Brainscape's Knowledge GenomeTM

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


See full index

US > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Describe the fetal circulation?

A

1) Blood entering fetus through ombilical vein is conducted via the ductus venosus into the IVC bypassing the hepatic circulation
2) Highly oxygenated blood reaches the heart via the IVC and is directed through the foramen ovale (and pumped into the aorta to supply the head and body)
3) deoxygenated blood from the SVC passes through the RA and to the RV (through the main PA) and to the patent ductus arteriosus

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

What happens to baby physiology when the infant takes a breath?

A

Decrease in resistance of pulmonary vasculature

Increase left atrial pressure vs right atrial pressure

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

What causes closure of a ductus?

A

Increased O2 from respiration

Decrease in prostaglandins from placental seperation

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

What helps to close the PDA?

A

Indomethacin

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

What supplies the SA and AV node?

A

Usually the RCA

Infarct may cause nodal dysfunction

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

What is the percentage of right dominant?

A

85% of the PDA arises from the RCA

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

What is the percentage of left dominant?

A

8%, the PDA arises from the LCx

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

what does it mean to be codominent?

A

The PDA arises from both the LCx and the RCA

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

What is the most posterior part of the heart?

A

The left atrium
Enlargement can cause dysphagia (due to compression of the esophagus, or hoarseness due to left recurrent nerve (a branch of the vagus)

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

What are the three layers of the pericardium?

A

1) Fibrous pericardium
2) Parietal layer of the serous pericardium
3) Visceral layer of the serous pericardium

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

How to define the CO?

A

Stroke volume X heart rate

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

What is Fick principal?

A

CO = rate of O2 consumption / arterial O2 content-venous O2 content

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

What is the MAP?

A

The mean arterial pressure is CO X total periphereal resistance

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

What are the componenets of the MAP?

A

2/3 diastolic pressure + 1/3 systolic pressure

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

what is the pulse pressure?

A

systolic pressure-diastolic pressure

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

What is the SV (stroke volume)?

A

end-diastolic volume -end-systolic volume

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

what affects the stroke volume?

A

1) Contractility
2) Increase in preload
3) Decrease in afterload

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

What factors increase the contractility?

A

1) Catecholamines (increase Ca into the sarcoplasmic reticulum
2) Increase the preload
3) Decrease the afterload
4) Increase the intracellular Ca
5) Decrease the Na
6) Digitalis blocks the Na/K pump

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

How to estimate the preload?

A

By the EDV

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

How to approximate the afterload?

A

MAP

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

What is the ejection fraction?

A

EF = SV/EDV

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

what are the components of the heart sounds?

A

S1: mitral and tricuspid valve closure (loudest over the mitral)
S2: aortic and pulmonary valve closure (upper left)
S3 rapid ventricular filling phase (increase filling pressures mitral regurgitation and HF), can be normal in young patients
S4: Atrial kick (best heard at the apex with the patient in left lateral decubitus), consider abnormal at all ages

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

What are the components of the JVP?

A

a wave: atrial contraction
C wave: RV contraction (closed tricuspid valve against the bulging atrium)
x descent: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
v wave: Increased right atrial pressure due to filling
y descent: RA emptying into the RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Normal splitting
Wide splitting
Fixed splitting
Paradoxical splitting

A

Normal: P2 splits because of the drop in intrathoracic pressure with increase in venous return
S1–A2-P2
Wide Splitting: S1–A2–P2 (delay of Rv emptying) due to pulmonary stenosis and right bundle branch block
Fixed splitting: S1–A2–P2 (due to ASF and left to right shunting)
Paradoxical splitting: S1–P2-A2 (NOTE the P2 is before the A2, that is due to conditions when there is delay in the closure of the aortic valve (like aortic stenosis)

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

What type of murmure is aortic area?

A

Systolic murmure: Aortic stenosis

Flow murmure: aortic sclerosis

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

What types of mumure in the pulmonic area?

A

Systolic ejection murmure

Pulmonary stenosis

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

What type of murmure in the tricuspid area?

A 
Holosytolic murmure (TR) or VSD
Diastolic murmure: Tricuspid stenosis (atrial septal defect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Maneuver for heart sounds: Inspiration?

A

Increase intensity of the right heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Maneuver of the hand grip (increase afterload)?

