Cardiovascular Flashcards
1
Q
Question: What is cardiac output, and how is it calculated?
A
Answer: Cardiac output is the product of heart rate and ventricular stroke volume. It is calculated as CO = HR x SV.
2
Q
Question: What factors determine stroke volume?
A
Stroke volume is determined by the contractility of the ventricle, preload, and afterload.
3
Q
What is left ventricular ejection fraction (LVEF), and how is it defined?
A
LVEF is defined as stroke volume divided by end-diastolic volume. The normal range for LVEF is 50-70%.
4
Q
What is contractility, and what factors influence it?
A
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.
5
Q
How is preload defined clinically, and what determines it?
A
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.
6
Q
What is the Frank-Starling law, and how does it relate to preload?
A
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.
7
Q
Define afterload and its primary determinant.
A
Afterload is the load (pressure) that the ventricle must overcome before it can eject blood. It is primarily determined by systemic vascular resistance.
8
Q
What is the jugular venous pressure (JVP), and how is it observed?
A
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.
9
Q
Question: What are the upward deflections observed in JVP?
A
Answer: Upward deflections in JVP include the A wave (atrial contraction), C wave (ventricular isovolumetric contraction), and V wave (venous filling).
10
Q
Question: What are the downward deflections observed in JVP?
A
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).
11
Q
Question: How is the JVP interpreted, and what is the normal range?
A
The JVP is reported in centimeters above the sternal angle, regardless of elevation. The normal range is typically 2-4 cm.
12
Q
What is the significance of the Kussmaul sign in JVP?
A
If JVP increases on inspiration (Kussmaul sign), it may indicate conditions like constrictive pericarditis, tamponade, severe right heart failure, or restrictive cardiomyopathy.
13
Q
Question: How can hepatojugular reflux aid in identifying JVP?
A
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.
14
Q
Describe the visualization and location of the internal jugular vein.
A
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.
15
Q
How does JVP change with changes in posture and breathing?
A
JVP drops when elevated, drops with inspiration, and rises with expiration.
16
Q
Question: What can an absent ‘a’ wave in jugular venous pressure (JVP) indicate?
A
An absent ‘a’ wave in JVP is often associated with atrial fibrillation.
17
Q
What conditions can lead to an enlarged ‘a’ wave in JVP?
A
Conditions such as tricuspid stenosis, severe pulmonary stenosis, and pulmonary hypertension can cause an enlarged ‘a’ wave in JVP.
18
Q
Question: When might you observe an enlarged ‘v’ wave in JVP?
A
An enlarged ‘v’ wave in JVP can be indicative of tricuspid regurgitation.
19
Q
What are adrenergic receptors, and what neurotransmitters affect them?
A
Adrenergic receptors are a class of G protein-coupled receptors targeted by adrenaline and noradrenaline.
20
Q
How are adrenergic receptors classified?
A
Adrenergic receptors are classified into α receptors (sympathetic), β receptors (sympathetic), and muscarinic receptors (parasympathetic).
21
Q
What is the function of α1 adrenergic receptors?
A
α1 adrenergic receptors are responsible for smooth muscle contraction, leading to vasoconstriction, mydriasis (pupil dilation), and contraction of GI and urinary sphincters.
22
Q
What are the effects mediated by β1 adrenergic receptors?
A
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.
23
Q
What functions are attributed to β2 adrenergic receptors?
A
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.
24
Q
What are the typical coronary arteries that supply the heart?
A
The heart is typically supplied by the right and left coronary arteries, which originate from the root of the aorta.
25
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).
26
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.
27
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.
28
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.
29
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).
30
What does the PR interval signify in an ECG?
The PR interval represents conduction delay through the AV node.
31
What does the QT interval correspond to in an ECG?
The QT interval represents the mechanical contraction of the ventricles.
32
What is the T wave in an ECG a representation of?
The T wave represents ventricular repolarization.
33
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.
34
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
35
What is the "Rule of Fours" in ECG interpretation?
Review history/clinical picture.
Rate, Rhythm, Axis
36
What are some ECG findings associated with right ventricular infarcts?
ECG findings suggestive of right ventricular infarcts include ST elevation in V1,
37
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.
38
What are the common symptoms of Bradyarrhythmias?
Common symptoms of Bradyarrhythmias include signs of reduced cardiac output (such as dyspnea, angina, syncope) and palpitations.
39
What are the common signs of Bradyarrhythmias?
Common signs of Bradyarrhythmias include bradycardia, hypotension, and heart failure.
40
What is the typical heart rate range for Bradyarrhythmias?
