Disorders of CVS Flashcards
a) What electrolyte mediates SA and AV nodal cell current in comparison to atrial and ventricular myocytes? (how does this affect phase 0 of Action Potenbetwtial profile)
b) How are cells with properties of SA and AV nodal tissue connected to the remainder of the myocardium?
c) Why are cells in the SA node the dominant pacemakers in a normal heart?
a) SA and AV nodal cells are mediated by calcium. Atrial and ventricular myocytes are mediated by sodium current. Thus the action potential upstroke (phase 0) is slow in nodal tissue compared to atrial and ventricular cells.
b) SA and AV nodal cells are electrically conected to the remainder of the myocardium by cells with an electrophysiologic phenotype between that of nodal cells and atrial/ventricular myocytes.
c) Because cells in the SA node exhibit the most rapid phase 4 depolarision thus are the dominant pace makers.
IMAGE: Action potential profiles recorded in SA or AV nodal tissue compared with cells from atrial or ventricular myocardium. Nodal cell action potentials exhibit more depolarized resting membrane potentials, slower phase 0 upstrokes, and phase 4 diastolic depolarization.
a) What is the most common cause of pathologic Bradycardia?
b) In what decades of life should SA node dysfunction be considered and what are the symptoms?
c) What are some reversible aetiologies for bradycardia? & what is the only reliable therapy in the absence of the above reversible aetiologies?
a) SA node dysfunction and AV conduction block. (difficult to distinguish from physiologic bradycardia, particularly in the young/athletes)
b) 5th and 6th decades of life SA node dysfunctionm increases in frequency. Symptoms include fatigue, exercise intolerance, syncope all with sinus bradycardia.
c) Increased vagal tone/hypoxia/hypothermia and drugs. The ony reliable therapy is permanent pacemaking.
What are some of the most common aetiologies for bradycardia?
**Vascular: CAD, acute MI, collagen vascular disease
**Infectious/inflammation: Pericarditis, myocarditis (incl viral)
**Neoplastic: Increased Intracranial pressure
**Degenerative/Drugs:
Senile Amyloidosis, Sick Sinus Syndrome (SSS)
Beta blockers
Calcium channel blockers
Digoxin
Ivabradine
Antiarrhythmics (class I and III)
Adenosine
Clonidine (other sympatholytics)
Lithium carbonate
Cimetidine
Amitriptyline
Phenothiazines
Narcotics (methadone)
Pentamidine
**Iatrogenic: Radiation therapy/Postsurgical
**Congenital: Myotonic Dystrophy
**Autoimmune/Autonomic: Carotid sinus hypersensitivity. Vasovagal (cardioinhibitory) stimulation. Rheumatic heart disease. Endotracheal suctioning (vagal maneuvers)
**Traumatic: Chest trauma
**Endocrine/Metabolic: Hypothyroidism.
a) What shape are SN node cells and where exactly are they located in the right atrium?
b) What is the vascular source to the SA node and how is it innervated?
a) Fusiform shaped cells in the epicardium at the right atrial/SVC junction
b) SA nodal artery arises from the right CA in 55-60% & left circumflex artery in 40-45% of persons. SA node is richly innervated by sympathetic and parasympathetic nerves and ganglia
a) How is intrinsic SA node dysfunction characterised?
b) Describe an infiltrative disorder affecting SA node typically seen in the 9th decade of life
a) Characterised pathologically by fibrous replacement of the SA node or it’s connections to the atrium. Inflammatory processes will often ultimately produce replacment fibrosis.
b) Senile Amyloidosis. Deposition of Amyloid protein in the atrial myocardium can impair SA node function.
a) Describe a rare heritable form of sinus node disease, the types and pathophysiology
b) What conditions may hasten it’s onset?
c) Name/describe any other conditions you can think of that affect SA node.
a) Sick Sinus syndrome
SSS1: Autosomal recessive form with a prominent feature of atrial inexcitability and absence of P waves.
