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Pathophysiology - Cardiovascular > First Pass Miss > Flashcards

First Pass Miss Flashcards

1
Q

What is the formula for wall stress? What increases / decreases it?

A

Wall stress = (Pressure x Radius) / 2(wall thickness)
-> force with cardiomyocytes must push against

Increased by greater radius from center to wall of ventricle, and systolic pressure (afterload)

Stress is normalized via increasing wall thickness

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2
Q

Why is afterload approximated by mean arterial pressure?

A

Afterload can basically be thought of as the force per unit area the heart must push against

However, we assume that ventricular radius and wall thickness are pretty much constant, so pressure (in the numerator of wall stress equation) is a pretty good proxy.

Pressure = Force per area
Radius = length (i.e. cm)
Wall thickness = length (i.e. cm)

(F/A * cm) / cm = F/A, Laplace’s law

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3
Q

How does wall stress change during ejection?

A

It decreases because

  1. The size of the LV cavity decreases -> Radius decreases
  2. LV wall thickness increases -> more sarcomeres pushed together
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4
Q

Give a few conditions causing concentric hypertrophy?

A

Uncontrolled HTN
Aortic valve stenosis
Pulmonic valve stenosis (thickening of RV)

-> laying down of fibers in parallel to reduce wall stress by increasing thickness and reducing radius of ventricles

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5
Q

What does eccentric hypertrophy happen in response to, and what is its pathogenesis?

A

In response to chronically increased preload

  • > Lay down more sarcomeres in series to accommodate increased volume
  • > Increased volume increases wall stress (radius is larger)
  • > Lay down sarcomeres in parallel to increase wall thickness and decrease cavity size
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6
Q

Why is LV hypertrophy bad?

A
  1. Volume of myocytes increases disproportionately to capillary growth -> decreased coronary reserve in situations of high demand (i.e. tachycardia)
  2. Sarcomeres increase more than mitochondria -> inefficient energy use
  3. Decreased contraction efficiency in myosin ATPase
  4. Increased collagen deposition -> increased LV stiffness
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7
Q

What is the Fick equation and how is it used to measure cardiac output?

A

Cardiac output = VO2 (measured via inspiration / expiration, in mL/min) / AV oxygen difference (mL O2 / liter of blood)

Measure the patients arterial and venous O2 concentrations for the AV oxygen difference.

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8
Q

How is vascular resistance measured? Units?

A

Mean pressure difference across a vascular bed / mean blood flow (Delta P / CO = TPR)

Mean blood flow is measured in volume / time (cm^3/sec)

Thus, units are (Dynes/cm^2) / (cm^3 / sec) = dynesseccm^-5

Dyne is a force per unit area

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9
Q

What does pulmonary capillary wedge pressure (PCWP) approximate?

A

Left atrial pressure (diastolic pressure from a balloon catheter inserted into the pulmonary artery) -> LVEDP -> implies LVEDV -> preload

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10
Q

How is vascular resistance measured? Units?

A

Mean pressure difference across a vascular bed / mean blood flow (Delta P / CO = TPR)

Mean blood flow is measured in volume / time (cm^3/sec)

Thus, units are (Dynes/cm^2) / (cm^3 / sec) = dynesseccm^-5

Dyne is a force per unit area

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11
Q

What does pulmonary capillary wedge pressure (PCWP) approximate?

A

Left atrial pressure (diastolic pressure from a balloon catheter inserted into the pulmonary artery) -> LVEDP -> preload

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12
Q

How is the systemic vascular resistance calculated and what is the normal range?

A

SVR = (MAP - Mean RAP) / CO

RAP = right atrial pressure

Normal = 900-1300 dynesseccm^-5

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13
Q

What is the definition of hypertensive crisis?

A

SBP > 180
or
DBP > 110

Urgency = without end-organ damage
Emergency = with evidence of end-organ damage
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14
Q

How is the pulmonary vascular resistance calculated and what is the normal range?

A

PVR = (Mean PAP - Mean LAP) / CO

LAP = Left atrial pressure = PCWP

Normal = 40 to 90 dynesseccm^-5

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15
Q

Who is most likely to get fibromuscular dysplasia and renal artery stenosis?

A

Fibromuscular dysplasia -> especially young women, developmental defective in large and medium muscular arteries, especially affecting renal artery

Renal artery stenosis -> especially older men, due to atherosclerosis of renal arteries

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16
Q

Other than adrenal disorders, give four endocrine disorders or conditions which can cause hypertension?

A
  1. Acromegaly - GH excess
  2. Hypothyroidism -> Increases sodium, also increases lipid levels for hardening of arteries
  3. Hyperparathyroidism -> increases renin / kidney dysfunction
  4. Exogenous hormones -> steroids / oral contraceptives
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17
Q

What are the best antihypertensives to use post-MI and in heart failure / CAD?

A

Beta blocker and ACE inhibitor

Use diuretics in heart failure and CAD

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18
Q

What is the definition of resistant HTN? Causes?

A

Persistently elevated BP despite 3+ medications

Causes:
Noncompliance or medications at not max dose, use of other drugs which elevate BP, volume overload, or undiagnosed OSA

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19
Q

When are ACE inhibitors contraindicated?

A
  1. C1 esterase inhibitor deficiency (C1 esterase inhibitor also cleaves kallikrein, responsible for converting HMW kininogen to bradykinin. Only other enzyme which breaks down bradykinin is ACE)
  2. Bilateral renal artery stenosis -> angiotensin II is the only thing maintaining GFR by constricting efferent arteriole
  3. Pregnancy
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20
Q

What areas of the brain are most susceptible to microaneurysm rupture in systemic hypertension?

A

Putamen (BG), thalamus, and pons

Rupture.PPT

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21
Q

What can be seen pathologically in hyerplastic arteriolosclerosis? Grossly in kidney?

A

Concentric proliferation of myofibroblastic cells into intima - “onion-skin” appearance

Accompanied by fibrinoid necrosis and petechial hemorrhages.

Grossly: Kidney will have a flea-bitten appearance due to hemorrhages on cortical surface

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22
Q

How does benign nephrosclerosis appear microscopically in larger arteries? What is benign nephrosclerosis?

A

Larger arteries include interlobular and arcuate

Fibroelastic hyperplasia -> myofibroblast hyperplasia, reduplication of elastic lamina, medial smooth muscle hypertrophy, and luminal narrowing (large arteries respond somewhat like hyperplastic arteriolosclerosis)

Benign nephrosclerosis occurs in longstanding essential hypertension and diabetes mellitus

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23
Q

How does benign nephrosclerosis appear microscopically in small arteries / arterioles and renal parenchyma?

A

Small arteries / arterioles - hyaline arteriolosclerosis

Renal parenchyma - ischemic changes - interstitial / glomerular fibrosis and accompanying tubular atrophy

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24
Q

What are the microscopic features of malignant nephrosclerosis? (Grossly = flea-bitten appearance)

A

Small arteries / arterioles -> hyperplastic arteriolosclerosis with fibrinoid necrosis

Renal parenchyma -> infarction and/or ischemic atrophy (if you had prior benign hypertension) -> infarction due to rapid death of arterioles

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25
Q

As vascular walls weaken, forming microaneurysms and hemorrhages in the retina, how do you know if a hemorrhage is superficial vs deep?

