Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards > Cardiovascular > Flashcards

Cardiovascular Flashcards

0
Q

What are the three shunts in fetal circulation?

A 
1) Ductus venosus
Umbilical vein (oxygenated) --> IVC

2) Foramen ovale
RA (oxygenated) –> LA

3) Ductus arteriosus
Pulmonary artery (deoxygenated from SVC) --> Aorta (after the great vessels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Where does fetal erythropoiesis occur?

A

“Young Liver Synthesizes Blood”

Yolk sac (3-10 wk)
Liver (6 wk-birth)
Spleen (15-30 wk)
Bone marrow (22 wk+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is used to keep a PDA open?

To close it?

A

PGE keeeeeps it open

Indomethacin closes it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the umbilical vein become?

A

Ligamentum teres hepatis

within falciform ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do the umbilical arteries become?

A

Medial umbilical ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the ductus arteriosus become?

A

Ligamentum arteriosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the ductus venosus become?

A

Ligamentum venosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the foramen ovale become?

A

Fossa ovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does the urachus become?

A

Median umbilical ligament

Urachus is part of the allantoic duct (portion between bladder & umbilicus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the notochord become?

A

Nucleus pulposus of intervertebral disc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does it mean to be right heart dominant vs. left?

A

Right dominant (85%) - the posterior descending artery arises from the RCA

Left dominant (8%) - the PD arises from the Left circumflex

Codominant (7%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What heart chamber composes the back of the heart?

What can be seen with pathology?

A

The LA is the most posterior chamber. Enlargement can cause dysphagia (esophageal compression) or hoarseness (recurrent laryngeal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Myocardial infarction:
What leads will show alterations?
What artery is infarcted?
Left lateral wall

A

Leads I, AVL, V5, V6

LCX or LCA infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Myocardial infarction:
What leads will show alterations?
What artery is infarcted?
Anterior

A

Leads: V2-V4

LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Myocardial infarction:
What leads will show alterations?
What artery is infarcted?
Septal

A

Leads: V1,V2

LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Myocardial infarction:
What leads will show alterations?
What artery is infarcted?
Inferior

A

Leads: II,III,AVF

PDA or RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the equations for Cardiac Output?

A

CO = Stroke Volume * HR

CO =
O2 consumption rate)/(arterial O2 content - venous O2 content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the equations for mean arterial pressure?

A

MAP = (2/3)Diastolic + (1/3)Systolic

MAP = CO x TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What factors increase myocardial O2 consumption?

A

^Afterload
^Contractility
^HR
^Heart size (wall tension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does blood pH affect potassium levels?

A

Potassium moves the opposite direction of protons across cell membranes in order to maintain charge.Thus:

Acidosis –> hyperkalemia
Alkalosis –> hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What effect does insulin have on potassium?

A

INsulin causes K+ shift INto cells.

This is why DKA pts are hyperkalemic at first but may become hypokalemic with treatment. (Also because acidosis –> hyperkalemia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does acidosis decrease contractility?

A

H+ shifts into cardiac cells, so K+ shifts out –> hyperpolarization of the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are preload and afterload affected by dilating drugs?

A

vEnodilators decrease prEload

vAsodilators decrease Afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What can decrease contractility?

A 
Beta blockade
CHF
Acidosis
Hypoxia/Hypercapnia
Non-dihydropyridine CCB's
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the equation for ejection fraction?

What is a normal ejection fraction?

A

EF = (EDV - ESV)/EDV

Normal is >55%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What portion of the vasculature accounts for most of the resistance to flow?

A

Arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the total resistance of vessels in series?

In parallel?

A

Series:
Total = R1 + R2 + R3. . .

Parallel:
1/Total = 1/R1 + 1/R2 + 1/R3. . .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What factors determine resistance?

A

Viscosity & vessel length increase resistance

Radius decreases resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the waves on a jugular venous pulse tracing?

A 
a = RA contraction
c = RV contraction (valve bulges backward)
v = RA filling against closed tricuspid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What causes the dicrotic notch seen on aortic pressure tracings?

A

Transient backward flow back into the LV, which causes closure of the valve. The elastic recoil of the aorta can then exert its effects, causing an increase in pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When is an S3 heard?

A

Normal in children & pregnancy

Otherwise indicates ^filling pressures and/or a dilated LV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What causes wide splitting of S2?