SSS2: Autosomal dominant sinus node dysfunction with SVT (Tachy-brady variant).
SSS3: Variant in myosin heavy chain 6 increase in susceptibility of SSS.
NB: SSS in elderly also associated with fibrous tissue in SA node.
b) CAD, diabetes mellitis, HTN, cardiomyopathies and valvular diseases.
c) Neuromuscular diseases incl Kearns-Sayre syndrome (ophthalmoplegia, retinal disease, cardiomyopathy) and myotonic dystrophy have a predilection for the conducting system and SA node.
a) How could asymptomatic SA node dysfunction manifest on ECG?
b) What altered cardiac rhythms can be caused by SA node dysfunction?
a)Sinus bradycardia
Sinus arrest: No conduction from SA node to atria, thus no P wave causing long pauses, arrhythmia and possible fatal asystole.
Exit block: SA Node depolarises normally however impulses are blocked before they can be transmitted. Leads to intermittent dropped P waves
b)SVT, AFib, Bradycardia
a) What symptoms develop with SA Node dysfunction?
b) What are the risks of persistent AFib in a patient with SA Node dysfunction?
c) What is the risk with tachy/brady variant of SSS and what are the risks of this occuring?
a) Symptoms commonly only arise from SA Node dysfunction due to concomitant CVD. A minority of patients with SSS will develop heart failure due to fast/slow HRs.
b) Diabetes Mellites, HTN, left Ventricular dilatation, Valvular heart disease and Ventricular pacing
c) Thromboembolism with AFib. Greatest risk if patients >65, stroke, valvular heart diease, left ventricular dysfunction or atrial enlargement. These patients need to be anticoagulated
a) How many patients with SA Node dysfunction have concurrent AV Node dysfunction?
b) How many patients with SA Node dysfunction develop SVT, AFib or AFlutter?
a) Up to 25%, however only a minority will require treatment for the AV node.
b) One third to half of patients.
a) What is the definition of sinus bradycardia and what is gernally considered abnormal?
a) <60bpm is sinus bradycardia. Very common and typically benign. Generally <40bpm in the awake state in the absence of physical conditioning is considered abnormal.
a) Desribe first degree SA block
b) Describe type I second-degree (Mobitz I/Wenchebach) SA block, and
c) Describe how it appears on the ECG
d) Describe Type II second degree (Mobitz II) SA block on ECG
a) Delay between impulse generation in SA Node and transmission to the atrium (not detectable on surface ECG)
b) A progressive prologation of SA node conduction with intermittant failure of the impulses originating in the SA node to conduct to surrounding atrial tissue
c) Intermittent absence of P waves producing a regularly irregular rhythm. Subtly decreasing P-P intervals before the pause.
d) There is no change in SA node conduction, thus no change in P-P interval before the pause.
a) Describe third degree or complete heart block on ECG
b) How can the rhythm be maintained in third degree heart block?
c) What the most common causes of SA Exit block?
a) No SA Node impulses are conducted to the right atrium, thus a complete absence of P waves. May lead to fatal asystole.
b) Junctional escape rhythms
c) Sick sinus syndrome, increased vagal tone (athletes), vagal stimulation (surgery, pain), inferior MI, myocarditis, drugs (digoxin, beta-blockers, calcium channel blockers, amiodarone).
a) How is SA Node dysfunction diagnosed? and What diagnostic testing can be utilised?
b) How can SA Node disease be ruled out?
a) Diagnosis is commonly clinical with ECG correlation. Longer-term ECG measurements e.g. Holter monitor (~24hrs) may permit correlation of symptoms with cardiac rhythm.
b) SA Node dysfunction may be ruled out when symptoms occur in the absence of sinus bradyarrhythmias.
a) What are 2 differential diagnoses for SA Node dysfunction?
b) Define these conditions
c) How can they be differentiated from SA Node dysfunction?
a) Chronotropic Incompetence and Carotid Sinus Hypersensitivity.
b) Chronotropic incompetence is failure to increase HR with exercise, specifically failure to reach 85% HR max or failure to achieve a HR >100. Carotid sinus hypersensitivity (CSH) is defined by >3 sec pause (asystole-which can be present in asymptomatic elderly) and a decrease of 50mmHg BP or more with carotid sinus massage.
c) Exercise testing is useful to discriminate between chronotropic incompetence and resting bradycardia. Autonomic nervous system testing with carotid sinus massage can confirm CSH.