<60
41
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.
42
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.
43
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.
44
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.
45
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.
46
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.
47
What are the common symptoms of Tachyarrhythmias?
Common symptoms of Tachyarrhythmias include signs of reduced cardiac output (such as dyspnea, angina, syncope) and palpitations.
48
What are the typical heart rate thresholds for defining tachycardia?
>100
49
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.
50
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.
51
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)
52
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.
53
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.
54
How is AVNRT acutely treated?
Acute treatment of AVNRT may involve vagal maneuvers, Valsalva maneuver, carotid massage, adenosine, or rarely cardioversion.
55
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.
56
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.
57
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.
58
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.
59
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.
60
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.
61
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.
62
How should stable VT be treated?
Stable VT can be treated with medications like amiodarone.
63
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.
64
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.
65
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.
66
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.
67
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.
68
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).
69
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).
70
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.
71
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.
72
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.
73
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.
74
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.
75
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.
76
What is the ACLS protocol used for?
The ACLS protocol is primarily used for shockable rhythms (pulseless ventricular tachycardia and ventricular fibrillation)
77
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).
78
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.
79
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.
80
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).
81
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.
82
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).
83
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.
84
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
85
What are some common clinical signs for RHF?
Forward failure: tricuspid regurg
Backward: peripheral oedema, elevated JVP, hepatomegaly, ascites, pulsatile liver
86
What diagnostic tests are commonly used to evaluate heart failure?
Diagnostic tests for heart failure include laboratory tests (CBC, U&E, LFTs, HbA1c, lipids, TSH, BNP), ECG, chest X-ray (ABCDE criteria), and echocardiography.
87
What is the ABCDE signs of heart failure on CXR?
alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lope vessels
pleural Effusion
88
What is the treatment approach for acute heart failure (pulmonary edema)?
Answer: In acute heart failure with pulmonary edema, the treatment approach is PPPOND: BiPAP or CPAP, Position, vasoPressors, Oxygen, Nitrates, Diuresis, plus VTE prophylaxis.
89
What is the treatment approach for chronic heart failure?
The treatment of chronic heart failure includes lifestyle changes, pharmacologic therapy (beta-blockers, renin-angiotensin-aldosterone blockade, mineralocorticoid receptor antagonists, diuretics, cardiac glycosides, antiarrhythmic drugs), and advanced treatments (ICD, resynchronization therapy, LVAD, cardiac transplantation).
90
What is the treatment approach for chronic heart failure?
The treatment of chronic heart failure includes lifestyle changes, beta-blockers, renin-angiotensin-aldosterone blockade, mineralocorticoid (aldosterone) receptor antagonists
For some patients (but do not improve mortality):
diuretics, cardiac glycosides (digoxin), antiarrhythmic drugs if AF),
Advanced treatments (ICD, resynchronization therapy, LVAD, cardiac transplantation).
91
What is the NYHA functional classification for heart failure, and how is it used?
The NYHA functional classification stratifies heart failure patients based on their functional limitations: Class I (no symptoms) to Class IV (symptoms at rest). It helps estimate prognosis and guide treatment decisions.
92
What are some common complications of heart failure?
Common complications of heart failure include arrhythmias (e.g., atrial fibrillation), sleep-disordered breathing, systemic embolic phenomena (including stroke), and sudden cardiac death.
93
What are the major risk factors for IHD?
Major risk factors for IHD include diabetes mellitus, smoking, hypertension, dyslipidemia, and a family history of the disease.
94
What are the minor risk factors for IHD?
Minor risk factors for IHD include obesity, older age, being male (or post-menopausal female), heavy alcohol intake, and a sedentary lifestyle.
95
How is Angina Pectoris defined?
Angina Pectoris, or stable angina, is defined as substernal chest pain resulting from myocardial ischemia, typically lasting less than 20 minutes.
95
What is the classic triad of symptoms in Angina Pectoris?
The classic triad of symptoms in Angina Pectoris includes brief (<20 minutes) substernal chest pain (dull/pressure-like), precipitated by stress/exertion, and relieved by rest/nitrates.
95
What are some common associated symptoms with Angina Pectoris?
Angina Pectoris may be associated with symptoms like shortness of breath, nausea/vomiting, sweating, or light-headedness. In rare cases, it may occur when lying down at night, known as angina decubitus.
95
How is Angina Pectoris diagnosed?
Angina Pectoris is primarily diagnosed clinically, but other causes of chest pain (e.g., acute coronary syndrome, pericarditis, aortic dissection) must be ruled out. Diagnostic tools include ECG, stress testing, CXR, and lab tests like CBC, lipids, and glucose.