A

Wide splitting: varies with respiration but is always wider than expected.

Caused by pulmonic stenosis or RBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What causes fixed splitting of the S2 heart sound?

A

ASD is the only etiology

Left to right shunt causes splitting all of the time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What causes paradoxical splitting?

A

Inspiration: They close together
Expiration: P2 closes before A2

Aortic stenosis & LBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where is a HOCM murmur heard best?

A

Systolic murmur at the left sternal border (3rd intercostal space)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where are aortic & pulmonic regurgitation heard best?

A

Diastolic murmurs at the left sternal border (3rd intercostal space)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What can be heard with an ASD?

Where?

A

Pulmonary flow murmur & diastolic rumble heard best at pulmonic area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What effect does inspiration have on murmurs?

Expiration?

A

Inspiration –> ^intensity of right heart sounds

Expiration –> ^intensity of left heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What effect does the hand grip technique have on murmurs?

A

^systemic vascular resistance

Louder: AR, MR, VSD, MVP
Softer: AS, HOCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What effect does valsalva have on murmurs?

A

Decreases venous return

Louder: MVP, HOCM
Softer: Most murmurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What effect does rapid squatting have on murmurs?

A

Increases venous return

Softer: MVP, HOCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is heard with mitral/tricuspid regurgitation?

A

Mitral - Holosystolic blowing murmur loudest at apex & radiates to axilla.

Tricuspid - Holosystolic blowing murmur loudest at tricuspid area & radiates to RSB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does aortic stenosis sound?

What else is seen?

A

Systolic ejection click followed by crescendo-decrescendo murmur. Heard best at the aortic area & radiates to carotids.

“Pulsus parvus et tardus” = weak pulses w/ a delayed peak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What causes aortic stenosis?

What are the symptoms?

A

Causes:
Bicuspid aortic valve
Calcific aortic stenosis

Symptoms:
Syncope
Angina
Dyspnea on exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does a VSD sound?

What effect does size of the VSD have on the sound?

A

Holosystolic, harsh murmur loudest at tricuspid area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does mitral valve prolapse sound?

A

Midsystolic click then crescendo murmur. Heard bast at the apex.

Enhanced by decreased venous return (standing, valsalva).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What can cause mitral valve prolapse?

A

Often associated with young adult women. Caused by:
Myxomatous degeneration
Rheumatic fever
Chordae rupture

It ^susceptibility to infective endocarditis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What does aortic regurgitation sound like?

What else can be seen?

A

Immediate blowing diastolic decrescendo murmur. Heard best at LSB.

Wide “water hammer” pulse pressures & head bobbing can also be seen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What can cause aortic regurgitation?

A

Aortic root dilation (syphilis or idiopathic)
Bicuspid aortic valve
Endocarditis
Rheumatic fever (mitral always involved)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does mitral stenosis sound?

A

Diastolic opening snap, followed by rumbling late diastolic murmur.

99% are due to rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does a PDA sound like?

What causes it?

A

Continuous “machinery” murmur heard best at infraclavicular area.

Caused by congenital rubella or prematurity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the best prognostic indicator of mitral stenosis?

Aortic stenosis?

A

Time to opening snap (MS) or ejection click (AS)

Mitral: Early opening snap –> more severe

Aorta: Early ejection click –> less severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What channels are responsible for the slow diastolic depolarization seen in the SA & AV node?

A

If (funny) channels –> Na+ flows into the cell slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the resting membrane potentials of cardiac pacemaker cells?
Myocytes?

A

Pacemaker cells = -70 mV

Myocytes & His-Purkinje = -90 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What can cause the appearance of a U wave?

A

Hypokalemia

Bradycardia

55
Q

What ECG finding may lead to Torsades de pointes?

A

Anything that prolongs the QT interval.

56
Q

What is seen in Jervell and Lange-Neilsen syndrome?

A

Autosomal recessive syndrome causing congenital QT elongation & deafness

57
Q

What can cause transient isolated atrial fibrillation?

A

Binge EtOH consumption (“holiday heart”)
Sympathetic tone
Pericarditis

58
Q

What is the path of the aortic arch baroreceptors & the carotid sinus baroreceptors?

