2007 First Aid Ch 08 Cardiovascular

Front 1

Pregnant woman in 3rd trimester
has normal blood pressure when
standing and sitting. When supine,
blood pressure drops to 90/50.

Back 1

Compression of the IVC.

Front 2

35-year-old man has high blood
pressure in his arms and low
pressure in his legs.

Back 2

Coarctation of the aorta.

Front 3

5-year-old boy presents with
systolic murmur and wide,
fixed split S2.

Back 3

ASD.

Front 4

During a game, a young
football player collapses and
dies immediately.

Back 4

Hypertrophic cardiomyopathy.

Front 5

Patient has a stroke after
incurring multiple long bone
fractures in trauma stemming
from a motor vehicle accident.

Back 5

Fat emboli.

Front 6

Elderly woman presents with a
headache and jaw pain. Labs
show elevated ESR.

Back 6

Temporal arteritis.

Front 7

80-year-old man presents with a
systolic crescendo-decrescendo
murmur.

Back 7

Aortic stenosis.

Front 8

Man starts a medication for
hyperlipidemia. He then
develops a rash, pruritus, and
GI upset.

Back 8

Niacin.

Front 9

Patient develops a cough and
must discontinue captopril.
name good altenatives

Back 9

Losartan, an angiotensin II
receptor antagonist, does not ↑
bradykinin as captopril does.

Front 10

Carotid sheath structures

Back 10

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

Front 11

location of
Internal jugular Vein (lateral)
Common carotid Artery (medial)
Vagus Nerve (posterior)

Back 11

Carotid sheath

Front 12

In the majority of cases, the SA
and AV nodes are supplied
by

Back 12

the RCA.

Front 13

what supplies
the inferior portion of the
left ventricle

Back 13

80% of the time the RCA supplies
via the PD
= right dominant).

Front 14

Coronary artery
names

Back 14

Acute marginal artery
Left main coronary artery (LCA)
Circumflex artery (CFX)
Left anterior
descending
artery (LAD)
Posterior descending artery (PD)
Right coronary
artery (RCA)

Front 15

artery (= right dominant).
Coronary artery occlusion
occurs most commonly
in and supplies what?

Back 15

the LAD, which supplies
the anterior interventricular
septum.

Front 16

The most posterior part of the
heart is what and implications

Back 16

left atrium;
enlargement can cause
dysphagia.

Front 17

Where to listen to the Heart

Back 17

APTM
aortic: Right 2ndICS
Pulmonic:left 2ndICS
Tricuspid: left 4th ICS
Mitral: left 5th ICS lateral to left midclavicular line

Front 18

What is heard best at
Aortic area:

Back 18

Systolic murmur
• Aortic stenosis
• Flow murmur

Front 19

What is heard best at
Left sternal border:

Back 19

Diastolic murmur
• Aortic regurgitation
• Pulmonic regurgiation

Front 20

What is heard best at
Pulmonic area:

Back 20

Diastolic murmur
• Pulmonic stenosis
• Flow murmur

Front 21

What is heard best at
Tricuspid area:

Back 21

Pansystolic murmur
• Tricuspid regurgitation
• Ventricular septal defect
Diastolic murmur
• Tricuspid stenosis
• Atrial septal defect

Front 22

What is heard best at
Mitral area:

Back 22

Systolic murmur
• Mitral regurgitation
Diastolic murmur
• Mitrial stenosis

Front 23

Cardiac output (CO)=

Back 23

= (stroke volume) × (heart rate).

Front 24

CO in During exercise, CO ↑
initially as a result of an
↑ in SV. After prolonged
exercise, CO ↑ as a result
of an ↑ in HR.

Back 24

CO ↑
initially as a result of an
↑ in SV. After prolonged
exercise, CO ↑ as a result
of an ↑ in HR.

Front 25

fick principle

Back 25

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

Front 26

Mean arterial pressure =
= (cardiac output) × (total peripheral resistance)

Back 26

MAP = (co) × (TPR)

MAP = 2/3 diastolic + 1/3 systolic

Front 27

Pulse pressure =

Back 27

systolic - diastolic

and is proportional to SV

Front 28

equation for SV

Back 28

=CO/HR

also

=EDV-ESV

Front 29

Stroke Volume affected by

Back 29

SV CAP.
Stroke Volume affected by Contractility, Afterload,
and Preload. ↑ SV when ↑ preload, ↓ afterload,
or ↑ contractility.

Front 30

Contractility (and SV) ↑ with:

Back 30

1. Catecholamines (↑ activity of Ca2+pump
in sarcoplasmic reticulum)
2. ↑ intracellular calcium
3. ↓ extracellular sodium
4. Digitalis (↑ intracellular Na+, resulting
in ↑ Ca2+)
5.SV ↑ in anxiety, exercise,
and pregnancy.

Front 31

Contractility (and SV) ↓ with:

Back 31

1. β1 blockade
2. Heart failure
3. Acidosis
4. Hypoxia/hypercapnea
5. Ca2+ channel blockers

Front 32

Myocardial O2 demand is ↑ by:

Back 32

1. ↑ afterload (∝
diastolic BP)
2.↑ contractility
3. ↑ heart rate
4. ↑ heart size (↑ wall
tension)

Front 33

Preload and
afterload
aka's

Back 33

Preload = ventricular EDV.
Afterload = diastolic arterial pressure

Front 34

aka ventricular EDV.