A

Flame-shaped hemorrhages - more superficial, as the nerve fiber layer runs perpendicular to the rods and cones in the back of the retina, and the hemorrhage follows these.
(we are seeing their long axis).

Dot hemorrhages - more deep, as the hemorrhage runs between the plexiform layers which are parallel to the rods / cods in the retina.(we are seeing their short axis)

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26
Q

How serious are hard exudates in the retina and what are they? How about cotton wool spots?

A

Very serious -> represent a severe, acute increase in blood pressure which has resulted in the breakdown of the blood-retinal barrier

-> leakage of lipid and protein into the retina, causing small, yellow, oval lesions deep in the retina

Cotton wool spots are less serious microinfarcts of the nerve fiber layer leading to damaged “cytoid bodies”

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27
Q

What are the most severe findings of malignant hypertension in the retina? Will vision changes occur?

A

Optic disc swelling (papilledema), associated with macular star

-> macular star due to how nerve fibers are arranged around the fovea, and complete loss of outer blood-retinal barrier causing many hard exudates to deposit around.

Papilledema due to very high ICP.

-> this is where we will see blurred vision typically

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28
Q

What retinal changes of hyaline arteriolosclerosis can be seen very early on?

A
  1. Narrowing / tortuosity of retinal arteries
  2. Copper-wire / silver-wire appearance -> due to thickened wall and narrowed blood column, altering light reflex
  3. AV nicking
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29
Q

What are the four biochemical labs which, when elevated, are associated with atherosclerosis?

A
  1. C-reactive protein (inflammation)
  2. Homocysteine
  3. Lipoprotein (a)
  4. Plasminogen activator inhibitor (PAI) -> released by endothelial cells in prothrombotic states
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30
Q

What is an atheroma? How does it appear grossly?

A

Uncomplicated fibrofatty plaque (within the intima)

Grossly - raised, yellow-white lesion protruding into blood vessel

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31
Q

How do macrophages amplify the atherosclerosis response?

A

Increase IL-1/TNF levels to increase leukocyte adhesion, give chemotactic cytokines, and oxidize LDL via oxygen-free radicals. They also secrete growth factors.

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32
Q

What is the first stage of the increasing size of the atheroma / what is this called? When can the vessel lumen start getting smaller?

A

Positive remodeling -> vessel gets larger due to plaque formation, but the vessel is not stenosed at all
-> lumen shrinks once the plaque occupies greater than 40% of the circular intima

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33
Q

How do preload and afterload increases affect myocardial oxygen demand?

A

By increasing wall tension, they increase myocardial oxygen demand

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34
Q

What is a good, rapid measure of myocardial oxygen demand?

A

Rate Pressure Product (RPP)

RPP = HR * SBP

SBP = systolic blood pressure

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35
Q

How is unstable angina defined?

A

New onset angina of at least class III severity (within 2 months of initial presentation), increase in frequency or severity, or angina at REST.

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36
Q

What is the first stage of the increasing size of the atheroma / what is this called? When can the vessel lumen start getting smaller?

A

Positive remodeling -> vessel gets larger due to plaque formation, but the vessel is not stenosed at all
-> lumen shrinks once the plaque occupies greater than 40% of the circular intima

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37
Q

How do preload and afterload increases affect myocardial oxygen demand?

A

By increasing wall tension, they increase myocardial oxygen demand

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38
Q

What areas does the right coronary artery supply (other than the right / left dominant areas)?

A

Anterior right ventricle
-always, via the right marginal artery

Right dominant hearts usually have the posterior descending coronary artery, sometimes it comes off of left circumflex

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39
Q

What areas are supplied by either the left heart or the right heart depending on dominance?

A

Posterior descending coronary artery

  • > supplies posterior 1/3 of IV septum, posterior and inferior walls of left ventricle
  • > AV node and proximal HIS bundle
  • > posteromedial papillary muscle
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40
Q

What symptoms are most compatible with infarction due to ACS?

A

Prolonged chest discomfort >30 minutes, with radiation to left arm or neck.

  • > precipitated by exertion and relieved by rest / nitroglycerin
  • > nausea, vomiting, diaphoresis, palpitations are common

Women may have SHARP pain, fatigue, or weakness

Elderly may have AMS

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41
Q

What is the general treatment plan for chronic stable angina?

A

Beta blocker. Use non-DHP calcium channel blocker if not working or contraindicated

Use sublingual nitroglycerin for acute events

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42
Q

What areas does the right coronary artery supply (other than the right / left dominant areas?

A
  1. Anterior right ventricle
  2. Posterior 1/3 of interventricular sptum
  3. Posterior wall of LV
  4. Posteromedial papillary muscle of LV - near septum
    (anterolateral supplied by LAD / circumflex dual supply)
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43
Q

What areas are supplied by either the left heart or the right heart depending on dominance?

A

Inferior LV
Proximal HIS bundle
AV node
Posterior left bundle

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44
Q

What symptoms are most compatible with infarction due to ACS?

A

Prolonged chest discomfort >30 minutes, with radiation to left arm or neck.

  • > precipitated by exertion and relieved by rest / nitroglycerin
  • > nausea, vomiting, diaphoresis, palpitations are common
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45
Q

Should PCI be done in NSTEMI or unstable angina?

A

Yes, this is okay -> just no thrombolytic therapy unless STEMI

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46
Q

When myocardial ischemia occurs, how quick is function lost, and when does irreversible injury occur? When is infarct size determined?

A

Functional loss: within 1-2 minutes after myocardium has to switch to anaerobic glycolysis and lactic acid accumulates

-> organelle and cytosolic swelling occurs with loss of function and irritability

Irreversible injury: Begins at 30 minutes, infarct size is determined by around 6 hours

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47
Q

What is the general treatment plan for Prinzmetal angina?

A

Use DHP calcium channel blockers (i.e. amlodipine, relax the coronary arteries), with sublingual nitroglycerin for acute events.

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48
Q

In what ACS’s should thrombolytic therapy be used?

A

Only in STEMI, and only if PCI capability is unavailable for greater than 90 minutes.

Must be done within 12 hours of symptoms onset.

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49
Q

Should PCI be done in NSTEMI or unstable angina?

A

Yes, this is okay -> just no thrombolytic therapy unless STEMI

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50
Q

When myocardial ischemia occurs, how quick is function lost, and when does irreversible injury occur? When is infarct size determined?

A

Functional loss: within 1-2 minutes after myocardium has to switch to anaerobic glycolysis and lactic acid accumulates

-> organelle and cytosolic swelling occurs with loss of function and irritability

Irreversible injury: Begins at 30 minutes, infarct size is determined by around 6 hours

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51
Q

What are some reperfusion-induced injuries?

A
  1. Additional cell death
  2. Microvascular injury w/ endothelial swelling
  3. Cardiac arrhythmias
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52
Q

What is a likely complication 2-3 days after a transmural infarct? Why is it specific to this type of infarct?

A

Fibrinous percarditis, due to inflammatory response entering the pericardial sac

Subendocardial infarcts will not allow access of inflammatory cells to the pericardial sac

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53
Q

Other than rupture, what are a few other reasons for papillary muscle dysfunction in MI? What’s the result of all of these?

A

Mitral valve regurgitation is the outcome

  1. Acute ischemia -> can’t contract
  2. Chronic fibrosis and shortening -> due to healing with fibrosis post-MI
  3. LV dilatation -> weak, healing wall must dilate.