A

Aortic arch –> vagus nerve –> nucleus solitarius (medulla)

Carotid sinus –> glossopharyngeal nerve –> nucleus solitarius

Both of them show decreased firing rates in response to hypotension. The carotid body can respond to both increases or decreases in BP.

59
Q

What is the Cushing reaction?

What causes it?

A

Cushing reaction:
Hypertension
Bradycardia
Respiratory depression

Caused by ^ICP –> arteriole constriction –> cerebral ischemia –> compensatory hypertension –> baroreceptors cause bradycardia

60
Q

What do the central & peripheral chemoreceptors respond to?

A

Central - pH & PCO2

Peripheral (carotid & aortic bodies) - PO2 (<60 mmHg)

61
Q

What are normal pulmonary artery pressures?

A

25/10

Pulmonary capillary wedge pressure < 12

62
Q

What are normal LV & RV pressures?

A

LV = 130/10

RV = 25/5

63
Q

How is the heart autoregulated?

A

Local metabolites (CO2, Adenosine, NO)

64
Q

How is the brain autoregulated?

A

CO2 –> vasodilation

65
Q

How is the kidney autoregulated?

A

Myogenic & tubuloglomerular feedback

66
Q

How is skeletal muscle autoregulated?

A

Local metabolites (lactate, adenosine, K+)

67
Q

What congenital heart diseases cause early cyanosis?

A

5 T’s:

Tetralogy
Transposition
Truncus
Tricuspid
TAPVR
68
Q

What causes late cyanosis?

What is the mechanism?

A

Late cyanosis = Eisenmenger’s Syndrome

Uncorrected ASD, VSD, or PDA (L–>R shunt) causes eventual pulmonary vascular hypertrophy –> pulmonary HTN –> reversal of shunt –> late cyanosis, clubbing, & polycythemia.

69
Q

What is the most common congenital heart defect?

A

VSD

Associated with fetal alcohol syndrome.

70
Q

What type of ASD is most common?

A

Ostium secundum (90%)

Ostium primum type is found in Down Syndrome pts

71
Q

What is seen with ASD?

A

Fixed splitting
Paradoxical emboli
Late cyanosis

72
Q

What type of cyanosis is seen with a PDA?

A

Late cyanosis in the LOWER EXTREMITIES

PDA comes off after the great vessels

73
Q

What is seen in Persistent Truncus Arteriosus?

A

Truncus arteriosus does not divide into aorta & pulmonary trunk. Most patients have a VSD as well.

Presents with early cyanosis.

74
Q

What is seen with tricuspid atresia?

A

Absence of tricuspid valve (it’s sealed shut) & hypoplastic RV. Requires both an ASD & VSD for survival.

Presents with early cyanosis.

75
Q

What is seen with TAPVR?

A

Total Anomalous Pulmonary Venous Return

Pulmonary veins drain into right heart circulation. ASD (or rarely PDA) is required to sustain life. Presents with early cyanosis.

76
Q

What is seen in Tetralogy of Fallot?

A

1) Pulmonary infundibular stenosis (prognostic)
2) RVH (boot shaped heart on CXR)
3) VSD
4) Overriding aorta (overrides the VSD)

Presents with early cyanosis (pulmonic stenosis forces blood R–>L across the VSD).

77
Q

What congenital heart defect is associated with tet spells?

A

tet spells = cyanotic spells seen in Tetralogy of Fallot

Patients learn to squat –> ^TPR –> decreased R–>L shunt

78
Q

What causes transposition of the great vessels?

A

Failure of aorticopulmonary septum to spiral (associated with maternal diabetes) –> Aorta comes off RV & pulmonary trunk comes off LV –> Pulmonary & systemic circulations are separate

ASD, VSD, or PDA required for survival.

79
Q

What is the treatment for Transposition of the Great Vessels?

A

Keep the PDA open (PGE) until surgery can be performed

80
Q

What is seen with infantile coarctation of the aorta?

What other condition is it associated with?

A

Coarctation lies proximal to the PDA (preductal). Presents with early lower extremity cyanosis & weak femoral pulses.

It is associated with Turner syndrome.

INfantile = IN close to the heart

81
Q

What is seen in adult coarctation of the aorta?

What other condition is it associated with?

