Cardio 21-25 Flashcards
1
Q
- What is atrial fibrillation?
A
Atrial fibrillation is an irregular and often rapid heart rate that can increase the risk of strokes, heart failure, and other heart-related complications. During AF, the atria beat irregularly and out of coordination with the ventricles, leading to quivering.
2
Q
What is the primary pathologic change in atrial fibrillation?
A
The primary pathologic change in atrial fibrillation is progressive fibrosis of the atria, primarily due to atrial dilation. This may be influenced by genetic factors and inflammation.
3
Q
What are some common causes of atrial fibrillation?
A
Common causes include:
Valvular diseases (mitral stenosis, mitral regurgitation)
Hypertension
Congestive heart failure
Viral infections
4
Q
How does atrial dilation contribute to atrial fibrillation?
A
Atrial dilation increases stress on cardiomyocytes, leading to tissue heterogeneity where cells develop different properties, causing unpredictable conduction in the atria.
5
Q
What are the types of atrial fibrillation?
A
Paroxysmal AF: Comes and goes (< 1 week), self-terminating. Diagnosed by Holter monitoring.
Persistent AF: Repeated paroxysmal AF (> 1 week), not self-terminating.
Permanent AF: Lasts over 1 year and cannot be terminated. Diagnosed by ECG.
6
Q
What are the common symptoms of atrial fibrillation?
A
Symptoms include:
Heart palpitations
Shortness of breath
Weakness
Fatigue
Dizziness
Chest pain
7
Q
What is the most serious consequence of atrial fibrillation?
A
The most serious consequence of atrial fibrillation is thrombus formation due to stasis in the atria, leading to embolization, particularly to the cerebral circulation, which can result in ischemic stroke.
8
Q
What scoring systems are used to assess thromboembolic risk in atrial fibrillation?
A
The CHADS2 score and its updated version, the CHA2DS2-VASc score, are used to estimate the risk of stroke in patients with non-rheumatic atrial fibrillation.
9
Q
How is the CHADS2 and CHA2DS2-VASc score utilized?
A
These scores help determine whether treatment with anticoagulation therapy or antiplatelet therapy is required. A high score indicates a greater risk of stroke, while a low score indicates a lower risk.
10
Q
CHADS2
A
11
Q
CHA2DS2-VASc
A
12
Q
What is Buerger’s disease?
A
Buerger’s disease, also known as Thromboangiitis obliterans, is a recurring progressive inflammation and thrombosis of medium arteries and veins of the hands and feet. It is strongly associated with tobacco use, primarily from smoking.
13
Q
Who is most commonly affected by Buerger’s disease?
A
Buerger’s disease typically occurs in young males (under 40 years old) who are heavy cigarette smokers.
14
Q
What are the clinical manifestations of Buerger’s disease?
A
Clinical manifestations include:
Severe circulatory insufficiency in distal extremities
Raynaud’s phenomenon
Potential need for amputation if there is gangrene.
15
Q
What is the primary treatment for Buerger’s disease?
A
The primary treatment for Buerger’s disease is smoking cessation.
16
Q
What is vasculitis?
A
Vasculitis is a group of disorders characterized by inflammation that destroys blood vessels, affecting both arteries and veins, often due to autoimmune disorders that damage the endothelium.
17
Q
What are general symptoms of vasculitis?
A
General symptoms include:
Fever
Weight loss
Fatigue
18
Q
What are the mechanisms of systemic vasculitis?
A
Immune complex deposition: e.g., Polyarteritis nodosa (PAN), Henoch-Schönlein purpura
Autoantibodies (ANCA): e.g., Wegener’s granulomatosis, Microscopic polyangiitis, Churg-Strauss syndrome
T-cell mediated (CD4+ T cells): e.g., Takayasu arteritis, Giant cell arteritis
19
Q
What are the types of great vessel vasculitis?
A
The main types of great vessel vasculitis include:
Giant cell arteritis (temporal arteritis)
Takayasu arteritis
20
Q
What treatment options are available for vasculitis?
A
Treatment options include:
Corticosteroids (e.g., prednisone)
Aspirin
Methotrexate
Cyclophosphamide
IL-6 inhibitors (e.g., tocilizumab)
Revascularization when needed
21
Q
What is the role of corticosteroids in treating vasculitis?
A
Corticosteroids are used to reduce inflammation and suppress the immune response in various forms of vasculitis.
