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Block 4 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

During pregnancy - What happens to

  1. systemic vascular resistance
  2. cardiac output
  3. plasma volume
A
  1. decrease in systemic vascular resistance
  2. increase in cardiac output
  3. increase in plasma volume - eventually reaches an increase of about 45% above non-pregnant values
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2
Q

What causes anemia of pregnancy?

A
  1. there is a large increase in plasma volume and a slight increase in RBC
  2. due to this ratio of small RBC to large plasma volume there is lower hematocrit → anemia
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3
Q

Why is there an increase in plasma volume in pregnant women?

A

to protect them from blood loss that happens at delivery

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4
Q

What happens to coagulation in pregnant women?

A

Hyper coagulable state during pregnancy helps prepare for hemostasis after delivery

*can predispose women to venous thrombosis

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5
Q

What is

  • cardiac output
  • stroke volume
  • ejection fraction
A
  1. liters/min
  2. volume ejected from left ventricle on every beat
  3. % of blood in heart ejected on each beat
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6
Q

During delivery -What happens to

  • stroke volume
  • cardiac output
A
  • both further increase
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7
Q

What happens to vena cava when pregnant women lay down?

A

When laying down - the weight of the gravid uterus can compress inferior vena cava and cause reduction in venous return to heart

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8
Q

What is cardiac tamponade?

A

filling of the pericardial space with fluid which puts pressure on the outside of the heart → heart is unable to pump normal and blood flow is obstructed

  • can be caused by trauma, heart surgery, aortic dissection, etc
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9
Q

What side of the heart fails in cardiac tamponade? Explain

A

Right sided

  1. Heart does not stretch out fully between contractions so chambers don’t fill properly → leads to less cardiac output → hypotension
  2. Since chambers don’t fill properly then blood builds up on venous side
  3. Right heart failure - leads to JVD
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10
Q

What is pulses paradoxus?

A
  1. Decrease systolic blood pressure (more than 10 mmHg) during inspiration
  2. Inspiration increases right ventricular filling, shifting interventricular septum toward the left, reducing LV filling and LV stroke volume
  3. This is exaggerated in tamponade because right ventricle can’t stretch against pericardium so it fills up faster pushing on septum more and further reduces LV filling and stroke volume → reducing systolic blood pressure
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11
Q

What is becks triad and in what condition is it found in?

A
  1. Distended jugular veins
  2. Hypotension
  3. Distant heart sounds

cardiac tamponade

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12
Q

What ECG findings are found in cardiac tamponade?

A

Low QRS complex voltage

QRS have differing heights - electrical alternans

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13
Q
  1. What is endocarditis?
  2. What does this mostly affect?
A
  1. inflammation of the endocardium (inner lining of heart) and largely of bacterial etiology
  2. Valves
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14
Q

What is the pathogenesis of endocarditis?

A
  1. alteration of valve surface due to degeneration (wear and tear), trauma, immune destruction
  2. Deposition of platelets and fibrin (inflammation and thrombus at valves) → making NBTE (non-bacterial thrombotic endocarditis)
  3. transient bacteremia - somehow bacteria get into bloodstream and colonize on this injured valve surface. Organisms adhere to NBTE
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15
Q

Left or right valves are affected more in endocarditis?

A

left sided valves

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16
Q

What are specific symptoms found with endocarditis? (3)

-2 other unique symptoms but not specific to endocarditis

A
  1. Roth spots
  2. Osler nodes
  3. Janeway lesions
  • splinter hemorrhages
  • Conjunctival petechiae
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17
Q

What are roth spots?

A

Retinal lesions, red with pale/white center (which is fibrin) - white center is shiny

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18
Q

What are osler nodes

A
  • painful bumps on the pads of fingers and toes
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19
Q

What are janeway lesions?

A

nontender red macules on palms and soles

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20
Q

What are splinter hemorrhages?

A

Red-brown lines under fingernails. Painless.

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21
Q

What is the Duke/Direct Criteria for infective endocarditis?