In 2/3 the valve leaflets won’t be able to reach to close.

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54
Q

What is a left ventricular aneurysm? When after an MI does this occur? What is the most likely complication?

A

Occurs very late, after an anterior, transmural myocardial infarct. The wall repairs via fibrous scarring and stretches outward.

Likely complication -> mural thrombosis (Due to exposed collagen) but NOT rupture because it is dense collagen (vs false aneurysm)

-> rupture causing hemopericardium or false aneurysm is most likely 4-5 days post MI

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55
Q

How should a patient coming in with ACS be treated with aspirin?

A

An initial loading dose of 2-4 baby aspirins (81mg each) should be given, via chewing an uncoated pill
-> rapid antithrombic effect due to almost complete inhibition of TXA2

-> contraindicated in In patients >60 years of age with peptic ulcer bleeding

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56
Q

What are some reperfusion-induced injuries?

A
  1. Additional cell death
  2. Microvascular injury w/ endothelial swelling
  3. Cardiac arrhythmias
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57
Q

What are the contraindications for nitroglycerin? There are four, three were covered in sketchy, the other is intuitive, but be specific about it.

A
  1. Hypotension (SBP < 90 mmHg) -> avoid when this may be possible, as it will worsen this
  2. Right ventricular infarction -> reduction in preload may cause cardiogenic shock (think of sketchy no right turn sign)
  3. Aortic stenosis -> Need the preload into the left heart to maintain blood flow -> think of the curled smokestack in sketchy
  4. Phosphodiesterase inhibitors (PDE5) taken within the last 24 hours -> i.e. sildenafil -> fill = coal truck in sketchy
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58
Q

What are the beta blockers of choice for ACS? How quickly should they be started? What types should be used?

A

Cardioselective agents: Metoprolol and Atenolol
Should be started within 24 hours

Early: Use short-acting and low dose, titrating upwards for tighter control
Discharge: Give long-acting beta blockers

-> give IV for hypertensive emergencies or Afib with RVR

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59
Q

What are the anticoagulant therapies of choice for early hospital care in ACS? When are these used?

A
  1. Enoxaparin (think of the pair of foxes held by fido for fondaparinux or enoxaparin)
    - > inhibit the factor Xa fox by holding it in close association with ATIII
  2. Unfractionated heparin can also hold onto thrombin

Only in thrombus related NSTEMI -> not indicated for STEMI

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60
Q

What is the typical secondary prevention therapy for ACS?

A
  1. Dual therapy for 1 year: aspirin / P2Y12
  2. Beta blockers
  3. Ace inhibitor / ARB - if indicated (HTN, Diabetes, or HFrEF)
  4. Statin
  5. Standard risk factor management
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61
Q

Where are the precordial / chest leads placed?

A

V1: Right 4th intercostal space
V2: Left 4th intercostal space
V3: Between V2 and V4
V4: Midclavicular line, 5th intercostal space
V5: Between V4 and V6, anterior axillary line
V6: Midaxillary line, 5th intercostal space

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62
Q

How does ticagrelor differ from prasugrel? How is it similar?

A

Differs - binds REVERSIBLY -> clopidogrel and prasugrel are irreversible

Similar - rapid onset, more intense inhibition, same contraindications:

Prior TIA or stroke
>75 years of age (elderly)

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63
Q

When are GP IIb/IIIa inhibitors used? Which one is recommended?

A

Used for patients undergoing early cardiac catheterization to prevent thrombus formation

Eptifibatide - think TIED score in sketchy

Preferred over abciximab or TIrofiban - “tie”

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64
Q

What are the common causes of prolonged QT?

A

Drugs (macrolides, Class IA and III antiarrhythmics, antipsychotics, TCAs, ondansetron)

Hypomagnesia, hypokalemia, hypocalcemia

Congenital long QT syndrome

Increased ICP

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65
Q

What is a normal P wave duration, and what leads should always be up or down?

A

80-200 msec

Upright in leads I and II
Inverted in aVR

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66
Q

What is the definition of Mobitz I, second degree AV block?

A

Also called Wenckebach
-> Mobitz 1 cuz its my #1 favorite arrhythmia

Gradually lengthening PR intervals, until QRS is dropped. Longest PR interval just before dropped beat, shortest after dropping a beat.

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67
Q

What is the ECG definition for left atrial enlargement?

A

This is the criteria of 1s.

  1. P wave in V1 is -1.0 mm in depth for at least 1 small box
  2. P wave is notched (humped) in lead I with a duration of >120 msec (3 small boxes).
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68
Q

What is the ECG definition for right atrial enlargement?

A

P wave is tall and peaked, with a height of 2.5 mm or more in leads II, II, and aVF (all inferior leads).

-> P wave is >2.5 small boxes in inferior leads

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69
Q

How is atrial flutter diagnosed via ECG?

A
  1. Narrow QRS tachycardia - usually around 150 bpm. May be slower if on medications to slow AV node conduction
  2. Regular atrial activity at about 300 bpm
  3. Flutter waves “saw tooth” seen in leads II, III, and aVF
    (inferior leads)
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70
Q

What is a normal P wave duration, and what leads should always be up or down?

A

80-200 msec

Upright in leads I and II
Inverted in aVR

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71
Q

What is the primary toxicity of concern with class Ib antiarrhythmics?

A

Brain hat on the trucker -> neurologic issues

Lowers the seizure threshold, tremor, slurred speech, convulsions

Includes Mexiletine and Lidocaine

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72
Q

What is the primary interval on ECG which class IC drugs will prolongate? What is their use?

A

Primarily the QRS interval -> strongly bind Na+ channels, leaving K+ channels untouched (curtain untouched) -> no QT effect really

Use: Atrial fibrillation rhythm control - guy sitting in bed changing channel on TV (2nd line to amiodarone)’

-> Propafenone and Flecainide

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73
Q

What is the ECG definition for right atrial enlargement?

A

P wave is tall and peaked, with a height of 2.5 mm or more in leads II, II, and aVF (all inferior leads).

-> P wave is >2.5 small boxes in inferior leads

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74
Q

How is atrial flutter diagnosed via ECG?

A
  1. Narrow QRS tachycardia - usually around 150 bpm. May be slower if on medications to slow AV node conduction
  2. Regular atrial activity at about 300 bpm
  3. Flutter waves “saw tooth” seen in leads II, III, and aVF
    (inferior leads)
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75
Q

What are the ECG characteristics of multifocal atrial tachycardia?

A
  1. At least 3 different P wave forms in the same lead, with no dominant atrial pacemaker
  2. Atrial rate > 100 bmp.
  3. PR and RR intervals will vary, but P waves are more obvious than in atrial fibrillation and are ALL transmitted to the ventricles

-> seen in COPD / asthma

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76
Q

What is the primary toxicity of concern with class Ib antiarrhythmics?

A

Brain hat on the trucker -> neurologic issues

Lowers the seizure threshold, tremor, slurred speech, convulsions

Includes Mexiletine and Lidocaine

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77
Q

What is the primary interval on ECG which class IC drugs will prolongate? What is their use?

