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STEP > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Patient presents with BP of 200/120 mm hg,, has dyspnea and is hyperemic. Chest Xray shows pulmonary edema and ECG shows inverted T waves in the inferolateral leads. Which medication should be used?

A

Nitroglycerin

  • A direct venous dilator that reduces preload
  • Has vasodilator effects on coronary vessels
  • Should be used in the setting of acute cardiac ischemia and pulmonary edema
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2
Q

28 YO pregnant woman is brought to the ER due to elevated BP of 180/90 mm Hg. She is asymptomatic and has a history of preeclampsia. What medication should be given?

A

Labetalol

  • Combined alpha/beta adrenergic blocker
  • Safe to use in pregnancy
  • Also used in aortic dissection
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3
Q

Preferred medications for patients with preeclampsia or eclampsia?

A

Labetalol and Nifedipine

Magnesium sulfate is also given IV to avoid seizures

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4
Q

What is the target goal for BP control in women with preeclampsia or eclampsia?
What if the platelet count is below 100,000?

A

< 160/110 mmHg

< 150/100 mmHg

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5
Q

What is the treatment of choice for cocaine associated acute coronary syndromes?

A

Alpha adrenergic antagonists

- Phentolamine

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6
Q

Preferred medications for treatment of acute intracerebral hemorrhage caused by hypertensive emergency? Which should be avoided?

A
  • Labetalol, Nicardipine or Esmolol

- Avoid Sodium Nitroprusside and Hydralazine

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7
Q

Preferred medications for treatment of aortic dissection caused by hypertensive emergency? Which should be avoided?

A
  • Labetalol, Nicardipine, Sodium Nitroprusside (add Beta-blocker), Esmolol and Morphine Sulfate
  • Avoid Beta-Blocker if aortic regurgitation or suspected cardiac tamponade
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8
Q

What is Fenoldopam used for?

- MOA

A
  • Hypertensive Emergency with Renal Insufficiency (AKI)
  • Short acting, selective, peripheral dopamine-1 receptor agonist
  • Little or no effect on alpha or beta adrenergic receptors
  • Dopamine-1 receptor agonism stimulates adenylyl cyclase and raises intracellular cyclic AMP
  • Results in vasodilation of most arterial beds with a decrease in systemic blood pressure
  • Renal vasodilation is prominent and increases renal perfusion, diuresis and natriuresis
  • IV
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9
Q

When does left ventricular myocardial perfusion occur? Why?

A
  • During diastole
  • Because during systole ventricular pressure and wall stress exceed the aortic pressure (120 mm Hg) preventing effective coronary perfusion
  • Relaxation during diastole decreases intraventricular pressure (10 mmHg) which is much lower than aortic diastolic pressure (80 mm Hg) providing for adequate perfusion
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10
Q

What happens in the coronary circulation with increased HR?

A
  • It shortens the time of ventricular relaxation
  • Time of diastole
  • Therefore time available for maximal coronary flow will decrease and becomes a major limiting factor for blood supply
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11
Q

What does phenytoin do to the gums?

A
  • Gingival hyperplasia
  • Increases expression of platelet derived growth factor
  • When macrophages are exposed to PDGF, they stimulate proliferation of gingival cells and alveolar bone
  • May regress after discontinuation of phenytoin
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12
Q

Most common bacterial causes of heart block?

A

HR is not as fast as we expect it to be

  • Legionella
  • Lyme disease
  • Chagas disease
  • Dipththeria
  • Typhoid fever
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13
Q

MI with Right Ventricular Failure

A
  • Occurs Acutely
  • Hypotension and clear lungs
  • Kussmaul sign
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14
Q

MI with Papillary Muscle Rupture

A
  • Occurs within 3-5 days
  • Acute, severe pulmonary edema
  • Severe mitral regurgitation with flail leaflet
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15
Q

MI with Interventricular Septum/Rupture Defect

A
  • Occurs within 3-5 days
  • New holosystolic murmur
  • Step up oxygen level between right atrium and ventricle
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16
Q

MI with free wall rupture

A
  • Within 5-14 days
  • Pericardial Tamponade
  • Jugular venous distension
  • Distant heart sounds
  • Profound Hypotension is usually cause of death
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17
Q

Where do you find Beta 1 receptors?