NB: Determining the intrinsic heart rate (IHR) with propranolol & atropine can also indicate SA disease.
NB: Electrophysiologic testing using invasive techniques can be used to rule out more malignant aetiologies of syncope e.g VTachyarrhythmias and AV conduction block.
a) Describe the treatment for symptomatic and asymptomatic SA Node dysfunction
b) What medications should be discontinued prior to decisions regarding the need for PPM?
NB: Since SA node dysfunction is not associated with increased mortality rates, aim of therapy is to alleviate symptoms
a) In symptomatic SA Node dysfunction, exclusion of extrinsic causes and correlation with symptoms is an essential part of initial management. PM implantation is the primary therapeutic intervention in patients with symptomatic SA Node dysfunction.
b) Cease beta blockers and calcium channel blockers, which increase SNRT (sinus node recovery time) & cease antiarrhymthic drugs with class I and III action that may promote SA Node exit block.
a) Is there a role for chronic pharmacotherapy is SA Node dysfunction?
b) Are there any medications for acute management of SA Node dysfuction?
c) What is the MOA of the above mentioned medications?
a) Chronic pharmacotherapy for sinus bradycardias is limited. Digitalis has been shown to shorten SNRT in patients with SA node dysfunction.
b) Isoprenaline or atropine can be used to increase SA firing rate acutely when bradyarrhythmia occurs with haemodynamic compromise. Atropine is short-acting, Isoprenaline can be given by prolonged infusion for a longer duration of action. PM is then preferred for persistent bradycardia.
c) Atropine functions to competitively block the action of acetylcholine at parasympathetic (muscarinic) sites in smooth muscle, secretory glands and the CNS. From a cardiac perspective, this increases CO by increasing HR and contractility.
NB: Theophylline has been used acutely & chronically to increase HR, however has risks for patients with tachy-brady syndrome, increasing risk of SVT and serious ventricular arrhythmias.
a) What is the primary indication of pacing in SA Nodal disease?
b) What are the indications for the use of pacemakers, as categorised by levels of evidence?
c) Describe what each class of evience means.
a) Pacing in SA Nodal disease is indicated to alleviate symptoms of bradycardia.
b) See table
c) Class I conditions are those for which there is evience or consensus of opinion that therapy is useful and effective.
Class II evidence there is conflicting evidence. e.g. Class IIa conditions the weight of evidence favours treatment; in class IIb conditions, efficacy is less well established by the evidene/opinion of experts.
Class III conditions the evidence suggests the therapy/treatment is not efficacious & may be harmful.
a) What is the long-term treatment option for CSH and Vasovagal Syncope?
a)CSH, if accompnied by a significant cardioinhibitory component, responds well to PM. The mechanism of vaso-vagal syncope is incompletely understood and several RCTs involving PM have shown inconclusive results.
a) What is the % of young adults affected by AV conduction block?
b) What is the incidence of AV block in adult populations?
c) Of the PM inplanted in America and Europe, how many for due to AV conduction disorders?
a) 10% of young adults suffer high vagal tone which can cause transient AV conduction block.
b) Estimated incidence of 200 per million population per year. With comorbidities such as MI, aging and fibrosis, persistent AV block is much more common.
c) ~50% of 160,000 PPM is the US and 70-80% of those in Europe.
a) Where is the AV Node located in relation to the lining of the heart, where is it located in relation to the R atrium? & what atrionodal bundles converge on it from the SA Node?