A

Increase intensity of MR, AR, VSD

MVP will have later onset of the click

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

Manuover of Valsalva? (decrease the preload)

A

1) Decrease the intensity of most murmers

2) Increase the intensity of hypertrophic cardiomyopathy

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

Maneouver of rapid squatting (increase venous return, increase preload, increase afterload)

A

Increase the intensity of AS murmure
MVP (late onset of click andmurmure)
Decrease the intensity of hypertrophic

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

What type pf murmure for aortic stenosis?

A

Cresecendo-descendo systolic ejection murmure (might have a click)
Pulsus parvus et tardus (weak pulse with a delayed peak)

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

What is the mitral/tricuspid regrugitation mumure?

S1——–S2

A

1) Holosystolic high pitched blowing murmure
2) Mitra area (loudest at apex and radiates toward the axilla)
3) Tricuspid: loudest in tricuspid area and radiates to the sternal border (RV dilatation)

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

What are characteristics of mitral valve prolapse?

S1 MC(clicK)——S2

A

Late systolic crescendo murmure with midsystolic click due to sudden tensing of the chordae tendinea

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

What is the murmure for VSD?

A

Holosystolic (Harsh sounding) Loudest in the tricuspid area

S1————-S2

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

What does the diastolic murmure of aortic regurgitation sound like?

A

S1 S2——— (early diastolic decrescendo murmure) Can have head bobbing when chronic
Wide pulse pressure

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

What does the murmure for mitral stenosis sound like?

A

S1 S2 OS——-
OS= opening snap

This is due to the abrupt halt in leaflet motion in diastole
Often second to rheumatic fever

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

What is the murmure of PDA?

A

S1——S1——
Continous machine like murmure
Loudest at S2

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

what are the phases of myocardial action potential?

A

Phase O: Rapid upstroke and depolarization
Phase 1: Initial repolarization (voltage Na channels open)
Phase 2: Plateau Ca 2+ influx through gated Ca channels with K efflux
Phase 3 Rapid repolarization, massice K efflux due to opening of voltage gated slow K+ channels
Phase 4: resting potential, high K permeability through K+ channels.

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

What are some differences between cardiac muscle action potential and skeletal muscle?

A

1) Cardiac muscle action potential which has a plateau (due to Ca2+ influx and K influx)
2) Cardiac muscle requires constant Ca 2+ influx from ECF
3) Cardiac myocytes are electrically coupled to each other by their gap junctions

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

What are the phases of the pacemaker action potential?

A 
Phase O: upstroke and opening of the voltage gated Ca 2+ channels
Phase 3 (no phase 1 and 2): Inactivation of Ca2+ channels and increased activation of K+ channels allowing K+ efflux 
Phase 4:slow spontaneous diastolic depolarization due to If channels (mixed Na/K inward current)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the conduction pathways?

A

SA to atria to AV node to bundle of HIS to right and left sided bundle branches to purkinje fibers to the ventricles (left bundle branch divides to the left anterior and posterior fascicles

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

What is the function of the SA node?

A

Pacemaker inherent dominence with the slow phase of the upstroke

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

What are the pacemaker rates (fastest to slowest)

A

SA> AV> Bundle of His )Purkinje/ventricles

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

What does the P wave of EKG correspond to?

A

Atrial repolarization

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

What does the PR interval?

A

Time from start of atrial depolzarization to start of ventricular depolarization (normally less then

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

what is the QRS complexe?

A

Ventricular depolarization

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

What is the QT interval?

A

Ventricular deploarization (mechanical contraction of the ventricles)

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

What is the T wave?

A

Ventricular repolarization (inversion might indicate recent MI)

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

what is a J point?

A

Junction between the end of the QRS and start of the ST segment

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

What is the ST segment?

A

Isoelectric, ventricle depolarization (U wave) prominent in hypokalemiz and bradycardia

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

What are torsades de points?

A

Polymorphic ventricular tachycardia (shifting sinusoidal form) Can progress to ventricular fibrillation

Long QT syndrome will predispose

Caused by decreased K and Mg levels

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

What drugs cause torsades de points?

A 
Anti arrythmic (Class I1, III)
Antibiotics (Macrolides) 
Antipyschotics (haldol) 
Antidepreseents (TCA) 
Antiemetics (Ondansetron)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the congenitial long QT syndromes?

