Usmle First Aide Cardiology 2006

Front 1

pregnant woman in 3rd trimester has normal BP when standing and sitting. When supine BP drops to 90/50. what is the dx?

Back 1

compression of the IVC

Front 2

35 y/o man has high BP in arms and lowBP in his legs. what is the dx

Back 2

coarction of teh aorta

Front 3

5 y/o boy presents with a systolic murmur and a wide fixed split S2. what is the dx

Back 3

ASD

Hint 3

None

Front 4

During a game a young football player collapses and dies immediately. What is the most likely type of cardiac dz

Back 4

hypoertrophic cardiomyopathy

Front 5

pt has a stroke after incurring multiple long bone fractures in trauma stemming from a MVA. What caused the infarct

Back 5

fat emboli

Front 6

elderly woman presents with a headache and jaw pain. labs show elevated ESR. what is teh dx

Back 6

temporal arteritis

Front 7

80 y/o man presents w/ systolic crescendo-decrescendo murmur. What is the most likely cause?

Back 7

aortic stenosis

Front 8

Man starts a medication for hyperlipidemia. He then develops a rash, pruritis, and GI upset. What drug was it

Back 8

Niacin

Front 9

Pt developes a cough and must discontinue captopril. What is a good replacement drug and why doesn't it have the same side effects?

Back 9

losartan, an angiotensin II receptor antagonist, does not increase bradykinin as captopril does.

Front 10

What are the 3 struct inside the carotid sheath

Back 10

1) Internal jugular Vein (lateral) 2) Common carotid Artery (medial) 3) Vagus Nerve (posterior) mneu: VAN

Front 11

In the majority of cases, the SA and AV nodes are supplied by this coronary artery?

Back 11

Right coronary artery

Front 12

80% of the time the ____ coronary artery is "dominant", suppplying the inferior left ventricle via the _________ branch

Back 12

RCA, Posterior descending artery

Front 13

Which coronary is most commonly occuluded? What does it supply?

Back 13

LAD, antierior interventricular septum

Front 14

Enlargement of this chamber may cause dysphagia?

Back 14

Left atrium (most posterior chamber)

Front 15

cardiac output =

Back 15

SVxHR

Front 16

During exercise, CO ↑ as a result of an ↑ in _____. After prolonged exercise, CO ↑ as a result of an ↑ in ____

Back 16

SV HR

Front 17

Mean arterial Pressure (MAP)= give 2 equasions: 1) CO, TPR 2) systolic, diastolic

Back 17

1) CO x TPR
2) 1/3Systolic + 2/3Diastolic

Hint 17

None

Back 18

2)1/3 systolic +2/3 diastolic

Front 19

(Fick’s Equation)

Back 19

rate of O2 consumption / ( aa O2 content-vv O2 content)

Front 20

Pulse pressure =

Back 20

systolic-diastolic

Hint 20

None

Front 21

SV= (2 equasions) 1) CO, HR 2)EDV,ESV

Back 21

1)=CO/HR 2)=EDV-ESV

Front 22

Stroke volume is affected by what 3 things

Back 22

Contractility, Afterload, and Preload

mneu: SV CAP

Hint 22

None

Front 23

↑Preload →__SV

Back 23

↑

Front 24

↑Afterload→ __SV

Back 24

↓

Front 25

↑contractility→ __SV

Back 25

↑

Front 26

SV ___ in anxiety, exercise, & pregnancy

Back 26

↑

Front 27

a failing heart has a ___ SV

Back 27

↓

Front 28

Contractality (and SV), ____ with catecholemines

Back 28

↑

Front 29

Contractality (and SV), ____ with ↑ intracellular Ca++

Back 29

↑

Front 30

Contractality (and SV), ____ with ↑ extracellular sodium

Back 30

↓ (think of how digoxin increases SV by retaining Na in cells)

Hint 30

None

Front 31

Contractality (and SV), ____ with digitalis

Back 31

↑

Front 32

Contractality (and SV), ____ with β1 blockade

Back 32

↓

Front 33

Contractality (and SV), ____ with heart failure

Back 33

↓

Front 34

Contractality (and SV), ____ with acidosis

Back 34

↓

Front 35

Contractality (and SV), ____ with hypoxia/hypercapnea

Back 35

↓

Front 36

Contractality (and SV), ____ with Ca++ channel blockers

Back 36

↓

Front 37

Myocardial demand is ___ by ↑ afterload (diastolic BP)

Back 37

↑

Front 38

Myocardial demand is ___ by ↑ contractility

Back 38

↑

Front 39

Myocardial demand is ___ by ↑ heart rate

Back 39

↑

Front 40

Myocardial demand is ___ by ↑ heart size

Back 40

↑

Front 41

ventricular EDV is equivalent to (preload or afterload?)

Back 41

Preload

Front 42

Systolic arterial pressure is equivalent to (preload or after?)

Back 42

afterload

Front 43

proportional to peripheral resistance (preload or afterload?)

Back 43

afterload

Front 44

venous dialators (example drug?) ↓ _______ (preload or afterload)

Back 44

preload : VENous dialator (nitroglycerine)

Front 45

vaso dialators (example drug?) ↓ _______ (preload or afterload)

Back 45

Afterload (hydralazine)

Front 46

______ ↑ w/ exercise, ↑ blood volume, exitement (sympathetics) (preload or afterload)

Back 46

Preload

Front 47

Starling Hypoth:

Back 47

Force of contraction is proportional to initial length of cardiac mm fiber (preload)

Front 48

contraction state of the myocardium is ____ by circulating catecholamines (+,-)

Back 48

+

Front 49

contraction state of the myocardium is ____ by digitalis (+,-)

Back 49

+

Front 50

contraction state of the myocardium is ____ by sympathetic stimulation (+,-)

Back 50

+

Front 51

contraction state of the myocardium is ____ by pharmacologic depressants (+,-)

Back 51

-

Front 52

contraction state of the myocardium is ____ by loss of myocardium (MI) (+,-)

Back 52

-

Front 53

EF= (give 2 equasions)

Back 53

1) SV/EDV 2) EDV-ESV/EDV

Front 54

this is an measurable index of ventricular contractility

Back 54

Ejection fraction

Front 55

EF is normally > ___%

Back 55

55

Front 56

Place condition on the Starling curve [pic p.219]

Back 56

1)exercise 2)CHF + digitalis 3)CHF

Front 57

(driving Pressure)ΔP= Q (flow) ,R (resistance)