A
  • Cardiac tissue

- Renal juxtaglomerular cells

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18
Q

What kind of receptors is a Beta 1 receptor?

A
  • A G protein coupled receptor
  • It is associated with Gs
  • Increases intracellular levels of cAMP
  • Blocking the receptor with a beta blocker decreases levels of cAMP in cardiac and renal tissue
  • No effect on vascular smooth muscle since it contains no Beta 1 receptors
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19
Q

How are the lymphatics of the extremities divided?

A
  1. Superficial lymphatic vessels
    - Follow the venous system
  2. Deep lymphatic vessels
    - Follow the arterial system
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20
Q

How are the lymphatics of the lower extremities divided?

A
  1. Medial track
    - Runs along the saphenous vein to the superficial inguinal lymph nodes
    - It bypasses the popliteal nodes
    - Lesion to medial track causes inguinal lymphadenopathy
  2. Lateral track
    - Communicates with the popliteal and inguinal lymph nodes
    - Lesion to the lateral track will cause popliteal and inguinal lymphadenopathy.
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21
Q

Where do the prostate lymphatics drain to?

A

Into the internal iliac lymph nodes

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22
Q

Where does the scrotum lymphatics drain to?

A

They drain into the superficial inguinal lymph nodes

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23
Q

Where do the testicular lymphatic drain to?

A

The para aortic lymph nodes

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24
Q

What are the cardiologic findings in Turner syndrome?

A
  • Bicuspid aortic valve is the most common
  • Creates aortic ejection sound, it presents as early systolic, high frequency click heard in the right second intercostal space, sternal border
  • The valve may be at risk for stenosis, insufficiency and infectious endocarditis
  • Coarctation of the aorta may also be seen in turner syndrome
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25
Q

What will EKG show if electrical impulses are generated below the AV node and his bundle?

A
  • HR can be as slow as 20 BPM

- ECG shows prolonged, abnormally shaped QRS complexes due to aberrant impulse conduction through the ventricles

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26
Q

When can the Av node become the pacemaker?

A
  • When conduction between the SA node and AV node is impaired
  • Such as third degree AV block (complete heart block)
  • SA node causes atrial contraction and AV causes ventricular contraction independant of each other
  • QRS complexes will be narrow since ventricular depolarization proceeds normally
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27
Q

What are the two signs of microembolism seen in infectious endocarditis?

A
  1. Splinter Hemorrhages
    - Flame shaped hemorrhagic streaks that occur under the nail bed
  2. Janeway lesions
    - Small, macular, erythematous or hemorrhagic, non tender lesions on the palms and soles
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28
Q

What are the three main causes of valvular aortic stenosis?

A
  1. Calcified normal valve (Most common in US)
  2. Rheumatic heart disease (Most common worldwide
  3. Congenitally abnormal valve with calcification
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29
Q

Name a few low molecular weight heparins?

What are they used for?

A
  • Enoxaparin and Dalteparin
  • Indirect thrombin inhibitors that bind to antithrombin and convert it from a slow to a rapid inactivator of thrombin and factor Xa.
  • Used in patients with acute coronary syndrome
  • Such as unstable angina or myocardial infarction
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30
Q

What does the truncus arteriosus give rise to?

A

Aorta and the pulmonary trunk

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31
Q

What does the bulbus cordis give rise to?

A

Smooth parts of the left and right ventricles (the outflow tract)

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32
Q

What does the endocardial tissue give rise to?

A
  • Atrial septum
  • Membranous Interventricular septu
  • AV and semilunar valves
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33
Q

What does the primitive atrium give rise to?

A

Trabeculated part of the left and right atria

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34
Q

What does the primitive ventricle give rise to?

