Conditions - Cardio&Haem Flashcards
STEMI Definition
Clinical event characterised by transmural myocardial ischaemia resulting in myocardial injury or necrosis.
The mismatch between myocardial oxygen demand and delivery is almost always caused by total occlusion of a coronary artery from atherosclerotic plaque rupture and subsequent thrombus formation. The severity is dependent on the size, location, and duration of the occlusion.
STEMI Signs and symptoms
Chest pain
Low-grade fever
Pale, cool and/or clammy skin
Signs of acute heart failure
Systolic murmur due to acute mitral regurgitation or ventricular septal rupture and/or pericardial rub
Chest pain described as:
Central or left-sided chest pain
Usually lasting > 15 minutes “Crescendo pain” with increasing severity over several minutes
Described as substernal pressure
Varying severity
Radiating to left arm, shoulders, neck, or jaw
STEMI investigations
12-lead ECG → ST segment elevation
STEMI ECG
Left anterior descending (LAD) occlusion produces ST elevation in the precordial leads (V1-3)
Right coronary artery (RCA) occlusions produce ST changes in the inferior leads (II-III-AVF)
Left circumflex artery (LCA) occlusions produce ST elevation in the lateral leads (I, AVL and V5-6)
STEMI Management
Morphine
Oxygen (saturations under 94%)
Nitrates
Aspirin (300mg loading dose)
Perfusion therapy (primary percutaneous coronary intervention if available <120 minutes of presentation or thrombolysis if PCI is not possible within 120 minutes)
NSTEMI About
There are more varied causes of mismatch including partial coronary artery obstruction from a ruptured plaque (most common), partial occlusion from a stable plaque, coronary artery vasospasm (Prinzmetal’s angina) or coronary arteritis.
Can lead to necrosis
NSTEMI Signs and symptoms
Sudden onset central crushing chest pain radiating to the left arm and/or jaw lasting longer than 20 minutes
Diaphoresis
Nausea
Shortness of breath
Signs of respiratory distress, pallor, diaphoresis, or fluid overload
Tachycardia
High or low blood pressure
S4 heart sound: due to reduced ATP production impairing left ventricular relaxation
Signs of papillary muscle dysfunction (e.g. mitral regurgitation)
Pulmonary oedema, due to acute left-sided heart failure
NSTEMI Investigations
12-lead ECG → ST segment depression
High sensitivity troponin → elevated
NSTEMI ECG
Regional ST-segment depression
T wave inversion or flattening
Any dynamic or new Q or T wave changes
NSTEMI Management
Antiplatelet therapy: aspirin 300mg
Analgesia: either GTN or intravenous opioids
Initial antithrombin therapy: fondaparinux if low bleeding risk and the patient is not undergoing immediate angiography. Unfractionated heparin can be used for patients with renal impairment.
Supplemental oxygen should be offered only to patients with SpO2 of less than 94%.
Coronary angiogram
Unstable Angina About
Defined by the absence of biochemical evidence of myocardial damage.
It is characterised by specific clinical findings of:
- prolonged (>20 minutes) angina at rest
- new onset of severe angina
- angina that is increasing in frequency, longer in duration, or lower in threshold
- angina that occurs after a recent episode of myocardial infarction
Unstable Angina Signs and symptoms
Chest pain
Unstable Angina Investigations
Diagnosis is based on clinical assessment
Unstable Angina ECG
May be normal
Unstable Angina management
Antiplatelet therapy: aspirin 300mg
Analgesia: either GTN or intravenous opioids
Initial antithrombin therapy: fondaparinux if low bleeding risk and the patient is not undergoing immediate angiography. Unfractionated heparin can be used for patients with renal impairment.
Supplemental oxygen should be offered only to patients with SpO2 of less than 94%.
Coronary angiogram
Systolic HF definition
Inability of the heart to contract efficiently to eject adequate volumes of blood to meet the body metabolic demand [most common].
Diastolic HF definition
Reduction in the heart compliance resulting in compromised ventricular filling and therefore ejection [pericardial disease, restrictive cardiomyopathy, tamponade]. Increasingly recognised as an important cause of heart failure – it is often present in elderly patients with a normal CXR and otherwise unexplained shortness of breath on exertion.
Left HF
Inability of the left ventricle to pump adequate amounts of blood, leading to pulmonary circulation congestions and pulmonary edema. Usually results in RHF due to pulmonary hypertension. Defined as an ejection fraction of <40%.
