Cardio T12-20 Flashcards
1
Q
- What is sudden cardiac death (SCD)?
A
Sudden cardiac death is an unexpected non-traumatic death occurring within one hour of symptom onset in a clinically stable patient, primarily caused by ventricular arrhythmias like ventricular fibrillation.
2
Q
How does sudden cardiac arrest differ from sudden cardiac death?
A
Sudden cardiac arrest is the sudden loss of cardiac output, which can potentially be reversible with prompt restoration of circulation and oxygenation, while sudden cardiac death refers to the actual death that occurs.
3
Q
What are the two major causes of sudden cardiac death?
A
The two major causes of sudden cardiac death are acute coronary syndrome and cardiomyopathies.
4
Q
What is the primary goal of cardiopulmonary resuscitation (CPR)?
A
The primary goal of CPR is to maintain circulation in patients experiencing sudden cardiac arrest until cardiac function can be restored.
5
Q
What are the two main protocols for CPR?
A
The two main protocols for CPR are Basic Life Support (BLS) for lay rescuers and Advanced Cardiac Life Support (ACLS) for medical professionals.
6
Q
What steps are included in Basic Life Support (BLS)?
A
BLS includes checking the patient’s responsiveness, calling for help, performing chest compressions and rescue breaths (30:2 ratio), and using an automated external defibrillator (AED) if available.
7
Q
What is the Chain of Survival in CPR?
A
The Chain of Survival includes:
Check responsiveness and call for help.
Immediate CPR.
Early defibrillation.
Early advanced life support.
8
Q
What are the steps in BLS regarding airway management?
A
In BLS, airway management involves clearing any obstruction and positioning the airway using head tilt or chin lift maneuvers.
9
Q
Describe the CPR compression technique.
A
CPR compressions should be at a rate of 100 compressions per minute and a depth of 5-6 cm. Compressions should continue until emergency medical services (EMS) arrive.
10
Q
How is an AED used in CPR?
A
Place one pad on the right chest above the nipple and the other pad on the left side below the nipple. Most AEDs are automatic and will provide prompts for shock delivery; continue CPR after any shock is administered.
11
Q
What is included in Advanced Life Support (ALS)?
A
ALS includes continuing CPR, activating the emergency response system, securing the airway (if needed), providing rescue breaths or artificial ventilation, and using a defibrillator for shockable rhythms.
12
Q
What medical therapy is administered in ALS if defibrillation is ineffective?
A
If defibrillation does not restore normal rhythm, administer 1 mg of IV epinephrine every 3-5 minutes.
13
Q
What are acute aortic syndromes (AAS)?
A
Acute aortic syndromes are emergency conditions involving the aorta that may lead to intramural hematoma, penetrating aortic ulcer, aortic dissection, or rupture.
14
Q
What is an aortic dissection?
A
Aortic dissection is a tear in the inner layer of the aorta, causing blood to accumulate in the intima-media space, resulting in a progressively growing hematoma.
15
Q
What are the main risk factors for aortic dissection?
A
Age and hypertension are the main risk factors for aortic dissection.
16
Q
How does a patient with aortic dissection typically present?
A
Patients with aortic dissection typically present with sudden onset severe pain radiating to the chest, back, or abdomen.
17
Q
What is a key finding on a chest X-ray in aortic dissection?
A
A widened mediastinum on chest X-ray is a characteristic finding in aortic dissection.
18
Q
How is the diagnosis of aortic dissection confirmed in stable vs. unstable patients?
A
In stable patients, diagnosis is confirmed with a CT angiogram, and in unstable patients, it is confirmed with transesophageal echocardiography (TEE).
19
Q
What are the treatment options for aortic dissection?
A
Treatment ranges from conservative measures like blood pressure control to surgery, such as aortic stent graft placement, depending on the severity and location of the dissection.
20
Q
What are common complications of aortic dissection?
A
Common complications include complete occlusion of branching vessels and aortic rupture.
21
Q
What are the two main classifications of aortic dissection?
A
The two main classifications of aortic dissection are the Stanford and DeBakey classifications.
22
Q
How does the Stanford classification system categorize aortic dissections?
A
The Stanford classification is based on whether the ascending aorta (Stanford type A) or descending aorta (Stanford type B) is involved.
23
Q
What is the DeBakey classification of aortic dissection?
A
The DeBakey classification categorizes aortic dissection based on its origin and extent:
Type I: involves the ascending aorta and extends beyond it.
Type II: confined to the ascending aorta.
Type III: confined to the descending aorta.
24
Q
A
25
What are common etiology/risk factors for acute aortic syndromes?
Hypertension or trauma
In rare cases, Ehlers-Danlos and Marfan syndrome
26
What is the pathophysiology of aortic dissection?
A transverse tear in the arterial intima leads to:
Blood entering the intima-media space, creating a false lumen
Hematoma formation that propagates longitudinally downwards
27
What are the clinical presentations and complications of aortic dissection?
Sudden and severe tearing/ripping chest pain
Asymmetrical blood pressure
Syncope, diaphoresis, confusion, agitation
28
How is aortic dissection diagnosed?
Echocardiography: Shows dissection flap, double lumen, pericardial effusion
CT (gold standard): Dissection flap, double lumen, dilatation, hematoma
MRI: Same findings as CT (used if CT is contraindicated)
X-ray: Widened mediastinum
29
What are the treatment options for aortic dissection?
Surgery:
Immediate for Stanford A or Stanford B with complications
Open surgery with replacement of the dissection with polyester graft
Endovascular aortic repair with stent implantation (in Stanford B with high operative risk)
30
What is the difference between true and false aneurysms?
True aneurysms: Involve all 3 layers of the arterial wall, can be fusiform or saccular.
False aneurysms: External hematomas with persistent communication to a leaking artery, often due to trauma.
31
What are aortic dissections?
Separation of the arterial wall layers caused by blood entering the intima-media space after a tear in the internal layer occurred.
32
How are aneurysms classified?
Aneurysms are classified by their location, such as cerebral, external carotid, iliofemoral, popliteal, and ventricular aneurysms.
33
What factors influence symptoms of aneurysms?
Symptoms depend on the location and size of the aneurysm.
34
What are the treatment options for aneurysms?
Surgical and endovascular treatments, depending on the type and whether symptoms or complications are present.
35
Thoracic Vs Abdominal aortic aneurysm
36
What is the treatment approach for unstable patients with ruptured aneurysms?
Emergency surgery within 90 minutes.
37
How should symptomatic patients with impending rupture or leaking aneurysms be treated?
Urgent repair within hours.
38
What is the recommended approach for asymptomatic patients with aneurysms?
Elective aneurysm repair or surveillance.
39
What is the general treatment strategy for all patients with aneurysms?
Reduction of atherosclerosis risk factors.
40
What is Endovascular Aneurysm Repair (EVAR)?
A minimally invasive procedure preferred over open surgery for most aneurysms, where an expandable stent graft is placed via the femoral or iliac arteries.
41
What is the procedure for open surgical repair of aneurysms?
Laparotomy is performed, and the dilated segment of the aorta is replaced with a tube graft.
42
13. What is the Vaughan-Williams classification used for?
The Vaughan-Williams classification is used to classify antiarrhythmic drugs based on their mechanism of action.
43
Why are Class I drugs in the Vaughan-Williams classification further subdivided?
Class I drugs are further subdivided because of subtle, yet important differences in their effects on action potentials.
44
What is the main purpose of the Vaughan-Williams classification?
The main purpose of the Vaughan-Williams classification is to categorize antiarrhythmic drugs by their mechanism of action and their effectiveness with certain types of arrhythmias.
45
46
What are the limitations of the Vaughan-Williams classification?