96
What is the initial treatment for Angina Pectoris during an episode?
Sublingual GTN (nitroglycerin) is used for immediate pain relief during an angina episode.
97
What is the recommended order of medications for angina prophylaxis?
The recommended order for angina prophylaxis medications is β-blocker (e.g., metoprolol), followed by calcium channel blocker (e.g., diltiazem), and then long-acting nitrate (e.g., isosorbide mononitrate).
98
Which medications have an impact on reducing mortality in Angina Pectoris?
Among the medications used for Angina Pectoris, only aspirin and β-blockers have an impact on reducing mortality.
99
What is Prinzmetal's (variant) angina?
Prinzmetal's angina mimics angina pectoris but is caused by vasospasm of coronary vessels. It typically affects young women at rest, early in the morning, and is associated with ST-elevation in the absence of cardiac enzyme rise. It can be treated with GTN and calcium channel blockers (e.g., diltiazem).
100
What is the spectrum of clinical syndromes encompassed by Acute Coronary Syndrome (ACS)?
It comprises stable angina, unstable angina, myocardial infarction, and sudden cardiac death.
101
How is Myocardial Infarction (MI) defined and diagnosed?
Myocardial Infarction (MI) is defined by evidence of myocardial necrosis and diagnosed by a rise/fall of serum cardiac markers (e.g., troponins or CK-MB), plus at least one of the following: symptoms of ischemia (chest discomfort, dyspnea), ECG changes (ST changes, new BBB, pathological Q waves), or imaging evidence.
102
What clinical criteria define Unstable Angina?
Unstable Angina is clinically defined by any of the following: new-onset angina, angina at rest, an accelerating pattern of pain (increased frequency/duration or decreased threshold/response to treatment), or angina post-MI or post-procedure. It signals the presence of possible impending infarction due to plaque instability.
103
What is NSTEMI, and how is it different from Unstable Angina?
NSTEMI (Non-ST-Elevation Myocardial Infarction) is defined as myocardial infarction without ST-elevation or new BBB.
104
What is STEMI, and how is it diagnosed?
STEMI (ST-Elevation Myocardial Infarction) is defined as myocardial infarction with ST-elevation or new BBB on the ECG. It is diagnosed based on clinical presentation, ECG changes (ST-elevation), and elevated cardiac markers (troponins or CK-MB).
105
What are the clinical presentations of ACS?
ACS typically presents with acute-onset substernal chest pain, often described as pressure or tightness, which may radiate to the left arm, neck, or jaw. Associated symptoms include nausea/vomiting, dyspnea, diaphoresis, palpitations, light-headedness, syncope, anxiety, and signs such as tachycardia, blood pressure changes, signs of heart failure, and more.
106
What are some atypical presentations of ACS?
Atypical presentations of ACS can occur, especially in the elderly and diabetics, and may include syncope, pulmonary edema, epigastric pain, vomiting, hypotension, oliguria, confusion, stroke, and hyperglycemia. Some patients may not report chest pain.
107
What is the initial treatment for all patients with suspected ACS?
Initial treatment for all patients with suspected ACS includes:
Basic first aid
ECGs
IV access + bloods (troponin, CBC, coag, U+E, Mg, glucose, lipids)
Administering 300mg aspirin orally. (STOP NSAIDS)
Sublingual GTN (nitroglycerin) for chest pain, hypertension, or heart failure. - CAUTION HYPOTENSION
Morphine or fentanyl for pain and anxiety if needed.
Supplemental oxygen only if O2 saturation is below 90%.
108
What are the life-threatening conditions that should always be considered in the differential diagnosis of chest pain?
Aortic dissection, pulmonary embolism, and tension pneumothorax.
109
What are the treatment guidelines for patients with unstable angina or NSTEMI?
P2Y inhibition: ticagrelor or clopidogrel (in addition to aspirin)
Treatment with invasive therapy (determined by risk stratification and within 72 hours of first medical contact)
IV UFH or LMWH for anticoagulation
Treatment with non-invasive therapy includes SC LMWH.
110
What are the treatment guidelines for patients with STEMI?
P2Y inhibition: ticagrelor or clopidogrel (in addition to aspirin)
Treatment with PCI (preferred if within 12 hours of symptom onset and performed within <90 minutes of first medical contact)
IV UFH or LMWH for anticoagulation
Transfer to CCU for 24-48 hours post-PCI
Treatment with fibrinolysis (performed within 12 hours of symptom onset and no active internal bleeding or history of stroke) includes immediate transfer for angiography or PCI within 24 hours.