A

Inherited disorders of myocardial repolarization

Typically due to ion channel defects (increase risk of sudden death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the types of congential QT syndrome?

A

Romano-Ward syndrome: autosomal dominent (pure cardiac phenotype, no deafness)

Jervell and Lange Nielsen syndrome: Autosomal recessive (sensorineural deafness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Brugada syndrome?

A

Automsomal dominent
Common in Asian males
Pseudo right bundle branch block with ST elevations in V1-V3
Prevent SCD with ICD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is wolf-parkinson white syndrome?

A

Preventricular excitation syndrome
Abnormal fast accessory conduction pathways
Ventricles depolarize quickly
Can have SVNRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is atrial fibrillation?

A

Chaotic baseline, no discret P waves (irregular, irregular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is atrial flutter?

A

Rapid back to back depolarization (sawtooth appearance with flutter waves)
Treat like Afib (abalation is the definitive treatment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is ventricular fibrillation?

A

Erratic rhythm with no identifiable waves

Fatal without CPR or defibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is a first degree block?

A

PR interval more then 200 msec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is a second degree block?

A

Mobitztype I : lengthening of PR inteval until a beat is dropped (assymptomatic)

Mobitz Type 2:Dropped beats that are not preceeded by a change in the length of the PR interval
May progress to 3rd degree block (often need pacemaker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is a 3rd degree block?

A

Atria and ventricules beat independently of one another.

The atrial rate is usually faster then the ventricular rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the Atrial Natriuretic peptide?

A

Released from atrial myocytes to increase the blood volume and the pressure
Acts as cGMP
Causes vasodilation and decrease Na 2+ absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is a B-type (brain natriuretic peptide)?

A

Released from the ventricular myocytes in response to increse in tension

BNP is used to diagnose heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the receptors for BP?

A

Aortic arch to the vagus nerve to respond to increase and decrease in the BP

Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How do baraoreceptors react to hypotension?

A

1) Decrease arterial pressure, decrease stretch
2) Leads to decrease efferent parasympathetic stimulation (vasoconstriction)
3) Can cause increase in HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How does the carotid massage work?

A

Increase in pressure of the carotid
Increase the stretch
Decrease the heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is Cushings’s reaction triad?

A

Hypertension, bradycardia and respiratory depression
Causes increase in intracranial pressure (constricts arterioles) causing cerebral ischemia

Increase the pCO2
Decrease the Ph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How do the chemoreceptors work?

A

1) Periphereal-carotid and aortic bodies stimulate by decreasing PO2

71
Q

How are chemorecpetors (central) stimulated?

A

changes in pH and PCO2 of the brain (DOES NOT RESPOND DIRECTLY TO PO2)

72
Q

What are the normal cardiac pressures?

A

PWCP is estimation of the left capillary wedge pressure

73
Q

What happens to the wedge pressure in mitral stenosis?

A

PCWP is higher then LV end diastolic pressure

74
Q

What autoregulates the blood flow of the heart?

A

NO, CO2 and decreased O2

75
Q

What autoregulates blood flow to the brain?

A

CO2 and PH

76
Q

What autoregulates the kidneys?

A

Myogenic and tubuloglomerular feedback

77
Q

What autoregulates the lungs?

A

Hypoxia causes vasoconstriction

78
Q

What autoregulates skeletal muscles?

A

Lactate
Adenosine
K+, H+ and Co 2

79
Q

What autoregulates the skin?

A

Sympathetic stimulation (usually temperature control)

80
Q

What are the starling factors for the capillary fluid exchange?

A

Capillary pressure pushes fluid out of the capillary
Interstitial fluid pressure: pushes fluid into capillary
Plasma oncotic prressure: pulls fluid into the capillary
Interstitial fluid colloid osmotic pressure (pulls fluid out of the capillary)

81
Q

How is edema caused?

A

Increased capillary pressure
Decrease in plasma proteins
Increase in capillary permeability
Increase in interstitial fluid and colloid osmotic pressure

82
Q

What is the long term consequences of VSD?

A

May lead to LV overload and heart failure

83
Q

What is the atrial septal defect cause?

A

Most common is ostium secondum

Will have increased O2 saturation in the RA, RV, and the pulmonary artery

84
Q

How to maintain the PDA?

A

PGE

Low O2 tension

85
Q

What are treatments to try and close the PDA?