22
Q
When is revascularization needed in the treatment of vasculitis?
A
Revascularization may be necessary in cases where there is significant vascular obstruction leading to ischemia or gangrene, especially in conditions like Buerger’s disease or severe cases of Takayasu arteritis.
23
Q
What are the two major types of large vessel vasculitis?
A
The two major types of large vessel vasculitis are:
Giant Cell Arteritis (Temporal Arteritis)
Takayasu Arteritis
24
Q
Who is most commonly affected by Giant Cell Arteritis?
A
Giant Cell Arteritis typically affects older individuals, particularly those over the age of 50.
25
Which arteries are most frequently involved in Giant Cell Arteritis?
The most frequently affected arteries are:
External carotid artery
Ophthalmic artery
Temporal artery
26
What is the suspected underlying cause of Giant Cell Arteritis?
The underlying cause is unknown, but it may be related to helper T-cell activation.
27
What are the key symptoms of Giant Cell Arteritis?
Key symptoms include:
Headache
Jaw claudication (pain in jaw when chewing)
Scalp tenderness
Visual abnormalities
Fever
28
How is Giant Cell Arteritis diagnosed?
Diagnosis involves:
Elevated CRP (C-reactive protein) and ESR (erythrocyte sedimentation rate)
Biopsy: Removing a small section of the affected artery to examine for giant cells infiltrating the tissue, specifically in the internal elastic lamina.
A long section is needed due to the segmental nature of the disease.
29
What is the main treatment for Giant Cell Arteritis?
The main treatment includes:
High-dose corticosteroids (e.g., prednisone)
Aspirin (100 mg)
Methotrexate
Anti-TNF therapy (e.g., infliximab)
30
Who is most commonly affected by Takayasu Arteritis?
Takayasu Arteritis primarily affects younger individuals, particularly women under 50, and is more common in Asian populations.
31
What is the pathophysiology of Takayasu Arteritis?
Takayasu Arteritis is a form of large vessel granulomatous vasculitis characterized by massive intimal fibrosis and vascular narrowing, mainly affecting the aorta and its branches, as well as the pulmonary arteries.
32
What are the key symptoms of Takayasu Arteritis?
Key symptoms include:
"Pulseless disease" (weaker pulses in the upper extremities)
Fever
Night sweats
Skin nodules
Ocular disturbances
33
How is Takayasu Arteritis diagnosed?
Diagnosis involves:
Elevated CRP and ESR
Magnetic Resonance Angiography (MRA) to visualize vascular lesions
34
What is the treatment for Takayasu Arteritis?
Treatment includes:
Corticosteroids (e.g., prednisone)
Methotrexate
Azathioprine
Tocilizumab (IL-6 inhibitor)
35
22. What are the primary treatment goals for atrial fibrillation?
The primary treatment goals for atrial fibrillation are:
Restoration and maintenance of sinus rhythm (if possible).
Ventricular rate control.
Prevention of blood clots and thromboembolism.
36
What is the purpose of cardioversion in atrial fibrillation treatment?
Cardioversion aims to reset the heart's normal rhythm, stopping the irregular electrical activity.
37
What are the two types of cardioversion used in atrial fibrillation?
Electrical cardioversion: An electrical shock (100-200J) is delivered to the heart to restore normal rhythm.
Chemical cardioversion: Medications such as amiodarone and procainamide are used to restore normal rhythm.
38
What anti-arrhythmic medications are used after electrical cardioversion?
After electrical cardioversion, anti-arrhythmic medications include:
Amiodarone
Sotalol
39
What medications are used for heart rate control in atrial fibrillation?
Beta-blockers (e.g., metoprolol, esmolol) to slow the heart rate.
Calcium channel blockers (e.g., verapamil, diltiazem) to control heart rate.
40
Describe catheter ablation for atrial fibrillation treatment.
Catheter ablation involves inserting long, thin tubes (catheters) through a vein or artery into the heart to destroy areas of heart tissue causing irregular heartbeats using radiofrequency energy or cryotherapy.
41
When is catheter ablation indicated for atrial fibrillation patients?
Catheter ablation is indicated after one failed anti-arrhythmic drug therapy or without previous drug therapy based on patient preference.
42
What is the success rate of catheter ablation in patients with paroxysmal/persistent atrial fibrillation?
In patients with paroxysmal/persistent atrial fibrillation, catheter ablation provides long-term symptom control in 70% to 80% of cases, especially with a structurally normal heart and normal-sized left atrium.
43
What is the Maze procedure in atrial fibrillation treatment?
The Maze procedure is an invasive surgical treatment that creates electrical blocks or barriers in the atria, forcing abnormal electrical impulses to travel uniformly to the ventricles, restoring normal rhythm.
44
Where do most thromboembolic events originate in atrial fibrillation?
The vast majority of thromboembolic events in atrial fibrillation originate from the left atrial appendage.
45
What is the most serious consequence of thromboembolism in atrial fibrillation?
The most serious consequence of thromboembolism in atrial fibrillation is an ischemic stroke.
46
How is thromboembolic risk assessed in patients with atrial fibrillation?
Thromboembolic risk is assessed using the CHA2DS2-VASc score:
A score of 2 or more indicates the need for long-term oral anticoagulant treatment.
A score of 0 generally requires no therapy.
47
What types of anticoagulants are used in the management of atrial fibrillation?
Vitamin K antagonists (e.g., warfarin)
NOACs (Non-Vitamin K Oral Anticoagulants), such as:
Dabigatran
Rivaroxaban
Apixaban
Edoxaban
48
What is the mechanism of action of Warfarin?
Warfarin is a vitamin K antagonist that inhibits the synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X) in the liver.
49
What are the key requirements for patients on Warfarin?
Patients on Warfarin require regular blood tests (INR monitoring) to ensure therapeutic levels and prevent bleeding complications.
50
Name two Factor Xa inhibitors used as anticoagulants.
Two Factor Xa inhibitors are Rivaroxaban and Apixaban.
51
How do Factor Xa inhibitors differ from Warfarin?
Factor Xa inhibitors are shorter-acting, usually do not require regular blood tests or monitoring, and have a more predictable pharmacokinetic profile than Warfarin.
52
What is the normal function of the pericardium?
The pericardium is a double-layered sac that surrounds the heart, consisting of a serous visceral layer and a fibrous parietal layer, separated by a small amount of fluid that acts as a lubricant.
53
Define pericarditis.
Pericarditis is the inflammation of the pericardium, the fibrous sac surrounding the heart.
54
How is pericarditis clinically classified based on duration?
Acute pericarditis: < 6 weeks
Fibrinous
Effusive
Subacute pericarditis: 6 weeks to 6 months
Effusive-constrictive
Constrictive
Chronic pericarditis: > 6 months
Constrictive
Effusive
Adhesive (non-constricted)
55
How is pericarditis classified etiologically?
Infectious pericarditis:
Viral (e.g., coxsackievirus, echovirus, HIV)
Pyogenic (e.g., pneumococcus, streptococcus)
TB
Fungal (e.g., histoplasmosis)
Non-infectious pericarditis:
Acute myocardial infarction
Uremia
Neoplasia
Aortic dissection
Autoimmune diseases (e.g., SLE, rheumatoid arthritis)
Drug-induced
Post-cardiac injury
56
What are common clinical features of pericarditis?
Severe, pleuritic chest pain (improves when sitting and leaning forward)
Pericardial friction rub on auscultation
Pericardial effusion visible on chest x-ray
57
What diagnostic methods are used for pericarditis?
Echocardiography (for suspected effusion)
CT/MRI
ECG: shows diffuse ST elevation (saddle-shaped) and PR depression
58
What ECG changes are associated with pericarditis?
Diffuse ST elevation (saddle-shaped)
PR segment depression
PR elevation in lead aVR
ST segment normalizes after about 1 week
T-wave inversion (not in all patients)
59
What is the first-line treatment for pericarditis?
The first-line treatment is bed rest and anti-inflammatory treatment with aspirin (with omeprazole for gastric protection).
60
What are the second and third lines of treatment for pericarditis?
Second line: NSAIDs
Third line: Colchicine (for inflammation and pain) and glucocorticoids (for 2-4 days).
61
Why should anticoagulants be avoided in pericarditis?
Anticoagulants should be avoided as they could cause bleeding into the pericardial cavity, leading to cardiac tamponade.
62
What are common complications of pericarditis?
Common complications include:
Cardiac tamponade
Pericardial effusion
63
What is constrictive pericarditis?
Constrictive pericarditis is a medical condition characterized by a thickened, fibrotic pericardium that forms a non-compliant shell around the heart, preventing it from expanding during diastolic filling.
64
How does constrictive pericarditis affect the heart's filling?
A rigid, fibrotic pericardium restricts diastolic filling. When intracardiac volume reaches the limit set by the noncompliant pericardium, ventricular filling is abruptly halted, unlike cardiac tamponade where filling is impeded throughout diastole.
65
What are common causes of constrictive pericarditis?
Thickened, rigid pericardium due to acute pericarditis.
Uremia
Radiation therapy
Tuberculosis
Chronic pericardial effusion
Tumor invasion
Connective tissue disorders
Histoplasmosis
Prior surgery involving the pericardium
66
What symptoms indicate fluid overload in constrictive pericarditis?
Symptoms of fluid overload include:
Jugular vein distention (most prominent finding)
Kussmaul sign: paradoxical rise in JVP on inspiration
Hepatomegaly
Peripheral edema and ascites
67
What symptoms indicate reduced cardiac output in constrictive pericarditis?
Symptoms of reduced cardiac output include:
Fatigue and dyspnea on exertion
Pericardial knock: a high-pitched early diastolic sound
Tachycardia
Pulsus paradoxus: decreased blood pressure amplitude during deep inspiration
68
What ECG changes are seen in constrictive pericarditis?
ECG may show nonspecific changes such as:
Low QRS voltages
Generalized T-wave flattening or inversion
Left atrial abnormalities
Atrial fibrillation may be seen in advanced disease (in fewer than half of patients).
69
What does an echocardiogram reveal in constrictive pericarditis?
Echocardiogram may show:
Increased pericardial thickness in about half of patients
Sharp halt in ventricular diastolic filling
Atrial enlargement
Evidence of septal bounce and reduced mitral inflow velocities with inspiration.
70
What findings can CT scan and MRI provide in constrictive pericarditis?
CT and MRI can show pericardial thickening and calcifications, aiding significantly in diagnosis.
71
What findings would cardiac catheterization show in constrictive pericarditis?
Cardiac catheterization would show:
Elevated and equal diastolic pressures in all chambers
Ventricular pressure tracing demonstrates a rapid y descent, described as a dip and plateau or square root sign.
72
What is the general approach to treating constrictive pericarditis?
Treat the underlying condition.
Diuretics may help relieve fluid overload symptoms.
Surgical pericardiectomy may be performed to remove part or all of the pericardium.
73
What is pericardial effusion?
Pericardial effusion is defined as the exudation of fluid into the pericardial space due to any cause of acute pericarditis. It can be asymptomatic and suspected based on the underlying condition.
74
What factors influence the physiologic importance of a pericardial effusion?
The speed of fluid accumulation is more important than the amount; large effusions that develop slowly may have no hemodynamic effects, while smaller effusions that accumulate rapidly can cause tamponade.
75
What are some nonspecific clinical features of pericardial effusion?
Clinical features may include:
Muffled heart sounds
Soft PMI (Point of Maximal Impulse)
Dullness at the left lung base (due to compression by pericardial fluid)
Pericardial friction rub (may or may not be present)
76
What is the imaging procedure of choice for diagnosing pericardial effusion?
Echocardiogram is the imaging procedure of choice; it can confirm the presence of a significant effusion, showing as little as 20 mL of fluid. It should be performed in all patients with acute pericarditis to rule out effusion.
77
What does a chest X-ray reveal in cases of pericardial effusion?
Chest X-ray can show:
Enlargement of the cardiac silhouette when >250 mL of fluid has accumulated.
A “water bottle” appearance of the cardiac silhouette.
An enlarged heart without pulmonary vascular congestion suggests pericardial effusion.
78
What ECG changes may be seen in pericardial effusion?
ECG may show:
Low QRS voltages
T-wave flattening (not used to diagnose pericardial effusion)
Electrical alternans (alternating QRS amplitude), which suggests a massive pericardial effusion and tamponade.
79
When are CT scans or MRIs indicated for pericardial effusion?
CT scans or MRIs are very accurate for diagnosing pericardial effusion but are often unnecessary due to the accuracy of echocardiograms. They can help in analyzing pericardial fluid if needed.
80
What analysis should be performed on pericardial fluid?
Pericardial fluid analysis may include:
Protein and glucose content
Cell count and differential
Cytology
Specific gravity
Hematocrit
Gram stain, acid-fast stains, mycobacterial PCR, fungal smear, cultures, LDH content.
81
What factors influence the treatment of pericardial effusion?
Treatment depends on the patient’s hemodynamic stability.
82
When is pericardiocentesis indicated in pericardial effusion?
Pericardiocentesis is indicated only when there is evidence of cardiac tamponade.
83
What is the management approach for small, clinically insignificant effusions?
For small, clinically insignificant effusions, a repeat echocardiogram in 1 to 2 weeks is appropriate.
84
What is cardiac tamponade?
Cardiac tamponade is the accumulation of fluid in the pericardial space in a quantity sufficient to obstruct blood inflow into the ventricles, potentially resulting in a fatal complication if not recognized and treated promptly.
85
What are the common causes of cardiac tamponade?
The most common cause is idiopathic pericarditis. Other causes include:
Bleeding into the pericardial space due to:
Aortic dissection
Myocardial infarction (MI)
Cardiac operations
Trauma (e.g., stabbing, car crash)
Treatment of acute pericarditis with anticoagulants.
86
What are the classic clinical features of cardiac tamponade?
Clinical features include:
Beck’s triad:
Hypotension
Soft or absent heart sounds
Jugular venous distension
Dyspnea and orthopnea
Hepatic engorgement
Pulsus paradoxus: A drop in systolic pressure greater than 10 mmHg during inhalation due to the interventricular septum shifting leftwards.
87
What diagnostic tools are used to identify cardiac tamponade?
Diagnostic tools include:
Echocardiogram (TTE, TEE) to visualize excess fluid and heart movement in the pericardial cavity.
ECG showing reduced amplitude of QRS complexes, tachycardia, and electrical alternans in P, QRS, or T waves.
Doppler ultrasound
CT scan
MRI
88
What is the primary treatment for cardiac tamponade?
The primary treatment is pericardiocentesis, which involves analyzing the pericardial effusion for red and white blood cells, performing cytologic studies, and obtaining cultures.
89
23. What is abnormal impulse generation in the context of arrhythmias?
Abnormal impulse generation refers to arrhythmias originating from the SA node, which is the heart’s natural pacemaker responsible for the rhythm of heartbeats.
90
What are the two types of sinus arrhythmias?
Sinus Tachycardia: Heart rate exceeds 100 beats per minute.
Sinus Bradycardia: Heart rate is less than 60 beats per minute.
91
What is Sick Sinus Syndrome?
Sick Sinus Syndrome (SSS), also known as sinus node dysfunction or Brady-Tachy syndrome, is characterized by alternating slow and fast rhythms due to malfunction of the SA node, often with long pauses (asystole) between heartbeats.
92
What conditions are associated with Sick Sinus Syndrome?
SSS is associated with ischemic heart disease and valvular disease.
93
What are the symptoms of Sick Sinus Syndrome?
Symptoms may include fatigue, dizziness, shortness of breath, chest pain, and palpitations (sensation of rapid, fluttering heartbeats).
94
What is abnormal impulse conduction?
Abnormal impulse conduction refers to issues in the electrical conduction system of the heart, which includes blockages at the SA node, AV node, and bundle branches. This can be caused by structural heart problems or congenital disorders.
95
What is AV Block?
In AV block, the electrical signal from the SA node is either delayed or completely blocked at the AV node. If completely blocked, the ventricles generate their own electrical signals, leading to a much slower heart rate.
96
What are the three main types of AV block?
First Degree AV Block: Prolonged delay in conduction at the AV node (PR interval > 200 msec), but no complete block.
Can be caused by parasympathetic drugs and calcium channel blockers.
Second Degree AV Block: Intermittent failure of conduction (Type I or Type II).
Third Degree AV Block: Complete heart block where no signals from the atria reach the ventricles.
97
What symptoms might indicate the need for treatment in cases of bradycardia?
Symptoms include dizziness, fatigue, shortness of breath, and syncope. Treatment may be indicated when symptoms are present or if the heart rate falls below a certain threshold.
98
What are common ECG findings associated with abnormal impulse generation and conduction?
Common findings include:
Sinus bradycardia: heart rate < 60 bpm.
Sinus tachycardia: heart rate > 100 bpm.
First-degree AV block: PR interval > 200 msec.
Sick sinus syndrome: irregular heart rhythms with long pauses.
99
What characterizes Second Degree AV Block?
Second Degree AV Block occurs when the electrical signal between the atria and ventricles is impaired, leading to occasional skipped beats due to failed conduction of impulses.
100
What are the two types of Second Degree AV Block?
Mobitz Type I (Wenckebach):
Characterized by progressive prolongation of the PR interval until a beat is dropped (missing QRS).
This is a reversible block at the AV node.
Mobitz Type II:
Characterized by a sudden failure of the His-Purkinje system to conduct the impulse.
The PR interval remains constant, but there are unexpected dropped beats (missing QRS). This block is infra-nodal.
101
How can Mobitz Type I (Wenckebach) be identified on an ECG?
Mobitz Type I is identified by a gradual prolongation of the PR interval until a QRS complex is dropped. The pattern repeats.
102
How can Mobitz Type II be identified on an ECG?
Mobitz Type II is identified by a constant PR interval with sudden, unexpected drops in QRS complexes. This indicates the failure of conduction without prior warning.
103
What is Third Degree AV Block?
Third Degree AV Block occurs when there is a complete block of electrical signals between the atria and ventricles, resulting in no communication between the two. The atria pace independently of the ventricles.
104
What is the consequence of Third Degree AV Block on heart rhythm?
The consequence is AV dissociation, where the atria and ventricles beat independently. An automaticity focus takes over to pace the ventricles, leading to a slower ventricular rate.
105
How can Third Degree AV Block be identified on an ECG?
On ECG, there is no relationship between P waves and QRS complexes; they do not occur in a 1:1 ratio, indicating a complete dissociation between atrial and ventricular activity.
106
What is the pacing of the atria and ventricles in Third Degree AV Block?
In Third Degree AV Block, the atria are paced by the SA node while the ventricles are paced by an escape rhythm from an automaticity focus, which can be located in the AV node or below it.
107
What is the mechanism of action of aspirin in antiplatelet therapy?
Aspirin is an irreversible COX inhibitor that decreases thromboxane A2 production, reducing platelet activation and aggregation.
108
What are the primary indications for aspirin use?
Aspirin is indicated for acute coronary syndrome, ischemic stroke, and primary and secondary prevention of cardiovascular disease.
109
What are common side effects associated with aspirin?
Common side effects include gastrointestinal upset, aspirin exacerbated respiratory disease, and Reye syndrome.
110
What class of drugs does clopidogrel belong to, and what is its mechanism of action?
Clopidogrel is an ADP receptor inhibitor that prevents platelet activation and aggregation by irreversibly binding to the P2Y12 receptor.
111
What are the indications for using ADP receptor inhibitors like clopidogrel?
Indications include dual antiplatelet therapy (with aspirin), STEMI, unstable angina/NSTEMI, and before percutaneous coronary intervention (PCI).
112
What are the potential side effects of ADP receptor inhibitors?
Side effects include allergic reactions and hemorrhage.
113
What are glycoprotein IIb/IIIa inhibitors, and when are they used?
Glycoprotein IIb/IIIa inhibitors (e.g., abciximab, eptifibatide, tirofiban) are used in high-risk patients with unstable angina/NSTEMI before undergoing PCI.
114
What are the side effects of glycoprotein IIb/IIIa inhibitors?
Side effects include acute thrombocytopenia and hemorrhage.
115
What are the two main types of oral anticoagulants?
The two main types of oral anticoagulants are Vitamin K antagonists (e.g., warfarin) and non-VKA oral anticoagulants (NOACs).
116
How do vitamin K antagonists like warfarin work?
Warfarin inhibits vitamin K epoxide reductase, leading to decreased synthesis of clotting factors II, VII, IX, X, and proteins C and S.
117
What are the advantages of using warfarin?
Advantages include well-known effects and side effects, low cost, and the availability of an antidote (vitamin K, fresh frozen plasma).
118
What are the disadvantages of using warfarin?
Disadvantages include a long half-life, the need for regular monitoring of PT/INR, and a broad range of interactions. Complications can include skin necrosis.
119
What is a key benefit of non-VKA oral anticoagulants (NOACs)?
NOACs do not require regular monitoring of coagulation parameters, making them easier to manage.
120
Name some direct oral anticoagulants (DOACs) and their mechanisms.
Dabigatran: Direct thrombin inhibitor.
Apixaban, Rivaroxaban, Edoxaban: Direct inhibitors of factor Xa
121
What are the antidotes for NOACs in case of life-threatening bleeding?
Antidotes include idarucizumab for dabigatran and andexanet alfa for factor Xa inhibitors (apixaban, rivaroxaban, edoxaban).
122
What are the types of parenteral anticoagulants?
Parenteral anticoagulants include unfractionated heparin (sodium heparin), low molecular weight heparin (e.g., enoxaparin, dalteparin), and direct thrombin inhibitors (e.g., argatroban, bivalirudin).
123
What is the mechanism of action of unfractionated heparin?
Unfractionated heparin enhances the action of antithrombin III, leading to the inhibition of the intrinsic coagulation pathway.
124
What is a key complication associated with unfractionated heparin?
A key complication is heparin-induced thrombocytopenia (HIT).
125
What are the types of thrombolytic agents?
Fibrin-specific agents: Tissue plasminogen activator (alteplase).
Non-fibrin specific agents: Streptokinase, Urokinase.
126
What are the primary indications for thrombolytic therapy?
Indications include early STEMI, early ischemic shock, and massive pulmonary embolism (PE).
127
What are the contraindications for thrombolytic therapy?
Contraindications include prior intracranial hemorrhage, recent surgery, severe hypertension, and active bleeding
128
24. What is syncope?
Syncope is a loss of consciousness and muscle strength due to reduced cerebral perfusion, characterized by a fast onset, short duration, and spontaneous recovery.
129
How does syncope differ from unconsciousness?
Syncope involves spontaneous recovery after loss of consciousness, whereas unconsciousness is defined as loss of consciousness without spontaneous recovery.
130
What are the three broad categories of syncope causes?
Neural mediated syncope (reflex syncope)
Orthostatic (postural) hypotension
Cardiac syncope
131
What is neural mediated syncope?
Neural mediated syncope is caused by parasympathetic hyperactivity (excessive vagal tone), leading to reduced blood pressure and cerebral perfusion.
132
What is carotid sinus syndrome?
Carotid sinus syndrome causes syncope due to hypotension from excessive vagal tone, where baroreceptors in the carotid sinus activate the vagus nerve, reducing blood pressure.
133
How is carotid sinus hypersensitivity treated?
Carotid sinus hypersensitivity can be treated with carotid massage, which helps restore normal blood pressure.
134
What triggers vasovagal syncope?
Vasovagal syncope may occur in response to triggers such as stress, fear, embarrassment, blood drawing, or other high-stress situations.
135
What causes orthostatic hypotension?
Orthostatic hypotension is primarily caused by a significant drop in blood pressure when standing up from a lying or sitting position, often due to gravity's effect on blood flow.
136
What medications commonly cause orthostatic hypotension?
Common medications causing orthostatic hypotension include diuretics, beta-blockers, and vasodilators.
137
What are some heart-related causes of cardiac syncope?
Causes include arrhythmias (bradycardia, tachycardia, sick sinus syndrome, AV block), heart valve disease (aortic stenosis), hypertrophic obstructive cardiomyopathy, pulmonary embolism, and aortic dissection.
138
What are the diagnostic steps for evaluating syncope?
Physical examination (blood pressure measurement, carotid artery examination)
ECG (to check for arrhythmias, long QT, AV block)
Echocardiography (if initial tests are non-diagnostic)
Tilt table test (to simulate standing up)
139
What conditions can mimic syncope?
Conditions that can mimic syncope include seizures, hypoglycemia, and certain types of strokes, although they do not meet the definition of syncope.
140
What are the primary treatments for syncope?
Treatments include volume expanders, hydration, and vasoconstrictors.
141
What is Peripheral Arterial Occlusive Disease (PAOD)?
PAOD is a condition caused mainly by atherosclerotic or inflammatory processes that narrow the arterial lumen (stenosis) or lead to thrombus formation.
142
What are common risk factors for PAOD?
Risk factors include smoking, diabetes mellitus, hyperlipidemia, and hypertension.
143
What are common sites for PAOD?
The most common sites for PAOD are the femoral artery and popliteal artery in the leg.
144
What are the two main categories of treatment for PAOD?
The two main categories are conservative treatment and interventional/surgical treatment.
145
What lifestyle changes are recommended in conservative treatment for PAOD?
Stop smoking
Increase physical activity
Maintain normal body weight
Avoid trauma and infections
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What medications are used in the conservative treatment of PAOD?
Diabetes management (e.g., metformin)
Hypertension management (e.g., ACE inhibitors, beta-blockers)
Hypercholesterolemia management (e.g., statins)
Antiplatelet drugs (e.g., aspirin, clopidogrel)
Fibrinolytic therapy
Cilostazol (a PDE-III inhibitor for vasodilation and improved walking distance in claudication)
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What is vascular bypass surgery, and when is it indicated?
Vascular bypass surgery is indicated for progressive intermittent claudication and involves creating a bypass around the blocked artery.
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What is thromboendarterectomy?
Thromboendarterectomy is a surgical procedure that removes atherosclerotic plaques from the arteries.
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What is angioplasty?
Angioplasty is a procedure that uses a balloon to widen narrowed arteries, and may involve placing a stent (bare metal or PTFE).
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What is cryoplasty?
Cryoplasty combines balloon dilation with cryotherapy to open arteries, effectively treating the narrowing.
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When is amputation necessary in the context of PAOD?
Amputation may be required when revascularization is not possible or in cases of severe necrosis and infection of the tissue.
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25. What is a cardiac electrophysiology study?
A minimally invasive procedure using catheters to record electrical activity within the heart, aimed at investigating abnormal heart rhythms.
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What are the goals of an electrophysiology (EP) study?
Definitive diagnosis of an arrhythmia.
Establish the etiology for syncope (bradyarrhythmia or tachyarrhythmia).
Stratification for risk of sudden cardiac death.
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Where is an EP study typically performed?
In a catheterization lab equipped with an X-ray machine, ECG recording equipment, and ablation equipment.
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What vessels are commonly accessed for an EP study?
The femoral or subclavian veins and sometimes the femoral artery.
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What is the purpose of placing electrodes in the heart during an EP study?
To sense the electrical signals in different areas of the heart and to view them on ECG monitors.
157
Describe the incremental pacing technique.
The pacing interval is started just below the sinus interval and lowered in 10 ms steps until block occurs.
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What is extrastimulus pacing?
A paced beat introduced at a shorter coupling interval following a train of 8 paced beats at a fixed cycle length
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What is burst pacing?
Pacing at a fixed cycle length for a predetermined time.
160
What is catheter ablation?
A treatment that removes misfiring cells in the heart by using high-energy radio frequencies to heat the abnormal cells, forming scar tissue.
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What is cryoablation?
A newer method of ablation that freezes the affected area in the heart, considered less risky and painful than traditional ablation.
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How have EP procedures evolved?
They have become more complex, leading to longer procedures with greater X-ray exposure, necessitating non-fluoroscopic electroanatomical mapping systems for 3D imaging.
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What is primary prevention?
Steps taken to prevent the onset of disease, achieved through healthy lifestyle choices such as diet and exercise.
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What dietary changes are recommended for primary prevention?
A diet low in saturated fatty acids and caloric intake to achieve optimal body weight.
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What lifestyle change is crucial for primary prevention in cardiology?
Cessation of cigarette smoking.
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How should hypertension be managed in primary prevention?
By monitoring and controlling with medications like diuretics, beta-blockers, vasodilators, and ACE inhibitors.
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Why is diabetes management important in primary prevention?
Diabetes accelerates coronary and peripheral atherosclerosis; controlling diabetes helps prevent related complications.
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How can hyperlipidemia be managed for primary prevention?
By reducing dietary fat intake and using medications to lower LDL levels, such as statins, niacin, and fibrates.
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What role does physical activity play in primary prevention?
Regular physical activity is essential for maintaining cardiovascular health and preventing disease onset.
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What is secondary prevention?
Focuses on reducing the impact of a disease through early diagnosis to avoid permanent damage and life-threatening situations.
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What is the most critical step in secondary prevention of CVD?
Early diagnosis, which allows medical professionals to provide necessary care and improve the quality of life for patients.
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How does early diagnosis benefit patients?
It enables timely intervention, directing patients to required treatments that afford a higher quality of life.
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What is the recommended antiplatelet therapy for secondary prevention in CVD?
Low-dose aspirin: 81 mg daily.
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What anticoagulation therapy is recommended for patients with mechanical heart valves?
Warfarin.
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What medications are used for blood pressure control in secondary prevention?
Beta-blockers and ACE inhibitors, which are given to all post-myocardial infarction (post-MI) patients.
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What type of therapy is recommended to lower lipid levels in secondary prevention?
Lipid-lowering therapy with statins.