111
What is the long-term management of ACS (Acute Coronary Syndrome)?
Low-dose aspirin (100-150mg/day) indefinitely (clopidogrel if contraindicated)
Dual antiplatelet therapy (clopidogrel or ticagrelor) for 12 months or more
High-dose statin early and indefinitely (irrespective of cholesterol levels)
β-blockers early and indefinitely (unless heart failure or cardiogenic shock)
ACEIs should be considered in all patients (unless contraindicated)
Perform repeat echocardiography, angiography, ECG, or stress test if indicated
Automatic two-week stand-down from driving.
112
When is fibrinolysis considered in STEMI treatment, and what should follow?
Fibrinolysis is considered within 12 hours of symptom onset, followed by immediate transfer for angiography or PCI within 24 hours.
113
What is the definition of sudden cardiac death?
Sudden cardiac death is unanticipated, non-traumatic cardiac death in a stable patient that occurs within 1 hour of symptom onset. It is most commonly due to ventricular fibrillation or other ventricular arrhythmias.
114
What are some common causes or etiologies of sudden cardiac death?
Primary cardiac pathology
Myocardial infarction
Severe left ventricular dysfunction
Severe ventricular hypertrophy (e.g., HOCM or AS)
Congenital heart disease
Channelopathies (e.g., long QT syndrome)
115
116
What are the two main classifications of coronary revascularization procedures, and how do they differ?
Percutaneous coronary intervention (PCI), which includes balloon angioplasty and intracoronary stenting. It can be performed more rapidly than coronary artery bypass graft surgery (CABG).
CABG, or coronary artery bypass graft surgery, is indicated in cases of severe left main disease, triple vessel disease, or diffuse disease (e.g., severe diabetes mellitus).
117
What are the graft options for CABG, and which is considered first-line?
Graft options for CABG include the left internal thoracic/mammary artery (considered first-line due to excellent patency) and saphenous vein grafts (used when arterial grafts are not available or multiple grafts are required).
118
What is the general outcome comparison between PCI and CABG, and what advantage does CABG offer?
PCI and CABG have similar outcomes, although CABG is associated with a decreased need for repeat revascularization procedures.
119
What causes rheumatic fever, and how does it relate to Lancefield group A β-haemolytic streptococci?
Rheumatic fever is caused by pharyngeal infection with GAS (Group A Streptococcus) and occurs weeks later.
120
What's the pathophysiology of rheumatic fever?
Antibodies to GAS cross-react with cardiac tissue (antigen mimicry), causing damage.
Acute: carditis, pericarditis, valvulitis, arrhythmia.
Chronic: valvular heart disease, infectious endocarditis, thromboembolism.
121
Who's most affected by rheumatic fever, and the common age group?
Most common in ages 5-15, with higher prevalence in Pacific, Maori, and certain ethnic groups.
122
What are the major and minor signs/symptoms for diagnosing acute rheumatic fever, and the acronym for major signs?
Major (J♥NES): Joints, Carditis, Nodules, Erythema marginatum, Sydenham chorea.
Minor: Fever, Raised ESR/CRP, Arthralgia, Prolonged PR interval, Previous rheumatic fever.
123
How's rheumatic fever diagnosed (Revised Jones Criteria), and what confirms a previous streptococcal infection?
Diagnosis: One major criterion plus one other major or two minor criteria. Evidence: GAS pharyngitis culture, anti-streptolysin O titre, clinical history.
124
What's the treatment for acute rheumatic fever?
Admission, notifiable illness. Oral penicillin V initially, then IM benzathine penicillin. NSAIDs for arthritis. Prednisone for severe carditis.
125
What's the secondary prophylaxis for rheumatic fever, and how long is it administered?
IM benzathine penicillin every 28 days for a minimum of 10 years or until age 21. PO penicillin V for compliance issues.
126
What is myocarditis?
Myocarditis is an inflammatory process involving the myocardium, which is a significant cause of dilated cardiomyopathy.
127
What are the common causes (etiology) of myocarditis?
Idiopathic
Infectious (especially Coxsackie B virus)
Toxic (e.g., catecholamines, chemotherapy, cocaine)
Systemic diseases (e.g., rheumatic fever, giant cell myocarditis)
128
What are the typical clinical symptoms of myocarditis?
Myocarditis typically follows a minor feverish illness and presents with non-specific constitutional or cardiac symptoms such as acute congestive heart failure, chest pain, arrhythmia, and syncope.
129
How is myocarditis diagnosed?