A

Endomethacin

86
Q

What happens with chronic left to right shunt?

A

1) VSD, ASD and PDA
2) Increased in pulmonary blood flow
3) Remodelling of pulmonary vasculature
4) Pulmonary HTN
5) Leads to cyanosis and clubbing

87
Q

What are some problems associated with coarctation of the aorta?

A

1) Associated with a bicuspid valve
2) Turner’s syndrome
3) Other heart defects
4) Will have HTN in extemties and weak, delayed pulses in the lower extremities
5) With age will have intercoastal arteries that enlage, and notched appearence on X ray

88
Q

What are complications associated with a coarctation?

A

Heart failure
Cerebral hemorrhage
Aortic rupture
Endocarditis

89
Q

What congenital cardiac defects are asssociated with ETOH?

A

VSD, PDA, ASD, tetralogy of fallot

90
Q

Heart defects associated with congenital rubella?

A

PDA
Pulmonary artery stenosis
Septal defects

91
Q

Defects associated with down’s syndrome?

A

AVSD
VSD
ASD

92
Q

Heart defects associated with diabetic mother?

A

Transposition of the great vessels

93
Q

Defects associated with Marfan’s disease?

A

MVP
Thoracis aortic aneurysms
Dissected aorta
Aortic regurgitation

94
Q

Defects associated with lithium exposure?

A

Ebstein’s anomaly

95
Q

Defect associated with Turner’s syndrome?

A

Bicuspid aortic valve

Coarctation of the aorta

96
Q

Defect associated with Williams syndrome?

A

Supravalvular aortic stenosis

97
Q

Defect associated with 22q11 syndrome?

A

Truncus arteriosus

Tetralogy of fallot

98
Q

What is hypertension?

A

BP more then 140 mmHg

Bp > 90 mmhg

99
Q

what are risk factors for hypertension?

A 
Increased age
Diabetes
Physical inactivity
Too much salt
Too much ETOH
Family history
African American
100
Q

What is the most common type of hypertension?

A

Essential HTN associated with increased CO or increased total periphereal resistance

101
Q

What are the other type of HTN?

A 
Renovascular disease and muscular dysplasia  (10%)
And hyperaldosteron (usually found in younger women)
102
Q

What is categorized as a hypertensive urgency?

A

180/120, can lead to acute end organ damage

103
Q

What is categorized as a hypertensive emergency?

A 
Severe HTN with evidence of end organ damage
Encephalopathy
Stroke
Retinal damage
Exudates
Papilledema
104
Q

What does HTN predispose to?

A 
CAD
LVH
HF
aortic dissection
Aneurysm
Stroke
Chronic kidney disease 
Hypertensive nephropathy
Retinopathy
105
Q

What are signs of hyperlipidemia?

A

Xanthomas: nodules or lipd-laden histocytes in the skin (especially on the eyelids)

Tendinous xanthomas: lipid deposirs on the tendon (usually the Achilles)

Corneal Arcus: lipid deposit in the cornea

106
Q

What are the signs of arteriosclerosis?

A

Hardening of the arteries

107
Q

What are the two types of arteriosclerosis?

A

Hyperplastic (onion skinning) if have severe hypertnesion

Hyaline (thickening of the vessel walls in essential hypertension) or diabetes

108
Q

What are monckeberg sclerosis (medial calcific sclerosis)

A

Medium sized arteries are affected
Vascular stiffening without obstruction
Pipestem appearance on x-ray

109
Q

what are the common sites of atherosclerosis?

A

aabdominal aorta (most common) > coronary artery > poplitel artery > carotid artery

110
Q

What are the modifiable factors?

A

Smoking
HTN
Hyperlipidemia
Diabetes

Sex
Age
Family history

111
Q

What is the process of the formation?

A

endothelial cell dysfunction to macrophages to foam cell formation to fatty streaks to smooth muscle migration to proliferation and extracellular matrix deposition and formation of fibrous plaques and atheromas

112
Q

Risk factors for abdominal aneurysm?

A

Tobacco use
Age
Male sex

113
Q

What are risk factors for thoracic aortic aneurysms?

A 
Cystic medial degeneration 
Hypertension 
Bicuspid aortic valve 
Connective tissue disease 
Can be associated with syphlis
114
Q

What are traumatic rupture of the aorta?

A

Trauma or deceleration injury

Aortic isthmus

115
Q

What is variant, prinzmetal angina?