A

Trabeculated part of the left and right ventricles

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35
Q

What does the primitive pulmonary vein give rise to?

A

Smooth part of the left atrium

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36
Q

What does the left horn of the sinus venosus give rise to?

A

Coronary sinus

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37
Q

What does the right horn of the sinus venosus give rise to?

A

Smooth part of right atrium (sinus venarum)

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38
Q

What does the right common cardinal vein and right anterior cardinal vein give rise to?

A

Superior vena cava

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39
Q

What is the first functional organ in embryos and when does it begin to work?

A

The heart and it beats spontaneously by week 4 of development

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40
Q

When does the heart begin to loop and establish its polarity?
What defects can result during this?

A
  • In week 4 of gestation, the primary heart loops to establish the left and right sides
  • Defect in left to right dyenin (in L/R asymmetry) can lead to dextrocardia, seen in Kartagener syndrome (primary ciliary dyskinesia)
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41
Q

Describe the septation of the chambers?

A
  1. Septum primum grows toward endocardial cushions, narrowing the foramen primum.
  2. Foramen secundum forms in septum primum (foramen primum disappears)
  3. Septum secundum develops as foramen secundum maintains right to left shunt
  4. Septum secundum expands and covers most of the foramen secundum. The residual foramen is the foramen ovale
  5. Remaining portion of the septum primum forms valve of foramen ovale
  6. Septum secundum and septum primum fuse to form the atrial septum
  7. Foramen ovale usually closes soon after birth because of increase in LA pressure
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42
Q

What is patent foramen ovale?

A
  • Failure of septum primum and septum secundum to fuse after birth
  • Most are left untreated
  • Can lead to paradoxical emboli (venous thromboemboli that enters systemic arterial circulation) similar to those resulting from an ASD
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43
Q

Describe how the ventricles form?

A
  1. Muscular interventricular septum forms, the opening is called the interventricular foramne
  2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum closing interventricular foramen
    3 Growth of endocardial cushions seperates atria from ventricles and contributes to both atrial septation and membranou sportion of the interventricular septum.
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44
Q

What is a ventral septal defect?

A
  • Most common congenital cardiac anomality

- Usually occurs in the membranous septum

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45
Q

How does the outlfow tract form?

A
  1. Neural crest and endocardial cells migrate
  2. Truncal and bulbar ridges spiral and fuse to form the aorticopulmonary septum.
    3, Ascending aorta and pulmonary trunk form
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46
Q

What are conotruncal abnormalities associated with failure of neural crest cells to migrate?

A
  • Transposition of the great vessels
  • Tetrology of Fallot
  • Persistent truncus arteriosus
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47
Q

How do the valves develop?

A
  • Aortic/pumonary are derived from the endocardial cushions of the outflow tract
  • Mitral/tricuspid are derived from fused endocardial cushions of the AV canal
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48
Q

What causes Pericarditis?

What are the features?

A

Most commonly caused by viral infections
Also caused by MI (dresslers syndrome), radiation to the chest, metastatic cancer, systemic diseases particularly SLE, other autoimmune disorders and uremia
- Damage leads to the inflammatory process
- Inflammed pericardium reasults in positional and pleuritic chest pain
- Pain is releaved by sitting up
- Pericardium becomes stiff and noncompliant
- You will hear the hearts motion across the pericardium, like a grating noise

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49
Q

Isolated Systolic Hypertension

A
  • Seen in patients over 60 years old
  • Responsible for 60-80% of hypertension in this population
  • SBP > 140 mmHg is an important modifiable risk factor for stroke and heart disease
  • Aging leads to increased arterial stiffness by endothelial dysfunction and change in extracellular matrix composition
  • Due to decreased elastin and increased collagen deposition
  • There is decreased compliance of the aorta and major peripheral arteries
  • ISH can also result from increased cardiac output in aortic regurgitation or systemic causes such as anemia or hyperthyroidism
50
Q