  • 2 major criteria
  • 5 minor criteria

What combination leads to diagnosis?

A
  1. MAJOR: positive blood culture for endocarditis (persistent bacteremia, typical organisms on blood cultures, etc)
  2. MAJOR: Evidence of endocardial involvement (positive echo for vegetations, prosthetic dehiscence OR new regurgitant murmur)
  3. MINOR: predisposition for cardiac disease or IVDU
  4. MINOR: high temp
  5. MINOR: vascular phenomena (arterial embolus, PE, etc)
  6. MINOR: immunologic phenomena (glomerulonephritis, osler’s, roth’s)
  7. MINOR: Microbiologic events (only 1 out 3 positive blood culture, or serological evidence of organism that causes IE)
  • Both 1 and 2 - dx
  • Either 1 or 2 + 3 minor criteria
  • All 5 minor criteria
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22
Q

What are the (top 2) common causative organisms associated with infective endocarditis

A
  1. staph aureus (IVDU have much larger risk)
  2. viridans strep (typically after dental procedure - affects damaged valves)
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23
Q

What does this show?

A

What vegetations on valves in infective endocarditis look under microscope

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24
Q

In IE due to staph aureus what antibiotic is used for

  1. methicillin sensitive
  2. methicillin resistant
A
  1. Beta lactams
  2. vancomycin or daptomycin if vanco is not tolerated
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25
Q

In IE due to Strep species what antibiotic is used

A
  1. beta lactam plus aminoglycoside for shorter course (2 weeks)
  2. vancomycin if there is beta lactam allergy
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26
Q

In IE due to enterococci what antibiotic is used for

  1. symptoms <3 months
  2. symptoms >3 months
  3. allergies
A
  1. penicillin or ampicillin plus gentamicin for 4 wks
  2. penicillin or ampicillin plus gentamicin for 6 wks
  3. with beta lactam or penicillin resistance → use vanco plus gentamicin for 6 weeks
  4. Penicillin resistant → use ampicillin plus gentamicin for 6 weeks
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27
Q

In IE due to HACEK/AACEK what antibiotic is used for

  1. No beta lactam allergy
  2. beta lactam allergy
A
  1. ceftriaxone for 4 weeks
  2. fluoroquinalone for 4 weeks
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28
Q

In IE due to culture negative endocarditis what antibiotic is used for

  1. if acute (days)
  2. subacute (weeks)
A
  1. vanco plus cefepine for 4-6 weeks
  2. vanco plus ampicillin-sulbactam for 4-6 weeks
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29
Q
  1. With what predispositions would prophylaxis be needed for infective endocarditis
  2. what is prophylaxis medicine and dose
A
  1. patients with prosthetic valves
  2. patients with prior IE
  3. procedures such as dental work or pulmonary procedures
  • amoxicillin 2 grams
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30
Q

What is myocarditis

A

inflammation of the myocardium (frequently with pericarditis)

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31
Q

Are viruses or bacteria more likely to be cause of infection in myocarditis?

A
  1. viral infection (adenovirus, herpes virus 6, enterovirus family, influenza)
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32
Q

What are some causes for myocarditis?

A
  1. infection (mostly viral)
  2. inflammatory reactions (drug reactions, rheumatic fever, lupus)
  3. can happen as result of transplant rejection
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33
Q

How does myocarditis present in young children/teenagers vs older adults

A
  1. young children/teenagers - more acute presentation
  2. older adults- more subtle and insidious symptoms
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34
Q

What clinical findings are seen with left sided failure myocarditis?

A
  1. crackles on auscultation due to blood backing up into pulmonary vasculature
  2. Softer S1 and S2 - positive S3
  3. displaced point of maximal impulse
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35
Q

What clinical findings are seen with right sided failure myocarditis?

A
  1. increased JVD
  2. hepatojugular reflux (when pushing on abdomen and jugular vein becomes more pronounced)
  3. peripheral edema
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36
Q

What x ray findings are seen with myocarditis?