A

Due to coronary spasm
Can have transient ST elevation on ECG
Triggered by tobacco, cocaine, and triptophans

Treatmant Calcium blockers

116
Q

What causes unstab;e angina?

A

Thrombosis of the coronary artery with ST depression or T wave inversion of ECG but no increase in biomarkers

117
Q

What is coronary steal syndrome?

A

Distal to stenosis, vessels are maximally dilated at baseling

When you give vasodilators, it shunts blood to well perfused areas.

Can have decreased flow and ischemia in poststenotic regions

118
Q

What are the causes of sudden cardiac death?

A 
Death within 1 hour of symptoms
Usually arrythmia VF
Associated with CAD within 70% of cases 
Cardiomyopathy
Long QT
Burgada
119
Q

What are characteristics of ST MI?

A

Transmural
Full thickness of the myocardial wall
ST elevation of ECG and Q waves

120
Q

What are NON ST segment MI (NSTEMI)?

A

Subendocardial infarcts
Subendocardium (inner 1/3) in areas
ST depression

121
Q

What are the most commonly occluded coronary arteries?

A

LAD > RCA > circumflex

122
Q

What is seen 0-24 after infarct? (microscopy and CX)

A

Coagulative necrosis, edema, hemorrahe
Can have reperfusion injury with free radicals

Cx: Ventricular arrythmias and cardiogenic shock

123
Q

What is seen 1-3 after infarct? (mico and CX)

A

Coaguative necrosis

Postinfarction fibrinous pericarditis

124
Q

What is seen 3-14 after infarct (micro and CX)

A

Free wall rupture
Tamponade (papillary muscle rupture)
Acute MR
LV pseudoaneurysm with risk to rupture

125
Q

What is seen 2 weeks to several months?

A 
Contracted scar complete
Dressler syndrome
HF
Arrythmias 
True ventricular aneurysm 
Risk of mural thrombus
126
Q

In first 6 hours, after MI, what is gold standard?

A

EKG

127
Q

When do trops rise?

A

4 hours (peak at 24 hours)

128
Q

When do CK MB rise?

A 
6 hours (peak at 16-24 hours) 
Most useful in diagnosing reinfarction following an acute MI (and return to normal after 48 hours)
129
Q

Where is CK-MB found?

A

Predominantly in the myocardium but some from skeletal

130
Q

What are the ECG infarct location?

A 
LAD: V1 to V2
Distal LAD V3 to V4
Anterolateral LAD or CX: V5 to V6
Lateral I to aVL
Inferior RCA: II, III and aVF
PosterioR PDA V7-V9, ST depression in V1 to V3 and tall R wave
131
Q

What are the most common cardiomyopathy?

A

90% is idiopathic or familial

132
Q

What are other etiologies of cardiomyopathies?

A 
Beriberi
Coxsackie 
Chronic cocaine use
Chagas disease
Doxrubin toxicity
Hemochromacytosis 
Sarcoidosis 
Peripartum
133
Q

Dilated cardiomyopathy, is it eccentric or concentric hypertrophy?

A

eccentric

134
Q

How should dilated cadiomyopathy be treated?

A 
Na restriction
ACE inhibition 
B Blockers
diuretics
Digoxin
ICD
Heart transplant
135
Q

What are causes of hypertrophic cardiomyopathy?

A

70% is familial and autosomal (usually B chain myosin)

136
Q

How to treat hypertrophic cardiomyopathy?

A

Cessation of athletics
B blocker of C blocker
ICD

137
Q

How does obstuctive hypertrophic cardiomyopathy work?

A

Assymmetric septal hypertrophy
Have systolic anterior motion of the mitral valve
Outflow obstruction
Syncope

138
Q

What are causes of restrictive/infiltrative cardiomyopathy?

A 
Sarccoidosis
Postradiation fribosis
Endocardial fibroelastosis
Loeffler syndrome (eosinophils)
139
Q

Restrictive cardiomyopathy ECK?

A

Have low voltage EKG (despite thick myocardium)

140
Q

what are signs of left heart failure?

A

1) Orthopnea (shortness of breath when supine)
2) PND: breathless awakening from sleep (due to redistribution of blood)
3) Pulmonary edema: increased pulmonary venous distention and transudation of fluid

141
Q

What are signs of right heart failure?

