Copilot Exam 4 - Notes Week 1 to 5 Flashcards
(184 cards)
1
Q
Questions
A
Answers
2
Q
What are the contents of the thoracic cavity?
A
Mediastinum: Heart, thymus, trachea, esophagus, major vessels. Pleural Cavities: Lungs, pleural membranes.
3
Q
What are the boundaries and divisions of the mediastinum?
A
Boundaries: Superior (thoracic inlet), Inferior (diaphragm), Anterior (sternum), Posterior (vertebral column), Lateral (pleural cavities). Divisions: Superior and Inferior (Anterior, Middle, Posterior).
4
Q
What are the contents of each division of the mediastinum?
A
Superior: Thymus, great vessels, trachea, esophagus, vagus & phrenic nerves. Inferior—Anterior: Fat, lymph nodes. Middle: Heart, pericardium, great vessels. Posterior: Esophagus, descending aorta, thoracic duct.
5
Q
Describe the structure, blood supply, and innervation of the pericardium.
A
Structure: Fibrous (outer) + Serous (parietal & visceral with fluid). Blood supply: Pericardiophrenic, bronchial & esophageal arteries. Innervation: Phrenic, vagus, sympathetic trunks.
6
Q
What are the functions of the pericardium?
A
Protects heart, reduces friction, prevents overdistension, anchors heart.
7
Q
Describe the structure and great vessels of the heart.
A
Structure: 4 chambers, valves (tricuspid, mitral, pulmonary, aortic), layers (endocardium, myocardium, epicardium). Great Vessels: Vena cava, pulmonary arteries/veins, aorta.
8
Q
Describe the branches and distribution of the coronary arteries.
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Right: Marginal & posterior interventricular (supplies RA, RV, LV, septum). Left: Circumflex & LAD (supplies LA, LV, septum).
9
Q
Explain the direction of blood flow in the heart.
A
Deoxygenated: Body → RA → RV → Lungs. Oxygenated: Lungs → LA → LV → Body.
10
Q
Compare the structure of the right and left sides of the heart.
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Right: Thin walls, low-pressure (lungs). Left: Thick walls, high-pressure (body).
11
Q
Describe the location and position of the heart and its chambers.
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In mediastinum, behind sternum, rests on diaphragm. Apex at 5th intercostal space.
12
Q
Describe the location and position of major vessels.
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Aorta: Ascends, arches, descends. Pulmonary trunk: From RV, splits. Vena cava: Drains into RA.
13
Q
Identify the relevant areas for palpation in the cardiovascular system.
A
Carotid (neck), radial/ulnar (wrist), apical impulse (5th ICS), femoral, popliteal.
14
Q
Identify the sites for auscultation of the heart.
A
Aortic: R 2nd ICS. Pulmonary: L 2nd ICS. Tricuspid: L 4th ICS near sternum. Mitral: L 5th ICS midclavicular.
15
Q
What are the phases of the cardiac cycle?
A
Atrial systole (atria contract). Ventricular systole (contraction & ejection). Diastole (relaxation & filling).
16
Q
Describe the structure of the myocardium.
A
Cardiomyocytes arranged in spiral bundles, intercalated discs for synchronized contraction.
17
Q
Describe the structure and function of cardiomyocytes.
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Striated, central nucleus, rich in mitochondria, connected via intercalated discs.
18
Q
Explain cardiac output and its determinants.
A
CO = HR × SV. Influenced by HR, preload, afterload, contractility.
19
Q
Discuss factors affecting venous return.
A
Muscle pump, respiration, venous valves, blood volume, venous tone.
20
Q
Discuss the anatomy and histology of heart valves.
A
AV: Tricuspid (right), Mitral (left), supported by chordae tendineae & papillary muscles. Semilunar: Pulmonary & Aortic (pocket-like cusps).
21
Q
What generates heart sounds?
A
S1: AV valves closure. S2: Semilunar valves closure.
22
Q
Explain the consequences of insufficient valvular function.
A
Regurgitation (backflow), stenosis (restricted flow).