A
  1. cardiomegaly
  2. kerly B lines
  3. cephalization of vessels in lungs (you can see vessels in lungs)
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37
Q

Treatment of myocarditis

A
  1. supportive care to maintain cardiac output (beta blockers, ACE inhibits, ARBs, etc)
  2. manage arrhythmias, heart block, heart condition
  3. Antimicrobial agents (rare)
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38
Q

Right image is abnormal and shows what condition

lymphocytic infiltration w/destruction of myocytes

A

myocarditis

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39
Q

What is pericarditis?

A

Inflammation of pericardial sac

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40
Q

What are causes of pericarditis?

A
  1. infections (viral infections most common but also bacterial)
  2. Post injury (MI can lead to dying of pericardium, radiation, pericardiotomy)
  3. drugs/toxins
  4. idiopathic (MOST COMMON)
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41
Q

What 5 clinical manifestations represent pericarditis?

A
  1. sharp chest pain worse when supine (laying down) because pericardium pushes on the spine
  2. pericardial friction rub (left lower sternal border - can hear rub at ventricular systole, ventricular diastole, atrial systole)
  3. ECG - shows diffuse ST elevation everywhere (not STEMI) + PR depression
  4. Echo will show swinging heart
  5. Muffled heart sounds (S1 and S2)
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42
Q

What is the treatment of pericarditis?

A

NSAIDS for decrease inflammation and symptom control

  • NSAIDS + colchicine has better results
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43
Q

What is restrictive cardiomyopathy?

A

Heart muscles are stiffened and less compliant but muscles and sizes of ventricles stay the same or slightly enlarged

  • ventricles can’t stretch when filling because less compliant (diastolic heart failure)
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44
Q

What is seen in EKG with restrictive cardiomyopathy?

A
  1. low amplitude QRS complex
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45
Q

What happens to atria in restrictive cardiomyopathy?

A

atria end up being dilated due to restriction in ventricles

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46
Q

What causes restrictive cardiomyopathy? (8 reasons)

A
  1. amyloidosis - misfolded proteins that are insoluble and can deposit in heart making it less compliant
  2. sarcoidosis - formation of granulomas (collection of immune cells)
  3. endocardial fibroelastosis - fibrosis of endocardium and subendocardium
  4. Loeffler endomyocarditis - eosinophils accumulate in lung tissue which can also affect heart
  5. Hemochromatosis - iron overload can lead to iron deposited in heart tissue
  6. Radiation - makes ROS which leads to inflammation and eventual fibrosis of heart tissue
  7. Endomyocardial fibrosis (not common in US) - linked to nutritional deficiencies and/or inflammation related to helminthic infections
  8. Genetic mutation in troponin
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47
Q

What does loeffler endomyocarditis look like under microscope?

A

orange cells are eosinophils

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48
Q

What does restrictive cardiomyopathy look like in gross anatomy?

A
  • atria are dilated
  • white lining on ventricles is abnormal
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49
Q

How do you detect amyloids in between myocytes (for restrictive cardiomyopathy) under microscope

A
  1. amyloids will stain red congo red staining
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50
Q
  1. What is hypertrophic cardiomyopathy?
  2. What changes happen to blood flow
  3. Diastolic or systolic heart failure?
A

When heart muscle gets thick and heavy - muscles grow much larger

  • LV is most affected and muscle growth (sarcomeres in parallel) is asymmetrical so that the interventricular septum grows inward towards LV - less blood filling in LV
  • Leads to smaller outflow tract - due to venturi effect the mitral valve moves closer to overgrowth muscle wall and creates even smaller LV outflow tract

diastolic heart failure

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51
Q

What different heart sounds do you hear with hypertrophic cardiomyopathy?

A
  1. crescendo-decrescendo murmur - due to aortic/pulmonary stenosis that is causing ventricle to work harder
  2. may hear an S4 sound - blood is hitting stiff muscle when going into ventricle
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52
Q

What are the two types of amyloidosis?

A
  1. familial amyloid cardiomyopathy (TTR misfolded protein gets deposited in heart)
  2. Senile cardiac amyloidosis - seen in elderly where normal TTR is deposited in heart
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53
Q

Hypertrophic cardiomyopathy can be inherited. What are the two types of inherited disorders?