A

Hepatomegaly: increased CV and can lead to cirrhosis
JVP distended
Peripheral edema due to fluid transudation

142
Q

What are the characteristics of hypovolemic shock?

A

Decreased PCWP
Decreased CO
Increased SVR
Treatement with IV fluid

143
Q

What are characteristics of cardiogenic shock?

A

Increased PCWP
Decreased CO
Increased SVR

Treatement with inotropes

144
Q

What are characteristics of distributive shock?

A

Decreased PCWP
Decreased CO
Decreased SVR

145
Q

what is the most common valve involved in endocarditis?

A

Mitral valve

146
Q

What is the endocarditis of prosthetic valves?

A

S. Epidermis

147
Q

Which bug is associated with colon cancer endocarditis?

A

S. Bovis gallolyticus

148
Q

What causes Rheumatic fever?

A

B hemolytic strep

149
Q

Which heart valves are most often affected in Rheumatic fever?

A

Mitral > aortic > tricuspid

150
Q

What are the early lesions of rheumatic fever?

A

Mitral regurgitation

151
Q

what are the criteria for the rhuematic fever?

A

Joint pain, migratory
Nodules on the skin
Erythema
Sydenham chorea

152
Q

What are causes of acute pericarditis?

A 
Inflammation
Neoplasia
Autoimmune
Viral 
Infection
SLE
153
Q

What is pulsus paradoxus?

A 
Decrease in amplitude BP > 10 mmHG during inspiration 
Seen in cardiac tamponade
asthma
Sleep apnea
Pericarditis 
Croup
154
Q

What are consequences of syhilitic heart disease?

A

Disrupts the vasa vasorum of the aorta causing dilatation of the aorta

Can lead to the aneurysm of the ascending aorta and insufficiency

155
Q

What are the most common cardiac tumors?

A

Most common is metastasis

Myxomas are primary tumor (90% are in the atria)

156
Q

What are most common tumor in children?

A

Rhabdomyomas

157
Q

What is Kussmaul’s sign?

A

High JVD
Inspiration leads to neagtive intrathoracic pressure that is not transmitted to the heart, and imparied filling of the right ventricle.

158
Q

What are the large vessel vascultis (epi and path)?

A

1) Giant cell : elderly female, and unilateral temporal artery

Focal granulomatous inflammation, increased ESR
Usually the branches of the carotid

2)Takayasu arteritis: Asian females less then 40 years old
(weak extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules)

PAth: granulomatous thickening and narrowing of the aortic arch

Treat with corticosteroids

159
Q

what are medium vasculitis with path characteristics?

A

1) Polyarteritis nodosa: Young adult, Hep B, presents with abdominal pain, melena

HTN, neurological dysfunction and renal damage

Transmural inflammation with renal microaneurysms
Treat with corticosteroids

2) Kawasaki disease: Asian children less then 4 years old. Conjunctival infection, with rash, and adenopathy.

Strawberry tongue and hand-foot changes

Can develope coronary aneurysm

3) Buerger disease: heavy smokers

160
Q

What are examples of small vessel vasculitis?

A 
1) Granulomatosis with polyangiitis 
Triad of Focal 
a) necrotizing vasculitis
b) Necrotizing granulomas 
c)Necrotizing glomerulonephritis
d) PR3-ANCA, c-ANCA

2) Microscopic polyangiitis
Necrotizing vasculitis involving the lungs, kidney and skin
No granulomas
MPO-ANCA

3)Eosinophilic granulomatosis polyangitis (Churg-Strauss)

Granulomatous, necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA
Increased IgE level

4) Henoch-Schonlein purpura: most commonly childhood vasculitis (following URI)

Triad:
Skin (papable purpura)
Arthalgias
Abdominal Pain
Vasculitis secondary to IgA (associated with IgA nephropathy)
161
Q

What are the treatments for HTN?

A

1) Primary: Thiazide diuretics,ACE, angiotensin II receptor blockers, Calcium channel blockers
2) HTN with heart failure: diuretics, ACE, ARB, B blockers (if stable)
3) HTN with DM: Ace/ARB, CA +blockers, thiazide, diuretics
4) HTN with pregnancy: Hydralazine, labetalol, methyldopa

162
Q

What conditions are dihydropyridines used to treat? (calcium channel blocker)

A

HTN, Angina, Raynauds

163
Q

What conditions are nimodipine used to treat?