A

Primarily the QRS interval -> strongly bind Na+ channels, leaving K+ channels untouched (curtain untouched) -> no QT effect really

Use: Atrial fibrillation rhythm control - guy sitting in bed changing channel on TV (2nd line to amiodarone)’

-> Propafenone and Flecainide

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78
Q

What drugs can be used for pharmacological cardioversion?

A

Class 1C = Flecainide, propafenone

Class 3 = Dofetilide, Ibutilide, amiodarone

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79
Q

What is the first line treatment for Rate control in Afib with and without heart failure?

A

Afib w/ heart failure = Digoxin, add beta-blocker if needed

Afib w/o heart failure = non-DHP CCBs, add digoxin if needed

Can consider Beta blockers instead of CCBs for Afib w/o HF, but not calcium channel blockers in heart failure (think of guy holding balloon outside sketchy)

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80
Q

What is the primary use of amiodarone, and what are its drug interactions / half life?

A

Use - Most effective anti-arrhythmic for maintaining sinus rhythm in AF, as well as termination of ventricular tachycardias

  • > Inhibits many CYP450s -> think of the CYP450 truck holding cow, especially warfarin problem
  • > Half life ~60 days = need a huge loading dose.
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81
Q

Why might Dronedarone be preferred to amiodarone, and when should it be avoided?

A

Has a shorter halflife due to lack of iodine moieties, good for non-permanent Afib (paroxysmal <7 days or persistent >7 days but cardiovertable)

Avoid: HFrEF, and PERMANENT Afib (dumb)

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82
Q

When can you or can you not simply directly electrically cardiovert a patient’s Atrial fibrillation / flutter? What is the protocol for when you cannot? Why?

A

<48 hours: Go for it
>48 hours: Must be anticoagulated for 3 weeks prior and 4 weeks post cardioversion for fear that a mural thrombus formed in atria from blood stasus

4 weeks post because there is myocardial stunning which occurs which may not directly restore sinus rhythm until months after the electrical cardioversion

83
Q

What secondary changes often occur in mitral valve prolapse?

A

Friction-induced fibrosis of left atria, with possible thrombi in left atria (due to leaflets hitting endocardium of left atrium)

Friction induced fibrosis of LV endocardium (due to chordae tendinae snapping against the walls of LV)

84
Q

What is the first line treatment for Rate control in Afib with and without heart failure?

A

Afib w/ heart failure = Digoxin, add beta-blocker if needed

Afib w/o heart failure = non-DHP CCBs, add digoxin if needed

Can consider Beta blockers instead of CCBs for Afib w/o HF, but not calcium channel blockers in heart failure (think of guy holding balloon outside sketchy)

85
Q

What are the three layers of normal valves (aside from the endothelial covering)? What layer faces the highest stress portion (i.e. would face venticular side in AV valves and large vessel side in semilunar valves)

A
  1. Fibrosa - dense collagen layer to which supporting structures attach (chordae tendinae) -> face high stress portion
  2. Spongiosa - central core of loose connective tissue with proteoglycans
  3. Elastin-rich layer - on inflow surface (atrialis or ventricularis)
86
Q

What is Marantic Endocarditis also called and what are the usual causes? Will there be inflammation?

A

Nonbacterial Thrombotic Endocarditis (NBTE)

  • > Hypercoagulability state associated with debilitating disease like malignancies (especially mucinous adenocarcinoma of pancreas)
  • > endocardial injury, often due to intracardiac catheter

Marantic = Marasmus

Only endocarditis w/o significant inflammation

87
Q

How does it sound to auscultate a mitral valve prolapse? What accounts for this sound?

A

Midsystolic click, typically heard in young women (myxomatous degeneration)

Due to long, thin chordae tendinae snapping against the wall during systole

88
Q

What secondary changes often occur in mitral valve prolapse?

A

Friction-induced fibrosis of left atria, with possible thrombi in left atria (due to leaflets hitting endocardium of left atrium)

Friction induced fibrosis of LV endocardium (due to chordae tendinae snapping against the walls of LV)

89
Q

What condition is characterized by systemic flushing, diarrhea, and wheezing, with thickened endocardium due to accumulation of mucopolysaccharide-rich matrix containing smooth muscle cells? What side of the heart does this affect and why?

A

Carcinoid heart disease -> part of carcinoid syndrome in some neoplasms, due to ectopic serotonin production

Affects the right side of the heart only, since serotonin from venous circulation is broken down in the lungs

90
Q

What is the most common cause of IE in previously disease valves?

A

S. viridans

Note: S. epidermidis tends to grow on prosthetic valves

91
Q

Why are the symptoms of mitral stenosis worse during exercise?

A

Less passive filling of LV during diastole in tachycardia -> need to push more blood through stenotic valve during exercise, leading to increased pressure and atrial dilatation

+Afib is very common

92
Q

What does acute rheumatic heart disease do to the endocardium? What side of the heart does it affect?

A

Small, sterile thrombi (vegetations) along lines of closure of valves

Affects especially left side of heart, mitral > aortic valve.

93
Q

What will happen to the pulse pressure and pulse in aortic stenosis?

A

Pulse pressure narrows (opposite of aortic regurgitation)

Pulse is weak and delayed (parvus et tardus)

  • > due to less increase in systolic BP (explains narrowed pulse pressure)
  • > takes longer for valves to swing open (delayed pulse as compared to heart beat)
94
Q

What abnormal heart sounds will be associated with aortic stenosis?

A
  1. Systolic ejection click - which can go away with worsening stenosis (due to ventricles not being able to whip valve open fast enough anymore)
  2. Crescendo-decrescendo systolic murmur - sometimes with palpable thrill
  3. S4 - due to diastolic dysfunction of atrial contraction
  4. Paradoxical splitting of S2 -> lengthening of LV ejection time makes A2 happen after P2
95
Q

How can the pressure in the left ventricle be estimated non-invasively in valvular stenosis?

A

Modified Bernoulli Equation

Pressure will be ~4 v^2, where the velocity can be measured on ultrasound. You are measuring the velocity of the blood coming into the aorta, and determining the LV pressure based on this.

96
Q

Why are the symptoms of mitral stenosis worse during exercise?

A

Less passive filling of LV during diastole in tachycardia -> need to push more blood through stenotic valve during exercise, leading to increased pressure and atrial dilatation

+Afib is very common

97
Q

What causes an “Austin-Flint” murmur?

A

Diastolic rumble -> due to diastolic jet from aortic regurgitation blocking the opening of the mitral valve
-> impaired opening of mitral valve

98
Q

What will happen to the pulse pressure and pulse in aortic stenosis?

A

Pulse pressure narrows (opposite of aortic regurgitation)

Pulse is weak and delayed (parvus et tardus)

  • > due to less increase in systolic BP (explains narrowed pulse pressure)
  • > takes longer for valves to swing open (delayed pulse as compared to heart beat)
99
Q

What are the key physical exam findings of aortic regurgitation?

A

Wide pulse pressure
Hyperdynamic precordium (like mitral regurgitation)
Diastolic decrescendo (high frequency on left sternal border)
Bobbing head

100
Q

What heart sound findings are associated with mitral regurgitation due to mitral prolapse, and how are they changed with LV preload?

A

Late systolic murmur associated with midsystolic click

Click and murmur begin later (closer to S2) with increasing LV preload (Chordae tendinae are too long in prolapse. Distention of LV will make them the more appropriate size until some contraction has occurred)

Remember, mitral prolapse is the most common cause of mitral regurg

101
Q

What are the major and minor criteria for acute rheumatic fever?