A
  1. Missense mutations - mutation for a gene that encodes proteins in the sarcomere in heart muscle (for muscle growth)
  2. Mutation in beta myosin heavy chain
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54
Q

What does hypertrophic cardiomyopathy look like in gross anatomy?

A
  1. has banana shaped outflow tract
55
Q

What does hypertrophic cardiomyopathy look like under microscope?

A
  1. larger myocyte size
  2. Myocyte disarray where myocytes don’t align in parallel fashion like usually do
56
Q
  1. What is dilated cardiomyopathy?
  2. What changes to heart muscle occur
  3. diastolic or systolic heart failure?
A
  1. leads to all 4 chambers of the heart to dilate or get bigger
  2. sarcomeres are added in series which leads to larger chambers but thinner muscle → leads to weak contractions, less blood is pumped out
  3. Systolic heart failure
57
Q
  1. What murmurs can cause dilated cardiomyopathy?
  2. What is the murmur described as?
A
  1. mitral valve regurgitation
  2. tricuspid valve regurgitation
  3. holosystolic murmur
58
Q

What causes dilated cardiomyopathy? (4)

A
  1. commonly idiopathic
  2. genetic mutations or disorders (like duchenne or hemochromatosis)
  3. Infection (coxsackivirus B or chagas disease)
  4. mutation in titin
  5. and more…
59
Q

What does dilated cardiomyopathy look like in gross anatomy?

A
60
Q

What is contractility?

A

The ability of heart muscle cells to contract

61
Q

What is preload vs afterload?

A
  1. preload- initial stretching of the cardiac myocytes (muscle cells) prior to contraction
  2. Afterload - the force or load against which the heart has to contract to eject the blood. Decreased afterload increases stroke volume.
62
Q

What is the equation for cardiac ouput?

A

CO = heart rate X stroke volume

measured in L/min

63
Q
  1. What is HFrEF?
  2. What two things can cause HRrEF?
A
  1. heart failure with reduced ejection fraction due to
  2. Excessive afterload or impaired contractility
64
Q

What changes to pressure volume curve happen with HRrEF?

  • afterload
  • stroke volume
  • systolic pressure
A
  1. increased afterload
  2. decreased stroke volume
  3. decreased systolic pressure
65
Q
  1. What is HFpEF
A
  1. heart failure with normal ejection fraction due to impaired diastolic filling
66
Q

What changes to pressure volume curve happen with HFpEF?

  • preload
  • stroke volume
A
  1. less preload
  2. less stroke volume
67
Q

What is right sided heart failure?

A

Right ventricle is unable to accommodate sudden onset increases in after-load and can lead to acute right ventricle failure - pushing blood back into vena cava and body edema

  • this is because RV is thin walled and typically fills at low pressures and ejects against low resistance
68
Q

What is the overall function of the RAAS system?

A

to increase blood pressure in environment where low cardiac output due to heart failure is occuring

69
Q

Difference between eccentric vs concentric ventricular remodeling?

A
  1. Eccentric - sarcomeres growing in series which makes the heart lining thin
  2. Concentric - sarcomeres grow in parallel making the heart lining thick
70
Q

What is left sided heart failure? and what does it present like?

A
  • will show with pulmonary symptoms since blood is backing up into the lungs and causing problems (congestions and pulmonary edema)
  • Left ventricle is weakened and cannot pump properly
71
Q

Left sided heart failure has what classical lesion seen under microscope?

A

Heart failure cells - With pulmonary edema it leads to RBC diapedesis (RBC going through capillary walls) → then macrophage engulfment of these RBC which creates heart failure cells in lungs

72
Q
  1. What symptoms are seen with right sided failure?
  2. What classical lesion is seen?
A
  1. systemic, vascular symptoms such as elevated JVD and peripheral pitting edema (blood pools in vena cava which leads to increased hydrostatic pressure)
  2. Blood backs up into systemic vasculature and can lead to hepatic congestion (hepatic vein) - leads to NUTMEG LIVER (mottled appearance of liver)
73
Q

What is aortic stenosis?