Right HF definition
Inability of the right ventricle to pump adequate amounts of blood, leading to systemic venous congestion, therefore peripheral edema and hepatic congestion and tenderness. Most commonly the result of respiratory disease – especially COPD. The presence of raised JVP and peripheral oedema are suggestive of right HF in particular.
Congestive HF definition
Failure of both right and left ventricles, which is common.
Low-output HF definition
Heart failure resulting from reduced cardiac output [most common type] – also referred to as HFrEF (Heart Failure reduced Ejection Fractions).’Pump dysfunction’. Systolic heart failure. Causes decreased contractability (e.g. MI, myocarditis), decreased blood supply to the heart, increased afterload (e.g. hypertension) and impaired mechanical function (e.g. valve disease).
High-output HF definition
Heart failure that occurs in normal or high cardiac output due to metabolic demand and supply mismatch, either due to reduced blood oxygen carrying capacity [anaemia] or increase body metabolic demand [thyrotoxicosis] – also referred to as HFpEF (Heart Failure preserved Ejection Fraction). ‘Filling dysfunction’. Diastolic heart failure. Causes restrictive cardiomyopathy (‘stiff heart’ (amyloid, sarcoid), valve disease, hypertension)
Acute HF definition
Acute onset of symptom presentation often, but not always due to an acute event [MI, persistent arrhythmia, mechanical event (ruptured valve, ventricular aneurysm)]. Often an acute presentation to hospital. May be the first presentation, or may be “acute-on-chronic”.
Chronic HF definition
Slow symptoms presentation usually due to slow progressive underlying disease [CAD, HTN].
Acute-on-chronic HF definition
Acute deterioration of a chronic condition, usually following an acute event [anaemia, infections, arrhythmias, MI].
Right Bundle Branch Block Pathophysiology
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation through the bundle of His occurs only via the left bundle branch. The left branch still depolarises the septum as normal.
The left ventricular wall depolarises as normal.
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway.
Right Bundle Branch Block Diagnostic Criteria
Broad QRS complex: >120 ms (3 small squares)
RSR’ pattern in V1-V3: an initial small upward deflection (R wave), a larger downward deflection (S wave), then another large upward deflection (a second R wave, which is indicated as R’)
Wide, slurred S wave in lateral leads: I, aVL, V5-V6
Right Bundle Branch Block Clinical Relevance
RBBB can be either physiological or the result of damage to the right bundle branch. Causes of damage include underlying lung pathology (COPD, pulmonary emboli, cor pulmonale), primary heart muscle disease (ARVC), congenital heart disease (e.g. ASD), ischaemic heart disease and primary degeneration of the right bundle.
Left Bundle Branch Block Pathophysiology
The sino-atrial node acts as the initial pacemaker
Depolarisation reaches the atrioventricular node
Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.
The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.
Left Bundle Branch Block Diagnostic criteria
Broad QRS complex: >120 ms (3 small squares)
Dominant S wave in V1
Broad, monophasic R wave in lateral leads: I, aVL, V5-V6
Absence of Q waves in lateral leads
Prolonged R wave >60ms in leads V5-V6
Left Bundle Branch Block Clinical relevance
LBBB is always pathological. Left bundle branch block may be due to conduction system degeneration or myocardial pathologies such as ischaemic heart disease, cardiomyopathy and valvular heart disease.
LBBB may also occur after cardiac procedures, which damage the left bundle branch or His bundle. A STEMI presenting as chest pain with LBBB is exceedingly rare.
Due to the relatively greater mass of the left ventricle, disruptions in the depolarisation of the left ventricular muscle can cause cardiac axis changes. The left bundle branch splits into anterior and posterior fascicles. Each branch of the left bundle branch may be damaged in isolation. Anterior fascicle block, which is much more common, causes left axis deviation. Posterior fascicle block may cause right axis deviation. However, the posterior fascicle does much less work than the anterior fascicle, so it can be blocked without any obvious ECG changes.
1st Degree Heart Block About
First-degree AV block involves the consistent prolongation of the PR interval (defined as >0.20 seconds) due to delayed conduction via the atrioventricular node.
Every P wave is followed by a QRS complex (i.e. there are no dropped QRS complexes, unlike some other forms of AV block discussed later).
First-degree AV block is common and can often be an incidental finding.