Aortic Dissection

A
  • A longitudinal intimal tear forming a false lumen
  • Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (Marfans)
  • Can present with tearing, sudden onset chest pain, radiating to the back
  • Blood pressure can be equal or unequal in arms
  • Chest X ray will show mediastinal widening
  • Can lead to organ ischemia, aortic rupture and death
    1. Stanford Type A
  • Proximal tear
  • Involves the ascending aorta
  • May extend into the aortic arch or descending aorta
  • May result in acute aortic regurgitation or cardiac tamponade
  • Treat with surgery
    2. Stanford Type B
  • Distal tear
  • Only involves the descending aorta
  • Below the ligamentum arteriosum (old ductus arteriosus)
  • Treat with beta blockers then vasodilators
51
Q

What is an aortic aneurysm?

What are the two main types?

A
  • Localized, pathologic dilatation of the aorta
  • May cause abdominal and or back pain which is a sign of leaking, dissection or imminent rupture
  • Can be Abdominal or Thoracic
52
Q

What is an abdominal aortic aneurysm?

A
  • Associated with atherosclerosis
  • History of tobacco use, increased age, males, and family history are increased risk factors
  • Presents as palpable, pulsatile abdominal mass
  • CT may show calcified aortic wall, with partial crescent shaped nonopacification of aorta due to flap/clot
53
Q

What is a thoracic aortic aneurysm?

A
  • Associated with cystic medial degeneration
  • Risk factors include hypertension, bicupsid aortic valve, connective tissue disease
  • Associated with tertiary syphilis, causes obliterative endarteritis of the vasa vasorum
  • Aortic root dilation may lead to aortic regurgitation
54
Q

What is a traumatic aortic rupture?

A
  • Due to trauma and or deceleration injury
  • Most commonly at the aortic isthmus, which is the proximal aorta just distal to the origin of the left subclavian artery
55
Q

Which medications have negative chronotropic effects on the heart?

A
  1. Beta-adrenergic blockers (Atenolol and Metoprolol)
  2. Nondihydropyridine Calcium Channel Blockers (Verapamil and Diltiazem)
  3. Glycosides (Digoxin)
  4. Amiodarone and Sotalol
  5. Cholinergic Agonist (Pilocarpine and Rivastigmine)
56
Q

When used concomitantly, Non-dihydropyridine type calcium channel blockers (Verapamil and Diltiazem) and beta-adrenergic blocking agents can have what effects on the heart?

A
  • Additive negative effects on heart rate, AV node conduction and myocardial contractility
  • Significant sinus bradycardia and hypotension may occur
57
Q

Nitroglycerin

A
  • Acts primarily as a venodilator at the lower doses used in angina patients
  • Decreases cardiac workload because blood is collected in the venous system decreasing preload
  • Decreased preload in the heart decreases ventricular wall stress and cardiac oxygen demand
  • Large veins are most susceptible to nitrogylcerin
58
Q

Cardiac arrest leads to rapid cessation of cerebral blood flow, when does irreversible vs reversible brain damage occur?
Which areas are damaged first during global cerebral ischemia?

A
  • If ischemia lasts longer than 5 minutes, irreversible damage to neurons occurs
  • The pyramidal cells of the hippocampus and neocortex and purkinje cells of the cerebellum are damaged first
  • The hippocampus is damaged first during global cerebral ischemia
  • Watershed infarction occurs if cerebral hypoperfusion continues, these are areas between perfusion zones of the major cerebral arteries
59
Q

What is ischemia?

A
  • Characterized by reduction of blood flow
  • Usually result of mechanical obstruction within the arterial system (thrombus)
  • If flow of blood to ischemic tissue is restored in a timely manner, reversibly injured cells will recover
60
Q

What is reperfusion injury?
How does the process occur?
What enzyme can be detected in the blood?

A
  • When cells within damages ischemic tissue paradoxically die at an accelerated pace through apoptosis or necrosis after resumption of blood flow
    1. Oxygen free radical generation by parenchymal cells, endothelial cells and leukocytes
    2. Severe irreversible mitochondrial damage, described as mitochondrial permeability transition
    3. Inflammation, which attracts circulating neutrophils that cause additional injury
    4. Activation of the complement pathway, causing cell injury and further inflammation
  • Creatine kinase leaks across the damaged cell membrane and into the circulation when cells within the heart, brain or skeletal muscle are injured.
61
Q

Primary essential hypertension treatment?

A

May use any of the following:

  • Thiazide diuretics
  • ACE inhibitors
  • Angiotensin II receptor blockers (ARBs)
  • Dihydropyridine Ca2+ channel blockers
62
Q

Hypertension with heart failure treatment?

A

May use any of the following:

  • Diuretics
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Beta-blockers (For compensated heart failure) are contraindicated in cardiogenic shock
  • Aldosterone antagonist (spironolactone)
63
Q

Hypertension with DM treatment?

A

May use any of the following:

  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Ca2+ channel blockers
  • Thiazide diuretic
  • Beta-blockers
  • ACE inhibitors/ARBs are protective against diabetic neuropathy
64
Q

Hypertension in pregnancy treatment?

A

May use any of the following:

  • Hydralazine (vasodilator arterioles > veins)
  • Labetalol
  • Methyldopa
  • Nifedipine (Ca2+ channel blocker)
65
Q

Dihydropyradine calcium channel blockers

A

Act on vascular smooth muscle

  • Amlodipine
  • Clevidipine
  • Nicardipine
  • Nifedipine
  • Nimodipine
66
Q

Non-dihydropyridine calcium channel blockers

A

Act on the heart

  • Diltiazem
  • Verapamil
67
Q

Calcium channel blockers

MOA

A
  • Block voltage-dependent L-type calcium channels of cardiac and smooth muscle
  • Decrease muscle contractility
  • Vascular smoothe muscle
68
Q

What are the most common causes of death in patients with Coarctation of the aorta?

A

Hypertension associated complications such as:

  1. Left ventricular failure
  2. Ruptured dissecting aortic aneurysm
  3. Intracranial hemorrhage
    - Increased risk for ruptured intracranial aneurysm because of increased incidence of congenital berry aneurysm of the circle of willis and aortic arch hypertension.
69
Q

5 year old boy presents for cyanosis with minimal exertion that gets better when he squats, what is the most likely diagnosis?

A

Tetralogy of Fallot

70
Q

What causes tetralogy of Fallot?

A
  • Abnormal neural crest cell migration that leads to anterior and cephalad deviation of the infundibular septum during embryologic development
  • Results in malaligned ventral septal defect and overriding aorta over the left and right ventricles
71
Q

What are the features of Tetralogy of Fallot?

A
  • Overriding Aorta
  • Ventricular Septal Defect
  • Right Ventricular Outflow Tract Obstruction (Pulmonary Stenosis)
  • Right Ventricular Hypertrophy
72
Q

Why is there a harsh, systolic ejection murmur heard over the mid-to-left upper sternal border in patients with Tetralogy of Fallot?

A
  • Due to the Right Ventricular Outflow Tract obstruction

- Can be due to subvalvular, pulmonary valve stenosis or supravalvular narrowing in the main pulmonary artery.

73
Q

Why does squatting make patients fell better in Tetralogy of Fallot?

A
  • Because it increases peripheral systemic vascular resistance (afterload)
  • Decreases right-to-left shunting across the VSD decreasing cyanosis (because LV has higher pressure and doesn’t allow lower pressure blood from RV to come in)
74
Q

What is afterload?

A
  • LV pressure or LV wall stress
  • The resistance the left ventricle must overcome to circulate the blood
  • Simply the systolic blood pressure
75
Q

A holosystolic murmur heard at the 2nd and 3rd intercostal spaces that becomes louder during inspiration?

A

Tricuspid regurgitation

76
Q

A holosystolic murmur best heard at the apex and radiates to the axilla?