Back 57

ΔP = Q x R (V=IR)

Front 58

Resisitance (R) = Give 2 equasions: 1)ΔP(driving pressure),flow(Q) 2)Poiselle's Eqn

Back 58

1)=ΔP/Q 2)8nxl/Πr(^4) (poiselles’s)

Hint 58

None

Front 59

viscosity depends mostly on _______

Back 59

hematocrit

Front 60

increased viscosity in 3 conditions:

Back 60

1) Polycythemia 2) Hyperproteinemic states (e.g., multiple myeloma (IgG)) 3) hereditary spherocytosis

Front 61

resistance is ________ to viscosity (proportional or inversely proportional)

Back 61

proportional

Front 62

resistance is ________ to the radius to the 4th power (proportional or inversely proportional)

Back 62

inversely proportional

Front 63

cardiac and vascular fx curves [pic p.219]

Back 63

1) (+) inotropy 2) (-) inotropy 3) (↑) blood volume 4) (↓) blood volume

Front 64

cardiac cycle image [p. 220]

Back 64

1)isovolumetric contraction 2) aortic valve opens 3) ejection 4) aortic valve closes 5) isovolumetric relaxation 6) mitral valve opens 7)ventricular filling 8) mitral valve closes

Front 65

Name the phase of the cardiac cycle: period between mitral valve closure and aortic valve opening.

Back 65

isovolumetric contraction

Front 66

Name the phase of the cardiac cycle: period of highest O2 consumption

Back 66

isovolumetric contraction

Front 67

Name the phase of the cardiac cycle: period between aortic valve opening and closing

Back 67

systolic ejection

Front 68

Name the phase of the cardiac cycle: period between aortic valve closing and mitral valve opening

Back 68

isovolumetric relaxation

Front 69

Name the phase of the cardiac cycle: period just after mitral valve opening

Back 69

rapid filling

Front 70

Name the phase of the cardiac cycle: period just before mitral valve closure

Back 70

slow filling

Front 71

name the event at: S1

Back 71

mitral and tricuspid valve closure

Front 72

name the heart sound: aortic and pulmonary valve closure

Back 72

S2

Front 73

name the event causing the sound: S3

Back 73

at the end of rapid ventricular filling

Front 74

What causes S4 sound?

Back 74

high atrial pressure/stiff ventricle

Front 75

this heart sound is associated w/ dilated CHF

Back 75

S3

Front 76

this heart sound is associated with a hypertrophic ventricle

Back 76

S4

Front 77

Jugular venous pulse waves: a wave

Back 77

Atrial contraction

Front 78

Jugular venous pulse waves: c wave

Back 78

RV Contraction (tricuspid valve bulging into atrium)

* Remeber jugular venous pressure is based on RIGHT HEART since that is where the vena cava drains!

Hint 78

None

Front 79

Jugular venous pulse waves: v wave

Back 79

increaseed atrial pressure due to filling against closed tricuspid Valve

Front 80

jugular venous distention is seen in ___________

Back 80

right heart failure

Front 81

What happens when S2 splitting occurs? (which valve is closing first)

Back 81

the aortic valve closes before the pulmonic this heart sound abnormality results

Hint 81

None

Front 82

S2 splitting is increased upon ________

Back 82

inspiration

Front 83

Paradoxical splitting (S2 split increasd upon expiration is associated with what?

Back 83

aortic stenosis

Front 84

pressure volume relationship [pic p. 221]

Back 84

--

Front 85

cardiac mm contraction is dependent on extracellular ________, which enters the cells during plateau of action potential and stimulates ______ release from the cardiac mm sarcoplasm reticulum.

Back 85

calcium calcium calcium induced calcium release

Front 86

In contrast to skeletal mm, cardiac mm action potential has a plateau, which is due to ____ influx.

Back 86

Ca+

Front 87

In contrast to skeletal mm, cardiac nodal cells ________ depolarize, resulting in automaticity

Back 87

spontaneously

Front 88

In contrast to skeletal mm, cardiac myocytes are electrically coupled to each other by ________

Back 88

gap junctions

Front 89

myocardial action potential occurs in what cells?

Back 89

atrial, ventricular, and perkinje fibers

Hint 89

None

Front 90

In a myocardial action potential, this phase is the rapid upstroke, when voltage gated ______ open

Back 90

phase 0, Na+ channels

Hint 90

None

Front 91

In a myocardial action potential, this phase is the initial repolarization-inactivation of voltage0gated Na+ channels. Voltage gated K+ channels begin to open

Back 91

Phase 1

Front 92

In a myocardial action potential, this phase is the plateu--Ca++ influx through voltage-gated Ca++ channels balances K+ efflux. Ca++ influx triggers another Ca++ release from sarcoplasmic reticulum and myocyte contraction.

Back 92

phase 2

Front 93

In a myocardial action potential, this phase is the rapid repolarization--massive K+ efflux due to opening of voltage-gated slow K_ channels and closure of voltage gated Ca++ channels.

Back 93

Phase 3

Front 94

In a myocardial action potential, this phase is the resting potential--high K+ permeability through K+ channels.

Back 94

phase 4

Front 95

Pacemaker action potentials occur where

Back 95

SA & AV nodes

Front 96

In a pacemaker action potential this phase is the upstroke phase--it involves opening of voltage-gated Ca++ channels. These cells lack fast voltage-gated Na+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

Back 96

phase 0

Front 97

In a pacemaker action potential this phase, the plateau is absent.

Back 97

phase 2 (both 1 and 2 are absent in pacemaker cells)

Hint 97

None

Front 98

In a pacemaker action potential this phase, the slow diastolic depololarization results in membrane potential spontaneously depolarizing as Na+ conductance increases. This accounts for automaticity of SA and AV nodes. The slope of this phase in the SA node determines the heart rate. ACh decreases and catecholamines increasee the rate of diastolic depolarization decreasing or increasing heart rate respectively.