First Degree Heart Block Causes
Enhanced vagal tone (often seen in athletes)
Post myocardial infarction
Lyme disease
Systemic lupus erythematosus
Congenital
Myocarditis
Electrolyte derangements
Drugs, particularly AV blocking drugs
Thyroid dysfunction
First Degree Heart Block Signs and symptoms
Usually asymptomatic
First Degree Heart Block Investigations
12-lead ECG
First Degree Heart Block ECG
Rhythm: regular
P wave: every P wave is present and followed by a QRS complex
PR interval: prolonged >0.2 seconds (5 small squares)
QRS complex: normal morphology and duration (<0.12 seconds)
First Degree Heart Block Management
If symptomatic, pacemaker may be considered
2nd Degree Heart Block Mobitz I About
Also known as the Wenckebach phenomenon.
Typical ECG findings in Mobitz type 1 AV block include progressive prolongation of the PR interval until eventually the atrial impulse is not conducted and the QRS complex is dropped.
AV nodal conduction resumes with the next beat and the sequence of progressive PR interval prolongation and the eventual dropping of a QRS complex repeats itself.
2nd Degree Heart Block Mobitz I Causes
Increased vagal tone (often seen in athletes)
Drugs, particularly AV blocking drugs
infarction
Myocarditis
Cardiac surgery
2nd Degree Heart Block Mobitz I Signs and Symptoms
Usually asymptomatic
Some can develop symptomatic bradycardia and present with symptoms such as pre-syncope and syncope
Irregular pulse
2nd Degree Heart Block Mobitz I Investigations
12-lead ECG
2nd Degree Heart Block Mobitz I ECG
Rhythm: irregular
P wave: every P wave is present, but not all are followed by a QRS complex
PR interval: progressively lengthens before a QRS complex is dropped
QRS complex: normal morphology and duration (<0.12 seconds), but are occasionally dropped
2nd Degree Heart Block Mobitz I Management
AV blocking drugs should be stopped.
Usually, no intervention is required if the patient is asymptomatic.
If the patient is symptomatic a pacemaker may be considered.
2nd Degree Heart Block Mobitz II About
Typical ECG findings in Mobitz type 2 AV block include a consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.
The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave.
Mobitz type 2 AV block is always pathological, with the block typically occurring at either the bundle of His (20%) or the bundle branches (80%).
2nd Degree Heart Block Mobitz II Causes
Myocardial infarction
Idiopathic fibrosis
Cardiac surgery
Inflammatory conditions
Autoimmune
Infiltrative myocardial disease
Hyperkalaemia
Drugs, particularly AV blocking drugs
Thyroid dysfunction
2nd Degree Heart Block Mobitz II Signs and symptoms
Palpitations
Pre-syncope/Syncope
Regular irregular pulse
2nd Degree Heart Block Mobitz II Investigations
12-lead ECG
2nd Degree Heart Block Mobitz II ECG
Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)
P wave: present but there are more P waves than QRS complexes
PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes
QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)
The QRS complex will be broad if the conduction failure is located distal to the bundle of His
2nd Degree Heart Block Mobitz II Management
Patients should be placed on a cardiac monitor as soon as possible.
Treatment of underlying cause
Temporary pacing or isoprenaline may be required if the patient is haemodynamically compromised due to bradycardia.
A permanent pacemaker is usually inserted if there are no reversible causes identified.
3rd Degree Heart Block About
Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction. Cardiac function is maintained by a junctional or ventricular pacemaker.
Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.
3rd Degree Heart Block Causes
Congenital structural heart disease
Idiopathic fibrosis
Ischaemic heart disease
Non-ischaemic heart disease
Iatrogenic, e.g. post-ablative therapies and pacemaker implantation, post-cardiac surgery
Drugs, particularly AV blocking drugs
Infections
Autoimmune conditions
3rd Degree Heart Block Signs and symptoms
Palpitations
Pre-syncope/syncope
Confusion
Shortness of breath
Chest pain
Sudden cardiac death
Irregular pulse
Profound bradycardia
Haemodynamic compromise (e.g. prolonged capillary refill time and hypotension)
3rd Degree Heart Block Investigations
12-lead ECG
3rd Degree Heart Block ECG
Rhythm: variable
P wave: present but not associated with QRS complexes
PR interval: absent (as there is atrioventricular dissociation)
QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm
Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His. A typical heart rate would be >40bpm.
Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His. These escape rhythms produce slower, less reliable heart rates and more significant clinical features (e.g. heart failure, syncope).