A

Cerebral vasospasm (subarachnoid hemorrage)

164
Q

what are the conditions used to treat clevidipine?

A

HTN emergency

165
Q

What are conditions treated with non-dihydropyridine?

A

HTN, angina, atrial fibrillation/flutter

166
Q

What are the adverse effects of non-dihydropyridine?

A

Cardiac depression, AV block, hyperprolactemia, constipation

167
Q

What is the mechanism of Hydralazine? Clincal use, adverse effects?

A 
Increase cAMP (increase smooth muscle relaxation) 
Vasodilates arterioles > veins (afterload reduction)

Clinical use: Severe HTN, HF due to organic nitrate (safe during pregnancy)

Can lead to compensatory tachycardia (contra-indicated in angina/CAD) fluid retention, headache, lupus

168
Q

what are the drugs used in HTN emergency?

A

1) Nitroprusside: short acting cGMP (direct release of NO) can use with cyanide toxicity
2) Fenoldopam: Dopamine receptor agonist: coronary, periphereal, renal and splanic vasodilation
3) Nitrates: vasodilates by NO in vascular smooth muscle, dilates the veins more then arteries and decreases the preload

Clinical uses: reflex tachycardia, B blockers, HTN, flushng, headaches, can have tolerace that developes.

169
Q

Mechanism and use of Ranolazine?

A

1) Inhibits the late phase of sodium current, reducinf diastolic wall tension and oxygen consumption

Clinical use: angina refractory to other medical
Adverse effects: Constipation, dizziness, headache, nausea, QT prolongation.

170
Q

what are 4 types of lipid lowering agents?

A

1) HMG-CoA reductase inhibitors (lovastatin, pravastatin), decrease LDL, increase LDL, decrease triglycerides

Adverse effects: Heptatoxicity

Decreases mortality in CAD patients

2) Bile acid resins (Cholestryramine, colestipol, colesevelam) decrease LDL, HDL higher

Prevents intestinal reasoption of bile acids. Liver must use cholesterol to make more

Adverse effect: decrease absorption of other drugs and fat soluable vitamins

3) Ezetimibe: decrease LDL, prevent cholesterol absorption at small intestine
4) Fibrates: decrease LDL, increase HDL, decrease triglycerides

Cause myopathy, cholesterol and gallstones

5) Niacin: decrease LDL, increase LDL, decrease triglycerides

inhibits lipolysis (hormone sensitive

171
Q

What are cardiac glycosides?

A

Digoxin
Inhibits Na/K ATP ase
Increase Ca + for positive inotropy

Uses:
Increase contractility
Decrease atrial fibrillation
Can lead to hyperkalemia (poor prognosis)

Antidote: Normalize K, Cardiac pacer, digibind

172
Q

What are the classes of anti-arrythmics? What are the adverse effects?

A

1) Sodium channel blocker, used for atrial and ventricular arrythmias

Examples: Quinidine, procanamide

Adverse effects: Cinchonism, Heat failure, torsades, QT interval

2) Decrease the action potential duration (lidocaine, mexileTine)

Clinically used within ventricular arrythmias

Venticular arrythmias

Can cause CNS depression

3) Class IC (flecanide, propafenone)

Medication: prolongs the ERP in AV node and accessory bypass tracts

Last resort in refractory VT
Can be proarrythmic especially post MI
Contra-indicated in structural and ishchemic heart disease

4) Class II (B blockers) Metroprolol, esmolol, timolol

Decrease the SA and the AV node activity
Uses:SVT and rate control for afib and atrial flutter
Adverse effects: metroprolol causes dyslipidemia
Propranolol can have vasospasm.

5) Class III (Potassium channel blocker) amiodarone and sotalol.
1) Use with afib, aflutter
2) Sideffects of amio: fiborisis, heptatoxicity, corneal deposits, grey skin

Need to check the PFT, LFT, TFT

6) Calcium Channel Blockers
Verapamil , diltiazem
Uses: prevents nodal arrythmias, and rate control in afib
Adverse effects include: flushing, edema, etc.

173
Q

What type of anti-arrythmic is adenosine?

A

Potassium out of the cell, hyperpolarizing.
Very short acting
Effective in torsades de pointes and digoxin toxicity

US (17 decks)

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