Back 98

phase 4

Front 99

myocardial action potential [pic p. 221]

Back 99

--

Front 100

Pacemaker action potential [pic p 222]

Back 100

--

Front 101

electrocardiogram: atrial depolarization

Back 101

P wave

Front 102

electrocardiogram: conduction delay through AV node (normally < ____ msec)

Back 102

PR INTERVAL. Less than 200 ms

Hint 102

None

Front 103

electrocardiogram: vetricular depolarization (normally < ____ msec)

Back 103

QRS complex. Less than 120 ms

Hint 103

None

Front 104

electrocardiogram: mechanical contraction of the ventricles

Back 104

QT interval

Front 105

electrocardiogram: ventricular repolarization

Back 105

T wave

Front 106

electrocardiogram: atrial repolarization is masked by _______

Back 106

QRS complex

Front 107

electrocardiogram: isoelectric, ventricles depolarized

Back 107

ST segment

Front 108

electrocardiogram: These waves caused by hypokalemia

Back 108

U wave

Front 109

image ECG p. 223

Back 109

--

Front 110

Wolff-Parkinson-White syndrome
- what causes it
- how does it appear on EKG
- complication

Back 110

this syndrome is caused by an accessory conduction pathway from atria to vetricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic DELTA wave on ECG!! May result in reentry current leading to supraventricular tachycardia [image p.223]

Hint 110

None

Front 111

This ECG tracing has a chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes (pic. p 224)

Back 111

Atrial fibrillation

Front 112

This ECG tracing has a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves. (pic. p 224)

Back 112

Atrial flutter

Front 113

In this condition PR interval is prolonged (>200 msec). Asymptomatic. (pic. p 224)

Back 113

1st degree AV block.

Front 114

Progressive lenthening of the PR interval until a beat is "dropped" (a P wave not followed by a QRS complex). Usually asymptomatic. (pic. p 224)

Back 114

2nd degree AV block Mobitz type I (Wenckebach)

Front 115

On ECG shows dropped beats that are not preceded by a change in the length of the PR interval. These abrupt, nonconducted P waves result in a pathologic condition. It is often found as a 2:1 block, where there are 2 P waves to 1 QRS response. May progress to 3rd degree block.(pic. p 225)

Back 115

Mobitz type II AV block

Front 116

In this condition, the atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treat with pacemaker.

Back 116

3rd degree AV block (complete)

Front 117

completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation. (pic. p 225)

Back 117

Ventricular Fibrillation

Front 118

control of mean arterial pressure [pic. p 226]

Back 118

--

Front 119

What do aortic arch baroreceptors respond to? Through what nn. and to where is this relayed?

Back 119

transmits via vagus nn to medulla (responds only to increase blood pressure)

Hint 119

None

Front 120

How does the carotid sinus function in baroreception?

Back 120

1. Decreases firing with decrease in BP.
2. Signals via CN 9 (glossopharyngeal nn.)
3. Transmits to medulla. (Medulla then increases SNS and decreases PNS)

Hint 120

None

Front 121

decreased firing by aroreceptors during hypotension results in an increase in efferent ________ firing

Back 121

sympathetic

Front 122

In a carotid massage, the increased pressure on carotid aa results in increased stretch and ____ in heart rate

Back 122

decrease

Front 123

Peripheral chemoreceptors in the carotid and aortic bodies respond to (3 things)

Back 123

decreased PO2 (<60mmHg), increased PCO2 and decreased pH of blood

Front 124

Central chemoreceptors respond to what changes (2)

Back 124

changes in pH and Pco2 (not Po2)

Front 125

This chemoreceptor is responsible for Cushing reaction?

What is the cushing response?

Back 125

Central chemoreceptor

response to cerebral ischemia, response to increase intracranial pressure leads to hypertension (sympathetic response) and bradycardia (parasympathetic response)

Hint 125

None

Front 126

Baroreceptors & Chemoreceptors image p. 226

Back 126

--

Front 127

This orgen gets the largest share of systemic cardiac output

Back 127

liver

Front 128

this organ gets the highest blood flow per gram of tissue

Back 128

kidney

Front 129

this orgen has a large arteriovenous O2 differnece. Increased O2 demand is met by increased blood flow, not by increased extraction of O2.

Back 129

heart

Hint 129

None

Front 130

Normal pressure of the heart chambesr (image p.227)

Back 130

--

Front 131

this is a good approximation of L atrial pressure and measured with a Swan-Ganz catheter

Back 131

Pulmonary capillary wedge pressure

Front 132

blood flow is altered to meet demands of tissue

Back 132

autoregulation

Front 133

Name the organ regulated by the local metabolites: O2 adenosine, NO

Back 133

heart

Front 134

Name the organ regulated by the local metabolites: CO2 (pH)

Back 134

brain

Front 135

Name the organ regulated by the local metabolites: Myogenic and tubuloglomerular feedback

Back 135

kidneys

Front 136

Name the organ regulated by the local metabolites: hypoxia causes vasoconstriction

Back 136

lungs

Front 137

_______ vasculature is unique in that hypoxia causes vasoconstriction (in other organs hypoxia causes vasodilation)

Back 137

pulmonary

Front 138

Name the organ regulated by the local metabolites: lactate, adenosine, K+

Back 138

skeletal mm

Front 139

Name the organ regulated by the local metabolites: sympathetic stimulation most important mechanism--temp control

Back 139

skin

Front 140

______ forces determine fluid movement by osmosis throug capillary membranes

Back 140

starling

Front 141

moves fluid out of capillary

Back 141

P(c) capillary pressure

Front 142

moves fluid into capillary

Back 142

P(i) interstitial fluid pressue

Front 143

moves fluid into capillary

Back 143

π(c) plasma colloid osmotic pressure

Front 144

moves fluid out of capillary

Back 144

π(i) interstitial fluid colloid osmotic pressure

Front 145

net filtration pressure=Pnet=

Back 145

[Pc-Pi)-(πc-πi)] capillary pressure -interstitial pressure - plasma colloid osmotic presure - interstitual fluid colloid osmotic pressures

Front 146

Kf=

Back 146

filtration constant (capillary permeability)

Front 147

excess fluid outflow into interstitium

Back 147

edema

Front 148

edema is commonly caued by ___ capillary pressure (give example)

Back 148

↑ P(c) Heart failure

Front 149

edema is commonly caued by ___ plasma protiens(give example)

Back 149

↓π(c) plasma proteins (nephrotic syndrome, liver failure)

Front 150

edema is commonly caused by ___ capillary permeability (give example)

Back 150

↑Kf infections, burns

Front 151

edema is commonly caued by ___ interstitial fluid colloid osmotic pressure (give example)

Back 151

↑ πi lymphatic blockage

Front 152

capillary fluid exchange [pic p. 227]

Back 152

--

Front 153

right-to-left shunts (early cyanoisis) "blue babies"

Back 153

3 Ts Tetrology Transposition Truncus

Front 154

Children with this type of shunt may squat to increase venous return

Back 154

right to left shunts

Front 155

capillary fluid exchange [pic p. 227]

Back 155

--

Front 156

Right-to Left shunts (early cyanosis) - "blue babies"

Back 156

1) Tetrology of fallot 2) Transposition of great vessels 3) Truncus arteriosis The 3 Ts

Front 157

children with this type of shunt may squat to increase venous return.

Back 157

right to left shunt

Front 158

Left to right shunts (late cyanosis) - "blue kids"

Back 158

1) VSD 2) ASD 3) PDA

Front 159

this is the most common cause of early cyanosis

Back 159

tetralogy of fallot

Front 160

this is the most common congenital cardiac anomaly

Back 160

VSD

Front 161

this congenital heart dz manifests itself with a loud S1 and a wide, fixed split S2

Back 161

ASD

Front 162

this congenital heart defect is closed with indomethacin

Back 162

PDA

Front 163

give the frequency of occurance with PDA VSD ASD

Back 163

VSD>ASD>PDA

Front 164

eisenmenger's syndrome
- what is it caused by
- what happens

Back 164

eisenmenger's syndrome

Uncorrected VSD, ASD or PDA leads to progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from L to R to R to L, which causes late cyanosis (clubbing & polycythemia). [pic p. 228]

Hint 164

None

Front 165

Tetrology of Fallot [pic. p 228]

Back 165

1) Pulmonary stenosis 2)RVH 3) Overiding aorta (overides VSD) 4) VSD mneu: PROVe

Front 166

most important determinant for prognosis of tetrology of fallot

Back 166

pulmonary stenosis

Front 167

ON x-ray Tetrology of Fallot looks ________

Back 167

boot shaped

Hint 167

None

Front 168

give the frequency of occurance with PDA VSD ASD

Back 168

VSD>ASD>PDA

Front 169

Transposition of great vessels
- What is the physiology?
- How does it present?
- When can a patient survive?

Back 169

One of the 3T's (R->L shunts!) Blue baby.

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)leading to separation of systemic and pulmonary circulations.

Must have an ASD, VSD, or PDA for this to be compatible with life.

Hint 169

None

Front 170

Transposition is not compatable with life unless a _____is present to allow adequate mixing of blood [pic p. 229]

Back 170

shunt (e.g. VSD, PDA or patent foramen ovale)

Front 171

transposition of great vessels is due to failure of the _________ septum to spiral

Back 171

aorticopulmonary

Front 172

this type of coarction of aorta is aortic stenosis proximal to insertion of ductus arteriosus (preductal)

Back 172

infantile INfantile: IN close to the heart

Front 173

What occurs in "Adult" form of Coarctation of the Aorta?
- findings
- location of coarctation
- imaging

Back 173

this type of coarction of aorta is aortic stenosis is distal to ductus arteriosus (postductal) it is associated with notching of the ribs, hypertension in upper extremities, weak pulses in lower extremities.

Hint 173

None

Front 174

Coarction of aorta has a male: female ratio of ____

Back 174

3:01

Front 175

what is best way to diagnose coartation of aorta

Back 175

femoral pulses on pysical exam

Front 176

In fetal period, shunt is right to left. In neonatal period, lung resistance decreases and shunt becomes L to R w/ subsequent RVH and failure. [pic p. 229]

Back 176

patent ductus arteriosis

Front 177

______ is used to closed a PDA

Back 177

indomethacin

Front 178

______ is used to keep a PDA open, which may be necessary to sustain life in conditions such as transposition of the great vessels

Back 178

PGE

Front 179

Congenital cardiac defect associations: 22q11

Back 179

truncus arteriosus, tetralogy of Fallot

Front 180

Congenital cardiac defect associations: Down syndrome

Back 180

ASD, VSD

Front 181

Congenital cardiac defect associations: Congenital rubella

Back 181

septal defects, PDA

Front 182

Congenital cardiac defect associations: Turners syndrome

Back 182

coarctation of aorta

Front 183

Congenital cardiac defect associations: Marfan's syndrome

Back 183

aortic insufficiency

Front 184

Congenital cardiac defect associations: Offspring of diabetic mother

Back 184

transposition of great vessels

Front 185

Hypertension

Back 185

BP >140/90

Front 186

HTN risk factors

Back 186

increase age, obesity, diabetes, smoing, genetics, blck>white>asians

Front 187

90% of hypertension is this kind

Back 187

essential

Front 188

essentail hypertention is related to either one of these two factors

Back 188

increased CO or TPR

Front 189

10% of HTN is mostly secondary to ______ dz

Back 189

renal

Front 190

this type of HTN is severe and rapidly progressing

Back 190

malignant

Front 191

HTN predisposes pts to (give 3)

Back 191

athrosclerosis, stroke, CHF, renal failure, retinopathy, & aortic dissection

Front 192

Hyperlipidemia signs: Plaques in blood vessel walls

Back 192

Atheromata

Front 193

Hyperlipidemia signs: plaques or nodules composed of lipid-laden histocytes in the skin, especially the eyelids

Back 193

Xanthoma

Front 194

Hyperlipidemia signs: lipid deposits in the tendon, esp. the achilles

Back 194

Tendinous xanthoma

Front 195

Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)

Back 195

corneal arcus

Front 196

This type of arteriosclerosis is in the media of the arteries, esp radial or ulnar. Usually benign.

Back 196

Monckeberg

Front 197

This type of arteriosclerosis is hyalin thickening of small arteries in essential hypertension. Hyperplastic "onion skinning" in malignant hypertension.

Back 197

Arteriolosclerosis

Front 198

This type of arteriosclerosis is when fibrous plaques and atheromas form in intima of arteries

Back 198

atherosclerosis

Front 199

this is a disease of elastic arteries and large and medium sized mm arteries (image 79)

Back 199

atherosclerosis

Front 200

risk factors for atherosclerosis

Back 200

smoking, hypertension, dbts, hyperlipidemia, family hx

Front 201

progression of atherosclerosis complex atheromas, fatty streaks, proliferative plaque

Back 201

fatty streaks to proliferative plaque to complex atheromas

Front 202

complications of atherosclerosis (give 3)

Back 202

aneurisms, ischemia, infarcts, peripheral vascular dz, thrombus, emboli

Front 203

most common location of atherosclerosis

Back 203

abdominal aorta> coronary artery>popliteal artery>carotid artery

Front 204

symptoms of atherosclerosis

Back 204

angina, claudication, but can be asymptomatic

Front 205

CAD narrowing >75%

Back 205

angina

Front 206

retrosternal chest pain with exertion , mostly secondary to atherosclerosis

Back 206

stable angina

Front 207

chest pain occurring at rest secondary to corony artery spasm

Back 207

prinzmetal's variant (unstable angina)

Front 208

worsening of chest paiin due to thrombosis but no necrosis

Back 208

unstable/crescendo angina

Front 209

most often acute thrombosis due to coronary artery atherosclerosis. Results in myocyte necrosis

Back 209

myocardial infarction

Front 210

death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrythmia

Back 210

sudden cardiac death

Front 211

progressive onset of CHF over many years due to chronic ischemic myocardial damage

Back 211

chronic ischemic heart dz

Front 212

infarcts occuring in loose tissues with collaterals, such as lungs, intestine, or follwing reperfusion

Back 212

red (hemorrhagic) infarcts REd=REperfusion

Front 213

infarcts occur in solid tissues with single blood supply, such as brain, heart, kidney and spleen.

Back 213

pale infacts

Front 214

give order of highest frequency of coronary artery occlusion CFX, LAD, RCA

Back 214

LAD>RCA>CFX

Front 215

symptoms of MI (give 4)

Back 215

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm or jaw, shortness of breath, fatigue, adrenergic symptoms.

Front 216

color image 80.

Back 216

--

Front 217

How long ago did the MI occur? Occluded artery but no visable change by light microscopy

Back 217

2-4 hours

Front 218

How long ago did the MI occur? Gross: dark mottling; pale with tetrazolium stain. Micro: coagulative nocrosis. coagulation bands visable. release of contents of necrotic cells into bloodstream and the begining of neutrophil emigration.

Back 218

after 4 hrs. 1st day

Front 219

How long ago did the MI occur? Gross: hyperemic border; central yellow-brown softening. Micro: outer zone (ingrowth of granulation tissue), macrophages, & neutrophils

Back 219

5-10 D

Front 220

How long ago did the MI occur? Gross: grey-white Micro: scar complete

Back 220

7 weeks

Front 221

dx of MI what is gold standard in the 1st 6 hrs

Back 221

ECG

Front 222

This lab test rises after 4 hours and is elevated for 7-10D.

Back 222

troponin I

Front 223

this lab test is more specific than other protein markers

Back 223

troponin I

Front 224

This is predominantly found in myocardium but can also be relased from skeletal mm

Back 224

CK-MB

Front 225

This is nonspecific and can be found in cardiac, liver and skeletal mm cells

Back 225

AST

Front 226

lab image p.233

Back 226

1)troponin 2) CK-MB 3)AST 4)LDH

Front 227

ECG changes include ST elevation which indicates

Back 227

transmural infarct

Front 228

ECG changes include ST depression which indicates

Back 228

subendocardial infarct

Front 229

ECG changes include pathological Q waves

Back 229

transmural infact

Front 230

This MI complication is the most important cause of death before reaching hosptial; it is common in the 1st few days

Back 230

cardiac arrhythmia

Front 231

This MI complication results in pulmonary edema

Back 231

LV failure

Front 232

This MI complication has a high risk of mortanilty and occurs when there is a large infarct

Back 232

cardiogenic shock

Front 233

Rupture of ventricular free wall, interventricular septum, or paillary mm, usually occurs _____ post MI

Back 233

4-10D

Front 234

This MI complication of an MI results in decreased CO, a risk of arrythmia, and embolus from mural thrombus

Back 234

aneurism formation

Front 235

this MI complication is also known as a friction rub and occurs 3-5 D post MI

Back 235

fibrinous pericarditis

Front 236

This MI complication is an autoimmune phenomenon resulting in fibrinous pericarditis, several weeks post-MI

Back 236

dresslers syndrome

Front 237

This is the most common cardiomyopathy (90%)

Back 237

dialated (congestive) cardiomyopathy

Front 238

In dialated (congestive) cardiomyopathy ________ dysfunction ensues

Back 238

systolic

Front 239

In this type of cardiomyopathy, the heart looks like a baloon on chest x-ray

Back 239

dialated (congestive) cardiomyopathy

Front 240

etiology of dialated (congestive) cardiomyopathy

Back 240

Alcohol Beriberi Coxsackie B Cocaine Chagas dz Doxorubicin peripartum hemochromatosis

Front 241

this type of cardiomyopathy often involves an asymetric enlargement of the intraventricular septum

Back 241

hypertrophic cardiomyopathy

Front 242

In hypertrophic cardiomyopathy ______ diastolic disfunction occurs

Back 242

diastolic

Front 243

hypertrophic cardiomyopathy is a __________ trait, and 50% are familial

Back 243

autosomal dominant

Front 244

This is a very common cause of sudden death in young athletes.

Back 244

hypertrophic cardiomyopathy

Front 245

What are the heart sound findings with hypertrophic cardiomyopathy

Back 245

loud S4, apical impulses, systolic murmur

Front 246

How do you tx hypertrophic cardiomyopathy

Back 246

Beta blocker

Front 247

major causes of this type of cardiomyopathy include sarcoidosis, amyloidoss, postratdiation fibrosis, endocarrdial fibroelastosis, and endomyocardial fibrosis (Loffler's)

Back 247

restrictive/obliterative cardiomyopathy

Front 248

Heart Murmurs: holostolic, high piched "blowing murmur" loudest at apex[pic. p 234]

Back 248

mitral regurgitation

Front 249

Heart Murmurs: crecendo-decrescendo systolic ejection murmur following ejection click. radiates to carotids/apesx. "pulsus parvus et tardus" pulses weak compared to heart sounds [pic. p 234]

Back 249

aortic stenosis

Front 250

Heart Murmurs: holosystolic murmur [pic. p 234]

Back 250

VSD

Front 251

Heart Murmurs: Late systolic murmur with midsystolic click. Most frequent valvular lesion [pic. p 234]

Back 251

mitral prolapse

Front 252

Heart Murmurs: immediate high-pitched "blowing" diastolic murmur. Wide puse pressure [pic. p 234]

Back 252

aortic regurgitation

Front 253

Heart Murmurs: follows opening snap. delayed rumbling late diastolic murmur. [pic. p 234]

Back 253

mitral stenosis

Front 254

Heart Murmurs: Continuous machine like murmur. Loudest at time of S2 [pic. p 234]

Back 254

PDA

Front 255

most common primary cardiac tumor in adults. Usually described as a "ball-valve" obstruction in the LA

Back 255

myxomas.

Front 256

90% of myxomas occur in the _____

Back 256

atria (mostly LA)

Front 257

Most frequent primary cardiac tumor in children, associated with tuberous sclerosis

Back 257

rhabdomyomas

Front 258

Most common heat tumor (see color image 88)

Back 258

metasteses

Front 259

Given the pathophysiology tell me the symptom of CHF: failure of LV output to increase during exercise

Back 259

dyspnea on exertion

Front 260

Given the pathophysiology tell me the symptom of CHF: greater ventricular end-diastolic volume

Back 260

cardiac dilation

Front 261

Given the pathophysiology tell me the symptom of CHF: Lv ventrical failure leads to increased pulmonary venous pressure which leads to pulmonary venous distention and transudation of fluid.

Back 261

pulmonary edema (paroxysmal nocturnal dyspnea)

Front 262

this CHF abnormality is associated with presence of hemosiderin-laden macrophages

Back 262

pulmonary edema

Front 263

Given the pathophysiology tell me the symptom of CHF: increase venous return in supine position exacerbates pulmonary vascular congestion

Back 263

orthopnea (shortness of breath when supine)

Front 264

Given the pathophysiology tell me the symptom of CHF: increased central venous pressure leading to increased resistance to portal flow.

Back 264

hepatomegaly (nutmeg liver)

Front 265

Given the pathophysiology tell me the symptom of CHF: RV failure leads to increased venous pressure which leads to fluid transudation

Back 265

ankle , sacral edema

Front 266

embolus types

Back 266

Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor mneu: an embolus moves like a a FAT BAT

Front 267

CHF [pic p. 235]

Back 267

--

Front 268

this type of emboli are associated with long bone fractures and liposuction.

Back 268

fat

Front 269

approximately 95% of pulmonary emboli arise from where?

Back 269

deep leg veins

Front 270

this type of emboli can lead to DIC, especially postpartum

Back 270

amniotic fluid

Front 271

this type of embolus is associated with chest pain, tachypnea, and dyspnea

Back 271

pulmoary embolus

Front 272

compression of heart by fluid (i.e.,blood) in pericardium, leading to decreased cardiac output and equilibration of pressures in all four chambers.

Back 272

cardiac tamponade

Front 273

youre pt presents with hypotension, JVD, and distant heart sounds. He shows pulsus paradoxus and ECG shows electrical alternans

Back 273

cardiac tampanad

Front 274

pulsus paradoxus

Back 274

(exaggeration of nml variation in the systemic arterial pulse volume with respiration-- becoming weaker with inspiration and stronger with expiration)

Front 275

electrical alternans

Back 275

(beat to beat alterations in QRS complex height)

Front 276

Symptoms of bacterial endocarditis

Back 276

Fever Roth spots osler nodes Murmur (new) Janeway lesions Anemia Nail-bed hemorrhage Emboli mneu: bacteria FROM JANE

Front 277

osler nodes

Back 277

tender raised lesions on finger or toe pads

Front 278

Roth's spots

Back 278

round white spotss on retina surrounded by hemorrhage

Front 279

Janeway lesions

Back 279

small erythematous lesions on palm or sole

Front 280

What is the most frequently involved valve in bacterial endocarditis

Back 280

mitral valve

Front 281

What valve is associated with endocarditis associated with IV drug abuse

Back 281

tricuspid valce

Front 282

what are some of the complications associated with bacterial endocartitis (give 2)

Back 282

chordae rupture glomerulonephritis supportive pericarditis emboli

Front 283

acute endocarditis has a rapid onset. It results from large vegetations on previously normal valves. It is most often caused by this bug.

Back 283

S. aureus (high virulence)

Front 284

Subacute bacterial endocarditis has a more insidious onset. It consists of smaller vegetations on congentitally abnormal or diseased valves. It can be a sequela of dental procedures. Often caused by this bug

Back 284

viridans streptococcus (low virulence)

Front 285

endocarditis may also be nonbacterial and secondary to these 2 conditions

Back 285

metastasis or renal failure (marantic/ thrombotic endocarditis)

Front 286

In this condition, associated with lupus, vegetations develop on both sides of valve leading to mitral valve stenosis but do not embolize

Back 286

libman-sacks endocarditis mneu: SLE causes LSE

Front 287

Rhematic heart dz is a late consequence of pharyngeal infection with this organism

Back 287

a beta hemolytic streptococci

Front 288

rhematic heart dz affects heart valves in this order

Back 288

mitral>aortic>>tricuspid mneu: high pressure valves associated most.

Front 289

Give the symptoms of rheumatic heart dz

Back 289

Fever Erythema marginatum Valvular damage ESR (high) Red-hot joints (polyartheritis) Subcutaneous nodules St. Vitus' dance (chorea) mneu: FEVERSS

Front 290

This is associated with Aschoff bodies, migratory polyarthritis, erythema marginatum, elevated ASO titers.

Back 290

Rheumatic heart dz

Front 291

is rheumatic heart dz immune mediated or the direct effect of bacteria

Back 291

immune mediated

Front 292

Associated ith Aschoff bodies and Anitschkow's cells

Back 292

rheumatic heart dz mneu: think of 2 RHussians with RHeumatic heart dz (Aschoff & Anischkow)

Front 293

Aschoff bodies

Back 293

granuloma with giant cell

Front 294

Anitschkow's cells

Back 294

activated histiocytes

Front 295

This condition presents with pericardial pain, friction rub, ECG changes (diffuse ST elevation in all leads) pulsus paradoxus, distant heart sounds

Back 295

pericarditis

Front 296

pericarditis can resolve without scarring however, scarring can lead to this

Back 296

chronic adhesive or chronic constrictive pericarditis

Front 297

this type of pericarditis is caused by SLE, rheumatoid arthritis, infection, or uremia

Back 297

serous pericarditis

Front 298

this type of pericarditis is caused by uremia, MI, rheumatic fever

Back 298

fibrinous pericarditis

Front 299

this type of pericarditis is caused by TB or malignancy (e.g., melanoma)

Back 299

hemorrhagic

Front 300

this dz disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring. It often effects the aortic root and results in calcification of ascending arch of the aorta

Back 300

syphalitic heart dz (tertiary syphalis)

Front 301

This dz can result in aneurism of the ascending aorta or aortic arch and aortic valve incompetence.