A

Mitral regurgitation

77
Q

A holosystolic murmur best heard at the 3rd and 4th intercostal spaces, usually loud and accompanied by a thrill?

A

Ventral septal defect

78
Q

A year after a myocardial function, what type of collagen is present in the scar?

A

Type I Collagen
- The same collagen that is present in dermis, bones, tendons, ligaments, dentin, cornea, blood vessels and other scar tissue

79
Q

What type of collagen is present within 7 days of a myocardial infarction?

A

Granulation tissue which is made up of Type III collagen.

80
Q

Patient presents with dyspnea, bibasilar crackles and presence of S3 after a recent myocardial infarction with stent placement in the LAD artery, what is the most likely diagnosis?

A

Left sided heart failure

  • If infarction occure in LAD, then large area of myocardium is affected
  • Decreases left ventricular contractility and reduces left ventricular output.
  • Results in high end diastolic pressure which impairs return of diastolic blood from the pulmonary veins and capillaries
  • Leads to increased hydrostatic pressure in the pulmonary circulation causing transudation of fluid from the pulmonary capillaries into the lung interstitium
81
Q

Patient presents with uncomfortable heart beat sensation at night when he sleeps on his left side. He has mild shortness of breath with exertion for the past 6 months but no chest pain. Has been told he has a murmur before. Exam reveals bounding femoral pulses and carotid pulsations accompanied by head bobbing. What is most likely diagnosis?

A

Aortic regurgitation

82
Q

Aortic regurgitation presents with what?

A
  • Increase in total stroke volume
  • Abrupt distension and rapid falloff of peripheral arterial pulses
  • Results in wide pulse pressure
  • Bounding peripheral pulses and head bobbing with each heartbeat.
83
Q

When auscultating the aortic area of the heart, right 2nd intercostal space, what pathological murmur can you hear?
What 3 pathologies can cause that murmur?

A

Systolic murmur

  • Aortic stenosis (obstruction of flow)
  • Flow murmur (physiological murmur)
  • Aortic valve sclerosis
84
Q

When auscultating the pulmonic area of the heart (left 2nd intercostal) what pathological murmur do you expect to hear?
What are 2 pathologies that can cause this murmur?

A

Systolic ejection murmur

  • Pulmonic stenosis
  • Flow murmur (physiological murmur)
85
Q

When listening to the tricuspid area of the heart (left 4th intercostal space) what two murmurs can you expect to hear?

A
  1. Holosystolic murmur
    - Tricuspid regurgitation
    - Ventricular septal defect
  2. Diastolic murmur
    - Tricuspid stenosis
    - Atrial septal defect (increased flow across tricuspid valve)
86
Q

The _____ side of the heart has low pressure and resistance. Therefore it opens first and closes second.

A

Right

87
Q

The _____ side of the heart has high pressure and resistance. Therefore it opens second and closes first.

A

Left

88
Q

S1 is _____ of the _____ and _____ valves

A

Closure
Mitral
Tricuspid

89
Q

At S1, _____ closes first and _____ closes second.

A

Mitral

Tricuspid

90
Q

After isovolumetric contraction, _____ valve opens first and then _____ valve opens second

A

Pulmonary

Aortic

91
Q

S2, _____ valve closes first and then _____ valve closes second.

A

Aortic

Pulmonary

92
Q

After isovolumetric relaxation _____ valve opens first and then _____ valve opens second.

A

Tricuspid

Mitral

93
Q

What is Eisenmenger’s syndrome?

A

Left to right shunt

94
Q

A valve that is popping open during diastole is called an _____. It can be _____ or _____.

A

Opening snap
Mitral Stenosis
Tricuspid Stenosis

95
Q

A valve that is popping open during systole is called an _____. It can be due to _____ or _____.

A

Ejection click
Aortic Stenosis
Pulmonary Stenosis

96
Q

A midsystolic click is due to _____

A

Mitral valve prolapse

97
Q

During systole, the _____ and _____ valves close.

A

Mitral

Tricuspid

98
Q

During diastole, the _____ and _____ valves close.

A

Pulmonic

Aortic

99
Q

If you have a soft S1, what does that mean?

What can it be?

A
  • That one of the valves is not closing
    Tricuspid regurgitation
    Mitral regurgitation
    Valve is absent (Tricuspid or Mitral Atresia)
100
Q

If you have a loud S1, what does that mean?

What can it be?

A

-You have a stiff valve that bangs shut or ventricle is contracting harder
Tricuspid stenosis
Mitral stenosis

101
Q

If you have a soft S2, what does that mean?

What can it be?

A

One of the two valves is not closing properly
Aortic regurgitation
Pulmonary regurgitation
Valve is absent (Aortic or Pulmonary atresia)

102
Q

If you have a loud S2, what does that mean?

A

Either one of the valves is stiff and bangs shut when it tries to open
Aortic stenosis
Pulmonary stenosis
High pressure in front of the valves (systemic or pulmonary hypertension)

103
Q

What happens during S1?

Where is it loudest?

A 
Mitral valve and tricuspid valve close
Mitral area (Apex)
104
Q

What happens during S2?

Where is it loudest?

A

Aortic and pulmonary valve close

Left upper sternal border (Pulmonic area)

105
Q

What is an S3?

A
  • Heart sound heard early in diastole during rapid ventricular filling phase
  • Associated with increased filling pressures
  • Ex. Mitral regurgitation and heart failure or dilated ventricles
  • May be normal in kids
106
Q

What is an S4?

How is it best heard?

A
  • Atrial kick heard late in diastole
  • Patient in left lateral decubitus position and auscultaed in the apex
  • Associated with ventrical noncompliance such as hypertrophy
  • Left atrium must push against a stiff LV wall
  • Always abnormal
107
Q

Crescendo decrescendo murmur during systole?

A

Aortic stenosis

108
Q

Holosystolic high pitched murmur or blowing murmur?

A

Mitral or tricuspid regurgitation

109
Q

Holosystolic murmur heard at the apex and radiates to the axila?

A

Mitral regurgitation

110
Q

Holosystolic murmur heard in the tricuspid area?

A

Tricuspid regurgitation

111
Q

What causes mitral regurgitation?

A
  • Ischemic heart disease after an MI
  • Mitral valve prolapse
  • Left ventricular dilation
  • Rheumatic fever
  • Infective endocarditis
112
Q

What causes tricuspid regurgitation?

A
  • Right ventricle dilation
  • Rheumatic fever
  • Infective endocarditis
113
Q

Late systolic crescendo murmur with midsystolic click?

A
  • Mitral valve prolapse
114
Q

What causes the midsystolic click in mitral valve prolapse?

A

Sudden tensing of chordae tendineae

115
Q

Where is mitral valve prolapse best heard?

A

Over the apex, loudest just before S2.

  • Usually benign but can predispose to infective endocarditis.
  • Common in Marfan or Ehlers-Danlos syndrome
116
Q

Holosystolic harsh murmur heard at the tricuspid area?

A

Ventricular septal defect

117
Q

High pitched blowing early diastolic decresendo murmur?

A

Aortic regurgitation

118
Q

What are the features of aortic regurgitation?

A
  • Long diastolic murmur
  • Hyperdynamic pulse
  • Head bobbing in severe cases
  • Wide pulse pressure
  • Usually due to aortic root dilation, bicuspid aortic valve, endocarditis or rheumatic fever
  • Progresses to left heart failure
119
Q

Follows opening snap, delayed rumbling mid-to-late diastolic murmur

A

Mitral stenosis

120
Q

What are the features of mitral stenosis?

A

Follows opening snap

  • OS due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips
  • LA&raquo_space;LV pressure during diastole
  • A late sequela of rheumatic fever
  • If chronic can result in LA dilation

STEP (28 decks)

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