A

2 major or 1 major and 2 minor required
Major: JONES
Minor: Fever, Labs: increased ESR, increased CRP, arthralgias (if no J, aka just pain no inflammation), and prolonged PR interval

102
Q

What are the most common cardiac findings in Marfan syndrome?

A

Mitral valve prolapse and aortic root dilatation, leading to the following abnormalities

  1. Mitral valve prolapse
  2. Mitral regurgitation
  3. Aortic regurgitation

Treat with beta blockers and ACE inhibitors

103
Q

What are the three major jugular waves and what causes them? Which one is most liable to be absent?

A

These are transient rises in venous pressure seen as bulging
a wave = atrial contraction
c wave = carotid pulse pressing against vein / bulging of triscupid valve into atrium
v wave = venous return into left atrium peaking just before AV valves open during early diastole

C wave often absent, so it will just look like two pulses

104
Q

What does a large a wave indicate? When will the a wave disappear?

What does a large v wave mean?

A

Large a wave -> Tricuspid stenosis -> trying to contract the atria through a stenotic valve

a wave disappears in atrial fibrillation -> no atrial contraction

Triscupid regurgitation will cause a large v wave

105
Q

What will the EKG and Echo show for aortic regurgitation?

A

EKG - Left axis deviation, LV hypertrophy, LV strain pattern (ST depression and T wave inversion in I, aVL, and V5/V6)

Echo: Mechanism of AR, LV size, and LV ejection fraction

106
Q

What are the major and minor criteria for acute rheumatic fever?

A

Major: JONES
Minor: Fever, Labs: increased ESR, increased CRP, arthralgias (if no J, aka just pain no inflammation), and prolonged PR interval

107
Q

What is paradoxical splitting of S2 and why does it happen?

A

When S2 splits during expiration, happens due to conditions where A2 closes later than usual, as in aortic stenosis or left bundle branch block

108
Q

What are the three major jugular waves and what causes them? Which one is most liable to be absent?

A

These are transient rises in venous pressure seen as bulging
a wave = atrial contraction
c wave = carotid pulse pressing against vein / bulging of triscupid valve into atrium
v wave = venous return into left atrium peaking just before AV valves open during early diastole

C wave often absent, so it will just look like two pulses

109
Q

What does a large a wave indicate? When will the a wave disappear?

A

Large a wave -> Tricuspid stenosis -> blood backs up during atrial contraction

a wave disappears in atrial fibrillation -> no atrial contraction

110
Q

What type of valvular problem is indicated via palpable thrills? Anything else? Where are they best felt?

A

Stenosis -> pulmonic or aortic. These are vibrations

Also small VSDs with turbulent flow

Best felt at left sternal border

111
Q

What murmur is associated with chronic mitral regurgitation? Where is it best heard? Does it radiate?

A

Holosystolic, blowing murmur

Best heard at the apex, mediumpitched so audible no matter what.

Radiates to axilla

Aortic stenosis radiates to carotids

112
Q

What is paradoxical splitting of S2 and why does it happen?

A

When S2 splits during expiration, happens due to conditions where A2 closes later than usual, as in aortic stenosis or left bundle branch block

113
Q

What is wide splitting and why does it happen?

A

Exaggerating normal splitting -> splitting heard on expiration and even more on inspiration

Happens due to conditions causing a delay in RV emptying, including pulmonic stenosis and right bundle branch block

114
Q

What is fixed splitting and why does it happen?

A

Closure of pulmonic valve is consistently delayed, with no regard for inspiration / expiration

Happens typically due to atrial septal defect causing a left to right shunt

115
Q

What murmur is mitral valve prolapse with mitral regurgitation associated with? How and where is it best heard? Does it radiate?

A

Late systolic crescendo murmur following mid-systolic click

Heard best via the diaphragm at the apex (high pressure = high pitch)

Does not radiate

116
Q

What murmur is associated with chronic mitral regurgitation? Where is it best heard? Does it radiate?

A

Holosystolic, blowing murmur

Best heard at the apex, mediumpitched so audible no matter what.

Radiates to axilla

Aortic stenosis radiates to carotids

117
Q

What murmur is associated with mitral stenosis? Where and how is it best heard? Does it radiate?

A

Low-pitched, diastolic rumble best heard at apex in LLDP

Associated with an opening snap best heard in same place, but with diaphragm (high pitch)

118
Q

What heart sounds can result from a VSD?

A

More exaggerated RV S3 due to left-right shunt, also flow rumble at left ventricular apex due to shunt.

119
Q

What causes knocks and when do they occur? What is their frequency? Best heard?

A

High frequency, sharp diastolic sounds best heard at apex, occurring early in diastole (similar timing to S3)

Thus, they may confused with an opening snap
-> sudden tensing of pericardium during rapid filling, as in constrictive pericarditis

120
Q

What is the most common type of pericarditis and what are some common causes?

A

Fibrinous pericarditis

Causes:

  1. Same as serous -
    Uremia, autoimmune disorders
2. Things which will cause clotting - 
s/p myocardial infarction 
s/p cardiac surgery 
s/p radiation exposure 
early bacterial infection (i.e. group A strept)
121
Q

What are the causes of hemorrhagic pericarditis?

A
  1. Metastatic malignancy (due to angiogenesis)
  2. Infections i.e. TB, early on which are destructive
  3. Coagulopathies
  4. s/p cardiac surgery
122
Q

What is the most common type of chronic pericarditis, and what does it result from? What is it?

A

Adhesive pericarditis -> follows serous or fibrinous pericarditis

It is residual strands of fibrous connective tissue extending between the pericardial surfaces (like the bread and butter)

Soldier’s plaques = collagenous & calcified in local spots

123
Q

What is the most frequent chronic pericarditis which results from purulent or caseous pericarditis? Describe.

A

Constrictive pericarditis

-> replacement of pericardial space with a dense collagen or calcified collagen (dense shell)

124
Q

What is adhesive mediastinopericarditis and what does it follow?

A

Fibrous attachment of parietal pericardium to surrounding mediastinal structures, forcing an incresaed cardiac workload, causing cardiac hypertrophy / dilatation

Most often follows mediastinal radiation / surgery (which most often starts with fibrinous pericarditis), but can follow purulent / caseous pericarditis

125
Q

What are the possible complications of myxoma?

A
  1. Valvular obstruction / injury - seems like mitral stenosis, can injure like a wrecking ball
  2. Tumor embolization -
  3. Cytokine-mediated symptoms - inflammation caused by immune response
126
Q

What is the most common cardiac tumor in children? Describe it. What disease is associated?

A

Rhabdomyoma - bulging, intramyocardial hamartoma (derived from cardiac myocytes)

  • Tuberous sclerosis is the common association
  • > arrhythmias and outflow obstruction
127
Q

When tumors metastasize to the heart, where do they most commonly spread to and what are the complications of this?

A

Lung, breast cancers, melanoma, lymphomas / leukemias

Typically the pericardial surfaces

Complications -> cardiac constriction, or hemorrhagic pericardial effusion due to formation of new blood vessels

128
Q

What are the three primary etiologies of congestive heart failure (in a broad sense)?