23
Q
Identify the structures in the cardiac conduction pathway.
A
SA node → AV node → Bundle of His → Bundle branches → Purkinje fibers.
24
Q
Describe the spread of electrical activity across the heart.
A
SA node initiates → AV node delays → Bundle of His → Bundle branches → Purkinje fibers (ventricles contract).
25
What triggers cardiac myocyte contraction?
Ca²⁺ influx triggers SR calcium release → Actin-myosin interaction → Contraction.
26
What are the characteristics of ventricular action potential?
Long duration (~200 ms), plateau phase for sustained contraction.
27
What are the characteristics of pacemaker action potential?
Spontaneous depolarization, no true resting potential, key ions: Na, K, Ca.
28
What describes cardiac autonomic control?
Sympathetic: Increases HR & contractility. Parasympathetic (vagus): Decreases HR.
29
Which heart sound corresponds to aortic & pulmonary valve closure?
S2.
30
Which channels drive repolarization in cardiac AP?
Potassium channels.
31
What structure separates the heart's diaphragmatic surface from the base?
Coronary sulcus.
32
What structure describes the histology of AV valves?
Three parts: Collagen, fibrous ligaments, papillary muscles.
33
What ECG wave corresponds to ventricular repolarization?
T wave.
34
What differentiates pacemaker vs. cardiac muscle action potentials?
Pacemaker AP: SA/AV nodes, driven by funny current, automatic. Cardiac AP: Non-pacemaker, stimulus-driven.
35
When the LV stroke volume is 40 ml/beat and HR is 80 bpm, what is cardiac output?
CO = SV × HR → 40 × 80 = 3.2 L/min.
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Questions
Answers
37
Identify major arteries, veins, and lymphatics.
Arteries: Aorta, carotid, subclavian, renal, femoral. Veins: SVC, IVC, jugular, femoral, renal. Lymphatics: Thoracic duct, nodes near vessels.
38
Describe conducting, distributing, and small arteries.
Conducting: Large, elastic (e.g., aorta), maintain flow. Distributing: Muscular, direct blood to organs. Small arteries/arterioles: Regulate resistance, control BP.
39
Describe venules, medium veins, and large veins.
Venules: Small, collect blood. Medium veins: Valves prevent backflow. Large veins: Thick walls, large lumen (e.g., SVC, IVC).
40
Compare arterial and venous walls.
Arteries: Thick tunica media, elastic fibers, narrow lumen. Veins: Thin tunica media, wider lumen, valves present.
41
Explain pressure, volume, resistance, and flow.
Flow = Pressure difference ÷ Resistance. High pressure or low resistance increases flow.
42
Define preload and afterload.
Preload: Ventricular volume at end-diastole. Afterload: Resistance ventricles must overcome.
43
Define cardiac output (CO).
CO = HR × SV. Influenced by preload, contractility, afterload, HR.
44
Define mean arterial pressure (MAP).
MAP = Diastolic Pressure + (1/3 × Pulse Pressure).
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Identify parameters affecting MAP.
CO: HR × SV. TPR: Resistance in circulation. SV: Blood per beat. HR: Beats per minute.
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Describe effects of parameter changes on MAP.
↑ CO or TPR → ↑ MAP. ↓ CO or TPR → ↓ MAP.
47
Define basal vascular tone.
Continuous partial smooth muscle contraction, regulated by autonomic input.
48
Describe extrinsic arterial regulators.
Sympathetic & hormones (e.g., adrenaline, angiotensin II) influence vasoconstriction or dilation.
49
Describe intrinsic arterial regulators.
O2, CO2, lactic acid, nitric oxide, endothelin-1 regulate local vascular tone.
50
Explain autoregulation in organs.
Heart: Maintains flow. Brain: Responds to CO2. Kidneys: Adjusts filtration. Lungs: Reacts to O2.
51
Locate baroreceptors and their function.
Carotid sinus, aortic arch—detect BP changes, adjust autonomic response.
52
Describe autonomic control of BP.
Sympathetic ↑ BP, parasympathetic ↓ BP.