b) What is the name and anatomic borders of a prominent atrial triangle?
c) Describe the names and course of the electrical conduction system of the heart once it leaves the AV Node.
a) AV Node located in the subendocardial structure of the heart (transitional zone). It is in the posterior-inferior aspect of the right atrium. Superior, medial and posterior transitional atrionodal bundles converge on the AV Node.
b) Triangle of Koch, bordered by coronary sinus ostium posteriorly, septal tricuspid valve anteriorly, and the t_endon of Todaro superiorly_.
c) AV Node > central fibrous body > annulus fibrosis > bundle of His > Splits
RBB > travels around R ventricle (moderator band)
LBB > expands into broad subendocardial sheet of tissue in L ventricle.
Purkinje fibres emerge from RBB and LBB and ramifies (branches out) on the endocardial surface of the R & L ventricles.
a) Describe the blood supply and innervation to AV Node & bundle branches.
b) Describe in simple terms the cellular make up of the AV Node and conducting system.
a) AV nodal artery and first septal perforator of LAD supply AV Node. Bundle branches have dual supply from septal LAD perforators and branches from PDA.
- AV Node is highly innervated by postganglionic sympathetic and parasympathetic nerves. The bundle of His and distal conducting system are minimally influenced by autonomic tone.
b) AV Node cells are heterogenous with a range of action potential profiles. Fast and slow AV nodal pathways have been described but it is controversial whether these are anatomically distinct or represent two different regions of the AV nodal complex. The His bundle and BB are insulated from ventricular myocardium. The most rapid conduction is observed in these tissues.
a) In what simple way can AV Node disorders be classified?
b) List some possible causes for AV Node dysfunction
c) What infectious, autoimmune and neuromuscular diseases have a particular predilection for the conduction system and may affect the AV Node?
a) May be classified as functional or structural, functional causes are more likely to be reversible. Structural changes e.g. with fibrosis are generally permanent (often associated with normal aging)
b) Use VINDICATE acronym. See table
c) See table
NB: AV block may also occur during valve surgery or as a consequence of catheter ablation.
a) In what percentage of patients with acute MI does AV block develop?
b) How does inferior MI affect the AV node and at what level?
c) How does anterior MI affect the AV node and at what level?
a) 10-15%
b) Level of block tends to be in the AV node with stable, narrow escape rhythms.
c) Level of block at the distal AV nodal complex, His bundle, or bundle branches. Results in wide complex, unstable escape rhythms and worse prognosis with high mortality.
a) How does AV conduction block manifest on ECG?
b) What does the width of the QRS say about the location of the block?
c) Where does Type II second degree (Mobitz II) typically occur in the conduction system?
d) What is it called when there is a series of non-conducted P-waves?
a) Slow conduction on ECG in it’s mildest form and complete failure to conduct intermittently or persistently in it’s more severe form.
b) Narrow QRS suggests delay in AV node or Bundle of His. Wide QRS suggests delay in distal conduction system.
c) Typically in the distal of infra-His conduction system, often assoc with intraventricular conduction delays (e.g. BBB). More likely to proceed to higher grades of AV block.
NB: Mobitz II-Intermittent non-conducted P waves without progressive prolongation of PR interval.
d) Paroxysmal AV block, implies significant conduction disease and is an indication for PPM.
a) What is the primary aim of diagnostic tests for the AV Node and why is this important?
b) How can location of AV Node block be identified and
c) What can be used to do this?
d) Where is the block commonly located in type II second-degree (mobitz II) block?
e) What electrophysiologic testing is available and how does this change the management?
a) Testing is aimed at determining the level of conduction block, particularly in asymptomatic patients. Prognosis and therapy depend on this.
b) Location can be identified through the differences in innervation of AV Node & infranodal conduction system
c) Vagal stimulation and carotid sinus massage slow conduction in the AV Node. Atropine/Isoprenaline, and exercise improve conduction through AV Node and impair inranodal conduction.
