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USMLE Step 1 > Cardio > Flashcards

Cardio Flashcards

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USMLE® Step 1 flashcards
1
Q

What causes a patent foramen ovale?

A

Failure of septum primum and septum secundum to fuse after birth

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2
Q

What is the most common congenital cardiac anomolay?

A

Ventricular septal defect

most commonly occurs in the membraneous septum

best heard at the left sternal border

harsh/blowing holosytolic murmur

(harshness is inversely porportional to severity)

VSD is caused by defects in the septum of the atrioventricular canal, in the muscular septum, or in the distal conal septum in the developing fetal heart, resulting in a left-to-right

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3
Q

What is pulsus paradoxus and what is this associated with (5)

A

> 10mm Hg difference in systolic BP during inspiration

seen with: Cardiac tamponae, asthma, coup, OSA, pericarditis

CAPOT

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4
Q

What is beck’s triad for cardiac tamponae?

A

Muffled heart sounds

hypotension

jugular venous distension

also can see: pulsus paradoxus

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5
Q

You study blood flow in a rat’s capillaries. You find that arteriolar dilators change the TPR and thus capillary blood flow. Why is this?

A

Arterioles regulate capillary flow and account for most of TPR

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6
Q

A pt undergoes nephrectomy. How will the pt’s cardiac output be affected?

A

Cardiac output will decrease, as removal of organs in parallel arrangements results in

increased TPR

decreasing cardiac output

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7
Q

How do catecholamines or digoxin cause increased cardiac output (CO)?

A

They increase contractility

–> CO increases for a given right atrial pressure

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8
Q

In a cardiac cycle:

When is the period of maximal O2 consumption?

A

max O2 consumption: isovolumetric contraction

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9
Q

What is S3 associated with?

What is an S4 associated with?

Can any of these extra heart sounds be normal?

A

S3: associated with increased filling pressures; heard in early diastole, during rapid ventricular filling

indicative of: mitral regurg, HF, and more common in dialted ventrilces

NL: pregnant women and children

S4: associated with ventricular noncompliance/hypertrophy, left atrium must push against a stiff ventricle thus heard best in late distole

“Atrial kick” – high atrial pressure

best heard at the apex, when pt is in the left decubitus position, intensified during expiration due to increased blood flow from the lungs to right atrium

most always pathological (perhaps ok in older individuals)

use bell to listen to either of these sounds as they are low-frequency

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10
Q

During which phase of the cardiac cycle is ventricular volume the highest?

The lowest?

A

Highest: atrial systole

Lowest: isovolumetric relaxation

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11
Q

Jugular venous pressure curve:

What changes are seen with tricupsid regurg?

The a, c, and v waves of the jugular venous pulse are associated with which physiologic events, respectively?

The y descent on the jugular venous pulse represents what? The x descent?

A

Tricuspid regurg –> X decent

[vs: tricuspid]

a wave: Atrial contraction [absent in a fib]

c wave: right ventricular contraction

v wave: filling against a closed tricuspid valve

y = flow of blood from right atrium to right ventricle; x = atrial relaxation & displacement of tricuspid during ventricular contraction

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12
Q

What condition causes fixed spliting of S2?

A

ASD

Left to right shunt –> INC RA and RV volumes –> increasing the flow through the pulmonic valve, in which no matter with inspiration or not, you will have a split due to this increased flow through the valve.

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13
Q

What is paradoxical splitting?

Under what conditions cause paradoxical splitting?

A

Delay in the aortic valve –> paradoxical split (usually, the aortic valve closes before the pulmonic valve), but there is a reversal to have the pulmonic valve closing first.

Therefore, on inspiration, instead of the S2 being split, the heart sounds of valve closure come closer together.

Split is heard during expiration.

Heard in conditions that delay the aortic valve from closing - aortic stenosis, left bundle branch block

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14
Q

What is wide splitting?

Under what conditions could we hear wide splitting occuring?

A

Exaggerated splitting of S2 -

Seen in conditions that delay RV emptying - pulmonic stenosis, right bundle branch block.

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15
Q

Ventricular septal defect is most common seen at?

A

Most commonly occurs in the membranous septum

It is the #1 congenital cardiac anomaly

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16
Q

How does ejection fraction change in heart failure?

A

DECRASES in SYSTOLIC HF

NORMAL in DIASTOLIC HF

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17
Q

How do the following changes affect heart sounds?