Diagnosis is often by exclusion. Diagnostic tests may include troponin levels, non-specific ECG findings, and echocardiography to assess ventricular function. Myocardial biopsy can provide a definitive diagnosis but is rarely performed unless the condition is severe.
130
What is the treatment approach for myocarditis?
Treatment includes supportive care to manage complications, activity restriction (reducing exercise until cardiac biomarkers improve), avoiding exacerbating factors such as NSAIDs and alcohol, and considering anticoagulation when appropriate.
131
What is cardiomyopathy?
Cardiomyopathy is primary myocardial disease not due to congenital, hypertensive, coronary, valvular, or pericardial disease.
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What characterizes dilated cardiomyopathy?
Dilated cardiomyopathy is unexplained dilation and impaired systolic function in one or both ventricles.
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What are some potential causes of dilated cardiomyopathy?
Idiopathic, Myocarditis, toxins (e.g., alcohol or cocaine), drugs (e.g., steroids or chemotherapy), collagen vascular disease, and thiamine deficiency
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What is the clinical presentation of dilated cardiomyopathy?
May present as congestive heart failure (CHF) with reduced ejection fraction (EF), arrhythmia, systemic or pulmonary emboli, or sudden death.
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How is dilated cardiomyopathy diagnosed?
Labs: High BNP, creatinine, LFTs; Low bicarbonate, sodium. CXR shows global cardiomegaly and CHF signs. Echocardiography is diagnostic.
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What is the treatment for dilated cardiomyopathy?
Treat underlying cause, treat heart failure, and consider anticoagulation.
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What is the prognosis for dilated cardiomyopathy?
Poor prognosis, often leading to death due to CHF or sudden cardiac death (SCD).
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What characterizes hypertrophic cardiomyopathy?
Hypertrophic cardiomyopathy is unexplained ventricular hypertrophy, often due to a genetic defect involving cardiac sarcomere proteins.
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What are the clinical signs and symptoms of hypertrophic cardiomyopathy?
Typically asymptomatic or presents with symptoms of left ventricular outflow obstruction. Clinical signs include high volume jerky pulse, pulsus bisferiens, heaving apex, and a systolic murmur.
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How is hypertrophic cardiomyopathy diagnosed?
ECG shows evidence of left ventricular hypertrophy (LVH). Echocardiography is diagnostic. Screening involves resting ECG and echocardiography.
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What is the treatment for hypertrophic cardiomyopathy?
Avoid competitive sports.
For obstructive HCM, use β-blockers or calcium channel blockers. Avoid nitrates, diuretics, and ACE inhibitors. Surgery (myectomy or alcohol septal ablation) may be needed. Consider an ICD for high-risk cases.
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What characterizes restrictive cardiomyopathy?
Restrictive cardiomyopathy involves impaired ventricular filling with preserved EF in a non-dilated, non-hypertrophied ventricle due to factors decreasing myocardial compliance.
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How is restrictive cardiomyopathy diagnosed?
Echocardiography is diagnostic.
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What drug do we use to thrombolyse if PCI cannot be done within 90 mins
Tenecteplase
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What is the most common form of cardiac tumor?
Myxoma, accounting for over 50% of cardiac tumors.
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In which heart chamber does myxoma most commonly occur?
Approximately 75% of myxomas occur in the left atrium.
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Is myxoma typically benign or malignant?
Myxoma is a benign tumor (approximately 80% of cardiac primary tumors are benign).
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What is the classical clinical presentation of myxoma?
The classical triad includes heart failure, embolic disease (increasing thromboembolism risk), and constitutional symptoms.
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How does the murmur of a myxoma typically present?
It may mimic mitral stenosis, with loudness and location varying with body position.
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What other conditions or symptoms are associated with myxoma?
Atrial fibrillation, clubbing, and Raynaud syndrome.
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What is the treatment for myxoma?
Surgical excision.
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What are some complications or conditions associated with hypertension?
Hypertension is a risk factor for ischemic heart disease (IHD), congestive heart failure (CHF), cardiovascular disease (CVD), chronic kidney disease (CKD), and peripheral vascular disease (PVD).
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What percentage of hypertension cases are considered primary (no identifiable cause)?
Approximately 95% of hypertension cases are primary, likely due to genetic and lifestyle factors, including impaired sodium handling.
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What are some potential causes of secondary hypertension?
Secondary hypertension causes include renal disease (renovascular hypertension or renal parenchymal hypertension), Cushing's syndrome, hyperaldosteronism, aortic coarctation, certain drugs (e.g., OCP, steroids), renal artery stenosis, and pheochromocytoma.