A

Coarctation is distal to the ligamentum arteriosum (postductal). Presents with:
Notching of the ribs (collateral circulation from great vessels)
HTN in UE’s & weak pulses in LE’s

It is associated with bicuspid aortic valve.

82
Q 
What congenital cardiac defects are seen with the following conditions?
22q11 syndromes
Down syndrome
Congenital rubella
Turner syndrome
Marfan's syndrome
Maternal diabetes
A

22q11 syndromes –> Persistent truncus arteriosus, ToF
Down syndrome –> ASD (ostium primum), VSD, cushion defect
Congenital rubella –> PDA
Turner syndrome –> Preductal coarctation of aorta
Marfan’s syndrome –> Aortic regurgitation, dissection
Maternal diabetes –> Transposition of great vessels
Fetal alcohol syndrome –> VSD

83
Q

What is the cutoff for HTN?

Malignant HTN?

A

HTN = 140/90

Malignant = 180/120

84
Q

What are the signs of hyperlipidemia?

A

Atheromas
Xanthomas (xanthelasma - on/around the eye)
Tendinous xanthomas (Achilles is common)
Corneal arcus (nonspecific)

85
Q

What are the 3 types of arteriosclerosis?

A

Monckeberg Medial Calcific Sclerosis - calcification of the media. Can be seen on x-ray

Arteriolosclerosis - hyaline (HTN & DM) & hyperplastic (malignant HTN)

Atherosclerosis - atheromas within the intima

86
Q

What are the types of arteriolosclerosis & their causes?

A

Hyaline - caused by essential HTN or diabetes. Pink amorphous hyaline material

Hyperplastic - caused by malignant HTN. “Onion skin” appearance

87
Q

What are the risk factors for atherosclerosis?

A

Modifiable: Smoking, Hypertension, Hyperlipidemia, Diabetes

Non-modifiable:
Age
Gender (^men & postmenopausal women)
Family history

88
Q

What is the pathogenesis of an atheroma?

A

1) Damage to endothelium allows lipid entry into intima
2) Lipids are oxidized and consumed by macs –> foam cells
3) Inflammation & healing with fibrosis & smooth muscle cell migration

The result is an atheroma composed of a necrotic lipid core & a fibromuscular cap.

89
Q

Where is atherosclerosis found in the body?

A

Abdominal aorta > Coronary > Popliteal > Carotid

90
Q

What causes AAA?

Where are they found?

A

Atherosclerosis –> prevents oxygenation of wall
Most frequently found in hypertensive male smokers > 50

They are usually infrarenal

91
Q

How does a ruptured AAA present?

A

Hypotension
Pulsatile abdominal mass
Flank pain

92
Q

What % of a vessel must be blocked to be symptomatic?

A

70%+

93
Q

What are the causes of thoracic aortic aneurysm?

A

Tertiary syphilis (tree bark appearance)
Cystic medial necrosis (Marfan’s)
Hypertension

Can lead to Aortic Regurgitation

94
Q

What causes aortic dissection?

A

Hypertension
Bicuspid aortic valve
Cystic medial necrosis (Marfan’s, Ehlers-Danlos)

95
Q

How does aortic dissection present?

What are the complications?

A

Tearing chest pain that radiates to the back. Widened mediastinum on CXR.

Complications:
Cardiac tamponade (most common COD)
Rupture
Death

96
Q

What is seen on ECG with the 3 types of angina?

A

Stable & Unstable –> ST depression

Prinzmetal –> ST elevation

97
Q

What are the causes of the 3 types of angina?

A

Stable - atherosclerosis –> ischemia with exertion

Prinzmetal’s - coronary artery vasospasm (at rest)

Stable - thrombosis w/ incomplete arterial occlusion (at rest)

98
Q

What is coronary steal?

A

When there is ischemic heart disease present, administration of vasodilators can cause increased perfusion to the healthier tissues, leaving the ischemic tissue even more ischemic.

99
Q

What are the causes of sudden cardiac death?

A

90% fatal arrhythmia secondary to CAD
HOCM (kids)
Mitral valve prolapse
Cocaine use

100
Q

What are the most commonly thrombosed coronary arteries?