The Vaughan-Williams classification has limitations due to the incomplete understanding of drug mechanisms when it was created. Many antiarrhythmic drugs, especially in Class I and III, have overlapping mechanisms of action that break the classification down, as they could fit into multiple classes.
47
How do Class III drugs like amiodarone challenge the Vaughan-Williams classification?
Amiodarone, a Class III antiarrhythmic, also blocks sodium and calcium channels, showing that drugs in one class can share mechanisms with drugs in other classes, complicating their classification.
48
Why do different sources sometimes classify antiarrhythmic drugs differently?
Different sources may classify antiarrhythmic drugs differently because many drugs exhibit multiple mechanisms of action, which makes it possible for them to be assigned to more than one class.
49
How do the efficacy and safety of antiarrhythmic drugs vary?
The efficacy and safety of antiarrhythmic drugs vary depending on the type of arrhythmia, with some drugs being more effective or safer for certain arrhythmias than others.
50
What does the table accompanying the Vaughan-Williams classification show?
The table provides an overview of drug classes, their associated arrhythmias, and includes antiarrhythmic agents that are not classified within the Vaughan-Williams scheme.
51
52
What has contributed to the increase in cardiac disease in pregnancy?
The increase in cardiac disease in pregnancy is partly due to women with congenital heart disease now having children, but the majority is from acquired heart conditions.
53
What cardiac conditions can be encountered during pregnancy?
Cardiac conditions encountered in pregnancy include valvular lesions, congenital heart disease, cardiomyopathies, arrhythmias, and ischemic heart disease.
54
How does pregnancy affect the maternal cardiovascular system?
Pregnancy increases cardiac output (CO), which can cause deterioration in conditions like aortic stenosis, where CO is fixed, while conditions like regurgitant lesions may be well tolerated.
55
Why is diagnosing cardiac disease during pregnancy challenging?
Many symptoms of cardiac disease, such as breathlessness, palpitations, and syncope, as well as cardiovascular signs like a systolic murmur, mimic normal pregnancy symptoms, making diagnosis difficult.
56
What are the risks for women with cardiac conditions during pregnancy?
Women with cardiac conditions during pregnancy are at risk for CHF, hypoxia, arrhythmias and sudden cardiac death (SCD), bacterial endocarditis, venous thromboembolism, angina, myocardial infarction (MI), and aortic dissection.
57
When is pregnancy not advised for women with cardiac conditions?
Pregnancy is not advised for women with poor cardiac function, particularly those with Eisenmenger syndrome or pulmonary hypertension, due to high maternal death risk.
58
Which cardiac conditions are relatively well tolerated during pregnancy?
Conditions like atrial septal defect (ASD), ventricular septal defect (VSD), repaired tetralogy of Fallot, and coarctation of the aorta are relatively well tolerated during pregnancy.
59
Which cardiac conditions pose a significant risk during pregnancy?
Marfan syndrome and bicuspid aortic valve carry significant risks during pregnancy.
60
What may need to be altered in women with cardiac conditions during pregnancy?
Medications may need to be altered, and anticoagulation may be required for some women with cardiac conditions during pregnancy.
61
What anticoagulation regimen is typically followed for mechanical valves during pregnancy?
Anticoagulation for mechanical valves during pregnancy usually involves using unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) in the 1st trimester, switching to vitamin K antagonists for the 2nd and 3rd trimesters. Before planned delivery (36 hours), UFH is reintroduced (aPTT>2 of control). UFH is stopped 4-6 hours before surgery and resumed 4-6 hours after the operation.
62
What are the first diagnostic tests used if cardiac problems arise during pregnancy?
ECG and echocardiography are the first diagnostic tests, as they are non-invasive and safe for the fetus. If insufficient, chest radiography, CT, MRI, and cardiac catheterization may be used.
63
How is hypertension in pregnancy divided?
Hypertension in pregnancy is divided into two major groups:
1. Hypertension without proteinuria: includes pre-existing chronic hypertension and gestational hypertension.
2. Hypertension with proteinuria: includes pre-eclampsia and eclampsia.
64
What is gestational hypertension?
Gestational hypertension is hypertension that occurs after 20 weeks of gestation without proteinuria. It typically returns to baseline within 12 weeks of delivery.
65
What are the risk factors for gestational hypertension?
Risk factors for gestational hypertension include chronic kidney disease, diabetes, first pregnancy, age over 40, obesity, and family history.
66
What is the management of gestational hypertension?
Management of gestational hypertension includes beta-blockers and calcium channel blockers. ACE inhibitors, ARBs, and diuretics are contraindicated.
67
What is pre-eclampsia?
Pre-eclampsia is a condition of widespread vascular endothelial dysfunction and vasospasm, defined by hypertension and proteinuria (>300 mg/day) after 20 weeks of gestation.
68
What are the risk factors for pre-eclampsia?
Risk factors for pre-eclampsia include age extremes (young or old), obesity, diabetes, and a family history of pre-eclampsia.
69
How is pre-eclampsia classified?
Pre-eclampsia is classified as:
1. Mild: Hypertension (>140/90) with proteinuria, presenting as asymptomatic, headache, or edema.
2. Severe: Hypertension (>160/110) with proteinuria and severe features such as hypertensive crisis, pulmonary edema, DIC, elevated liver enzymes, acute renal failure, hemolytic anemia, and others.
70
What is the management of pre-eclampsia?
The management of pre-eclampsia typically involves delivery. Antihypertensive therapy, such as methyldopa, nifedipine, beta-blockers (labetalol and metoprolol), and hydralazine, may also be used.
71
What is eclampsia?
Eclampsia is pre-eclampsia with seizures, which can occur in the pre-, intra-, or postpartum periods.
72
How is eclampsia managed?
Eclampsia management includes seizure control with IV magnesium sulfate and blood pressure control with labetalol and epidural analgesia to relieve pain and cause vasodilation in the lower extremities.
73
74
What is peripartum cardiomyopathy (PPCM)?
Peripartum cardiomyopathy (PPCM) is a rare form of dilated cardiomyopathy marked by left ventricular (LV) systolic dysfunction, occurring from 1 month before to 6 months after delivery, most commonly right after delivery.
75
What is the suspected cause of PPCM?
The cause of PPCM is unclear but is thought to involve an immunological component.
76
What is the prognosis for women with PPCM?
A little over half of women with PPCM make a complete recovery, but recurrence is common in subsequent pregnancies, especially if cardiac function has not fully recovered.
77
What are the signs and symptoms of PPCM?
The signs and symptoms of PPCM are often typical of chronic heart failure.
78
What are the four criteria for diagnosing PPCM?
The four criteria for diagnosing PPCM are:
1. Heart failure in the last month of gestation or within 5 months of delivery.
2. Absence of other identifiable cause for heart failure.
3. Absence of recognizable heart disease in the last month of pregnancy.
4. LV systolic dysfunction with an ejection fraction (EF) of less than 45%.
79
What is the treatment for PPCM?
The treatment for PPCM includes the termination of pregnancy as soon as possible. If after delivery, β-blockers, nitrates, and diuretics may be given if necessary.
80
14. What is aortic regurgitation (AR)?
Aortic regurgitation (AR) is a valvular heart disease characterized by incomplete closure of the aortic valve, leading to reflux of blood from the aorta into the left ventricle during diastole.
81
What are the two types of aortic regurgitation?
The two types of aortic regurgitation are acute and chronic AR.
82
What are common causes of acute aortic regurgitation (AR)?
Acute AR is commonly caused by infective endocarditis, aortic dissection, or chest trauma.
83
What are common causes of chronic aortic regurgitation (AR)?
Chronic AR is often caused by congenital bicuspid valve, rheumatic heart disease, and dilation of the aortic root (e.g., Marfan syndrome, Ehlers-Danlos syndrome, syphilis).
84
What happens in acute aortic regurgitation (AR) physiologically?
Acute AR often leads to rapid deterioration of left ventricular (LV) function, pulmonary edema, and cardiac decompensation.
85
What is a characteristic auscultatory finding in aortic regurgitation (AR)?
A characteristic auscultatory finding in AR is a high-pitched, decrescendo early diastolic murmur.
86
What is the significance of a widened pulse pressure in aortic regurgitation (AR)?
Widened pulse pressure is a diagnostic finding in AR and is often associated with a water hammer pulse, head bob with heartbeat, and pulsating carotid arteries.
87
How is aortic regurgitation (AR) diagnosed?
AR is primarily diagnosed using transthoracic echocardiography, which assesses LV function, aortic valve morphology, severity of regurgitation, and the condition of the aortic root and ascending aorta.
88
What is the main treatment for severe aortic regurgitation (AR)?
The main treatment for severe AR is aortic valve replacement, sometimes with long-term anticoagulation if a mechanical valve is used.
89
What is the medical management for patients with AR who have heart failure or hypertension?
ACE inhibitors, ARBs, and beta-blockers are useful in patients with AR who have heart failure or hypertension.
90
What is the indication for surgical intervention in aortic regurgitation (AR)?
Surgical intervention is indicated for symptomatic patients with severe AR or asymptomatic patients with significant AR if the resting LVEF is ≤50% or LV systolic diameter is >50 mm.
91
What are nonpharmacological treatments for hypertension?
Nonpharmacological treatments for hypertension include lifestyle changes such as diet modifications, exercise, and stress reduction.
92
When is pharmacological treatment initiated for hypertension?
Pharmacological treatment is initiated when nonpharmacological measures fail to control hypertension.
93
94
What are the ABCDs of pharmacological treatment for hypertension?
The ABCDs of pharmacological treatment are: A – ACE inhibitors or Angiotensin-receptor blockers (ARBs), B – β-blockers, C – Calcium Channel Blockers (CCBs), D – Diuretics.
95
What is the initial treatment approach for blood pressure (BP) below 150/90?
For BP below 150/90, one primary antihypertensive is used.
96
What is the treatment approach for blood pressure (BP) above 150/90?
For BP above 150/90, two primary antihypertensives are used.
97
How should antihypertensive choice be tailored to the patient?
The choice of antihypertensives should consider the patient's ethnicity, pregnancy status, comorbidities (e.g., diabetes), and age.
98
What is the follow-up procedure after initiating antihypertensive treatment?
Follow-up should occur one month after initiation. If BP is controlled, reassess in 3-6 months; if uncontrolled, adjust the treatment.
99
What is the next step if the BP goal is not reached with one drug?
If the BP goal is not reached with one drug, increase the dose or add a second drug.
100
What is a first-line drug for hypertensive patients with diabetes mellitus or renal disease?
ACE inhibitors (e.g., lisinopril, enalapril) or ARBs (e.g., losartan, valsartan) are preferred for patients with diabetes or renal disease.
101
What side effect is common with ACE inhibitors and ARBs, and when should they not be used?
ACE inhibitors and ARBs can increase potassium (K+) and should not be used in pregnant patients or together.
102
What are the side effects of thiazide diuretics?
Thiazide diuretics can reduce potassium (K+) and sodium (Na+), and increase glucose and cholesterol levels.
103
What are the side effects of Calcium Channel Blockers (CCBs) like nifedipine?
CCBs may cause headaches, constipation, and GERD.
104
What is a contraindication for using β-blockers in hypertensive patients?
β-blockers are contraindicated in patients with aortic regurgitation.
105
What are the side effects of β-blockers?
β-blockers can cause bronchoconstriction and increased triglycerides.
106
What is the use of loop diuretics in hypertension treatment?
Loop diuretics, such as furosemide, are used in patients with heart failure or chronic kidney disease (CKD).
107
What is a second-line drug for patients with primary hyperaldosteronism?
Aldosterone antagonists are used for patients with primary hyperaldosteronism.
108
Which drug should be avoided in combination with ACE inhibitors or ARBs?
Direct renin inhibitors should not be used with ACE inhibitors or ARBs.
109
What is the initial step of pharmacological treatment for hypertension?
The initial step combines an ACE inhibitor or ARB with a calcium antagonist or a diuretic (A + C/D).
110
What is the second step of pharmacological treatment for hypertension?
The second step combines an ACE inhibitor or ARB with a calcium antagonist and a diuretic (A + C + D).
111
What is the third step in hypertension therapy?
The third step adds an extra hypertensive agent (e.g., spironolactone, beta-blocker, or alpha-blocker) to the previous regimen.
112
What are examples of fixed combination antihypertensive drugs?
Examples include: Tarka (trandolapril/verapamil), Zestoretic (lisinopril/hydrochlorothiazide), Exforge (valsartan/amlodipine), Hyzaar (losartan/hydrochlorothiazide).
113
114
15. What are acyanotic heart defects?
Acyanotic heart defects are congenital cardiac malformations affecting atrial or ventricular walls, heart valves, or large blood vessels. They involve a left-to-right shunt, leading to pulmonary hypertension and right heart hypertrophy.
115
What are common causes of acyanotic heart defects?
Common causes include genetic defects (e.g., trisomies), maternal infections (e.g., rubella), and maternal use of drugs or alcohol during pregnancy.
116
How do acyanotic heart defects affect the heart physiologically?
Acyanotic heart defects cause a left-to-right shunt, leading to increased pulmonary blood flow, pulmonary hypertension, and right heart hypertrophy.
117
What are typical symptoms of acyanotic heart defects in infants?
Infants may be asymptomatic or present with exercise intolerance, failure to thrive, and symptoms of heart failure.
118
What is the role of heart murmurs in diagnosing acyanotic heart defects?
Characteristic heart murmurs are important clues for diagnosing acyanotic heart defects, which are confirmed via echocardiography.
119
What imaging techniques are used to diagnose and plan surgery for acyanotic heart defects?
Echocardiography, chest x-ray, MRI, and cardiac catheterization are used to diagnose and plan surgery for acyanotic heart defects.
120
What are the treatment options for acyanotic heart defects?
Acyanotic heart defects are treated via catheter procedures or surgery. Supportive therapy (e.g., diuretics, inotropic agents) is used in cases of heart failure or if surgery cannot be performed.
121
What are common complications of untreated acyanotic heart defects?
Common complications include arrhythmias, embolisms, and infective endocarditis, especially if treatment is delayed.
122
What are the types of atrial septal defect (ASD)?
The types of ASD include ostium primum ASD (15%), ostium secundum ASD (80%), and sinus venosus defect (5%).
123
What is the pathophysiology of atrial septal defect (ASD)?
ASD results from impaired growth or excessive resorption of the atrial septa in utero, causing a left-to-right shunt and sometimes paradoxical emboli.
124
What is an ostium primum ASD?
Ostium primum ASD (15%) is located near the crux of the heart and is often associated with malformed AV valves, resulting in varying degrees of regurgitation.
125
What is an ostium secundum ASD?
Ostium secundum ASD (80%) is located in the region of the fossa ovalis and is the most common type of atrial septal defect.
126
What is a sinus venosus defect?
Sinus venosus defect (5%) is located near the entry of the superior vena cava and is often associated with partial connection of right pulmonary veins to the right atrium.
127
How is atrial septal defect (ASD) diagnosed?
ASD is diagnosed using echocardiography.
128
What is the treatment for atrial septal defect (ASD)?
In children with ASD, spontaneous closure may occur. If needed, treatment involves surgical patch repair.
129
What is the most common congenital heart defect?
Ventricular septal defect (VSD) is the most common congenital heart defect.
130
What is the primary cause of ventricular septal defect (VSD)?
VSD is commonly associated with Down syndrome.
131
What are the two types of ventricular septal defect (VSD)?
The two types of VSD are perimembranous (80%), located in the membranous septum, and muscular (15-20%), completely surrounded by muscle.
132
What can happen if the left-to-right shunt in VSD is not treated?
If untreated, the increased blood volume from the left-to-right shunt can cause pulmonary hypertension, leading to Eisenmenger syndrome and cyanosis around the lips and fingertips.
133
How is ventricular septal defect (VSD) diagnosed?
VSD is diagnosed using echocardiography and can present with a holosystolic murmur.
134
What is the typical treatment for ventricular septal defect (VSD)?
VSD often heals spontaneously and rarely requires surgical intervention.
135
What is patent ductus arteriosus (PDA)?
Patent ductus arteriosus (PDA) is the failure of the ductus arteriosus to close postnatally, resulting in persistent communication between the left pulmonary artery and the descending aorta.
136
What are the common causes of patent ductus arteriosus (PDA)?
Common causes include prematurity, respiratory distress syndrome, and trisomies.
137
How does the ductus arteriosus function in utero, and what happens if it fails to close?
In utero, the ductus arteriosus allows blood to bypass the lungs. Failure to close after birth causes a left-to-right shunt, leading to volume overload of the pulmonary vessels and potential heart failure.
138
What is Eisenmenger syndrome in the context of PDA?
Eisenmenger syndrome occurs when pulmonary hypertension from a left-to-right shunt reverses the flow to a right-to-left shunt, leading to deoxygenated blood flowing into the aorta and cyanosis, especially in the lower extremities (differential cyanosis).
139
How is patent ductus arteriosus (PDA) diagnosed?
PDA is diagnosed using echocardiography.
140
What is the primary treatment for patent ductus arteriosus (PDA)?
Treatment for PDA involves inhibition of prostaglandin synthesis to induce closure of the ductus arteriosus.
141
What is coarctation of the aorta (CoA)?
Coarctation of the aorta (CoA) is a congenital narrowing of the aorta at the aortic isthmus, near the ductus arteriosus and left subclavian artery.
142
What is the etiology of coarctation of the aorta (CoA)?
The etiology of CoA is unclear.
143
What are the two types of coarctation of the aorta (CoA)?
The two types of CoA are preductal (narrowing proximal to the ligamentum arteriosum, causing cyanosis) and postductal (narrowing distal to the ligamentum arteriosum, causing high pressure in the upper extremities and low pressure in the lower extremities).
144
What is a potential complication of preductal coarctation of the aorta (CoA)?
Preductal CoA can cause a right-to-left shunt of blood, leading to cyanosis due to lower pressure below the narrowing.
145
What are potential complications of postductal coarctation of the aorta (CoA)?
Postductal CoA can cause increased pressure in the upper extremities and head, leading to berry aneurysm, and decreased pressure in the lower extremities, causing weak pulses.
146
What is the initial diagnostic test for coarctation of the aorta (CoA)?
The initial diagnostic test for CoA is blood pressure measurement.
147
What is the confirmatory test for coarctation of the aorta (CoA)?
Doppler echocardiography is the confirmatory test for CoA.
148
What is the initial management for coarctation of the aorta (CoA)?
Initial management involves infusion of prostaglandin E1 (PGE1) to keep the ductus arteriosus open.
149
What is the typical treatment for coarctation of the aorta (CoA) in children under 5?
Treatment for children under 5 typically involves surgical correction or balloon angioplasty.
150
What treatment options are available for older patients with coarctation of the aorta (CoA)?
Older patients may undergo transcatheter intervention with stent placement.
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152
16. What is the apex impulse, and where is it normally located?
The apex impulse is the outermost and lowermost cardiac impulse that is palpable on the chest wall. It is normally located in the 5th intercostal space, midclavicular line.
153
What are the major components of cardiovascular (CV) examination?
The major components of CV examination include observation, palpation, auscultation, blood pressure measurement, and various noninvasive tests like ECG and echocardiography.
154
What are the physiological heart sounds, and what do they represent?
S1 (onset of systole): Closure of the mitral and tricuspid valves.
S2 (onset of diastole): Closure of the aortic and pulmonary valves.
155
What are S3 and S4 heart sounds, and what conditions are they associated with?
S3: Rapid ventricular filling, associated with mitral regurgitation, heart failure, and dilated cardiomyopathy.
S4: Late atrial contraction, associated with ventricular hypertrophy (e.g., HTN, aortic stenosis), ischemic cardiomyopathy, and acute MI.
156
What is a crescendo-decrescendo murmur, and which conditions cause it?
A crescendo-decrescendo murmur increases and then decreases in intensity. It is associated with aortic stenosis and hypertrophic cardiomyopathy.
157
How is the intensity of heart murmurs graded?
Grade 1: Difficult to hear
Grade 2: Quiet
Grade 3: Easy to hear
Grade 4: Easy to hear with a palpable thrill
Grade 5: Audible with the stethoscope barely touching the chest
Grade 6: Audible with the stethoscope off the chest
158
What are the auscultation points for different heart valves?
Aortic region: 2nd intercostal space, right upper sternal border
Pulmonic region: 2nd intercostal space, left upper sternal border
Tricuspid region: 4th intercostal space, left lower sternal border
Mitral region: 5th intercostal space, midclavicular line
159
What is an ECG, and what does it assess?
An ECG (electrocardiogram) measures the electrical conduction of the heart and assesses axis, rate, rhythm, and abnormalities in heart function, diagnosing arrhythmias and structural alterations.
160
What are the common modes of echocardiography?
The common modes of echocardiography are M-mode, 2D, 3D, Doppler, and Color Doppler, primarily used to assess valve function, myocardial contractility, septal defects, aneurysms, thrombi, and vegetations.
161
What is a stress test, and when is it contraindicated?
A stress test evaluates the heart's ability to respond to stress, typically used to assess the probability of coronary artery disease (CAD). Contraindications include acute MI, unstable angina, severe aortic stenosis, and decompensated heart failure.
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163
What is the primary clinical manifestation of cyanotic heart defects?
The primary clinical manifestation is cyanosis (bluish skin), caused by hypoxemia. Other symptoms include failure to thrive, heart murmurs, and signs of heart failure.
164
What is a cyanotic heart defect, and what causes it?
Cyanotic heart defects are congenital malformations that often cause a right-to-left shunt, leading to deoxygenated blood entering the systemic circulation. Common causes include genetic defects, maternal infections, and maternal consumption of alcohol or drugs during pregnancy.
165
How are cyanotic heart defects diagnosed?
Cyanotic heart defects are diagnosed with echocardiography. Additional findings include low oxygen saturation and characteristic X-ray findings.
166
What is the most common cyanotic congenital heart defect?
The most common cyanotic congenital heart defect is Tetralogy of Fallot, accounting for 50-70% of cases.
167
What are the four defects that make up Tetralogy of Fallot?
Right ventricular outflow obstruction (narrowing of the valve or infundibulum)
Right ventricular hypertrophy
Ventricular septal defect (VSD)
Overriding aorta (positioned above the VSD)
168
What clinical sign can help reverse a "Tet spell" in Tetralogy of Fallot?
Squatting can reverse a "Tet spell" by increasing systemic pressure and reversing the right-to-left shunt, improving oxygenation.
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What are "Tet spells" and how do they manifest?
"Tet spells" are acute cyanotic episodes seen in Tetralogy of Fallot. They are characterized by increased cyanosis, irritability, and difficulty breathing, which can be relieved by squatting or placing the knees to the chest.
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How is Tetralogy of Fallot treated?
Tetralogy of Fallot is treated with cardiac repair surgery in the first year of life. Until surgery, intravenous prostaglandins are given to keep the ductus arteriosus open.