A
  1. Decreased myocardial contractility - i.e. ischemic heart disease, drug toxicities like doxorubicin
  2. Increased resistance to ventricular filling / ejection - cardiac tamponade, severe HTN, aortic stenosis, coarctation
  3. Systemic diseases - hyperthyroidism, severe anemia
129
Q

What are the five types of acute pericarditis (fluid accumulation in pericardial sac with associated inflammation)? Include fluid characteristics

A
  1. Serous - least extra cells in fluid
  2. Fibrinous - Extra fibrin + inflammatory cells
  3. Purulent / suppurative - worst, with acute inflammatory infiltrate
  4. Hemorrhagic - fibrinous + RBCs
  5. Caseous - caseous necrosis within pericardium
130
Q

What will characterize the subacute course of presentation of infective endocarditis?

A

Long illness, lasting weeks to months, with small vegetations involving previously DISEASED or ABNORMAL valves

  • > low grade fever, may be intermittent
  • > constitutional symptoms will be associated: fatigue, anorexia, wasting, night sweats, myalgias
  • > Immune complex deposition likely - causing arthritis / hematuria
131
Q

What are Janeway lesions and what organism is usually associated with them?

A

Small, PAINLESS, hemorrhagic macular lesions of PALMS and SOLES

->S. aureus is associated

132
Q

Petechiae -> small hemorrhages of skin or mucous membranes

A

What can be seen in IE due to immune complex deposition in small vessels, and will cover entire feet sometimes?

133
Q

What are the complications of IE caused by immune complex deposition?

A
  1. Glomerulonephritis -> acute renal failure
  2. Polyserositis -> arthritis
  3. Vasculitis -> rashes

-> typically subacute, acute is associated with more tumor emboli

134
Q

What are the minor duke criteria for IE?

A
  1. Predisposition factors for IE
  2. Fever
  3. Vascular phenomena - i.e. infarcts, mycotic aneurysms
  4. Immunologic phenomena - i.e. arthritis, GN
  5. One positive blood culture
135
Q

What patients are at high risk with transient bacteremia and should thus receive prophylaxis during cystoscopy or dental procedures?

A
  1. Prior history of endocarditis
  2. Prosthetic valves
  3. Cardiac transplant recipients
  4. Congenital heart diseases -> unrepaired cyanotic, prosthetic material within 6 months of repair surgery, or residual defect adjacent to prosthetic material from repair surgery
136
Q

What are some common metastatic infections which can occur as a result of septic emboli in the left heart?

A

Septic joints, and vertebral osteomyelitis (will manifest as back pain)

137
Q

What are the major duke criteria for infective endocarditis?

A

Major:

  1. Typical organisms identified from two separate blood cultures @ different locations
  2. Single positive blood culture with Coxiella burnetti
  3. New valvular regurgitation or positive TEE
138
Q

What are the viral causes of pericarditis? Especially in AIDS? How do you treat?

A

Coxsackievirus, adenovirus, echovirus

AIDS - CMV

These are usually self limiting

139
Q

What are the clinical symptoms of acute pericarditis?

A

Sharp or rubbing chest pain which is pleuritic, meaning it varies with intensity of chest wall movement or position such as sitting or lying down

Can mimic MI: Fever, tachycardia, dyspnea

Will hear a three part friction rub

140
Q

Who is most liable to getting tuberculous pericarditis? What does it progress to?

A

Most common in AIDS population, often progresses to constriction with calcification.

-> early on it is often hemorrhagic pericarditis

141
Q

What drugs are commonly associated with pericarditis?

A
  1. Minoxidil - HF vasodilation
  2. Hydralazine (lupus-induced)
  3. Isoniazid
  4. Cyclosporine
142
Q

What are the congenital causes of pericardial disease? What will these cause?

A
  1. Pericardial cyst - usually benign
  2. Congenital absence of pericardium -> risk of herniation of heart and sudden cardiac death, and possible coronary artery compression
143
Q

What is the general treatment for acute pericarditis?

A

2 weeks of NSAIDs for symptoms: Indomethacin or ibuprofen
Systemic steroids - if slow response
Colchicine - as an alternative to corticosteroids

In recurrent cases, lean more on colchicine than steroids

144
Q

What is the most essential treatment for bacterial pericarditis?

A

Early surgical drainage via pericardiocentesis

145
Q

What happens to the pulse in pericardial tamponade? Why?

A

Pulsus paradoxus - defined as >10 mmHg drop in blood pressure in systolic BP during inspiration

Due to greatly increased venous return to RV in inspiration, RV pushes septum into LV which is diastolically constricted as is -> causes a massive drop in preload and increase in afterload, dropping stroke volume and systolic BP

146
Q

What is Kussmaul’s sign? What causes it?

A

Sign of constrictive pericarditis -> rise in systemic VENOUS pressure during INSPIRATION (opposite normal)
-> due to increase in venous flow but no compliance of RV to accommodate increased venous volume (restrictive disease)

147
Q

What’s Ewart’s sign?

A

Dullness of breath sounds and egophony over posterior left lung field due to large pericardial effusion

148
Q

How will syphilitic aneurysm appear microscopically?

A

Intima - undamaged, will have ribbon-like effect w/alternating bulges into lumen

Media - scattered patches of smooth muscle cell loss with inflammation & subsequent fibrosis (ischemia)

Adventitia - Vasa vasorum surrounding by plasma cells and lymphocytes -> destruction via syphilis

149
Q

What are the possible complications of syphilitic aneurysm? What is notably absent?

A
  1. Aortic insufficiency - aneurysm increases aortic annulus size -> regurgitation and LV volume overload
  2. Superimposed atherosclerosis / ischemic heart disease - from tubulence
  3. Compression / erosion of adjacent structures (absent = bronchi, esophagus, recurrent laryngeal nerves, vertebrae)

Absent = Rupture -> media / adventitia is scarred so rupture is unlikely

150
Q

What is the most common, and two uncommon causes of aortic dissection?

A

Most common - hypertension

Uncommon - inherited connective tissue disorder (i.e. Marfan), or peripartum (due to volume shifts in pregnancy)

151
Q

What are the two types of antineutrophil cytoplasmic antibodies (ANCAs) and their targets?

A

cytoplasmic, c-ANCA - proteinase-3

perinuclear, p-ANCA - myeloperoxidase

p doesn’t go with p

152
Q

What is granulomatosis with polyangiitis also called, and what is the clinical triad?

A

Wegener’s granulomatosis

Triad:
1. Necrotizing granulomatous inflammation of upper / lower respiratory tract

  1. Necrotizing granulomatous vasculitis of small vessels of upper / lower respiratory tract
  2. Necrotizing, proliferative glomerulonephritis -> hematuria / proteinuria
153
Q

What causes varicose veins and what are the most common sites?

A

Long-standing increased intravenous pressure with poor wall support -> dilated veins with wall abnormalities

Sites:

  1. Superficial on lower extremities
    - > may cause thrombosis or edema, but NOT thromboembolism
  2. Submucosal veins - i.e. distal esophagus / rectum due to portal HTN
    - > may hemorrhage
154
Q

What carcinogens is angiosarcoma associated with?

A

polyvinyl chloride (PVC), Thorotrast (radiocontrast agent), arsenic (pesticides)

155
Q

When does microscopic polyangiitis typically develop and what does it look like clinically?