A

LAD > RCA > LCX

101
Q

<4h post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross - normal

Microscopic - normal

Risk - Arrhythmia, CHF, Cardiogenic shock

102
Q

4-12h post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross - Darkly mottled infarct

Microscopic - Early coagulative necrosis (no nuclei)

Complications: Arrhythmia

103
Q

12-24h post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross: Dark mottling of infarct

Microscopic:
Contraction bands (perpendicular to fibers)
Beginning of PMN infiltration

Complications: Arrhythmia

104
Q

1-3 days post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross: Hyperemia

Microscopic:
Coagulative necrosis
Dense PMN infiltration

Complications:
Fibrinous pericarditis (seen only with transmural infarct)
105
Q

3 days to 2 weeks post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross: Central yellow-brown softening w/ hyperemic border

Microscopic:
Macrophage infiltration w/ granulation tissue at the margins

Complications:
Free wall rupture –> tamponade
Papillary muscle rupture (RCA infarct; mitral regurgitation)
Interventricular septum rupture
Aneurysm (Mural thrombi; risk greatest at 1 week)

106
Q

2 weeks to several months post-MI
What is seen grossly?
What is seen microscopically?
What are the possible complications?

A

Gross: Gray-white scar (Type I collagen)

Microscopic: Collagen

Complications:
Dressler’s syndrome (autoimmune fibrinous pericarditis; 6-8 wks)

107
Q

How is MI diagnosed?

A

ECG is the gold standard within the first 6h
Troponin I - rises after 4h; specific
CK-MB - found in myocardium & skeletal muscle; useful in diagnosing reinfarction bc returns to baseline in 48h

108
Q

What causes contraction band necrosis?

A

When a cardiac infarct is reperfused, Ca2+ enters myocytes –> contraction.

109
Q

What are the causes of dilated cardiomyopathy?

A

ABCCCDE:

Alcohol abuse
Ber1Ber1 (wet)
Coxsackie B myocarditis
Chagas' disease
Cocaine (chronic)
Doxorubicin
Expectancy (pregnancy)
110
Q

What type of hypertrophy is seen in dilated vs hypertrophic cardiomyopathy?

A

Dilated = eccentric hypertrophy (sarcomeres added in series)

Hypertrophic = asymmetric concentric hypertrophy (in parallel)

111
Q

What is the cause of hypertrophic cardiomyopathy?

A

Most cases are familial.
Autosomal dominant sarcomere mutation (myosin heavy chain)
Associated with Friedrich’s Ataxia.

112
Q

What is the treatment for HOCM?

A

Beta blockers or non-dihydropyridine CCB’s

113
Q

What is the treatment for dilated cardiomyopathy?

A 
Salt restriction
ACE inhibitors
Diuretics
Digoxin
Transplant
114
Q

What can cause restrictive cardiomyopathy?

A 
Amyloidosis
Sarcoidosis
Endocardial fibroelastosis (children)
Loffler's syndrome (endomyocardial fibrosis w/ eosinophils)
Hemochromatosis (can cause dilated or restrictive)
115
Q

What CCB’s are cardioselective?

Vascular?

A

Cardioselective - Verapamil, Diltiazem

Vascular SM - Amlodipine, Nifedipine

116
Q

What toxicities are seen with CCB’s?

A

Peripheral edema
Flushing
Cardiac depression/AV block
Gingival hyperplasia (Verapamil)

117
Q

What is Hydralazine used for?

A

Vasodilates arterioles > veins –> afterload reduction

Used for:
HTN in pregnancy (with methyldopa)
CHF

Often used with a beta-blocker to prevent reflex tachycardia

118
Q

What toxicities are seen with hydralazine?

A

Reflex tachycardia (contraindicated in angina/CAD)
Fluid retention
Drug-induced lupus

119
Q

What drugs are used to treat malgnant HTN?

What are their mechanisms?

A

Nitroprusside - NO release –> vasodilation (slightly V > A)

Fenoldopam - D1 agonist –> vasodilation of all capillary beds –> decreased BP & natriuresis

120
Q

What are nitrates used for?

What side-effects are seen?

A

Nitroglycerin & isosorbide dinitrate

Used for angina or pulmonary edema.

Side effects - Reflex tachycardia, hypotension, flushing, HA

121
Q

What is Monday disease?

A

People exposed to occupational nitrates have tolerance to them during the week then lose the tolerance over the weekend. So on Monday’s, they get tachycardia, dizziness, & HA.