53
Explain the baroreceptor reflex.
Detects pressure change → Signals medulla → Adjusts HR & vascular tone.
54
Identify RAAS structures.
Kidneys: Renin. Liver: Angiotensinogen. Lungs: ACE. Adrenal: Aldosterone.
55
Describe RAAS function.
Regulates BP via vasoconstriction & sodium retention.
56
Describe the RAAS sequence.
Renin → Ang I → ACE → Ang II → Vasoconstriction + Aldosterone → Na/water retention.
57
Define hypertension & types.
Systolic ≥140 mmHg or diastolic ≥90 mmHg. Primary: No cause. Secondary: Disease-related.
58
List hypertension risk factors.
Obesity, inactivity, high salt, stress, genetics.
59
Describe essential hypertension pathophysiology.
↑ vascular resistance due to endothelial dysfunction & ↑ sympathetic tone.
60
Define hypertensive crisis.
BP ≥180/120 mmHg with potential organ damage.
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Classify hypertension stages.
Normal <120/80. Elevated 120–129/<80. Stage 1: 130–139/80–89. Stage 2: ≥140/90 mmHg.
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List hypertension symptoms.
Often asymptomatic. Advanced: Headache, dizziness, vision changes, chest pain.
63
Describe hypertension diagnosis.
Repeated BP measurements, ambulatory monitoring, end-organ damage assessment.
64
List first-line antihypertensives.
ACE inhibitors, ARBs, β-blockers, CCBs, thiazide diuretics.
65
Describe antihypertensive mechanisms.
ACE inhibitors: Block Ang I→II. ARBs: Block Ang II receptors. BBs: ↓ HR & contractility.
66
Define hypertensive emergency treatment.
IV antihypertensives (e.g., nitroprusside, labetalol). Gradual BP reduction.
67
List hypertension complications.
Cardiac (LV hypertrophy, HF), cerebral (stroke), renal (CKD), ocular (retinopathy).
68
Explain pathophysiology of hypertension complications.
Atherosclerosis (plaque), LV hypertrophy (↑ workload), HF (pump failure), stroke (ischemia).
69
List lifestyle modifications for BP control.
Weight loss, ↓ salt, exercise, DASH diet, stress reduction, smoking cessation.
70
Which hormone regulates BP via osmolarity?
ADH—released when plasma osmolarity rises.
71
Which vessel has the lowest flow velocity?
Capillaries—allow efficient exchange.
72
Which structure distinguishes arteries from veins?
Arteries: Thick, elastic walls, high pressure.
73
Which vessel constricts due to angiotensin II?
Arterioles—angiotensin II is a potent vasoconstrictor.
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Which BP regulation mechanism involves RAAS?
RAAS adjusts BP via vasoconstriction & fluid retention.
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Which factor alters blood flow resistance?
Hematocrit—↑ viscosity decreases flow.
76
Which medication affects electrolytes most?
ACE inhibitors—risk of hyperkalemia.
77
Which value decreases after hemorrhage compensation?
Venous compliance—sympathetic stimulation constricts veins.
78
Which drug impacts diabetes the most?
Thiazide diuretics—risk of hyperglycemia.
79
Which receptor does sympathetic stimulation target?
β1-adrenergic receptors—↑ cardiac output.
80
Which mechanism defines angiotensin II function?
Vasoconstriction + aldosterone release → ↑ BP.
81
Questions
Answers
82
What are the key features of capillary structure?
Single endothelial cell layer, basement membrane, no smooth muscle, pores for permeability.
83
What are the three main processes across the capillary wall?
Diffusion (solutes move down concentration gradient), Osmosis (water movement via osmotic gradients), Bulk Flow (filtration & reabsorption due to pressure differences).
84
What are the four forces determining capillary fluid movement?
Capillary hydrostatic pressure (CHP), Interstitial hydrostatic pressure (IFHP), Blood colloid osmotic pressure (BCOP), Interstitial fluid colloid osmotic pressure (IFCOP).
85
What does Starling’s Law explain?
Balance between hydrostatic and oncotic pressures controls fluid movement into/out of capillaries.
86
What is the role of the lymphatic system?
Removes excess fluid/proteins from interstitial space, prevents oedema, returns fluid to circulation.
87
What is oedema?
Excess fluid accumulation in interstitial space, causing tissue swelling.
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What are the four mechanisms of oedema?
↑ Capillary hydrostatic pressure, ↓ Plasma oncotic pressure, ↑ Capillary permeability, ↓ Lymphatic drainage.
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What conditions increase capillary hydrostatic pressure?
Heart failure, DVT, fluid overload, pregnancy (compression).
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What conditions reduce plasma oncotic pressure?
Liver disease (↓ albumin), nephrotic syndrome (protein loss), malnutrition.
91
What increases capillary permeability?
Inflammation, burns, allergic reactions, sepsis.
92
What conditions obstruct lymphatic drainage?
Tumors, infections (filariasis), post-surgical lymph node removal.
93
What are common clinical manifestations of oedema?
Swelling (legs, hands, face), weight gain, breathlessness, ascites, raised JVP.
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What is heart failure (HF)?
Inability of heart to pump effectively, leading to congestion or inadequate perfusion.
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What are the major risk factors for HF?
Hypertension, CAD, diabetes, valvular disease, obesity, smoking, sedentary lifestyle.
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What are the stages of HF?
AHA/ACC: A (risk), B (structural, no symptoms), C (symptomatic), D (refractory). NYHA: I (no limits), II (mild limits), III (marked limits), IV (symptoms at rest).
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What are the signs/symptoms of left-sided heart failure?
Dyspnoea, orthopnoea, PND, fatigue, crackles, tachypnoea, S3 gallop, pulmonary oedema.
98
What are the signs/symptoms of right-sided heart failure?
Peripheral oedema, raised JVP, hepatomegaly, ascites, weight gain, fatigue.
99
What is cardiac remodeling?
Structural and functional heart changes due to stress/injury (e.g., MI, hypertension).
100
What differentiates concentric vs. eccentric remodeling?
Concentric: Thick walls, reduced chamber size (pressure overload). Eccentric: Dilated chamber, thin walls (volume overload).
101
What are key diagnostic tests for HF?
ECG, BNP/NT-proBNP, troponin, CXR, echocardiogram, blood tests.
102
What are key CXR findings in HF?
Pulmonary oedema (batwing pattern), upper lobe blood diversion, cardiomegaly, pleural effusions, Kerley B lines.
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What are acute HF complications?
Pulmonary oedema, cardiogenic shock, arrhythmias, renal dysfunction.
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What are chronic HF complications?
Declining ejection fraction, thromboembolism, cardiac cirrhosis, cachexia, hyponatraemia.
105
What are the first-line medications for chronic HF?
ACE inhibitors, ARBs, ARNIs, β-blockers, MRAs, SGLT2 inhibitors, diuretics.
106
What defines shock?
Impaired tissue perfusion leading to cellular hypoxia and organ failure.
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What are the main types of shock?
Hypovolemic (low blood volume), Cardiogenic (pump failure), Distributive (vasodilation), Obstructive (blockage).
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What are the stages of shock?
Compensated (maintained BP), Progressive (organ dysfunction), Irreversible (multi-organ failure).
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What is cardiogenic shock?
Severe pump failure reducing cardiac output, leading to systemic hypoxia and metabolic acidosis.
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What are key treatments for cardiogenic shock?
Oxygen therapy, inotropes (dobutamine, milrinone), vasopressors (norepinephrine, dopamine), diuretics, mechanical support (IABP, LVAD).
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Questions
Answers
112
What are the key components of an ECG?
P wave: Atrial depolarization. QRS complex: Ventricular depolarization. T wave: Ventricular repolarization.
113
What are the intervals in an ECG and their significance?
PR: Atrial to ventricular depolarization. QT: Ventricular depolarization to repolarization.
114
How is a standard 12-lead ECG derived?
Limb leads (bipolar), augmented limb leads (unipolar), chest leads (unipolar) provide heart’s electrical activity from different angles.
115
What does cardiac axis represent?
Overall direction of ventricular depolarization in the frontal plane.
116
What determines ECG electrical deflection?
A wave moving toward a positive electrode produces an upward deflection.
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What is the systematic approach to ECG interpretation?
Rate, rhythm, axis, hypertrophy, ischemia.
118
What defines sinus rhythm?
Normal P wave before each QRS complex, regular R-R intervals, rate 60-100 bpm.
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What is sinus bradycardia?
Sinus rhythm with HR <60 bpm.
120
What is sinus tachycardia?
Sinus rhythm with HR >100 bpm.
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What are the types of axis deviation?
Left axis (-30° to -90°), right axis (+90° to +180°).
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What defines tachyarrhythmia?
Arrhythmia with HR >100 bpm.
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What are symptoms of tachyarrhythmia?
Palpitations, presyncope, syncope, chest pain, dyspnea.
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What are key ECG findings in ventricular tachycardia (VT)?
Wide QRS complexes, rate >100 bpm, regular rhythm.
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What defines ventricular fibrillation (VF)?
Chaotic, irregular ECG deflections, no distinct waves or complexes.
126
What are ECG findings in atrial fibrillation (AF)?
Irregularly irregular rhythm, absent P waves, variable R-R intervals.
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What characterizes atrial flutter?
Sawtooth flutter waves, often regular ventricular response.
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What defines supraventricular tachycardia (SVT)?
Narrow QRS tachycardia, often with hidden P waves.
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What defines bradyarrhythmia?
Arrhythmia with HR <60 bpm.
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What are symptoms of bradyarrhythmia?
Lethargy, syncope, palpitations, HF.
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What is 1st-degree heart block?
Prolonged PR interval (>200 ms).
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What defines Mobitz type I heart block?
Progressive PR prolongation until QRS drop.
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What defines Mobitz type II heart block?
Fixed PR intervals with intermittent QRS drop.
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What diagnostic modalities identify arrhythmias?
ECG, Holter monitor, loop recorder, pacemaker interrogation.
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What are tachyarrhythmia complications?
Hemodynamic instability, thromboembolism, HF.
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What are bradyarrhythmia complications?
Syncope, HF, cardiac arrest.
137
What pharmacologic treatments manage arrhythmias?
Na+ blockers, β-blockers, K+ blockers, Ca2+ blockers.
138
What defines Na+ channel blockers?
Slow conduction velocity by blocking sodium influx.
139
What defines β-blockers?
Decrease HR and contractility by blocking β-adrenergic receptors.
140
What defines K+ channel blockers?
Prolong repolarization via potassium channel blockade.
141
What defines Ca2+ channel blockers?
Reduce contractility and conduction.
142
What are interventional approaches to arrhythmia treatment?
Defibrillation, pacemakers (temporary/permanent), ablation.
143
What lifestyle modifications aid in arrhythmia prevention?
Control underlying conditions, avoid triggers (caffeine, alcohol), maintain healthy habits.
144
What drug is NOT a calcium channel blocker?
Amiodarone—acts on potassium channels.
145
What is the normal QRS duration?
0.06–0.10 secs.
146
What is the most likely ECG finding in a collapsed patient with no regular rhythm?
Ventricular fibrillation.
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What does the S wave indicate in ECG?
Depolarization of the heart near the base.
148
What causes atrial fibrillation?
Multiple circulating re-entrant excitation waves in the atria.
149
What defines first-degree heart block?
PR interval prolonged due to slowed AV node conduction.
150
What ECG component assesses atria-to-ventricle conduction?
PR interval.
151
What drug increases HR in sinus rhythm?
Atropine—blocks vagal effects, allowing sympathetic action.
152
What is the likely diagnosis for a patient with irregularly irregular HR and palpitations?
Paroxysmal atrial fibrillation.
153
What is the next diagnostic step for suspected atrial fibrillation?
Electrocardiogram (ECG).
154
What is the priority treatment for atrial fibrillation?
Anticoagulation and rate control.