171
What is the role of prostaglandins in the treatment of cyanotic heart defects?
Prostaglandins (e.g., PGE1) are used to maintain the patency of the ductus arteriosus in cyanotic heart defects until corrective surgery can be performed.
172
What are some other cyanotic heart defects not covered in detail?
Other cyanotic heart defects include Tricuspid valve atresia, Ebstein anomaly, hypoplastic left heart syndrome, and double aortic arch.
173
174
What is Transposition of the Great Vessels (TGV)?
Transposition of the Great Vessels (TGV) is a congenital defect where the aorta and pulmonary artery are anatomically reversed, causing deoxygenated blood to circulate through the body and oxygenated blood to return to the lungs.
175
What are the risk factors for the development of Transposition of the Great Vessels (TGV)?
Risk factors include maternal diabetes, maternal alcohol consumption, maternal age >40, and rubella infection during pregnancy.
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What are the primary clinical findings in Transposition of the Great Vessels (TGV)?
Clinical findings include postnatal cyanosis, tachypnea (rapid breathing), and a single loud S2 heart sound.
177
How is Transposition of the Great Vessels diagnosed?
Transposition of the Great Vessels is diagnosed using echocardiography to visualize the anatomical reversal of the aorta and pulmonary artery.
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What are the treatment options for Transposition of the Great Vessels (TGV)?
Prostaglandins to keep the ductus arteriosus open and maintain blood flow.
Surgical correction within the first two weeks of life. Without surgery, 90% of patients die within the first year.
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What is Persistent Truncus Arteriosus?
Persistent Truncus Arteriosus is a congenital heart defect where the aorta and pulmonary artery fail to separate during development, resulting in a single arterial trunk receiving blood from both ventricles. It is sometimes associated with DiGeorge syndrome.
180
What are the main clinical features of Persistent Truncus Arteriosus?
Cyanosis (bluish skin due to low oxygen)
Heart failure symptoms
A harsh systolic murmur and a loud S2 heart sound
181
How is Persistent Truncus Arteriosus diagnosed?
The condition is diagnosed using echocardiography, which visualizes the single arterial trunk arising from the heart.
182
What is the treatment for Persistent Truncus Arteriosus?
Surgical repair is the only treatment, and without it, 85% of patients die within the first year of life.
183
184
What happens when the heart fails to pump enough blood to meet the body's metabolic needs?
Heart failure occurs, leading to inadequate blood circulation to the tissues and insufficient oxygen supply.
185
What causes blood to back up in the lungs in left ventricular failure?
Failure of the left ventricle to pump oxygenated blood into the systemic circulation, causing blood to back up in the pulmonary circulation, leading to respiratory symptoms and fatigue.
186
What are common respiratory signs of left ventricular failure?
Increased rate of breathing (tachypnea), crackles in the lung bases, dyspnea (difficulty breathing), and pulmonary edema.
187
What is pulmonary edema?
Pulmonary edema is a condition caused by excess fluid in the lungs, which can result from either cardiac or non-cardiac causes.
188
What are the causes of cardiogenic pulmonary edema?
Cardiogenic pulmonary edema is caused by heart-related issues like congestive heart failure and hypertensive crisis.
189
What are the causes of non-cardiogenic pulmonary edema?
Non-cardiogenic pulmonary edema can result from conditions like pulmonary embolism and acute respiratory distress syndrome (ARDS).
190
What are the symptoms of pulmonary edema?
Symptoms include dyspnea at rest, tachypnea, tachycardia, severe hypoxia, crackles, and wheezing.
191
How is pulmonary edema diagnosed?
Pulmonary edema is diagnosed using echocardiography, ECG, chest X-ray (showing fluid in alveolar walls, Kerley B lines, and pleural effusions), and elevated BNP in cardiogenic cases.
192
What are common treatments for pulmonary edema?
Treatment includes oxygenation support, reduction of preload (using diuretics, nitrates, morphine, ACE inhibitors), and intra-aortic balloon counter-pulsation.
193
What role does morphine play in pulmonary edema treatment?
Morphine is highly effective in reducing symptoms in pulmonary edema and may help in less severe heart failure decompensations when the patient is uncomfortable.
194
Why are beta-blockers contraindicated in acute heart failure?
Beta-blockers should not be used in acute heart failure because they can further reduce heart function. However, they may be additive in chronic heart failure when used with drugs like levosimendan.
195
What is cardiogenic shock?
Cardiogenic shock is a medical emergency where the heart suddenly cannot pump enough blood to meet the body's needs, often due to severe heart dysfunction.
196
What is the main cause of cardiogenic shock in most cases?
The main cause is a lack of oxygen to the heart, usually from a myocardial infarction, which damages the left ventricle, weakening the heart muscle and leading to cardiogenic shock.
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What are other conditions associated with cardiogenic shock?
Cardiogenic shock is associated with acute coronary syndrome, left ventricular failure, hypotension, abnormal heart rhythms, cardiomyopathy, heart valve problems, and ventricular outflow obstruction.
198
What is the pathophysiology of cardiogenic shock?
Cardiogenic shock starts with heart dysfunction leading to heart failure, decreased cardiac output, and blood pressure, triggering a cascade involving catecholamine release, vasoconstriction, increased myocardial oxygen demand, activation of the renin-angiotensin-aldosterone system, and further vasoconstriction, causing peripheral organ underperfusion.
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What are the clinical features of cardiogenic shock?
Clinical features include a weak pulse, tachycardia, hypotension, dyspnea, cold and clammy extremities, poor capillary refill, elevated JVP, and distended neck veins.
200
What are the diagnostic tools used in cardiogenic shock?
Diagnostic tools include ECG (to identify myocardial infarction or arrhythmias), cardiac markers, echocardiography, and pulmonary artery catheterization to monitor hemodynamic parameters (increased PCWP, decreased CO, increased SVR).
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What is the main treatment approach for cardiogenic shock?
Treatment is based on the underlying cause and includes inotropic therapy to maintain perfusion. Intravenous fluid administration should be avoided as it worsens cardiogenic pulmonary edema.
202
What is diabetic peripheral angiopathy (DPA)?
DPA is a blood vessel disease caused by high blood glucose levels, affecting vessels that carry oxygenated blood. It leads to reduced blood and oxygen supply to organs, causing long-term damage.
203
What causes diabetic peripheral angiopathy?
High blood sugar leads to increased production of energy and reactive oxygen species (ROS) in endothelial cells, causing cell and tissue damage. Endothelial damage triggers inflammation and plaque formation, narrowing arteries and impairing blood flow.
204
What are the two main types of diabetic angiopathy?
The two types are:
Micro-angiopathy: Affects small blood vessels, making them thick and weak, slowing blood flow. It is dangerous in the kidneys, eyes, and nerves.
205
What is macro-angiopathy, and how does it affect the body?
Macro-angiopathy primarily affects large blood vessels, leading to blood clots in vessels of the brain, neck, coronary arteries, and large leg arteries. This prevents blood from reaching vital organs and increases the risk of heart attack or stroke.
206
What symptoms are associated with macro-angiopathy?
Symptoms depend on the affected blood vessels:
Micro-angiopathy of the kidney: High concentration of proteins (e.g., albumin) in excretion.
Eye: Retinopathy.
Macro-angiopathy: Weakened pulse in early stages, cold feet and hands, and pain when walking longer distances.
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How is macro-angiopathy diagnosed?
Diagnosis involves confirming diabetes (Type 1 or Type 2) and using Doppler ultrasound to detect blockages in the arteries.
208
What are the prevention strategies for diabetic angiopathy?
Prevention includes maintaining blood sugar control through daily checks and drug therapy, along with an active lifestyle.
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What are the treatment options for diabetic angiopathy?