A

Frequently following a drug exposure or malignancy

Involves small vessels of skin, kidneys, and lungs the most:
Palpable purpura on skin, hematuria, and hemoptysis

156
Q

What is the cause of most dilated cardiomyopathy? What is the second most common cause?

A
  1. Idiopathic - cause unknown
  2. Genetic abnormalities (1/3 of cases) - usually autosomal dominant, affecting structural proteins of the myocardial cytoskeleton
157
Q

What are some other important causes of dilated cardiomyopathy not in the top two?

A

Toxicities:
1. Alcoholism + thiamine deficiency (wet beriberi), leading to myocardial death
2. Drugs - i.e. doxorubicin
S/p myocarditis: usually enteroviruses like Coxsackievirus
3. Pregnancy related - due to hemodynamic alterations / nutritional factors
4. Hypothyroidism - increases Na+, giving volume overload

158
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

A distinctive form of dilated cardiomyopatthy characterized by RV replacement with fat & fibrous tissue

-> right-sided heart failure and arrhythmias

159
Q

How will patients with HCM present clinically?

A

Broad range of findings.

Arrhythmias -> diastolic dysfunction leads to LA dilatation and Afib

Systemic emboli from Afib

Progressive heart failure, angina, shortness of breath

May cause sudden cardiac death in young athletes from ventricular arrhythmias

160
Q

What are the important causes of restrictive cardiomyopathy?

A
  1. Amyloidosis
  2. Sarcoidosis (granulomatous)
  3. Radiation-induced fibrosis
  4. Hemochromatosis, Pompe disease
  5. Metastatic malignancy

-> causes diastolic filling impairment, and dilatation of LA / RA

161
Q

How will myocarditis look if it is due to a drug-induced hypersensitivity?

A

Inflammatory cell infiltrate will also have many eosinophils

162
Q

What is giant cell myocarditis?

A

An idiopathic, aggressive form of myocarditis characterized by widespread myocardial cell loss, mononuclear infiltrate, and multinucleated giant cells

NOT caused by TB

163
Q

What will be seen in cardiotoxicity caused by doxorubicin and cyclophosphamide?

A

Doxorubicin - Myocardial cell vacuolization & lysis, progressing to dilated cardiomyopathy

Cyclophosphamide - Myocardial hemorrhage (targets vessels more)

164
Q

What types of cardiomyopathy does iron overload cause and why?

A

Early - restrictive cardiomyopathy from accumulation in cardiomyocytes

Late - dilated cardiomyopathy from loss of cardiomyocytes from free radical damage

165
Q

What amyloidosis leads to amyloid accumulating only in the atrium?

A

Isolated atrial amyloidosis - derived from atrial natriuretic peptide, often in heart failure from volume overload

166
Q

What will happen microscopically in cardiac amyloidosis?

A

Extracellular accumulation of amorphous eosinophilic material -> hyaline accumulation of amyloid proteins which stain with Congo red

Accumulation -> pressure atrophy of neighboring cardiac myocytes. Leads to a thickened, weak wall.

167
Q

What will happen microscopically in cardiac amyloidosis?

A

Extracellular accumulation of amorphous eosinophilic material -> hyaline accumulation of amyloid proteins which stain with Congo red

Accumulation -> pressure atrophy of neighboring cardiac myocytes. Leads to a thickened, weak wall.

168
Q

What are the consequences of pulse wave velocity in young people and old people?

A

Young people - arterial wave will return more slowly, and augment coronary perfusion during diastole

Old people - arterial wave will return more rapidly, increase afterload towards the end of systole
-> increases systolic BP and makes for a **wide pulse pressure***********

169
Q

How does calcium handling of the myocardium change with age / what is the net result?

A

Delayed inactivation of L-type calcium channel, delayed SR-Ca+2 uptake, delayed repolarization via K+ channels

Result: Prolonged action potential, prolonged contraction and relaxation, leaving less time for early diastolic filling

-> bad with Afib which is common in these patients due to hypertension

170
Q

Why is diastolic heart failure more common in the elderly? Is mortality better in these patients than HFrEF?

A

They are more likely to have stiff ventricles and abnormal myocardial relaxation (takes longer to repolarize)

HFpEF is better in younger people, but the same mortality in elderly

171
Q

What changes in the myocardium with aging?

A

Myocardium becomes more restrictive and less responsive

  1. Increased Type 1:Type 3 collagen ratio, decreased elastin
  2. Myocardial death via apoptosis
  3. Hypertrophy of muscle cells
  4. Changes in myocardial calcium handling
172
Q

What are the consequences of pulse wave velocity in young people and old people?

A

Young people - arterial wave will return more slowly, and augment coronary perfusion during diastole

Old people - arterial wave will return more rapidly, increase afterload towards the end of systole
-> increases systolic BP and makes for a **wide pulse pressure***********

173
Q

How does calcium handling of the myocardium change with age / what is the net result?

A

Delayed inactivation of L-type calcium channel, delayed SR-Ca+2 uptake, delayed repolarization via K+ channels

Result: Prolonged action potential, prolonged contraction and relaxation, leaving less time for early diastolic filling

-> bad with Afib which is common in these patients due to hypertension

174
Q

What will happen in severe stenosis of the aorta before and after ductus arteriosus closes?

A

Before - some blood will move past isthmus via a right->left shunt which allows left heart to not work as hard against stenosis. Patient will be cyanotic since blood from right heart is deoxygenated

After - venous return from lungs increases, with massive increase in afterload and rapid progression to progressive heart failure + cardiogenic shock

175
Q

What are some of the common symptoms of CHF in CHD?

A

Dyspnea on exertion
Frequent respiratory infections (esp. left-to-right shunts causing pulmonary edema)
Irritability / decreased feeding volumes, and growth failure

Tachypnea, tachycardia, and hepatomegaly (RAA activation)

-> caused by poor ventricular function (usually obstructive i.e. HLHS, severe stenosis, severe coarctation) or VSD

176
Q

What changes in the myocardium with aging?

A

Myocardium becomes more restrictive and less responsive

  1. Increased Type 1:Type 3 collagen ratio, decreased elastin
  2. Myocardial death via apoptosis
  3. Hypertrophy of muscle cells
  4. Changes in myocardial calcium handling
177
Q

What is the general difference between central and peripheral cyanosis?

A

Central - Arterial O2 saturation is decreased

Peripheral - Blood flow to a local organ is decreased, causing cyanosis

178
Q

What factors lead to a persistent ductus arteriosus? When might you not want to close it?

A

Opposite of what closes it:

  1. Hypoxia conditions
  2. Persistently high vascular resistance (i.e. prematurity, pulmonary disease)
  3. Exposure to teratogens (i.e. congenital rubella)
  4. Elevated PGE2 from treatment

Might not want to close it if associated with other cardiac abnormalities (i.e. transposition of great vessels).

179
Q

What will happen in severe stenosis of the aorta before and after ductus arteriosus closes?

A

Before - some blood will move past isthmus via a right->left shunt which allows left heart to not work as hard against stenosis. Patient will be cyanotic since blood from right heart is deoxygenated

After - venous return from lungs increases, with massive increase in afterload and rapid progression to progressive heart failure + cardiogenic shock

180
Q

What are some of the common symptoms of CHF in CHD?