Inspiration:

Hand grip:

Valsalva / standing up

Rapid squatting:

A

Inspiration = INC venous return –> inc right heart sounds, physiological split

Hand grip = INC afterload –>

INC MR, AR, VSD murmurs

DEC HOCM, MVP click has later onset

Valsalva (phase II), standing up (DEC preload)

DEC intensity of most murmurs

INC HOCM

MVP - earlier click

Rapid squatting = INC venous return/preload

DEC HOCM, MVP later click

INC AS

18
Q

A man has a systolic murmur. You are not sure if it is aortic stenosis (AS) or hypertrophic cardiomyopathy (HCM). How do you differentiate?

A pt performs the Valsalva maneuver. Phase II is reached, and the pt is standing. What happens to the heart’s preload?

A

Have the pt perform the Valsalva maneuver (HCM intensifies; AS softens.)

or squat rapidly (HCM softens; AS intensifies.)

Preload decreases

valsava - decreases preload

squat - increases preload

19
Q

In what areas are the murmurs of aortic stenosis and aortic regurgitation best heard?

A

Aortic stenosis: aortic area (ie, right sternal border and second intercostal space);

aortic regurgitation: left sternal border

20
Q

Which murmurs are heard during systole?

Which five murmurs are heard during diastole?

A

@SYSTOLE: Aortic/pulmonic stenosis, flow murmurs, aortic valve sclerosis, mitral/tricuspid regurgitation, hypertrophic cardiomyopathy, VSD, MVP

@DIASTOLE: Aortic/pulmonic regurgitation, mitral stenosis, tricuspid stenosis, and ASD

21
Q

An increase in afterload will cause which three murmurs to increase in intensity?

A

Mitral regurgitation, aortic regurgitation, and ventricular septal defect

22
Q

A pt with a mitral valve prolapse squats down suddenly. What will happen to the timing of the pt’s murmur?

A pt with a mitral valve prolapse clenches his fists. What will happen to the timing of the pt’s murmur?

A pt with a mitral valve prolapse performs a Valsalva maneuver.

A

squating = increase venous return

The onset of the click/murmur will be later

clench fist = increase afterload

The onset of the click/murmur will be later

valsalva/decrease preload/decreaes fterload

The onset of the click/murmur will be earlier

23
Q

Which heart valve disease process is often due to age-related calcification and can be associated with syncope?

A

Aortic stenosis

which on exertion can present as Syncope, Angina, Dyspnea (SAD)

24
Q

What is the most common valvular lesion that causes a murmur?

Which heart murmur is usually benign but can predispose pts to infective endocarditis?

A

Mitral valve prolapse

25
Q

An 80-y/o woman reports that her mother told her she had rheumatic fever as a child. Which valvular abnormalities might she have?

A

Mitral stenosis, aortic regurgitation, mitral valve prolapse, mitral regurgitation, tricuspid regurgitation

26
Q

What effect does combing beta blockers with non-dihydropyridine calcium channel blockers have on the heart?

What effect do ACE inhibitors, nitrates, peripheral alpha 1 selective adrenergic blcokers have on the systemic system and heart?

A

Severe hypotension and bradycardia

Ace inhibitors, nitrates and peripheral alpha 1 selective adrenergic blockers- vasodilation and reflexive tachy cardia

27
Q

What congenital anomaly leads to atrial septal defect (ASD)

A

An Absence of either septum primium or septum segundum during development

Findings: fixed S2, HF, pulmonary hypertension, Eisenmenger Syndrome

[vs patent foramen ovale is failure of septum primium and septum segundum to fuse during develpemt]

28
Q

What effect can thiamine deficiency have?

A

Thiamine = B1

Primary function is the decarboxylation of the alpha keto acids for carbohydrate metabolism

A deficiency could lead to:

BeriBeri –> peripheraly neuropathy, HF

wet or dry depending if there is cardiac involvement (wet obvi = cardiac involvement)

Wernike-Korsakoff syndrome

*alcoholics

“In extreme cases, beriberi is associated with Wernicke-Korsakoff syndrome. Wernicke encephalopathy and Korsakoff syndrome are two forms of brain damage caused by thiamine deficiency. Wernicke encephalopathy damages regions of the brain called the thymus and hypothalamus. This condition can cause confusion, memory loss, loss of muscle coordination, and visual problems such as rapid eye movement and double vision. Korsakoff syndrome is the result of permanent damage to the region of the brain where memories form. This can cause loss of memory, the inability to form new memories, and hallucinations.”

29
Q

What effects does a person with Marfan’s syndrome have on their heart?

___ ____ necrosis

A

Marfan’s:

Auto dominant on Chrom 15, affecting fibrillin-1 gene and thus the elasticity

–> CYSTIC MEDIAL NECROSIS that leads to issues such as aortic dissection, aneurysm

MVP, aortic regurg.

30
Q

Tuberous sclerosis is associated with what cardiac condition?

A

1 cardiac tumor in children

Rhabdomyomas

TS is an autosomal dominant syndrome characterized by cutaneous angiofibromas (adenoma sebaceum), seizures and mental retardation

31
Q

What heart conditions does a person with turners have?

A

Turner: XO

Bicuspid aortic valve

PREductal coartcation of aorta (aortic narrowing before the insertion of the ductus arteriosus)

32
Q

What cardiac abnormality could a person with Friedreich ataxia be associated with?

A

FA is spinocerebellar dedegration marked by spinal ataxia

could produce difficulty walking/gait ataxia

auto RECEssive

associated with- hypertrophic cardiomyopathy

[lot of other stuff]

33
Q

What are signs/symptoms associated with brachiocephalic (innominate) vein?

What could this be due to?

What is a DDX?

A

Could be due to aplical lung tumor, thrombic occlusion..

ONE SIDED arm, face and neck swelling

VS: Superior Vena Cava Syndrome - you get BILATERAL arm, face and neck swelling

34
Q

Where is the AV node located?

What procedure is performed here?

A

The AV node is located on the endocardial surface of the right atrium, near the insertion of the septal leafet of the tricuspid valve and the orfice of the coronary sinus

Ablation could occur here to correct a fib that is non-responsive/intolerant to therapy

35
Q

What therapy could be used in a women PREGNANT with an acute venous thrombus event?

A

Low molecular weight heparins

such as enoxaprin

(NO warfarin; aspirin and clopidogrel have no effect on ACUTE VTE treatment)

36
Q

How does NO vasodilate?

A

Acetylcholine, bradykinin or shear stress can cause an increase in calcium –> NO formation via Arginine, NADPH and O2 –> NO + citrulline –> activation of GC and an increase in cGMP via GTP –> activates protein kinase C –> decrease in cytosolic calcium and relaxation of smooth muscle

37
Q

What is a difference in phase 0 between myocardial cells and pacemaker cells?

A

In pacemaker cells, phase 0 depolarization is primarily due to calcium influx

[also note, pacemaker cells do not have phase 1 and phase 2, and phase 4 is a slow depolarization, via I channels]

VS in myocardiocytes and purkinje cells, phase 0 depolarization is due to sodium influx

38
Q

What are the 4 characteristic findings in tetrology of fallot?

A

3rd and 4th phary. pouch

  • Caused by*: anterosuperior displacement of the infundibular septum
    1. overriding aorta
    2. ventricular septal defect

3. **pulmonic infundibular stenosis **

most important determinant for prognosis

  1. right ventricular hypertrophy
    * boot shaped heart on CXR*

“PROV”

Pulmonary stenosis forces right to left flow across VSD –> early cynatoic tet spells (blue baby syndrome)

relived by SQUATTING – increased systemic ventricular resistance, RED right to left shunt, improves cyanosis; a low SVR:PVR raion, allows the deoxy blood from the right ventricle to take the low resistance output to the system –> acute hypoxemia/tet spells; the squatting increases the SVR thus, forces blood through the pulmonic circulation

Treatment is early surgical correction

39
Q

What type of vascular change is associated with:

Abdominal aortic aneurysm:

Atherosclerotic change:

Aortic dissection

Marfan

Syphillis heart disease

A

AAA –> chronic transmural inflammation/transmural inflammation –> dedegration of elastin and collagen –> loss of elastin, and abnormal collagen remoldeling/cross-linking –> weakening and expansion of the aortic wall = aortic aneurysm

Atherosclerosis: intima changes

Aortic dissection: intimal tear with dissection of blood through media of the aortic wall

Marfan - cystic medial necrosis (predisposing to aortic dissection and AAA), characterized by loss of smooth muscle, collagen and elastin –> cystic mucoid spaces in the aortic media

Syphillis heart disease - vaso vasorum endarteritis/tree barking

40
Q

Atherosclerosis:

Key players:

Mxn:

A

Key players: endothelial cells, vascular smooth muscle cells, leukocytes

  1. Endethelial cell injury via chronic hemodynamic stress and hyperlipidemia
  2. INC expression of surface vascular cell adhesion molecules (VCAMs) –>
  3. migration of monocytes adn T-lymphocytes into intima
  4. infiltrating leukocytes and dysfunctional endothelium release cytokines and growth factors that promoate the migration and proliferation of smooth vascular muscle within the intima
  5. SVM, then promote extracellular matrix deposition and the formation of the fibrous cap

USMLE Step 1 (15 decks)

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