155
Questions
Answers
156
What causes murmurs?
Turbulent blood flow due to stenosis, regurgitation, high flow states, or structural defects.
157
How do maneuvers affect murmurs?
Inspiration ↑ right-sided murmurs. Expiration ↑ left-sided murmurs. Valsalva ↓ most murmurs except HCM/MVP. Handgrip ↑ regurgitant murmurs, ↓ stenotic murmurs.
158
What causes S3 and S4 sounds?
S3: Rapid filling into volume-overloaded ventricle. S4: Atrial contraction against stiff ventricle.
159
What are murmurs for left-sided valve lesions?
AS: Harsh systolic (RUSB → carotids). AR: Diastolic decrescendo (LUSB → left sternal border). MS: Low rumbling diastolic (apex). MR: Blowing holosystolic (apex → axilla).
160
What are murmurs for right-sided valve lesions?
PS: Harsh systolic (LUSB → shoulder). PR: Diastolic decrescendo (LUSB). TS: Low rumbling diastolic (LLSB). TR: Blowing holosystolic (LLSB → right sternal border).
161
What is aortic stenosis (AS)?
Narrowed aortic valve obstructs LV outflow, causing LV hypertrophy and reduced cardiac output.
162
What are common causes of AS?
Degenerative calcification (elderly), congenital bicuspid valve, rheumatic disease.
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What are symptoms of AS?
Classic triad: Angina, syncope, dyspnea. Other: Fatigue, palpitations, sudden death.
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What are key AS exam findings?
Harsh systolic ejection murmur (RUSB → carotids), pulsus parvus et tardus, narrow pulse pressure.
165
What are AS diagnostic tools?
Echocardiogram (valve area, gradient, LV function), ECG (LVH), CXR (post-stenotic dilation).
166
What is the definitive AS treatment?
Aortic valve replacement (Surgical AVR or TAVI).
167
What is mitral stenosis (MS)?
Narrowed mitral valve obstructs LA flow, causing LA enlargement, pulmonary hypertension, RV hypertrophy.
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What are key causes of MS?
Rheumatic heart disease (most common), congenital MS, carcinoid heart disease.
169
What are symptoms of MS?
Dyspnea, fatigue, palpitations, hemoptysis, systemic embolization.
170
What are key MS exam findings?
Loud S1, opening snap, low-pitched diastolic murmur (apex).
171
What are MS diagnostic tools?
Echocardiogram (valve area, pressure gradient, LA size), ECG (LA enlargement, AF), CXR (LA enlargement).
172
What is the preferred MS treatment?
Percutaneous mitral balloon valvuloplasty (PMBV) if suitable.
173
What is aortic regurgitation (AR)?
Backward flow of blood into LV during diastole, causing volume overload.
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What are common causes of AR?
Bicuspid valve, infective endocarditis, aortic root dilation, Marfan syndrome.
175
What are symptoms of AR?
Wide pulse pressure, bounding pulses, palpitations, dyspnea, angina.
176
What are key AR exam findings?
High-pitched diastolic murmur (LUSB), Austin Flint murmur, Corrigan’s pulse.
177
What are AR diagnostic tools?
Echocardiogram (valve regurgitation severity), ECG (LVH), CXR (cardiomegaly).
178
What is AR management?
Medical (vasodilators), surgical (AVR for severe cases).
179
What is mitral regurgitation (MR)?
Backward flow of blood into LA during systole, causing LA overload and LV dilation.
180
What are common causes of MR?
Mitral valve prolapse (MVP), ischemic heart disease, rheumatic disease, endocarditis.
181
What are symptoms of MR?
Dyspnea, fatigue, palpitations, orthopnea, heart failure.
182
What are key MR exam findings?
Blowing holosystolic murmur (apex → axilla), loud S3.
183
What are MR diagnostic tools?
Echocardiogram (valve regurgitation severity, LV function), ECG (LA enlargement, AF), CXR (cardiomegaly).
184
What is MR management?
Medical (ACE inhibitors, diuretics, beta-blockers), surgical (repair/replacement).
