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USMLE Step 1 > Cardiology - First Aid / Pathoma > Flashcards

Cardiology - First Aid / Pathoma Flashcards

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USMLE® Step 1 flashcards
1
Q

Myocardial Oxygen Demand

A 
Increased by: 
Increased contractility
Increased afterload
Increased heart rate
Increased wall tension (or increased diameter of ventricle wall)
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2
Q

How are pressure, flow, and resistance related?

A

∆Pressure = Flow x Resistance

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3
Q

Which vessels account for most of TPR

A

Arterioles

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4
Q

Which vessels have the lowest flow velocity?

A

Capillaries.

They have the highest total cross sectional area and the lowest flow velocity.

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5
Q

How is resistance measured?

A

8viscositylength / pi*radius^4

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6
Q

How are flow and radius related?

A

Flow is inversely proportional to resistance.
Resistance is inversely proportional to radius^4.
Therefore, flow is directly proportional to radius^4

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7
Q

Aortic Stenosis

A

Systolic murmur.
Best heard at right sternal border.
Cresendo-decresendo systolic ejection murmur.
Often causes angina, syncope, dyspnea on exertion (and LVH/CHF?).

Most often caused due to old age/calcifications, or due to early calcifications of bicuspid aortic valve

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8
Q

Mitral regurgitation

A

Holosystolic murmur.
Loudest at apex and radiates to axilla.
Often due to ischemic heart disease, MVP, LV dilatation

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9
Q

Tricuspid regurgitation

A

Holosystolic murmur.
Best heard at tricuspid area, radiates to right sternal border.
Commonly caused by RV dilatation

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10
Q

Aortic Regurgitation

A

Diastolic murmur.
Diastolic blow sound, early decresendo murmur.
Can be caused by aortic root dilatation, bicuspid aorta, endocarditis, RF.

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11
Q

Mitral Stenosis

A

Diastolic murmur.
Opening snap followed by delayed rumbling late diastolic murmur.
Commonly due to RF.

The pressure in the LA&raquo_space; LV; MS can cause LA dilatation.

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12
Q

Ventricular Septal Defect

A

Systolic murmur.
Harsh holosystolic murmur.
Loudest at tricuspid area (just like ASD is loudest at the tricuspid area)

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13
Q

Murmurs best heard at the left sternal border

A

Aortic regurgitation
Pulmonic regurgitation
Hypertrophic cardiomyopathy

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14
Q

Patent Ductus Arteriosus

A

Continuous - machine like murmur.
Loudest at S2.

PDA best heard at left infra clavicular space.
Commonly caused by congenital rubella infection.

Side note, triad of congenital rubella: PDA, sensorineural deafness, cataracts/blindness

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15
Q

Murmurs best heart at Tricuspid area

A

Systolic:
VSD
Tricuspid regurgitation

Diastolic:
Tricuspid stenosis
ASD

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16
Q

Atrial septal defect

A

ASD commonly presents w/ a pulmonary flow murmur (due to increased blood flow through the pulmonary valve) and a diastolic rumble (due to increased flow across tricuspid valve).

Blood flow across actual ASD doesn’t cause murmur bc there’s no significant pressure gradient.
The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilatation of the pulmonary artery

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17
Q

Describe 3 ways cardiac muscle is different from skeletal muscle

A
  1. Cardiac muscle AP has plateau due to Ca2+ influx and K+ efflux – note that the myocyte contraction is due to CICR.
  2. Cardiac nodal cells display automaticity due to If channels (Na channels that are open even at threshold)
  3. Cardiac myocytes are electrically coupled to each other by gap junctions.
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18
Q

Which phase of the Pacemaker AP determines HR?

A

Phase 4 – diastolic depolarization.

Note that this is responsible for the automaticity of the SA and AV nodes.

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19
Q

Which phases are not present in pacemaker APs?

A

Phase 1 and Phase 2

*There is no plateau like in the myocytes.

20
Q

What decreases rate of diastolic depolarization, and what would this result in?

A

ACh or Adenosine can decrease rate of diastolic depol.

This would result in decreased HR.

21
Q

What increases rate of diastolic depolarization, and what would this result in?

A

Catecholamines.
Increased HR.

*Note that sympathetic stimulation increases the chance that If channels are open, and thus increases HR.

22
Q

How many phases are there in myocardial cell APs?

A 
Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
23
Q

List fastest to slowest speed of conduction

A

Purkinje > Atria > Ventricles > AV node

Note that as size increases, internal resistance decreases.
Increased gap junctions increase conduction too.