A

Dyspnea on exertion
Frequent respiratory infections (esp. left-to-right shunts causing pulmonary edema)
Irritability / decreased feeding volumes, and growth failure

Tachypnea, tachycardia, and hepatomegaly (RAA activation)

181
Q

What are some examples of CHDs with PDA dependent pulmonary circulation? Which way is the shunting of the blood in PDA? How will the patient present?

A

Pulmonary atresia

Critical pulmonic stenosis

Shunting is left-to-right thru PDA to get to lungs

Patient presents with severe cyanosis (blood not getting to lungs)

182
Q

What is the result of non-cyanotic shunt lesions?

A

These are left-right shunts

Result is pulmonary congestion, as more blood enters pulmonary circulation than systemic circulation (regardless of shunt location)

183
Q

What are the physical exam findings of VSD?

A

Holosystolic murmur which is larger with smaller hole

Diastolic murmur from increased flow across mitral valve

Loud S2 narrowly split (high pulmonary and systemic pressures (both will be 120 to make sure systemic circulation can be perfused))

Tachycardia, tachypnea, hepatomegaly from fluid overload and pulmonary edema

184
Q

What syndrome is associated with common AV canal or atrioventricular septal defect? What is this condition basically?

A

Down syndrome (Trisomy 21)

Complete AVSD - primum ASD + inlet VSD (VSD at triscupid valve)

Some have just primum ASD with no VSD -> will not have pressure overload, just volume on right

-> made worse by AV valve regurgitation

185
Q

How do infants vs adults typically present with Tetralogy of Fallot?

A

Infants - heart murmur due to VSD & pulmonary stenosis

Adults - shortness of breath due to cyanosis

186
Q

What are TET spells? What causes them?

A

Hypercyanotic spells in Tetrology, where there is a sudden increase in right-to-left shunting, causing hypernea and even unconsciousness

Caused by an increase in pulmonary vascular resistance (crying) or decrease in systemic vascular resistance (fever, exercise)

-> PS murmur may even disappear due to this

187
Q

What is the result of non-cyanotic shunt lesions?

A

These are left-right shunts

Result is pulmonary congestion, as more blood enters pulmonary circulation than systemic circulation (regardless of shunt location)

188
Q

What are the EKG chamber size findings in tricuspid atresia?

A

Left axis deviation:

  1. Right atrial enlargement
  2. Left atrial enlargement
  3. LV hypertrophy
  4. Hypoplastic RV
189
Q

How is the systemic circulation supplied in HLHS if aortic valve is stenotic + ascending aorta is hypoplastic?

A

PDA is required for life

If closed -> cardiogenic shock, multi organ failure

RV = CVO

ASD is also required

190
Q

What are the stages of heart failure?

A

A - high risk for future HF
B - Structural disease w/ no symptoms
C - Previous symptoms, but medically managed
D - Refractory HF - special treatment required

191
Q

What is a BiV-ICD / CRT-D/CRT-P?

A

Biventricular implantable cardioverter defibrillator
or
Cardiac resyncronization therapy defibrillatory / pacemaker

Can pacemaker or defibrillate both ventricles if things get out of wack, depending on what patient prefers

This is used in place of an implantable cardioverter defibrillator which is #1 for the prevention of sudden cardiac death

192
Q

Who is Truncus arteriosus associated with? how many valves will there be and what arteries come from it?

A

Associations: Maternal diabetes and DiGeorge syndrome

Valves: One semilunar valve with trunk supplying systemic, pulmonic, and coronary circulations

-> always presents with VSD due to nature of malformation

193
Q

What are the EKG chamber size findings in tricuspid atresia?

A

Left axis deviation:

  1. Right atrial enlargement
  2. Left atrial enlargement
  3. LV hypertrophy
  4. Hypoplastic RV
194
Q

How is the systemic circulation supplied in HLHS if aortic valve is stenotic + ascending aorta is hypoplastic?

A

PDA is required for life

If closed -> cardiogenic shock, multi organ failure

RV = CVO

195
Q

What are the adverse effects of digoxin toxicity?

A
  1. Hyperkalemia - due to K+ not being able to be taken into cells acutely
  2. Nausea, vomiting, diarrhea - first manifestations are GI
  3. Bradycardia / AV block - vagal
  4. Arrhythmias such as PVCs / PACs
  5. Vision disturbances - seeing yellow like van Gogh
196
Q

What is a BiV-ICD / CRT-D/CRT-P?

A

Biventricular implantable cardioverter defibrillator
or
Cardiac resyncronization therapy defibrillatory / pacemaker

Can pacemaker or defibrillate both ventricles if things get out of wack, depending on what patient prefers

This is used in place of an implantable cardioverter defibrillator which is #1 for the prevention of sudden cardiac death

197
Q

What are the major side effects of furosemide?

A

Hypokalemia (due to increased reabsorption of Na+ via ENaC)
Hypomagnesia (due to lack of Mg+2 reabsorption)
Dehydration
Hyperuricemia (uric acid reabsorption is increased in hypovolemia) -> gout
**Deafness - think of the gong in sketchy

198
Q

What is spironolactone used for and why? What drug is similar?

A

Severe CHF -> aldosterone mediates myocardial fibrosis, and spironolactone antagonizes this effect of cardiac remodeling

  • > improves overall SURVIVAL in Stage C/D heart failure
  • > similar drug = eplerenone (apple)
199
Q

What are the drug interactions of spironolactone?

A

Digoxin - competes for secretion (despite hyperkalemia being good to prevent toxicity)
ACE / ARBs / Cyclosporine / Tacrolimus - addative hyperkalemia

Remember furosemide causes HYPOkalemia which is bad since there isn’t enough K+ to compete

200
Q

What are the adverse effects of digoxin toxicity?

A
  1. Hyperkalemia - due to K+ not being able to be taken into cells acutely
  2. Nausea, vomiting, diarrhea - first manifestations are GI
  3. Bradycardia / AV block - vagal
  4. Arrhythmias such as PVCs / PACs
  5. Vision disturbances - seeing yellow like van Gogh
201
Q

What are the symptoms of cyanide and thiocyanate toxicity?

A

Cyanide - drug will look like it stops working, cardiac output drops off and patient goes into lactic acidosis

Thiocyanate - CNS symptoms, abdominal pain, convulsions
-> from renal insufficiency or too much infusion quickly

202
Q

What does it mean when you find yourself in all of the following states / what do you need to do to get out of this?

  1. Normal cardiac index but increased pulmonary capillary wedge pressure
    - > pulmonary congestion
  2. Normal pulmonary capillary wedge pressure but decreased cardiac index
    - > hypoperfusion
  3. Decreased cardiac index with increased pulmonary capillary wedge pressure
    - > pulmonary congestion and hypoperfusion
A
  1. Pulmonary congestion -> volume overload despite adequate cardiac output
    Give diuretics / vasodilators
    -i.e. furosemide + nitroprusside
  2. Hypoperfusion -> stop giving diuretics!! CO is okay but fluids are low. Need IV fluids.
  3. Pulmonary congestion and hypoperfusion systemically -> need inotropes!
    - i.e. dobutamine, milrinone, dopamine
203
Q

What are the indications to use a pressor agent?

A

Systolic BP <90 mmHg WITHOUT hypovolemia
-> cardiogenic or septic shock

-> i.e. dopamine, NE, E

Pathophysiology - Cardiovascular (24 decks)

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