Cardiovascular Flashcards
Question: What is cardiac output, and how is it calculated?
Answer: Cardiac output is the product of heart rate and ventricular stroke volume. It is calculated as CO = HR x SV.
Question: What factors determine stroke volume?
Stroke volume is determined by the contractility of the ventricle, preload, and afterload.
What is left ventricular ejection fraction (LVEF), and how is it defined?
LVEF is defined as stroke volume divided by end-diastolic volume. The normal range for LVEF is 50-70%.
What is contractility, and what factors influence it?
Contractility is the intrinsic contractile state of the myocardium. Factors influencing contractility include the number of contractile elements, availability of essential cofactors, and inotropic agents.
How is preload defined clinically, and what determines it?
Preload is defined clinically as the ventricular end-diastolic volume. It is determined by venous return, which depends on venous tone, blood volume, and atrial contraction.
What is the Frank-Starling law, and how does it relate to preload?
The Frank-Starling law states that as ventricular end-diastolic volume increases, there is a progressive increase in the force of ventricular contraction (and stroke volume) up to an optimal end-diastolic volume. Further increases in preload lead to a fall in stroke volume.
Define afterload and its primary determinant.
Afterload is the load (pressure) that the ventricle must overcome before it can eject blood. It is primarily determined by systemic vascular resistance.
What is the jugular venous pressure (JVP), and how is it observed?
The JVP is the indirectly observed pressure of the venous system. It is observed through upward and downward deflections in the jugular vein caused by various cardiac events.
Question: What are the upward deflections observed in JVP?
Answer: Upward deflections in JVP include the A wave (atrial contraction), C wave (ventricular isovolumetric contraction), and V wave (venous filling).
Question: What are the downward deflections observed in JVP?
Answer: Downward deflections in JVP include the X descent (atrial relaxation and tricuspid valve movement downwards) and Y descent (filling of the ventricle after tricuspid valve opening).
Question: How is the JVP interpreted, and what is the normal range?
The JVP is reported in centimeters above the sternal angle, regardless of elevation. The normal range is typically 2-4 cm.
What is the significance of the Kussmaul sign in JVP?
If JVP increases on inspiration (Kussmaul sign), it may indicate conditions like constrictive pericarditis, tamponade, severe right heart failure, or restrictive cardiomyopathy.
Question: How can hepatojugular reflux aid in identifying JVP?
Hepatojugular reflux can help identify JVP by observing the response of JVP when pressure is applied to the liver, which causes a temporary rise in JVP.
Describe the visualization and location of the internal jugular vein.
The internal jugular vein is non-palpable, readily occludable, and fills superiorly. It is found between the sternal and clavicular heads of the sternocleidomastoid muscle, lateral to the carotid artery.
How does JVP change with changes in posture and breathing?
JVP drops when elevated, drops with inspiration, and rises with expiration.
Question: What can an absent ‘a’ wave in jugular venous pressure (JVP) indicate?
An absent ‘a’ wave in JVP is often associated with atrial fibrillation.
What conditions can lead to an enlarged ‘a’ wave in JVP?
Conditions such as tricuspid stenosis, severe pulmonary stenosis, and pulmonary hypertension can cause an enlarged ‘a’ wave in JVP.
Question: When might you observe an enlarged ‘v’ wave in JVP?
An enlarged ‘v’ wave in JVP can be indicative of tricuspid regurgitation.
What are adrenergic receptors, and what neurotransmitters affect them?
Adrenergic receptors are a class of G protein-coupled receptors targeted by adrenaline and noradrenaline.
How are adrenergic receptors classified?
Adrenergic receptors are classified into α receptors (sympathetic), β receptors (sympathetic), and muscarinic receptors (parasympathetic).
What is the function of α1 adrenergic receptors?
α1 adrenergic receptors are responsible for smooth muscle contraction, leading to vasoconstriction, mydriasis (pupil dilation), and contraction of GI and urinary sphincters.
What are the effects mediated by β1 adrenergic receptors?
β1 adrenergic receptors are associated with positive chronotropy (heart rate increase), inotropy (contractility increase), dromotropy (conduction velocity increase), lusitropy (relaxation rate increase), and stimulation of renin release.
What functions are attributed to β2 adrenergic receptors?
β2 adrenergic receptors are responsible for smooth muscle relaxation, leading to bronchodilation, relaxation of GI and urinary sphincters, and minor vasodilation. They also stimulate insulin release.
What are the typical coronary arteries that supply the heart?
The heart is typically supplied by the right and left coronary arteries, which originate from the root of the aorta.
What are the main branches of the right coronary artery (RCA)?
The RCA gives rise to acute marginal branches, atrioventricular nodal artery (60% of the time), and the posterior descending artery (PDA).
What are the main branches of the left main coronary artery (LCA)?
The LCA branches into the left anterior descending artery (LAD), septal branches, and diagonal branches.
What is the main branch of the left circumflex artery (LC)?
The LC runs in the atrioventricular groove and gives rise to obtuse marginal branches.
How is venous blood from the heart drained?
Most venous blood from the heart drains into the right atrium (RA) through the coronary sinus. However, a small amount drains through Thesbian veins into all four chambers.
What is the significance of “dominance of circulation” in coronary arteries?
Dominance of circulation refers to the predominant source of blood supply to the posterior descending artery (PDA).
What does the PR interval signify in an ECG?
The PR interval represents conduction delay through the AV node.
What does the QT interval correspond to in an ECG?
The QT interval represents the mechanical contraction of the ventricles.
What is the T wave in an ECG a representation of?
The T wave represents ventricular repolarization.
Describe the conduction pathway of the heart.
SA node ➔ atria ➔ AV node ➔ common bundle ➔ three bundle branches (left anterior/posterior and right bundle) ➔ Purkinje fibers ➔ ventricles.
What are the criteria for normal, left axis deviation, and right axis deviation in ECG?
Normal: Positive QRS in leads I and aVF (0 to +90 degrees).
Left Axis Deviation: Positive QRS in lead I and negative QRS in lead aVF
Right Axis Deviation: Negative QRS in lead I and positive QRS in lead aVF
What is the “Rule of Fours” in ECG interpretation?
Review history/clinical picture.
Rate, Rhythm, Axis
What are some ECG findings associated with right ventricular infarcts?
ECG findings suggestive of right ventricular infarcts include ST elevation in V1,
What are the ECG findings in hypothermia and hyperkalemia?
In hypothermia, you may observe sinus bradycardia with “J waves” at the J point of the ST segment.
In hyperkalemia, you may notice peaked T waves and a prolonged PR segment, followed by widened QRS complexes, loss of P waves, and potential development of sine waves and ventricular fibrillation/asystole.
What are the common symptoms of Bradyarrhythmias?
Common symptoms of Bradyarrhythmias include signs of reduced cardiac output (such as dyspnea, angina, syncope) and palpitations.
What are the common signs of Bradyarrhythmias?
Common signs of Bradyarrhythmias include bradycardia, hypotension, and heart failure.
What is the typical heart rate range for Bradyarrhythmias?
<60
What is the normal treatment approach for sinus bradycardia?
Sinus bradycardia typically requires no treatment unless caused by offending drugs. If necessary, atropine or a pacemaker may be considered.
What is the primary cause of first-degree AV block?
First-degree AV block can occur in normal individuals and may also result from increased vagal tone or the use of drugs like beta-blockers, calcium channel blockers, digoxin, or amiodarone.
What is the characteristic feature of second-degree AV block (Mobitz 1)?
Second-degree AV block (Mobitz 1) is characterized by progressive PR lengthening until a dropped beat occurs, and then the PR interval resets. Typically, no treatment is required unless it’s due to specific drugs or conditions.
How can you differentiate between Mobitz 1 and Mobitz 2 second-degree AV block?
Mobitz 1 (Wenckebach) displays progressive PR lengthening until a dropped beat occurs, while Mobitz 2 presents with unexpected dropped beats without a change in the PR interval. A pacemaker is typically required for Mobitz 2.
What is third-degree (complete) AV block, and how is it treated?
Third-degree AV block is characterized by the complete failure of conduction of supraventricular impulses to the ventricle, resulting in no P-QRS relationship. It is treated with a pacemaker.
What is sick sinus syndrome, and how is it managed?
Sick sinus syndrome is characterized by intermittent supraventricular tachyarrhythmias and bradyarrhythmias. Bradycardia in sick sinus syndrome is managed with a pacemaker, while tachycardia may be treated with beta-blockers.
What are the common symptoms of Tachyarrhythmias?
Common symptoms of Tachyarrhythmias include signs of reduced cardiac output (such as dyspnea, angina, syncope) and palpitations.
What are the typical heart rate thresholds for defining tachycardia?
> 100
What is the normal treatment approach for sinus tachycardia?
Sinus tachycardia typically requires treatment of the underlying cause. Beta-blockers or calcium channel blockers may be used if indicated.
What are the characteristic features of atrial fibrillation in an ECG?
Atrial fibrillation is characterized by an irregularly irregular rhythm, the absence of P waves, and fibrillatory waves. It can be classified as slow AF (<60 bpm), fast AF (>100 bpm), or normal.
What is the characteristic ECG pattern of atrial flutter?
Atrial flutter shows a “saw-tooth” pattern of flutter waves at an atrial rate of approximately 300 bpm. The ventricular rate depends on the degree of AV conduction block. (300, 150, 75)
What is the typical presentation of multifocal atrial tachycardia (MAT)?
Multifocal atrial tachycardia (MAT) is characterized by an irregularly irregular rhythm with at least three distinctive P wave morphologies. It often occurs in elderly patients with severe COPD or heart failure and should be treated by addressing the underlying cause.
What is the mechanism behind Atrioventricular Nodal Re-entry Tachycardia (AVNRT)?
AVNRT is caused by a re-entry circuit within the AV node involving dual pathways with differing refractory periods. It typically results in narrow-complex tachycardia.
How is AVNRT acutely treated?
Acute treatment of AVNRT may involve vagal maneuvers, Valsalva maneuver, carotid massage, adenosine, or rarely cardioversion.
What is the chronic treatment approach for AVNRT?
Chronic treatment for AVNRT includes beta-blockers or calcium channel blockers. In refractory cases, catheter ablation may be considered.
What is Wolff-Parkinson-White syndrome (WPW)?
WPW is a pre-excitation syndrome caused by an accessory pathway (Bundle of Kent) between the atria and ventricles. It can lead to paroxysmal tachycardia.
How can WPW-related paroxysmal tachycardia be classified, and what ECG features are associated with WPW?
WPW-related paroxysmal tachycardia can be orthodromic (retrograde atrial activity from ventricle) or antidromic (ventricular activity via accessory pathway). WPW is characterized by a wide-complex QRS with a delta wave and an upsloping PR segment.
What is Paroxysmal Atrial Tachycardia?
Paroxysmal Atrial Tachycardia is characterized by a single ectopic atrial pacemaker, resulting in typically narrow-complex tachycardia (unless there is a bundle branch block), with consistently abnormal P waves.
What are Premature Ventricular Contractions (PVCs)?
Premature Ventricular Contractions are ectopic beats originating in the ventricles and are characterized by a premature wide QRS complex, usually followed by a compensatory pause.
How are PVCs typically managed?
Typically, no treatment is required for PVCs unless they are caused by an underlying condition. In such cases, beta-blockers or calcium channel blockers may be used.
What is Ventricular Tachycardia (VT), and what are its characteristics?
Ventricular Tachycardia is a wide complex tachycardia associated with severe cardiac pathology. It can be sustained (lasting >30 seconds) or nonsustained, and can be hemodynamically stable or unstable. VT demonstrates AV dissociation.
How should stable VT be treated?
Stable VT can be treated with medications like amiodarone.
What is Ventricular Fibrillation (VF), and how is it characterized on an ECG?
Ventricular Fibrillation is characterized by a totally erratic wide-complex ECG tracing and is associated with severe cardiac pathology. It is fatal unless Advanced Cardiac Life Support (ACLS) measures are instituted.
What is Torsades de Pointes, and what are its triggers?
Torsades de Pointes is polymorphic ventricular tachycardia that occurs in the context of QT prolongation. It can be triggered by long QT syndrome, QT-prolonging medications, or electrolyte disorders.
How is Torsades de Pointes treated?
Treatment of Torsades de Pointes involves addressing the underlying cause of prolonged QT, administering IV magnesium, increasing heart rate (which shortens QT), temporary overdrive pacing, isoproterenol, and cardioversion if the patient is unstable.
How is Atrial Fibrillation (AF) diagnosed?
Diagnosis of AF is based on clinical symptoms, examination, and confirmation by ECG. Echocardiography is recommended to assess underlying causes and structural abnormalities.
What scoring systems are used to assess thromboembolic risk in AF patients?
CHA2DS2-VASc is used to assess thromboembolic risk, while HAS-BLED is used to assess bleeding risk.
What does CHA2DS2-VASc stand for, and what does it assess?
CHA2DS2-VASc assesses the risk of stroke in AF patients. It includes Congestive heart failure, Hypertension, Age (≥75 years = +2 points, 65-74 years = +1 point), Diabetes mellitus, Stroke/TIA/thromboembolism (+2 points), Vascular disease, Age 65-74 years, and Sex (female).
What is the classification of AF based on its duration?
AF can be classified as newly-detected, paroxysmal (sustained for <7 days), persistent (recurrent AF sustained for >7 days), or permanent (continuous AF >1 year unresponsive to cardioversion).
What are the major objectives of AF treatment (RACE)?
The major objectives of AF treatment are Rate control, Anticoagulation, Correction of underlying etiology, and Electrical Cardioversion when indicated.
How is rate control achieved in AF patients?
Rate control in AF patients is typically achieved using beta-blockers, calcium channel blockers (diltiazem or verapamil, only if LVEF >40%), and sometimes digoxin as an adjunct to beta-blockers in heart failure patients.
What anticoagulation options are available for AF patients?
Anticoagulation options for AF patients include dabigatran, rivaroxaban, and warfarin, with the choice based on the CHA2DS2-VASc score and balancing with the HAS-BLED score.
When is electrical cardioversion considered in AF patients?
Electrical cardioversion is considered in patients with new-onset AF or hemodynamic instability. If AF is present for less than 48 hours, cardioversion can often be done without anticoagulation.
What is the preferred treatment approach for paroxysmal or newly-detected AF?
Rhythm control is favored for paroxysmal or newly-detected AF, particularly in young patients (<65), those with poor symptom control, and certain types of structural heart disease. Medications like amiodarone, sotalol, or flecainide may be used, and in some cases, pulmonary vein ablation or surgery may be considered.
What are the major complications of AF?
The major complications of AF are thromboembolism (such as stroke) and rate-related cardiomyopathy, which can lead to congestive heart failure.
What is the ACLS protocol used for?
The ACLS protocol is primarily used for shockable rhythms (pulseless ventricular tachycardia and ventricular fibrillation)
What are the common reversible causes of pulseless electrical activity (PEA)?
The common reversible causes of PEA are categorized as the 4H’s (Hypoxia, Hypovolemia, Hydrogen ion [acidosis], Hypo/hyperkalemia) and the 4T’s (Tension pneumothorax, Tamponade, Toxins, Thrombosis - pulmonary or coronary).
What is catheter ablation, and what are its indications?
Catheter ablation is the destruction of aberrant cardiac electrical pathways using techniques like radiofrequency ablation or cryotherapy. It is considered in conditions like AVNRT, atrial flutter, atrial fibrillation, and, rarely, ventricular tachycardia.
What is heart failure?
Heart failure is a clinical syndrome characterized by the inability of the heart to pump enough blood to maintain fluid and metabolic homeostasis.
What are the common causes of heart failure?
Common causes of heart failure include hypertension (pressure overload), ischemic heart disease (volume overload), arrhythmias (volume overload), valvular heart disease (pressure or volume overload), and cardiomyopathy (volume overload, except for hypertrophic cardiomyopathy).
How is heart failure classified based on ejection fraction?
Heart failure can be classified into two types based on ejection fraction: Heart Failure with Reduced Ejection Fraction (HFrEF), also known as systolic failure, and Heart Failure with Preserved Ejection Fraction (HFpEF), also known as diastolic failure.
What is the pathophysiology of HFrEF (systolic failure)?
HFrEF is characterized by a failure of contraction, leading to reduced ejection fraction (EF), increased end-diastolic volume (EDV), and increased end-diastolic pressure (EDP).
What is the pathophysiology of HFpEF (diastolic failure)?
HFpEF is characterized by a failure of relaxation, leading to impaired left ventricular (LV) filling, normal EDV, compensatory increased EDP, and normal EF.
What are some common clinical signs of left heart failure?
Common clinical signs of left heart failure include
FORWARD FAILURE: fatigue, hypotension, syncope, cool extremities, slow capillary refill, peripheral cyanosis
BACKWARD CONGESTION: dyspnoea, orthopnoea, PND, pulmonary oedema, basal crepitations, cough, pleural effusion