Treatment options include:
Insulin injections (for Type 1 diabetes)
Lifestyle changes
Surgical interventions (removal of calcified plaque, balloon catheter dilation, bypass surgery, stent implantation)
210
What is diabetic foot, and why is it significant?
Diabetic foot is a serious complication of diabetes characterized by foot ulceration associated with peripheral arterial disease. It results from decreased blood flow to the foot, leading to gangrene and non-healing ulcers.
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What complications can arise from diabetic foot?
Complications include gangrene formation, infected ulcers, abscesses, and potentially necessary amputation of the foot or toes due to poor healing and loss of sensation from neuropathy.
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18. What are the four main types of cardiomyopathies?
1) Dilated Cardiomyopathy
2) Hypertrophic Cardiomyopathy
3) Restrictive Cardiomyopathy
4) Arrhythmogenic Right Ventricular Cardiomyopathy
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What is the definition of cardiomyopathies?
Cardiomyopathies are a collective name for cardiac diseases related to intrinsic myocardial dysfunction, which can be classified as primary (idiopathic) or secondary (due to identifiable cardiac injury).
215
What are the common causes of dilated cardiomyopathy?
1) Mostly idiopathic
2) Genetic predisposition (TTN gene mutation)
3) Viral infections (Coxsackie B virus)
4) Systemic disorders (sarcoidosis, hemochromatosis)
5) Toxic substances (alcohol, cocaine, doxorubicin)
6) Peripartum cardiomyopathy.
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What are the clinical features of dilated cardiomyopathy?
Slowly progressive heart failure, ineffective contractions, mitral regurgitation (systolic murmur), arrhythmias, exertional dyspnea, and edema.
217
How is dilated cardiomyopathy diagnosed?
Diagnosis is done through ECG, chest radiography (showing cardiomegaly), and echocardiography (showing dilated heart and reduced left ventricular ejection fraction).
218
What is the treatment for dilated cardiomyopathy?
Treatment includes ACE inhibitors, beta-blockers, diuretics, aldosterone receptor blockers, digoxin, heart transplant, and device therapy if needed.
219
What characterizes hypertrophic obstructive cardiomyopathy?
The myocardium becomes hypertrophied and hypercontractile, leading to filling dysfunction (diastolic heart failure) and left ventricular outflow obstruction due to hypertrophy.
220
What are the causes of hypertrophic obstructive cardiomyopathy?
Autosomal dominant missense mutations in genes encoding proteins that form the contractile apparatus of the sarcomere (myosin binding protein C, beta-myosin heavy chain).
221
What are the clinical features of hypertrophic obstructive cardiomyopathy?
Dyspnea, syncope, chest pain, and potential sudden death due to ventricular arrhythmias, especially in young athletes.
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How is hypertrophic obstructive cardiomyopathy diagnosed?
Diagnosis involves echocardiography (showing hypertrophied septum and obstruction), ECG (showing left ventricular hypertrophy), and chest X-ray (showing left atrial enlargement).
223
What is the treatment for hypertrophic obstructive cardiomyopathy?
Treatment includes beta-blockers, non-dihydropyridine calcium channel blockers (verapamil), and in advanced stages, cardiac surgery (septal myectomy) or catheter therapy (septal alcohol ablation).
224
What defines restrictive cardiomyopathy?
The myocardium becomes stiff with less compliance, leading to filling dysfunction (diastolic heart failure) while maintaining a normal heart size.
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What are the common causes of restrictive cardiomyopathy?
1) Amyloidosis
2) Endocardial fibroelastosis (primarily in children)
3) Löffler syndrome (eosinophilic infiltration leading to fibrosis).
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What are the clinical features and diagnosis of restrictive cardiomyopathy?
Signs of left and right heart failure. Diagnosis through echocardiography (normal ejection fraction but reduced diastolic filling).
227
What is the treatment for restrictive cardiomyopathy?
Treatment includes diuretics, beta-blockers, and heart transplantation.
227
What characterizes arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Primarily affects the right ventricle with fibrofatty replacement of myocardium, causing thinning and dilation. The hallmark finding is arrhythmia.
227
What causes arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Mutations in genes encoding for desmosome proteins that are part of the tight junction between cardiomyocytes.
228
What is the general treatment for arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Treatment includes amiodarone, sotalol, beta-blockers, ICD, and in selected cases, catheter ablation. All patients should avoid strenuous exercise.
228
What is microcirculation?
Microcirculation is the blood flow through the smallest vessels in the circulatory system, including arterioles, venules, and capillaries, and exists in all tissues and organs except for the cornea.
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What techniques are used to study microcirculation?
Techniques include laser Doppler imaging, laser scanners, and transcutaneous oxygen measurements.
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How does Laser Doppler imaging work?
Laser Doppler measures total local microcirculatory blood perfusion by detecting changes in wavelength of light particles that hit moving blood cells, which are converted to electrical readings or digital imaging.
231
What is Laser Speckle Contrast Analysis?
Laser Speckle Contrast Analysis visualizes tissue blood perfusion in the microcirculation instantaneously by creating a speckle pattern from backscattered light.
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What is transcutaneous oximetry?
Transcutaneous oximetry is a local, non-invasive measurement reflecting the amount of oxygen that has diffused from the capillaries through the epidermis, used for determining peripheral vascular oxygenation.
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What factors influence microcirculatory blood flow?
Factors include temperature, systemic blood pressure, general status (stress, food, medication, smoking), and physical activity.
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What is Raynaud phenomenon?
Raynaud phenomenon is a medical condition characterized by spasms of arteries that cause episodes of reduced blood flow, typically to the fingers and less commonly the toes, triggered by cold or emotional stress.
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What happens to the affected areas during an episode of Raynaud phenomenon?
The affected area turns white (ischemic phase), then blue (hypoxic phase), and finally red as blood flow returns (hyperemic phase), often accompanied by numbness or pain.
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How is Raynaud phenomenon classified?
It is classified as primary (idiopathic) and secondary.
Primary RP (Raynaud disease) occurs alone and is idiopathic, with vasospasm of digital arteries.
Secondary RP (Raynaud syndrome) occurs with another disease process, such as drugs, smoking, occupational trauma, vasculitis, or connective tissue diseases.
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What are the clinical features of primary and secondary Raynaud phenomenon?
Primary RP: Symmetrical, no ulceration or necrosis.
Secondary RP: Asymmetrical, severe pain, and ulceration.
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How is Raynaud phenomenon diagnosed?
Diagnosis is made by measuring digital artery pressures in the fingers before and after cooling; a decrease of at least 15 mmHg is diagnostic. Capillaroscopy can also be used to examine nail fold vasculature.
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What is the treatment for Raynaud phenomenon?
Treatment includes calcium channel blockers (e.g., nifedipine or amlodipine) for their vasodilation effect, along with avoiding triggers.
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19. What are supraventricular arrhythmias?
Supraventricular arrhythmias are conditions where the impulse originates from a point above the ventricles, typically in the junction or atria, and are characterized by the presence of a P wave on ECG.
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What is the significance of the P wave on an ECG in the context of arrhythmias?
The presence of a P wave indicates that the arrhythmia is supraventricular, while its absence suggests a ventricular origin
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How are sustained arrhythmias defined?
Sustained arrhythmias are defined as lasting for 30 seconds or more.
243
What is considered tachycardia?
Tachycardia is defined as three or more consecutive beats at a rhythm faster than 120 bpm.
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What is the most common sustained arrhythmia?
The most common sustained arrhythmia is atrial fibrillation.
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What is the most common non-sustained arrhythmia?
The most common non-sustained arrhythmia is ventricular extra-systole.
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How are supraventricular tachycardias (SVT) classified?
SVTs are classified into AV node-dependent SVTs and non-AV node-dependent SVTs.
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What are AV node-dependent SVTs?
AV node-dependent SVTs are arrhythmias that involve the AV node for conduction, such as atrioventricular reentrant tachycardia (AVRT) and atrioventricular nodal reentrant tachycardia (AVNRT).
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What are non-AV node-dependent SVTs?
Non-AV node-dependent SVTs originate from ectopic foci in the atria or junctional tissue and include conditions like atrial flutter and atrial fibrillation.
249
What is the role of ECG in diagnosing narrow QRS tachycardias?
The ECG helps differentiate between various types of narrow QRS tachycardias by identifying the presence of P waves and the characteristics of the tachycardia.
250
What does FBI tachycardia refer to?
FBI tachycardia refers to a specific type of tachycardia characterized by features on the ECG that help in its identification, although the term itself requires further clarification in the clinical context.
251
What are common medical treatments for supraventricular arrhythmias?
Medical treatments include antiarrhythmic medications, beta-blockers, calcium channel blockers, and anticoagulants for atrial fibrillation.
252
What is catheter ablation in the context of supraventricular arrhythmias?
Catheter ablation is a procedure used to destroy the abnormal electrical pathways causing the arrhythmias, thereby restoring normal heart rhythm.
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What is paroxysmal tachycardia?
Paroxysmal tachycardia is characterized by a sudden, irritable focus that paces rapidly, with a heart rate of 150-250 BPM, often due to sympathetic activation or hyperthyroidism.
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What is Paroxysmal Atrial Tachycardia?
Paroxysmal Atrial Tachycardia occurs when the heart's electrical impulse comes from an ectopic pacemaker in the atria instead of the SA node, leading to abnormal P wave shapes on ECG.
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What is Paroxysmal Junctional Tachycardia?
Paroxysmal Junctional Tachycardia originates from an irritable focus in the AV node, resulting in three potential P wave morphologies on ECG: inverted P' before, after, or buried within the QRS complex.
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What is AV Nodal Reentrant Tachycardia (AVNRT)?
AVNRT occurs when a reentrant circuit forms within or near the AV node, involving a fast and a slow pathway, with inverted P waves seen on ECG depending on the conduction pathways.
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What are the two types of AV Reentrant Tachycardia (AVRT)?
AVRT can be orthodromic (impulse moves antegrade through the AV node, normal QRS) or antidromic (impulse travels retrograde via an accessory pathway, resulting in wide QRS and delta wave).
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What are common treatments for paroxysmal tachycardia?
Treatments include carotid artery massage, medications like adenosine and calcium channel blockers (diltiazem, verapamil), and cardioversion (electrical current to the heart).
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What is Atrial Fibrillation (A-fib)?
A-fib is an arrhythmia characterized by rapid and irregular beating of the atrial chambers due to multiple irritable foci, leading to irregular stimulation of the AV node.
261
What cardiovascular factors are associated with A-fib?
Factors include high blood pressure, coronary artery disease, mitral valve stenosis, mitral regurgitation, left atrial enlargement, hypertrophic cardiomyopathy, and pericarditis.
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How does A-fib appear on an ECG?
A-fib is characterized by irregular intervals between QRS complexes and the absence of P waves.
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Where are the trigger foci of atrial fibrillation commonly found?
Trigger foci are most commonly found within the pulmonary veins, where muscle fibers of the left atrium grow into the veins, disrupting electrical barriers.
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What is FBI (Fast, Broad, Irregular) tachycardia?
FBI tachycardia occurs in A-fib when an accessory pathway is present, typically characterized by an atrial rate exceeding 300 beats per minute.
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What are the treatment options for A-fib?
Treatments include regular aerobic exercise, anticoagulants (e.g., warfarin), rate control drugs (beta-blockers like metoprolol, non-dihydropyridine calcium channel blockers), cardiac glycosides (digoxin), and catheter ablation.
266
What characterizes atrial flutter?
Atrial flutter is characterized by a sudden-onset, usually regular abnormal heart rhythm generated by a reentrant circuit around the annulus of the tricuspid valve, with an atrial rate of 250-350 BPM.
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How does atrial flutter affect the AV node?
In atrial flutter, the AV node doesn’t have enough time to repolarize, leading to the absence of P waves and irregular QRS complexes on the ECG.
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What is the ECG appearance of atrial flutter?
Atrial flutter shows flutter waves (F-waves) in a sawtooth pattern, with a common 4:1 pattern (four F-waves per QRS complex).
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What conditions are commonly associated with atrial flutter?
Common conditions include hypertension, obesity, and pulmonary diseases such as COPD.
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What is the treatment for atrial flutter?
Atrial flutter is managed similarly to atrial fibrillation, requiring anticoagulation or antiplatelet agents and medications to control heart rate (e.g., beta-blockers, calcium channel blockers).
271
What defines Multifocal Atrial Tachycardia (MAT)?
MAT is characterized by an irregular rhythm with an atrial rate above 100 BPM, resulting from random firing of multiple ectopic atrial foci.
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How is MAT diagnosed on an ECG?
Diagnosis of MAT requires identification of at least three different types of P waves, which vary in size and shape due to their different ectopic origins.
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What is Wandering Atrial Pacemaker?
Wandering Atrial Pacemaker is when the atrial rate is under 100 BPM, characterized by varying P waves due to shifting atrial foci.
274
What is the first-line treatment for MAT in patients with underlying pulmonary disease?
The first-line treatment for MAT in COPD patients is a non-dihydropyridine calcium channel blocker (e.g., verapamil, diltiazem) to suppress atrial rate and decrease AV conduction.
275
What is the primary cause of peripheral arterial disease (PAD)?
Most cases of PAD are atherosclerotic in origin, increasing the risk of myocardial infarction (MI) and stroke.
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What are the risk factors for PAD?
Risk factors include smoking, diabetes mellitus, hyperlipidemia, and hypertension.
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What are the clinical manifestations of PAD?
Clinical manifestations include asymptomatic stages, intermittent claudication (pain after walking 200-300 meters), and critical limb ischemia (rest pain, ulcers, gangrene).
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What is the Fontaine classification for clinical stages of PAD?
Stage 1: Asymptomatic
Stage 2a: Mild claudication
Stage 2b: Moderate to severe claudication
Stage 3: Ischemic rest pain
Stage 4: Ulceration or gangrene
279
How is PAD diagnosed?
Diagnosis involves patient history, physical examination, and the ankle-brachial index (ABI), which compares blood pressure in the ankle to that in the arm. An ABI ≤ 0.90 indicates PAD.
280
What is the gold standard for evaluating PAD?
The gold standard for evaluating PAD is angiography, while lower limb Doppler ultrasound is used to assess blood flow velocity and site of obstruction.
281
What are the treatment options for PAD?
Treatment includes lifestyle changes (quitting smoking, physical activity), medications (management of diabetes, hypertension, hypercholesterolemia, antiplatelet drugs), and revascularization procedures (angioplasty, bypass, amputation).
282
20. What are ventricular arrhythmias?
Ventricular arrhythmias are abnormal heartbeats that originate from the ventricles (below the AV node) and are characterized by a wide QRS complex (> 0.12 ms) on the ECG.
283
Why is the QRS complex wide in ventricular arrhythmias?
The QRS complex is wide because ectopic impulses spread outside the normal ventricular conduction system, causing slow ventricular depolarization.
284
What is required to define a ventricular rhythm?
A ventricular rhythm exists if there are three consecutive beats of ventricular origin.
285
What is a Premature Ventricular Contraction (PVC)?
PVCs are the most common ventricular arrhythmias caused by an irritable focus in the ventricles that leads to premature contraction, often due to hypoxia.
286
How are PVCs classified?
PVCs can be classified as:
Ventricular Bigeminy: 1 normal beat followed by 1 PVC.
Ventricular Trigeminy: 2 normal beats followed by 1 PVC.
Ventricular Quadrigeminy: 3 normal beats followed by 1 PVC.
287
What are the risks associated with PVCs?
Frequent PVCs or runs of 3 or more consecutive PVCs can lead to ventricular tachycardia (VT) or fibrillation, which can be life-threatening.
288
What is the R-on-T phenomenon?
The R-on-T phenomenon occurs when a PVC falls on the T wave of the previous beat, which is a vulnerable period in the cardiac cycle, potentially leading to dangerous arrhythmias.
289
What are the treatment options for PVCs?
Treatment options include:
Medications: Antiarrhythmic drugs, beta-blockers, and calcium channel blockers.
Electrolyte replacement: Magnesium and potassium supplements.
290
What defines Ventricular Tachycardia (VT)?
VT is defined as a run of three or more PVCs, typically with a heart rate greater than 120 BPM. It can be either non-sustained (3-6 PVCs) or sustained (> 6 PVCs).
291
What conditions can lead to Ventricular Tachycardia?
VT can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte imbalances (low magnesium and potassium), or following a heart attack.
292
How is Ventricular Tachycardia treated?
If the patient has a pulse: Cardioversion to avoid degeneration to ventricular fibrillation.
If the patient is pulseless: Defibrillation with a high-energy shock.
Medications: Procainamide (class IA antiarrhythmic), beta-blockers (e.g., carvedilol, metoprolol), and magnesium sulfate.
Catheter ablation may be considered for recurrent VT.
293
What is Ventricular Fibrillation (VF)?
VF is an irregular heart rhythm characterized by multiple foci firing, causing the heart to shake and not contract effectively, resulting in cardiac arrest, loss of consciousness, and no pulse.
294
What are common causes of Ventricular Fibrillation?
VF often occurs due to:
Coronary heart disease
Valvular heart disease
Cardiomyopathy
Electrolyte imbalances
It usually follows ventricular tachycardia.
295
How does Ventricular Fibrillation appear on an ECG?
On ECG, VF shows irregular, unformed QRS complexes without clear P waves, with a heart rate of 350-450 BPM.
296
What is an important differential diagnosis for Ventricular Fibrillation?
An important differential diagnosis for VF is "Torsades de Pointes."
297
What is the definitive treatment for Ventricular Fibrillation?
The definitive treatment for VF is defibrillation.
298
What is Torsades de Pointes (TdP)?
TdP is a unique form of polymorphic ventricular tachycardia characterized by twisting of the QRS complexes around the isoelectric baseline.
299
What are the causes of Torsades de Pointes?
TdP can be inherited or acquired, most often caused by:
Drugs (especially antiarrhythmic class III and IA)
Electrolyte disorders (leading to excessive lengthening of the QT interval)
Malnutrition and chronic alcoholism (due to potassium and magnesium deficiencies)
300
How does Torsades de Pointes appear on an ECG?
On ECG, TdP is characterized by a twisting pattern of QRS complexes around the isoelectric line.
301
What is the most effective treatment for Torsades de Pointes?
The most effective treatment is cardioversion. Additionally, magnesium sulfate is commonly used to suppress early afterdepolarizations (EADs).
302
What is Accelerated Idioventricular Rhythm (AIVR)?
AIVR is a ventricular rhythm primarily seen after the reperfusion of a coronary artery, characterized by a heart rate of 50-100 BPM.
303
How does Accelerated Idioventricular Rhythm start and terminate?
AIVR starts and terminates gradually and does not progress to ventricular tachycardia (VT) or ventricular fibrillation (VF).
304
What causes Accelerated Idioventricular Rhythm?
AIVR can be caused by:
Reperfusion of coronary arteries
Certain drugs
Electrolyte disturbances
305
What forms can valvular heart diseases take?
Valvular heart diseases can manifest as:
Stenosis: Narrowing of the valve
Insufficiency (regurgitation): Inability of the valve to close properly
Combination of both
306
What are the common causes of valvular heart diseases?
Valvular heart diseases can be acquired due to:
Infections
Underlying heart disease
Degenerative processes
Congenital conditions can also lead to valvular heart diseases.
307
Where are acquired defects primarily found?
Acquired defects are primarily found in the left heart due to higher pressure and mechanical strain on the left ventricle.
308
How do valvular stenosis and insufficiencies affect the heart?
Valvular stenosis leads to greater pressure load and concentric hypertrophy (thickening of the heart muscle).
Insufficiencies are characterized by volume overload and eccentric hypertrophy (dilation of the heart chambers).
309
What diagnostic procedures are typically used for valvular heart diseases?
Diagnostic procedures include:
ECG (Electrocardiogram)
Chest X-ray
Echocardiogram
310
What does the management of valvular heart diseases involve?
Management typically includes:
Interventional or surgical procedures to reconstruct or replace valves
Medical treatment for possible heart failure
311
What is the prevalence of tricuspid valve defects?
Tricuspid valve defects occur in less than 1% of the population.
312
Are pulmonary valve defects common?
Pulmonary valve defects are rare, except in cases of congenital conditions.
313
314
What is the most common cause of secondary tricuspid regurgitation?
Secondary tricuspid regurgitation is most commonly due to right ventricular dysfunction following pressure and/or volume overload.
315
What are the causes of primary tricuspid regurgitation?
Primary tricuspid regurgitation can be caused by:
Endocarditis (particularly in drug addicts)
Carcinoid syndrome
Myxomatous disease
Endomyocardial fibrosis
Ebstein’s anomaly
316
How is tricuspid stenosis often presented and associated?
Tricuspid stenosis is often:
Combined with tricuspid regurgitation, usually of rheumatic origin.
Almost always associated with left-sided valve lesions, particularly mitral stenosis, which typically dominates the clinical presentation.
317
What is a common problem associated with pulmonary valve diseases?
Pulmonary valve problems are usually congenital. Pulmonary hypertension may lead to secondary pulmonary valve insufficiency.
318
What are the clinical features of tricuspid regurgitation?
Holosystolic murmur: Louder with inspiration (Carvallo’s sign).
Symptoms of right-sided heart failure:
Distended neck veins
Lower extremity swelling
Hepatosplenomegaly
319
What are the clinical features of tricuspid stenosis?
Snap and diastolic rumble.
Symptoms of right-sided heart failure.
320
What are the clinical features of pulmonary regurgitation?
Graham Steel murmur: High-frequency decrescendo diastolic murmur.
321
What are the clinical features of pulmonary stenosis?
Crescendo-decrescendo systolic murmur.
322
What is the preferred method for diagnosing tricuspid valve problems?
Echocardiography is the preferred method for evaluating:
Degree of tricuspid valve deformation
Right ventricular (RV) function
Pulmonary pressures
Severity of regurgitation (grade I-IV)
Transvalvular gradient
323
When is tricuspid valve surgery indicated?
Tricuspid valve surgery is indicated in symptomatic patients with significant tricuspid regurgitation or severe tricuspid stenosis.
324
What is the role of diuretics in managing valve diseases?
Diuretics are useful in managing heart failure (HF) in patients with tricuspid and pulmonary valve diseases.
325
What is the primary diagnostic tool for tricuspid valve problems?
The primary diagnostic tool is the echocardiogram.
326
What are the treatment options for tricuspid regurgitation?
Maintain fluid balance.
Valve repair or replacement is rare.
327
What is the treatment for tricuspid stenosis?
Balloon valvuloplasty is the treatment for tricuspid stenosis.
328
What is the treatment for pulmonary regurgitation?
Valve replacement is the treatment for pulmonary regurgitation.
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What is the treatment for pulmonary stenosis?
Balloon valvuloplasty is the treatment for pulmonary stenosis.
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