Back 301

syphalitic heart dz (tertiary syphalis)

Front 302

pic p. 238

Back 302

1) + ionotropic drugs 2) B blockers 3) ACE-inhibitors 4) ATN II antagonists 5) diuretics 6)Vasodialtors

Front 303

This Rx used for HTN has the adverse effect of HYPOKALEMIA, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia

Back 303

hydrochlorothiazide (diuretic)

Front 304

This Rx used for HTN has the adverse effect of potassium wasting, metabolic alkalosis, hypotension, ototoxicity

Back 304

loop diuretics

Front 305

This sympathoplegic used in the tx of HTN has the adverse effect of dry mouth, sedation, severe rebound HTN

Back 305

clonidine

Front 306

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, positive Coomb's test

Back 306

methyldopa

Front 307

This sympathoplegic used in the tx of HTN has the adverse effect of severe orthostatic hypotension, blurred vision, constipation, sexual disfunction

Back 307

hexamethonium

Front 308

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, depression, nasal stuffiness, diarrhea

Back 308

reserpine

Front 309

This sympathoplegic used in the tx of HTN has the adverse effect of orthostatic and exercise hypotension, sexual dysfunction, diarrhea

Back 309

Guanethidie

Front 310

This sympathoplegic used in the tx of HTN has the adverse effect of 1st dose orthostatic hypotension, dizziness, headache

Back 310

Prazosin

Front 311

This sympathoplegic used in the tx of HTN has the adverse effect of impotence, asthma, bradycardia, CHF, AV block, sedation & sleep alterations

Back 311

B blockers

Front 312

This vasodialator used in the tx of HTN has the adverse effect of nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retension

Back 312

hydralazine

Front 313

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

Back 313

minoxidil

Front 314

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

Back 314

nifidipine, veripamil (constipation)

Front 315

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

Back 315

nitroprusside

Front 316

This ACE inhibitor used in the tx of HTN has the adverse effect of Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

Back 316

Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

Front 317

This angiotensin II receptor inhibitor has theadverse effect of fetal renal toxicity, hyperkalemia

Back 317

Losartan

Front 318

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

Back 318

minoxidil

Front 319

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

Back 319

nifidipine, veripamil (constipation)

Front 320

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

Back 320

nitroprusside

Front 321

This ACE inhibitor used in the tx of HTN has the adverse effect of Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

Back 321

Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

Front 322

The MOA of this drug used for severe HTN & CHF is that it increases cGMP leading to smooth mm relaxation. It vasodilates arterioles > veins resulting in a reduction of afterload

Back 322

hydralazine

Front 323

Toxicity of this drug for severe HTN & CHF include compensitory tachycardia, fluid retension, & lupus like syndrome

Back 323

hydralazine

Front 324

The druges Nifedipine, verapamil & diltiazem belong to this category

Back 324

calcium channel blockers

Front 325

The MOA of these drugs is that they block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce mm contractilty

Back 325

calcium channel blockers

Front 326

give the order of potency of the 3 CCBs (nifedipine, verapamil, diltiazem) in 1) the heart 2)vascular smooth mm

Back 326

heart-verapamil>diltiazem>nifedipine vascular sm mm-- nifedipine>diltiazem>verapamil

Front 327

CCBs are used in hypertension but also in these 2 conditions

Back 327

angina, arrhytias (not nifedipine)

Front 328

These drugs produce a toxicity of cardiac depression, peripheral edema, flushing, dizziness, & constipation

Back 328

CCBs

Front 329

These 2 drugs used for angina, pulmonary edema, and as an erection enhancer have a MOA of vasodilating by releasing NO in smooth mm, causing an increase in cGMP and smooth mm relaxation. They dialate vv>>arteries resulting in a decrease in preload

Back 329

nitroglycerine, isosorbide dinitrate

Front 330

toxicity of these drugs include tachycardia, hypotension, headache, "Monday dz" in industrial exposure, development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting intahycardia, dizziness, and headache.

Back 330

nitroglycerin, isosorbide dinitrate

Front 331

What are the 2 major Rxs used in the tx of antianginal therapy

Back 331

nitrates & B blockers

Front 332

In antianginal therapy the goal is to due what?

Back 332

reduce myocardial O2 consumption.

Front 333

In order to reduce myocardial O2 consumption you need to decrease 1 or more of the determinants of MVO2 which are give 2(5)

Back 333

1)EDV 2)BP 3)HR 4) contractility 5) ejection time

Front 334

Used for antianginal therapy Nitrates reduce _______ (preload or afterload)

Back 334

preload

Front 335

Used for antianginal therapy B-blockers reduce _______ (preload or afterload)

Back 335

afterload

Front 336

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. EDV

Back 336

N (preload):↓ BB (afternoad):↑ C: no effect or ↓

Front 337

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. BP

Back 337

N (preload):↓ BB (afternoad):↓ C:↓

Front 338

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Contractility

Back 338

N (preload):↑ (reflex response) BB (afternoad):↓ C:little or no effect

Front 339

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. HR

Back 339

N (preload):↑ reflex response BB (afternoad):↓ C:↓

Front 340

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Ejection time

Back 340

N (preload):↓ BB (afternoad):↑ C:little or no effect

Front 341

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. MVO2

Back 341

N (preload): ↓ BB (afternoad): ↓ C: ↓↓

Front 342

CCBs: Nifedipine is similar to ________ (nitrates or B blockers); Verapamil is similar to ________nitrates or B blockers)

Back 342

Nitrates B blockers

Front 343

Cardiac drugs: sites of action

Back 343

1) Digitalis (-) 2) CCB (-) 3) B blockers 4) Ryanodine (+) 5) Ca++ sensitizers

Front 344

This cardiac drug inhibits Na+/K+ ATP ase

Back 344

digitalis

Front 345

These 2 cardiac drugs inhibit on voltage gated Ca++ channels

Back 345

CCBs B blockers

Front 346

This cardiac drug sensitizes Ca++ release channel in the SR

Back 346

Ryanodine

Front 347

These cardiac drug is a site of Ca+ interaction with troponin-tropomyosin system

Back 347

Ca++ sensitizers

Front 348

This cardiac glycoside has 75% bioavalibility, is 20-40% protein bound, has a half life of 40 hours and is excreted in the urine

Back 348

digoxin

Front 349

the MOA of this drug is that it inhibits the Na+/K+ ATPase of the cardiac sarcomere, causing an increase in intracellular Na+. Na+-Ca++antiport does not function as efficiently, casing an increase in intracellular Ca++, leading to positive inotropy.