122
Q

What is the mechanism of statins?

What are their toxicities?

A

Statins inhibit HMG-CoA Reductase. Also an ^ in peripheral LDLR is seen.

Toxicities:
Hepatotoxic
Rhabdomyolysis

123
Q

What is the mechanism of Niacin in lowering blood lipids?

What are the toxicities?

A

Inhibits lipolysis in adipose tissue & reduces VLDL secretion by the liver. Increases HDL substantially.

Toxicities:
Facial flushing
Hyperglycemia
Hyperuricemia

124
Q

What is the mechanism of Ezetimibe?

What toxicities are seen?

A

Ezetimibe blocks cholesterol reabsorption in the intestine.

Toxicities:
Rare ^LFT’s
Diarrhea

125
Q

What is the mechanism of Fibrates?

What toxicities are seen?

A

Fibrates upregulate Lipoprotein lipase –> ^TG clearance
They are most effective for lowering Triglycerides

Gemfibrozil, Fenofibrate, Clofibrate, Bezafibrate

Toxicities:
Myositis
Hepatotoxic
Cholesterol gallstones
Don't use w/ statins, if you must - use Fenofibrate
126
Q

What is the mechanism of digoxin?

What are its uses?

A

Inhibits Na+/K+ ATPase –> Impaired Na+/Ca2+ exchanger –> increased intracellular Ca2+ –> positive inotropy
Also stimulates vagus nerve to decrease HR

Used for:
CHF (inotropy)
A-fib (slows AV nodal conduction)

127
Q

What toxicities are seen with Digoxin?

A

Cholinergic - N/V, diarrhea, blurred yellow vision
ECG - ^PR, short QT, AV block, ST scooping, T inversion
Hyperkalemia

Factors causing toxicity:
Renal failure
Hypokalemia (Digoxin binds K+ site on ATPase)
Quinidine

128
Q

What are the classes of antiarrhythmics?

A

Class I = Na+ channel blockers
Class II = Beta blockers
Class III = K+ channel blockers
Class IV = Ca2+ channel blockers

129
Q

What are the Class Ia antiarrhythmics?
What is their effect?
What are their toxicities?

A

Quinidine, Procainamide, Disopyramide

They ^AP duration, effective refractory period, & QT interval

Toxicity:
Quinidine - Cinchonism (HA, tinnitus)
Procainamide - drug induced SLE
Disopyramide - CHF
Torsades
130
Q

What are the Class Ib antiarrhythmics?
What is their effect?
What are their toxicities?

A

Lidocaine, Mexiletine, Tocainide

They decrease AP duration in ischemic tissue. Useful in acute ischemic arrhythmias & Digoxin toxicity.

Toxicity:
Cardiac depression
CNS stimulation/depression

131
Q

What are the Class Ic antiarrhythmics?
What is their effect?
What are their toxicities?

A

Flecainide, Propafenone

No affect on AP duration. Only used as a last resort for intractable Vtach, Vfib, or SVT and only if heart is structurally normal.

Toxicity:
Pro-arrhythmic
^^AV node refractory period

132
Q

What arrhythmias are beta blockers (Class II antiarrhythmics) used to treat?

A

Vtach
SVT
Afib/flutter w/ RVR

133
Q

What are the Class III antiarrhythmics?
What is their effect?
What are their toxicities?

A

AIDS: Amiodarone, Ibutilide, Dofetilide, Sotalol

^AP duration & refractory period

Toxicity:
Sotalol - torsades, excessive beta block
Ibutilide - torsades
Amiodarone:
Pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism
(must check LFT’s, PFT’s, & TFT’s when using amiodarone)
Corneal/skin deposits –> photodermatitis
Neurologic effects
Heart block

134
Q

What is adenosine used for?
What is its mechanism?
What are its toxicities?

A

It is the drug of choice in treating SVT. Only lasts for ~15 seconds.

Adenosine causes K+ release from cells –> hyperpolarization
Its effects are blocked by Theophylline & Caffeine

Toxicities: Flushing, hypotension, chest pain

135
Q

What is the use of magnesium as an antiarrhythmic agent?

A

It is used in torsades & digoxin toxicity.

136
Q

What is seen in hyperkalemia on ECG?

A

U waves
Peaked T waves
Arrhythmia

Boards (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions