capacity
Signs:
- Early diastolic murmur
- Increased pulse pressure: head bobbing and pulsating nailbeds
- Collapsing pulse (due to sudden fall of diastolic pressure)
- Signs of HF (elevated JVP, peripheral oedema)
Describe the pathophysiology of mitral regurgitation
Occurings during ventricular systole
- Volume overload on LHS
- LV and LA dilatation
- Pulmonary hypertension
- Secondary right heart disease: back pressure from hypertensive pulmonary circulation
- Atrial fibrillation
List the symptoms and signs of mitral regurgitation
Symptoms:
- SOB
- palpatations (due to AF)
- right HF symptoms
Signs:
- pansystolic murmur
- quiet first heart sound
- displaced apex beat
- signs of HF
List 3 causes of mitral regurgitation
- mitral valve prolapse
- MI
- rheumatic fever
- LVHF
Describe the pathophysiology of mitral stenosis
Occurs during ventricular diastole
- makes it hard for blood to travel LA to LV, leading to increased volume and therefore pressure in the LA
- Causes LA dilatation and causes blood to back-up into the pulmonary circulation (pulmonary congestion, hypertension and oedema)
- Causes higher pressures in pulmonary circulation, making it harder for the right ventrcile to pump blood to the lungs
- Over time can get RV hypertrophy and right sided HF
List the symptoms and signs seen with mitral stenosis
Symptoms
- SOB and dyspnoea
- Palpatations
- Chest pain
- Haemoptysis and right heart failure symptoms
Signs
- diastolic murmur
- heaving apex
- signs of HF
How are valvular lesions treated?
Surgical intervention (preferential to medication)
- valve repair
- valve replacement: mechanical or tissue valves dependent on durability (age of pt/life expectancy) and anticoagulation (compliance to medication). Tissue valves don’t last as long
Procedural Intervention
- TAVI (Transcather Aortic Valve Implantation): minimally invasive, repairing the valve without removing the old, damaged valve. Used if unfit for surgery
- Mitraclip: used for mitral regurgitation
- Valvuloplasty: aka balloon valvotomy, repairing a heart valve with a narrowed opening
If a patient presents with both heart failure and subsequent atrial fibrillation, what is the treatment plan?
Initial: control rate first
- oxygen
- IV diuretics (furosemide)
- AF: digoxin (rate), amiodarone (rhythm), anti-coagulant (LMWH)
Next:
- regular oral diuretic (furosemide)
- bisoprolol and ramipril
- aldosterone antagonist (spironactone)
What is the CHA2-DS2-vasc score and what features are involved within in
Outline the clinical significance of the scoring
CHA2-DS2-vasc score is the most commonly used method of predicting thromboembolic risk in atrial fibrillation, and determines need for an anti-coagulant
- Cardiac failure / Congestive HF
- Hypertension
- Age >75 (x2 points)
- Diabetes
- Previous Stroke (x2 points)
- Vascular disease
- Age 65-74
- Sex (female)
Max score: 9
Score >2: put on a DOAC
What are the types of acute coronary syndrome (ACS)?
- Unstable angina
- STEMI
- NSTEMI
Outline the immediate management of acute coronary syndrome
MONARCH
- Morphine
- Oxygen
- Nitrate
- Aspirin
- Re-perfusion ie. thrombolysis or PCI (percutaneous coronary intervention, done unless >2 hours have passed)
- Clopidogrel
- Heparin
Outline the longer-term management for acute coronary syndrome
BASIC
- Beta-blocker
- Aspirin
- Statin
- Inhibitors of angiotensin-II (ACEi)
- Correction of RFs (smoking cessation, diet, exercise)
Identify three complications of acute coronary syndrome
- heart failure
- atrial fibrillation
- cardiogenic shock
- left bundle branch block
- LV mural thrombus
- myocardial rupture