Back 349

digoxin

Front 350

this drug may cause an elevated PR, a depressed QT, a scooping of ST segment, and a T-wave inversion on ECG

Back 350

digoxin

Front 351

The clinical uses for this drug include 1) ________ due to increased contractility 2) _______ due to decreased conduction at AV node

Back 351

1) CHF 3) atrial fibrillation

Front 352

toxicity of this drug includes N/V/D. Blurry yellow vision. Arrhythmia.

Back 352

digoxin

Front 353

Digoxins toxicities are increased by _________(decreased excretion), _______(potentiates drug's effects) , and _________ (decreases digoxin clearance and displaces dignoxin from tissue binding sites

Back 353

renal failure hypokalemia quinidine

Front 354

What is the treatment for digoxin toxicity

Back 354

slowly normalize K+ lidocaine cardiac pacer anti-dig Fab fragments

Front 355

antiarrythmics (Class I) are _____ channel blockers

Back 355

Na+

Front 356

antiarrythmics (Class II) are _____ blockers

Back 356

Beta

Front 357

antiarrythmics (Class III) are _____ channel blockers

Back 357

K+

Front 358

Thhs class of antiarrhthmics are local anesthetics. They act by slow or decreasd conduction. They decrese the slope of phase 4 ddepolarization and increase threshhold for firing in abnormal pacemaker cells.

Back 358

antiarrhythmics-Na+ channel blockers (class I)

Front 359

antiarrhythmics-Na+ channel blockers (class I) are state dependent meaning what

Back 359

they selectively depress tissue that is frequently depolarized (e.g., tachycardia

Front 360

this class of antiarrhythmics has 3 subcategories A, B, & C

Back 360

antiarrhythmics-Na+channel blockers (class I)

Front 361

this class of antiarrythmics includes Quinidine, Amiodarone, Procainamide, Disopyramide.

Back 361

Class IA mneu: Queen Amy Proclaims Diso's PYRAMID

Front 362

This class of antiarrhytmics has an ↑ AP duration, ↑ effective refractory period (EERP, ↑ QT interval. It can affect both atrial and ventricular arrhythmias

Back 362

IA

Front 363

This member of class IA antiarrhytmics has toxicities that include (cinchonism-headache, tinnitis, thrombocytopenia, torsades de pointes due to prolonged QT interva)

Back 363

quinidine

Front 364

This member of class IA antiarrhytmics has toxicities that include reverible SLE-like syndrome

Back 364

procainamide

Front 365

This class of antiarrythmics include lidocaine mexiletine, tocainide

Back 365

IB (Na+ channel blockers)

Front 366

this class of antiarrythmics acts to decrease AP duration. It effects ischemic or depolarized purkinje and ventricular tussue. It is useful in acute ventricular arrhytmias (especially post-MI) and i digitalis-induced arrhythmias.

Back 366

IB (Na+ channel blockers)

Front 367

This class of antiarrhytmics has toxicities that include local anesthetic effects, CNS stimulation/depression, cardiovascular depression

Back 367

IB (Na+ channel blockers)

Front 368

This class of antiarrhythmics includes flecainide, encainide, propafenone.

Back 368

class IC (Na+ channel blockers.

Front 369

This class of antiarrhythmics has no effect on AP duration. It is useful in V-tachs that progress to VF and intractable SVT. Usually used only as last result in refractory tachyarrythmias.

Back 369

class IC (Na+ channel blockers.

Front 370

Toxicities of this class of antiarrhythmics includes arrythmias, especially post MI (CONTRAINDICATED)

Back 370

class IC (Na+ channel blockers.

Front 371

picture p. 242 Class I antiarrythmics (Na+ channel blockers)

Back 371

1) IA 2) IB 3) IC

Front 372

This clas of antiarrythmics includes propanolol, esmolol, metroprolol, atenolol, timool.

Back 372

Beta Blockers (Class II)

Front 373

This class of antiarrythmics acts by ↓ cAMP, ↓ Ca+ currents, and by supressing abnormal pacemakers by ↓ slope of phase 4. The AV node is particularly sensitive resulting in increaed PR interval

Back 373

B-blockers (Class II antiarrythmics)

Front 374

this is the shortest acting B blocker

Back 374

esmolol

Front 375

Toxicities of this class of antiarrythmics include impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). It may mask signs of hypoglycemia.

Back 375

B-blockers (Class II antiarrythmics)

Front 376

This class of antiarrythmics includes Sotalol, ibutilide, bretylium, & amiodarone

Back 376

K+ channel blockers (class III)

Front 377

This class of antiarrythmics acts by ↑ AP duration, ↑ERP. It thends to ↑ QT interval. It is used when other antiarrhythmics fail.

Back 377

K+ channel blockers (class III)

Front 378

This class III antiarrythmic has toxicities which include torsades de pointes and excessive beta block

Back 378

sotalol

Front 379

This class III antiarrythmic has toxicities which include new arrhytmias& hypotension

Back 379

bretylium

Front 380

This class III antiarrythmic has toxicities which include PULMONARY FIBROSIS, HEPATOTOXICITY, HYPOTHYROIDSIM/HYPERTHYROIDISM, corneal deposits, skin depsits resulting in photodermatiitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF

Back 380

amiodarone mneu: remember to check PFTs, LFTs, and TFTs when using amiodarone.

Front 381

class III antiarrythmics [pic.p.243]

Back 381

--

Front 382

This class of antiarrythmics include the drugs verapamil, and diltiazem.

Back 382

Ca++ channel blockers (class IV)

Front 383

The MOA of this class of antiarrythmics is primarily on AV nodal cells. They ↓ conduction velocity, ↑ ERP, ↑ PR interval.

Back 383

Ca++ channel blockers (class IV)

Front 384

this class of antiarrythmics is used in prevention of nodal arrhythmias (e.g., SVT)

Back 384

Ca++ channel blockers (class IV)

Front 385

Toxicity of this class of antiarrythmics can include constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression, & torsades de pointes.

Back 385

Ca++ channel blockers (class IV)

Front 386

Ca++ channel blockers (class IV) [pic.p244]

Back 386

--

Front 387

Other antiarrythmics: this antiarrhythmic is the drug of choice in diagnosing/abolishing AV nodal arrhythmias

Back 387

adenosine

Front 388

Other antiarrythmics: this antiarrhythmic depresses ectopic pacemakers, especially in digoxin doxicity

Back 388

K+

Front 389

Other antiarrythmics: this antiarrhythmic is effective in torsades de pointes and digoxin toxiciity

Back 389

Mg+