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What are the blood pressure classification stages for hypertension?
Stage 1 (mild): >140/90mmHg
Stage 2 (moderate): >160/100mmHg
Stage 3 (severe): >180/110mmHg
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What diagnostic tests are commonly used for hypertensive patients?
Tests include ambulatory monitoring, resting ECG, echocardiography, U&E, HbA1c, lipids, urinalysis with ACR, fundoscopy, and specific tests based on suspected causes.
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What are the treatment goals for hypertension?
Blood pressure goals are <140/90mmHg or <130/80mmHg if the patient has comorbidity (e.g., diabetes, IHD, CVD).
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What is the first-line approach to treating hypertension?
Lifestyle modifications, including reducing salt intake, increasing exercise, limiting alcohol, quitting smoking, and weight management.
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What medications are commonly used to treat hypertension, and when are they prescribed?
Prescribing depends on age. If <55yo, ACEI or CCB may be used. If >55yo, CCB or ACEI. Thiazide diuretics are added if needed.
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What should be considered in cases of resistant hypertension?
Consider adding mineralocorticoid receptor antagonists (MRA), alpha-blockers, or beta-blockers. Reassess for secondary causes and consider referral.
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What defines a hypertensive emergency?
A hypertensive emergency (hypertensive crisis) is hypertension with acute end-organ damage, typically with a blood pressure >220/120mmHg.
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What are some clinical presentations of hypertensive emergencies?
Hypertensive emergencies may present with headache, visual disturbances, or confusion (hypertensive encephalopathy). Fundoscopy may reveal papilloedema and bilateral retinal hemorrhages.
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What conditions are associated with hypertensive emergencies?
Hypertensive emergencies are associated with malignant hypertension, cerebrovascular complications (encephalopathy or stroke), cardiac issues (aortic dissection, myocardial infarction, or heart failure), and renal complications (acute kidney injury).
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How are hypertensive emergencies typically treated?
IV anti-hypertensives are administered, aiming for slow control over one to two hours.
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What is pericarditis, and how can it affect the heart?
Pericarditis is inflammation of the pericardial sac, which can compromise cardiac output through conditions like tamponade or constrictive pericarditis.
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What are some common causes of pericarditis?
Common causes of pericarditis include idiopathic (presumed viral), viral infections (especially Coxsackie B virus), uraemia, drugs, neoplasms, radiation, trauma, aortic dissection, and it can also occur after a myocardial infarction (MI) or open-heart surgery.
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What is the diagnostic triad associated with pericarditis?What is the diagnostic triad associated with pericarditis?
The diagnostic triad for pericarditis consists of pleuritic chest pain, a pericardial rub, and characteristic ECG changes.
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What are the typical ECG changes seen in pericarditis?
Typical ECG changes in pericarditis include widespread concave ST elevation, PR depression, and sometimes reciprocal changes in aVR, with or without V1. Sinus tachycardia is also common.
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How is pericarditis diagnosed, and what initial tests are conducted?
Pericarditis is diagnosed through initial tests like chest X-ray (CXR), ECG, and echocardiogram to exclude acute coronary syndrome (ACS) or pneumonia. Echocardiography helps identify pericardial effusion or thickening.
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What is the treatment for pericarditis?
Treatment for pericarditis involves addressing the underlying cause or relieving symptoms. It may include activity restriction, aspirin for post-MI pericarditis, NSAIDs for viral pericarditis, and pericardiocentesis for pericardial effusion if it causes tamponade.
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What complications can arise from pericarditis?
Complications of pericarditis may include recurrent episodes of pericarditis, pericardial effusion, cardiac tamponade, constrictive pericarditis, and atrial arrhythmias.
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What is constrictive pericarditis, and what causes it?
Constrictive pericarditis results from a fibrosed, thickened, adherent, and/or calcified pericardium, often due to recurrent acute pericarditis.
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What are the clinical presentations of constrictive pericarditis, and how can it be mistaken for another condition?
Constrictive pericarditis may mimic congestive heart failure (CHF), especially right-sided heart failure (HF). It is also difficult to differentiate from cardiac tamponade. In some cases, a pericardial knock may be heard, resembling S3 but occurring earlier and louder.How is constrictive pericarditis diagnosed, and what diagnostic tools are used?
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How is constrictive pericarditis diagnosed, and what diagnostic tools are used?
Constrictive pericarditis is diagnosed using imaging techniques such as echocardiography, CT scan, or MRI, which can reveal pericardial thickening. However, cardiac catheterization is considered the definitive diagnostic tool.
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What are the treatment options for constrictive pericarditis?
The treatment for constrictive pericarditis can be medical or surgical. Medical treatment includes the use of diuretics and sodium/water restriction to manage symptoms. In refractory cases, surgical intervention may be required in the form of pericardiectomy.
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What is cardiac tamponade, and what are its common causes?
Cardiac tamponade is a clinical diagnosis resulting from a rapidly accumulating pericardial effusion. It can be caused by pericarditis (especially trauma, malignancy, uraemia, and aortic dissection).
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What is the pathophysiology of cardiac tamponade, and how does it affect the heart?
Cardiac tamponade leads to high intra-pericardial pressure, which reduces venous return, ventricular filling, cardiac output, and can result in hypotension and venous congestion.
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What are the clinical presentations of cardiac tamponade, and what is Beck's triad?
Cardiac tamponade may mimic congestive heart failure (CHF), especially right-sided HF, and cardiogenic shock. Beck's triad includes hypotension, increased jugular venous pressure (JVP), and muffled heart sounds. Other signs may include tachycardia, pulsus paradoxus, and Kussmaul sign.
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How is cardiac tamponade diagnosed, and what diagnostic tools are used?
ECG: Look for electrical alternans, which is a pathognomonic variation in R wave amplitude.
Echo: Identify pericardial effusion with compression of cardiac chambers (especially right atrium and right ventricle) during diastole.
CXR: Observe an enlarged heart shadow without pulmonary edema.
Cardiac catheterization may be used for confirmation.
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hat are the treatment options for cardiac tamponade?
Treatment for cardiac tamponade involves addressing the underlying cause, echo-guided pericardiocentesis to drain the effusion, and intravenous fluids to increase cardiac output. Diuretics and vasodilators should be avoided, as they can reduce venous return and preload, further decreasing cardiac output.
181
What are the common causes of aortic stenosis?
Common causes of aortic stenosis include calcification in the elderly, aortic sclerosis (senile valve degeneration), congenital factors (such as bicuspid and unicuspid valves), and rheumatic heart disease.
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What is the pathophysiology of aortic stenosis, and how does it affect the heart?
Aortic stenosis leads to outflow obstruction, increasing end-diastolic pressure (EDP), causing concentric left ventricular hypertrophy (LVH), LV failure, myocardial ischemia, and eventually heart faWhat are the clinical presentations of aortic stenosis?ilure.
183
What are the clinical presentations of aortic stenosis?
Aortic stenosis is initially asymptomatic but can progress to symptoms of outflow obstruction, including angina, syncope, and heart failure, whicWhat diagnostic investigations can help diagnose aortic stenosis?h worsen the prognosis.
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What diagnostic investigations can help diagnose aortic stenosis?
Diagnostic investigations for aortic stenosis include echocardiography , ECG and CXR
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What physical examination findings are associated with aortic stenosis?
Physical examination findings for aortic stenosis include a harsh systolic ejection murmur with a crescendo-decrescendo pattern, sometimes accompanied by an aortic ejection click.
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What are the treatment options for aortic stenosis?
he treatment for aortic stenosis depends on the symptoms:
Asymptomatic: Serial echocardiography and avoidance of exertion.
Symptomatic: Aortic valve replacement (before left ventricular dysfunction occurs).
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What are the common causes of aortic regurgitation?
Aortic regurgitation can be caused by various factors, including acute conditions like infective endocarditis, aortic dissection, and trauma, as well as chronic conditions such as congenital issues (e.g., bicuspid valve), rheumatic heart disease, infective endocarditis, and connective tissue disorders like Marfan's syndrome.
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What is the pathophysiology of aortic regurgitation, and how does it affect the heart?
Aortic regurgitation results in regurgitation of blood into the left ventricle during diastole, leading to volume overload, left ventricular (LV) dilation
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What are the physical examination findings associated with aortic regurgitation?
Physical examination findings for aortic regurgitation include an early diastolic decrescendo murmur ("blowing" sound), which is best heard when the patient is sitting forward. Other signs include a widened pulse pressure, water-hammer pulse,
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What are the treatment options for aortic regurgitation?
The treatment for aortic regurgitation depends on symptoms:
Asymptomatic: Serial echocardiography and afterload reduction (e.g., ACEIs or CCBs).
Symptomatic: Avoid exertion and consider aortic valve replacement if the regurgitation is severe.
191
What is the typical cause of mitral stenosis?
Mitral stenosis is typically caused by rheumatic fever.
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What is the pathophysiology of mitral stenosis, and how does it affect the heart?