A

when aortic valve narrows and makes heart work harder to get blood through small narrowing

74
Q
  1. What happens to heart muscle in aortic stenosis?
  2. What triad (symptoms) is seen in patients with aortic stenosis
A
  1. LV hypertrophy concentric (sarcomeres replicating in parallel), LV stiffness and decreased LV filling
  2. SAD (syncope, angina, dyspnea)
75
Q

What equation can you use to determine how compensation occurs when valve dysfunction occurs?

A

T = (P X R)/ (2 X Th)

T= wall tension/stress

P=pressure

R=radius

Th=thickness

ex: with aortic stenosis - there is more pressure in left ventricle then to compensate and bring back T down then thickness in ventricle increases

76
Q
  1. What physical findings are found in aortic stenosis
  2. What type of murmur is seen in aortic stenosis?
A
  1. elevated JVP (indirect measure of vena cava pressure), delayed carotid upstroke with reduced volume, sustained LV impulse
  2. long late peaking crescendo-decrescendo ejection murmur
77
Q
  1. What is aortic regurgitation?
A
  1. AV leaflets fail to close completely so blood flows from the aorta into the LV after ejection/during diastole
78
Q
  1. What happens in blood flow with aortic regurgitation?
  2. What type of LV hypertrophy happens?
A
  • During diastole - there is greater LV filling due to blood coming back from aorta and left atrium.
  • Leads to greater than normal stroke volume into aorta
  • Increases atrial pressure and back blood up into the lungs (pulmonary congestion)
  • Eccentric LV hypertrophy (sarcomeres replicating in series)
79
Q
  1. What is the murmur
A
  1. Diastolic blowing murmur (diastolic decrescendo)

* seen with pulmonary/aortic regurgitation

80
Q
  1. What is mitral stenosis?
  2. What is the changes in blood flow for mitral stenosis
A
  1. narrowing of the mitral valve opening- between left aorta and left ventricle
  2. → blood backs up into the left aorta and leads to left atrium enlarging and hypertrophying;; → reduced LV filling causes reduced LV stroke volume
81
Q

What murmur is found in mitral stenosis?

A
  1. Loud S1
  2. Opening snap sound
82
Q
  1. What is mitral regurgitation?
  2. What changes to blood flow happen?
A
  1. Mitral valve fails to close completely during ventricular systole
  2. Blood regurgitates back into left atrium as the LV contracts. This engorges left atrium because blood comes from LV and pulmonary veins (lung). Left atrium dilates. Increased preload enables larger stroke volume
83
Q
  1. What murmur sound is heard from mitral regurgitation?
A
  1. Apical holosystolic plateau murmur - systole
84
Q

What is the path of blood in fetal circulation?

A
  1. From right atrium blood goes to right ventricle AND left atrium via foramen ovale
  2. From right ventricle blood goes to lungs via pulmonary arteries. (lungs have high amount of pressure so the blood doesn’t easily go to lungs) → due to this pressure the blood actually goes through ductus arteriosus shunt into aorta
  3. From left atrium blood can go to left ventricle and into aorta like normally
85
Q
  1. foramen ovale
  2. ductus arteriosus
  • Is this a right to left or left to right shunt?
A
  1. both are right to left shunts
86
Q
  1. How does a fetus get oxygenated blood and how does it get to the heart?
A
  1. Placenta provides oxygenated blood to the fetus via umbilical vein
  2. Umbilical vein travels to the fetal liver and within the liver it helps create ductus venosus (vein connecting umbilical circulation directly to the inferior vena cava - now mixed blood) →from vena cava it goes into the right atrium
  3. veins travel to placenta so fetus blood can get oxygenated again
87
Q
  1. Explain patent ductus arteriosus?
  2. What is direction of this shunt lesion?
A
  1. When the ductus arteriosus stays present even after birth so when blood goes from left ventricle to aorta and out to body → blood in aorta has option of going to lungs (connection to pulmonary arteries) or systemic circulation
  2. left to right shunt (at first)
88
Q

What negative outcomes arise from patent ductus arteriosus?

A
  1. there is increase in blood going to lungs which can leads to pulmonary hypertension (happens after years of having patent ductus arteriosus
89
Q

What are the causes of having ductus patent arteriosus for many years?

A
  1. There is increase in blood going to lungs (pulmonary hypertension)
  2. This leads to increase pressure in pulmonary arteries and pushing blood into aorta (now right to left shunt) → you have deoxygenated blood going into aorta and causing cyanosis
90
Q
  1. What is ventricular septal defect?
  2. What is the shunt direction of this?
A
  1. septum that separates ventricles has a gap in it ;;;;;; Blood from left ventricle (higher pressure + oxygenated) moves into right ventricle - takes another unnecessary trip to lungs
  2. Left to right shunt (at first)
91
Q

At first ventricular septal defect has left to right shunt but when and why does it change?

A
  • At first it is left to right - so eventually more and more blood goes to lungs causing pulmonary hypertension
  • This changes pressure differences so now right ventricle has higher pressure than left ventricle → making deoxygenated blood from right ventricle go into left ventricle leading to cyanosis
92
Q
  1. What is atrial septal defect?
  2. What is direction of shunt?
A
  1. Opening between the right and left atrium.
  2. Left atrium has greater pressure than right so blood gets shunted from LEFT TO RIGHT - so oxygenated blood moves to right atrium sending more blood to lung
93
Q

What are the 4 abnormalities seen in tetralogy of fallot?

A
  1. stenosis - narrowing of right ventricular outflow tract to lungs
  2. Right ventricular hypertrophy (need more muscle to push out through stenosis)
  3. Ventricular septal defect (RIGHT TO LEFT shunt- due to large pressure with stenosis)
  4. Aorta overrides septal defect or sometimes more centered on the left ventricle.
94
Q
  1. What is truncus arteriosus?
  2. What does this change in blood flow of deoxygenated and oxygenated?
A
  1. congenital malformation - there is one large giant artery instead of divided aorta from pulmonary arteries
  2. because there is no division - deoxygenated and oxygenated blood always get mixed when going into pulmonary arteries and aorta - leads to cyanosis
95
Q
  1. What is transposition of the great arteries?
A
  1. switching aorta and pulmonary arteries so basically forms two circuits → leads to death unless foramen ovale stays in place or there is ventricular septal defect to mix blood
96
Q

What is tricuspid atresia?

A

The tricuspid valve (between right atrium and right ventricle) doesn’t form at all

  • makes right ventricle be underdeveloped
97
Q

What is total anomalous pulmonary venous return?

A

All four pulmonary veins do not connect normally to left atrium. Instead they abnormally drain to the right atrium

98
Q

What is pulmonary atresia?

A

The pulmonary valve does not develop (or develop normally)

  • oxygenated blood from aorta moves into pulmonary arteries via ductus arteriosus
99
Q
  1. What is aortic coarctation?
  2. How is aortic coarctation different in fetus
  3. vs adult life
A
  1. narrowing of the aorta which occurs after aortic arch but before ductus arteriosus
  2. FETUS: Before ductus arteriosus there is high pressure in aorta due to coarctation but after it is low pressure due to low blood flow….after ductus arteriosus blood flows from right to left
  3. ADULT: there is no ductus arteriosus so no mixing of blood. Higher pressure before coarctation which leads to higher pressure in upper extremities and head. Low pressure after coarctation leads to low BP in lower extremities
100
Q

What is congenital aortic stenosis?

A

Aortic outflow tract is narrowed

101
Q

What is hypoplastic left heart?

A
  1. underdeveloped left heart (specifically left ventricle and ascending aorta) + aortic or mitral valve may be too small or absent
  2. This defect requires atrial septum defect and ductus ateriosus shunts → so oxygenated blood goes into right atrium (mixed blood) and then mixed blood can go into aorta via patent ductus arteriosus
102
Q

What is pulmonary valve stenosis?

A
  1. pulmonary valve has a small opening and doesn’t allow for complete/easy flow to pulmonary arteries
103
Q

What is bulk flow transport across membranes?

A

Typically movement of fluid

104
Q

What is fick’s law and the equation for this?

A
  1. Rate of diffusion
  • J= D * A * (DeltaP)/(DeltaX)
    • J = rate of diffusion
    • D= diffusion constant (solubility/permeability)
    • A= surface area
    • DeltaP= (P1-P2) partial pressure gradient
    • DeltaX= diffusion distance
105
Q

what has a larger influence on capillary hydrostatic pressure?

  1. arterial or venous pressure?
A

Venous pressure has larger influence because there are no measures that can protect capillaries from getting full force of venous back up. Increased arterial pressure can lead to constriction of metarterioles to reduce pressure going into capillaries

106
Q

What is narrative review (EBM)

A

a broad overview of the topic that proposes no question

107
Q

What is systemic review (EBM)

A

a clearly formulated question that uses systematic and reproducible methods to identify, select and critically appraise all relevant research, and to collect and analyse data from the studies that are included in the review

108
Q

What is meta-analysis (EBM)?

A

Used statistical methods to summarize results of many studies

109
Q
  1. Reporting bias?
  2. Publication bias?
A
  1. selective revealing or suppression of information
  2. when the outcome of a study influences the decision of whether or not to publish data
110
Q
  1. What is the mechanism of action of loop diuretics? (for acute heart failure)
A
  • rapid management of fluid overload
  • inhibit Na, K, Cl pump (which normally leads to water reabsorption) in the ascending loop of henle which results in WATER EXCRETION
111
Q
  1. name several loop diuretics?
A
  1. furosemide
  2. bumetanide
  3. torsemide
112
Q

What are major side effects of loop diuretics? (2)

A
  1. hypokalemia (loss of potassium) → which can increase risk for arrhythmias
  2. volume depletion
113
Q

What is the mechanism of action of inotropes (for acute heart failure)?

A
  • INCREASE BP- activates B1 pathway in myocytes which increases HR and contractility
  • Has small B2 effects in smooth muscle to cause vasodilation
114
Q

What are examples of some inotrope drugs?

  • and how do they differ in MOA
A
  1. dobutamine - B1 agonist to increase cardiac contractility + some B2 activation → can produce vasodilation at low doses
  2. dopamine - at low dose it stimulates D1 to increase renal blood flood and augment diuresis;; at medium dose it is B1 agonist;;; high dose it is an alpha agonist
  3. milrinone - Phosphodiesterase 3 inhibitor (Phosphodiesterase 3 usually degrades cAMP but by inhibiting its degradation you get more muscle contraction)
115
Q

What are side effects of dobutamine and dopamine (types of inotropes)?

A
  1. can lead to angina or arrhythmias
116
Q
  1. What are the names of several vasodilators?
A
  1. Nitrates
  2. Nitroglycerin
  3. Nitroprusside
117
Q

Explain mechanism of action of vasodilators? (2) (acute heart failure)

A
  1. decreases venous tone which decreases preload
  2. decreases arterial tone which decreases afterload
118
Q
  1. What is the mechanism of action of ACE inhibitors? (systolic chronic heart failure)
  2. How to identify which drugs are ACE inhibitors?
A
  1. Blocks conversion of angiotensin I to angiotensin 2. A2 is responsible for increasing preload, afterload, and remodeling of heart (increases BP)
  2. end in “-pril”
119
Q
  1. What are some side effects of ACE inhibitors? (4)
A
  1. Acute kidney injury
  2. Hyperkalemia (increased potassium due to decreased GFR and decreased aldosterone)
  3. dry persistent cough
  4. angioedema
120
Q
  1. What is the mechanism of action of ARBs inhibitors? (systolic chronic heart failure)
  2. How to identify which drugs are ARBs inhibitors?
A
  1. Inhibiting binding of angiotensin II in RAAS system.
  2. ARBs end in “-sartan”
121
Q

What are the side effects of ARBs?

A
  1. Same as ACE inhibitors
  2. Don’t combine ACE and ARB bc it increases risk for hyperkalemia and renal insufficiency
122
Q

Vasodilators for chronic heart failure

  1. drugs in this category
  2. mechanism of action of each
A
  1. Hydralazine AND isosorbide dinitrate (used together)
  2. Isosorbide dinitrate:::: relaxes venous smooth muscle which allows veins to hold more blood and decrease preload.
  3. Hydralazine::: directly vasodilates arterial smooth muscle to decrease afterload
  • both are used together when patient has true contraindications to ACE and ARB drugs
123
Q
  1. What is the mechanism of action of beta blockers? (systolic chronic heart failure)
  2. How to identify which drugs are beta blockers?
A
  1. Inhibit sympathetic mechanisms of epinephrine and NE (such as increased HR, contractility, preload, afterload)
  2. end in “-lol”
124
Q
  1. What is the mechanism of action of ARA (aldosterone receptor antagonist)? (systolic chronic heart failure)
  2. What drugs are in this category?
A
  1. ARA blocks the effects of aldosterone in the kidneys, heart, and vasculature. → therefore excreting more water and decreasing blood volume
  2. Spironolactone and eplerenone
125
Q

What are side effects of ARA (aldosterone receptor antagonists)?

A
  1. Hyperkalemia
  2. Blocks testosterone effects in men (erectile dysfunction in men)
126
Q
  1. What is the mechanism of action of cardiac glycosides (Digoxin) for systolic chronic heart failure
A
  1. Inhibits myocardial Na/K ATPase pump which leads to preservation of intracellular Ca → increase binding of Ca to troponin → increase myocyte contractility
127
Q

What is the mechanism of action of ivabradine for systolic chronic heart failure

A
  1. Inhibits the funny sodium channel to prolong the slow depolarization phase and slow SA node firing → slows heart rate causing a drop in BP
128
Q

How is diastolic chronic heart failure treated?

A
  • no specific therapies exist - you just treat the symptoms
  • Main goal is to control tachycardia to increase filling time by decreasing HR
129
Q

What drugs for systolic chronic heart failure are used to also decrease mortality? (5)

A
  1. ACE inhibitors (recommended for all pts w/o contraindications)
  2. ARBs (recommended for all pts w/o contraindications)
  3. Beta blockers (recommended for all pts w/o contraindications)
  4. ARA (recommended for all pts w/o contraindications)
  5. Vasodilators (decrease mortality for select patients)
130
Q

What findings are found in X-ray for cardiomegaly?

A
  • Ratio of heart to thoracic size is greater than 0.5
  • From lateral view - there is an overlap of anterior portion spine and the heart
131
Q

What findings are found in X-ray for pulmonary edema? (4)

A
  1. fluid accumulates in interstitial tissue surrounding bronchi (thickening of bronchial walls) → leads to ring like densities (doughnuts or cheerios)
  2. Kerley B lines (horizontal lines at base of lungs)
  3. Kerley A lines (horizontal lines found from hilum to upper lobes)
  4. Butterfly pattern, soft fluffy lesions, coalescing
132
Q

What findings are found in X-ray for pleural effusion?

A
  1. You can see blunting of costophrenic angle (yellow arrow)
133
Q

What findings are found in X-ray for pericardial effusion?

A
  1. water bottle sign - heart takes form of a water bottle
  2. Oreo cookie sign - space between retrosternal and subepicardial fat
134
Q

For what circumstances do you use CT, MR, or nuclear medicine imagining for diagnosis of chronic heart failure?

A
  1. CT is used for - patient with dyspnea due to heart failure and ischemia has NOT been ruled out
  2. MR is used for - pts with dyspnea due heart failure - regardless if ischemia is ruled out or not
  3. Nuclear medicine imaging - for pts with chronic heart failure only if ischemia has not been ruled out

Block 4 (8 decks)

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