e. g patients with CHB and narrow QRS, exercise typically increases HR, in contrast with acquired CHB with wide QRS, does not respond with change to HR.
d) Commonly infranodal in the His-Purkinje system.
e) His bundle electrogram can give more precise info about the location of the block/atrial and ventricular activation. This can be helpful in second degree blocks. With acquired CHB there is little indication as PPM is almost always indicated.
a) When is temporary pacing indicated? What are the causative factors?
b) What are some adjunctive therapies to PM?
c) What are the types of temporary pacing?
a) During acute haemodynamic compromise due to a transient causative factor.
Inferior MI, electrolyte derangement and ishcaemia, inhibition of excessive vagal tone, withholding of drugs with AV Nodal blocking qualities.
b) Atropine or Isoprenaline if block is in AV node.
c) Transcutaneous pacing for minutes/hours (cathode-Anterior & Anode-posterior) & Transvenous pacing for hours/days. Placed in jugular or subclavian and advanced to right ventricle.
a) Why are there no RCTs of pacing in patients with AV block?
b) What are the indications for PM?
c) Do patients who are asymptomatic get a PM?
a) High-grade AV block is potentially lethal.
b) Symptomatic bradycardia and irreversible second or third degree AV block (regardless of cause or level).
c) Therapy is individualised in this group. PM is indicated in aquired CHB with cardiac enlargement; left ventricular dysfunction and waking HR <40. Second degree AV block with wide QRS and intra or infra His block, profound first degree AV block and patients with neuromuscular diseases that have a predilection for the conduction system.
a) Describe the basic mechanism of ACS
b) When is a STEMI likely to develop in coronary vasculature and how does this happen?
c) Describe the factors associated with vascular injury?
d) Describe the cascade of events following vascular injury
a) Disruption of a vulnerable plaque results in a completely of subtotally occlusive thrombus, this may then result in ischaemic chest discomfort.
b) STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury.
c) cigarette smoking, HTN, and lipid accumulation.
d) STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted (exposing its contents to the blood) and conditions (local or systemic) favor thrombogenesis. The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the disrupted plaque. The coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands
a) What are the determinants of MI injury/severity?
b) What are some rare causes of STEMI?
a) -Vulnerable plaque and thrombogenic blood
- Coronary microvasculature dysfunction
- Cardiomyosite swelling, interstitial oedema, tissue inflammation.
b) Coronary emboli, congenital abnormalities, coronary spasm +many others
a) What are the 4 main ECG features of a Premature Ventricular Contraction (PVC)?
b) How are PVCs classified and what are the repeating patterns?
c) What electrolyte abnormalities are a high risk for VT in patients with STEMI? What level should their values be aimed?
a) Broad QRS complex >120ms, premature (e.g. earlier than the next SR is expected), Discordant ST segment and T wave changes (ST segment and T wave changes are directed oposite to the main vector of the QRS complex), usually followed by compensatory pause.
b) Unifocal (single ectopic focus), multifocal (two or more ectopic foci. Patterns include:
Bigeminy-Every other beat is PVC
Trigeminy-Every third beat is PVC
Quadrigeminy-Every fourth beat is PVC
Couplet-two consecutive PVCs
NSVT: 3-30 consecutive PVCs
c) Hypokalaemia and Hypomagnesaemia, aim for ~4.5mmol/L and 2.0mmol/L respectively.
a) What are the two most common complications that occur in survivors of DVT and PE?
b) What are the symptoms associated with the above diagnosis?
a) Chronic thromboembolic pulmonary HTN or Post thrombotic syndrome (aka chronic venous insufficiency)
b) Chronic thromboembolic pulmonary HTN causes breathless esp with exertion. Postthrombotic syndrome ankle/calf swelling and leg aching caused by damage to the venous valves of the leg. In severe cases it can cause skin ulceration.