Mitral stenosis leads to a fixed cardiac output, left atrial enlargement (LAE), increased left atrial pressure (LAP), pulmonary hypertension, and congestive heart failure (CHF).
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What are the clinical presentations of mitral stenosis?
Clinical presentations of mitral stenosis include signs of both left and right heart failure, infective endocarditis, atrial arrhythmias (with potential emboli), and in severe cases, a "mitral facies" characterized by malar flush and central cyanosis.
194
What are the physical examination findings associated with mitral stenosis?
Physical examination findings for mitral stenosis include a late low-pitched diastolic murmur with an opening snap, an irregularly irregular pulse (often due to atrial fibrillation), a palpable diastolic thrill at the apex, a left parasternal heave, and "mitral facies" (central cyanosis and malar flush) in severe cases.
195
What are the treatment options for mitral stenosis?
reatment for mitral stenosis includes supportive measures such as serial echocardiography, avoiding exertion, treating atrial fibrillation and congestive heart failure, and preventing recurrent rheumatic fever. To increase diastolic filling time, beta-blockers or digoxin may be used. In severe cases, surgical options such as mitral balloon valvotomy or valve replacement may be considered.
196
What is the significance of S3 (ventricular gallop)?
S3 is typically a normal finding in young patients, trained athletes, and during pregnancy. However, it becomes abnormal when associated with ventricular dilation, such as in systolic heart failure.
197
What is the significance of S4 (atrial gallop)?
S4 is almost always abnormal and is associated with a low-compliance ventricle. It can be heard in conditions like aortic or pulmonary stenosis, pulmonary hypertension, or hypertrophic obstructive cardiomyopathy (HOCM). Importantly, S4 is never heard in the presence of atrial fibrillation (AF) since it requires atrial contraction.
198
What is infectious endocarditis, and what parts of the heart does it commonly affect?
Infective endocarditis is an infection of the endocardium, often affecting the heart valves, especially the mitral valve. It typically occurs on already abnormal heart valves.
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How is infectious endocarditis classified, and what are some key classifications?
Infective endocarditis can be classified based on several factors:
Acute vs. subacute onset
Native vs. prosthetic valve involvement
Right vs. left-sided heart involvement
200
What are the risk factors for infectious endocarditis?
Risk factors for infectious endocarditis include rheumatic, congenital, or valvular heart disease, prior endocarditis, prosthetic heart valves, IV drug abuse, immunosuppression, and opportunities for bacteremia
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What are the common clinical presentations and signs/symptoms of infectious endocarditis?
"FROM JANE":
Fever
Roth spots (eye hemorrhages with a white center)
Osler nodes (painful, red, raised lesions on hands and feet)
Murmur
Janeway lesions (non-tender erythematous macules on palms and soles)
Anaemia (normochromic normocytic)
Nail hemorrhage
Emboli
Constitutional symptoms like fever, weight loss, and fatigue are also common, along with clubbing and splenomegaly. A fever and new murmur should raise suspicion for endocarditis.
202
What are the major criteria of the Duke criteria for diagnosing infectious endocarditis?
The major criteria of the Duke criteria include:
Positive blood cultures for infective endocarditis, with at least two separate cultures for typical organisms or persistent bacteremia with any organism (blood drawn more than 12 hours apart).
Evidence of endocardial involvement, such as a positive echocardiogram for infective endocarditis or the presence of a new valvular regurgitation (murmur).
203
What are the minor criteria of the Duke criteria for diagnosing infectious endocarditis?
(Need 0, 3 or 5)
Positive predisposing risk factors.
Fever.
Vascular phenomena like septic emboli, septic pulmonary infarcts/abscess, mycotic aneurysms, or Janeway lesions.
Immunologic phenomena such as glomerulonephritis, Osler nodes, or Roth spots.
Microbiologic evidence that does not meet the major criteria.
204
What is the initial treatment for infective endocarditis?
Start with empiric IV antibiotics (usually vancomycin + gentamicin) and adjust once the pathogen is identified.
205
When is acute valve replacement considered in infective endocarditis?
Consider acute valve replacement if there's refractory congestive heart failure or severe complications.
206
When is lifelong antibiotic prophylaxis needed for infective endocarditis prevention?
Lifelong prophylaxis may be needed in individuals with significant cardiac defects or those undergoing high-risk dental or tonsillectomy procedures.
207
What are the mortality rates for infective endocarditis based on different factors?
Mortality rates vary: Prosthetic valve (25-50%), non-IVDU S. aureus (30-45%), IVDU S. aureus or streptococcal (10-15%).