24
Q

What is Torsades de Pointes

A

Polymorphic ventricular tachycardia.
It can progress to ventricular fibrillation.

Long QT interval predisposes to this.

25
Q

What can cause long QT

A

Congenital, mc due to mutation of outward rectifying K+ channels that can lead to longer Phase 3 since they aren’t functioning as well.

Drugs: Antiarrythmics, antibiotics, antipsychotics, antidepressants, antiemetics

Decreased Mg
Decrease K

26
Q

Name some congenital LQTS

A

Romano-Ward syndrome. Autosomal dominant - just cardiac phenotype.

Jervell and Lange-Nielsen syndrome. Autorecessive. Cardiac phenotype and sensorineural deafness

27
Q

Normal PR interval length

A

= 200 ms

28
Q

Normal QRS complex duration

A

= 120 ms

29
Q

Atrial Natriuretic Peptide

A

ANP released by atrial myocytes in response to increased volume or increased pressure.

Causes vasodilation and decreases Na absorption at the renal collecting tubule.

Dilates afferent arteriole and constricts efferent arteriole. Promotes diuresis.
Also contributes to the “aldosterone escape” mechanism - which is the inability of an ACEi to suppress aldosterone release in a pt with CHF.

30
Q

B-type or Brain Natriuretic Peptide

A

BNP released by ventricular myocytes in response to increased tension!
Similar to ANP, but longer t1/2.

BNP blood test is used to dx CHF - very good NPV.
Note that a recombinant form (nesiritide) can be used to treat CHF.

31
Q

Baroreceptors and hypotension

A

Note baro rs located at carotid body and aorta.

Decreased afferent baro rs firing due to decreased stretch.
Decreased efferent parasympathetic firing.
Increased efferent sympathetic firing.

Important in severe hemorrhage/hypotension.

32
Q

Baroreceptors and Carotid massage

A

Increased baro rs firing due to increased stretch.
Increased AV node refractory period
Decreased HR

33
Q

Cushing Reaction

A

Increased intracranial pressure causes:

Increased Blood Pressure/HTN
Decreased Heart Rate
Respiratory distress syndrome

Why?
increased ICP leads to cerebral ischemia, to decreased pH, to central reflex sympathetic increase in perfusion pressure (HTN). The stretch leads to peripheral baro rs firing and bradycardia

34
Q

Chemoreceptors

A

Peripheral: carotid and aortic bodies are stimulated by decreased PO2, increased PCO2 and decreased pH

Central: stimulated by change in pH/PCO2 of brain interstitial fluid (which are influenced by arterial CO2 - since only CO2 can cross BBB and H+ ions can’t). Central rs do NOT response to PO2

35
Q

Normal Pressures in the heart

A

LV: 130/10
LA:

36
Q

What is Autoregulation

A

Blood flow to an organ remaining constant over a wide range of perfusion pressures.

37
Q

What is the only vasculature that vasoconstricts in hypoxia?

A

Pulmonary vasculature.

Only well-ventilated areas are perfused.

38
Q

What 6 things determine net fluid flow (into, or out of, a capillary)?

A 
Pc
Pi
πc
πi
Kf (permeability of a capillary)
ç (permeability of capillary to protein)
39
Q

Congenital Heart Defects with Right to Left shunts

A 
Truncus arteriosus.
Tricuspid atresia.
Transposition of Great Vessels.
Tetralogy of Fallot.
TAPVR (Total anamalous pulmonary venous return).
40
Q

Congenital Heart Defects with Left to Right Shunts

A

Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus.

41
Q

Name 2 types of coarctation of the aorta

A

Infant

Adult

42
Q

What is the Beck Triad

A

hypotension
distended neck veins
distant heart sounds

**Found in cardiac tamponade

43
Q

What are some findings of cardiac tamponade?

A

Beck triad.
Increased HR.
Pulsus paradoxus.
ECG shows low-voltage QRS and electrical alternans

44
Q

Electrical alternans

A

Finding on ECG.

“Swinging” movement of the heart in large effusion of pericardial sac (like in cardiac tamponade).

45
Q

Pulsus paradoxus

A

Decrease in amplitude of systolic BP by more than 10mmHg during inspiration. Occurs because during inspiration right ventricle has increased blood return, left ventricle does not. In an condition like Cardiac Tamponade, the RV can’t extend out, so it pushes into the left ventricle - this decreases SV?
On clinical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse

Seen in cardiac tamponade, asthma/COPD, obstructive sleep apnea, pericarditis, croup.

46
Q

Pulsus Parvus et tardus

A

Pulses are weak with delayed peak.

Seen in aortic stenosis.

USMLE Step 1 (9 decks)

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