Back 34

Preload

Front 35

aka diastolic arterial pressure

Back 35

Afterload

Front 36

Preload and afterload
wrt dilators

Back 36

Venous dilators (e.g., nitroglycerin) ↓ preload.


Vasodilators (e.g., hydralazine) ↓ afterload.

Front 37

Preload increases with (3 things)

Back 37

Preload ↑ with exercise
(slightly), ↑ blood volume
(overtransfusion), and
excitement (sympathetics).
Preload pumps up the heart.

Front 38

Starling curve
Force of contraction is proportional to

Back 38

initial length of cardiac muscle fiber (preload).

Front 39

CONTRACTILE STATE OF MYOCARDIUM
+

Back 39

-Circulating catecholamines

-Digitalis

-Sympathetic stimulation

Front 40

CONTRACTILE STATE OF MYOCARDIUM
−

Back 40

-Pharmacologic depressants


-Loss of myocardium (MI)

Front 41

Ejection fraction (EF)
equation and description

Back 41

EF = SV/EDV = (EDV – ESV)/EDV

EF is an index of ventricular contractility.

Front 42

EF is normally

Back 42

≥ 55%.

Front 43

Resistance,
pressure, flow
∆P =

Back 43

Q × R

Front 44

Resistance =

Back 44

P/Q

or

8n(viscosity)(length)/(Pi)(R^4)

Front 45

Viscosity depends mostly on

Back 45

hematocrit.

Front 46

Viscosity ↑ in:

Back 46

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

Front 47

what vessels account for most of
total peripheral resistance
and how

Back 47

Arterioles
→ regulate capillary flow.

Front 48

Phases–left ventricle:
Isovolumetric contraction––

Back 48

period
between mitral valve closure and
aortic valve opening; period of
highest O2 consumption

Front 49

Phases–left ventricle:
period of
highest O2 consumption

Back 49

Isovolumetric contraction––

Front 50

Phases–left ventricle:
Systolic ejection–

Back 50

period between
aortic valve opening and closing

Front 51

Phases–left ventricle:
Isovolumetric relaxation

Back 51

––period
between aortic valve closing and
mitral valve opening

Front 52

Phases–left ventricle:
Rapid filling––

Back 52

period just after
mitral valve opening

Front 53

Phases–left ventricle:
Slow filling

Back 53

––period just before
mitral valve closure

Front 54

Phases–left ventricle: in order

Back 54

1. Isovolumetric contraction


2. Systolic ejection

3. Isovolumetric relaxation


4. Rapid filling

5. Slow filling

Front 55

heart sound events
S1
S2
S3
S4

Back 55

S1––mitral and tricuspid valve closure.
S2––aortic and pulmonary valve closure.
S3––at end of rapid ventricular filling.
S4––high atrial pressure/stiff ventricle.

Front 56

S3 is associated with

Back 56

dilated CHF.

Front 57

Heart sound associated with dilated CHF.

Back 57

S3

Front 58

Heart sound associated with (“atrial kick”)

Back 58

S4 (“atrial kick”)

Front 59

S4 (“atrial kick”)
is associated with

Back 59

a hypertrophic ventricle

Front 60

Heart sound associated with
hypertrophic ventricle.

Back 60

S4 (“atrial kick”)

Front 61

a wave=

Back 61

a wave––atrial contraction.

Front 62

c wave=

Back 62

c wave––RV contraction (tricuspid valve
bulging into atrium).

Front 63

v wave=

Back 63

v wave–– ↑ atrial pressure due to
filling against closed tricuspid valve.

Front 64

Normal S2 spliting

Back 64

S2 splitting: aortic valve closes before
pulmonic;
S1...A2.P2
inspiration ↑ this
difference.
s1...A2..P2

Front 65

Wide splitting (associated with

Back 65

Pulmonic stenosis
S1....A2(more time)P2

Front 66

Fixed splitting (associated with

Back 66

ASD

no change on inspiration

Front 67

Paradoxical splitting (associated with

Back 67

Aortic stenosis
S1...P2...A2 on expire
S1...P2.A2

Front 68

Cardiac muscle contraction is dependent on what Ion

Back 68

extracellular calcium,

Front 69

Cardiac muscle contraction is dependent on ?????? which enters the
cells during ?????? action potential and stimulates ???????from the cardiac
muscle ??????(?????????).

Back 69

extracellular calcium,

plateau of

calcium release

sarcoplasmic reticulum

calcium-induced calcium release

Front 70

Cardiac myocyte physiology in contrast to skeletal muscle

WRT Plateau

Back 70

Cardiac muscle action potential has a plateau, which is due to Ca2+ influx

Front 71

Cardiac myocyte physiology in contrast to skeletal muscle

WRT sponienaity

Back 71

Cardiac nodal cells spontaneously depolarize, resulting in automaticity

Front 72

Cardiac myocyte physiology in contrast to skeletal muscle

WRT coupling

Back 72

Cardiac myocytes are electrically coupled to each other by gap junctions

Front 73

Name 3 features of Cardiac myocyte physiology that contrast skeletal muscle

Back 73

1. has a plateau

2. spontaneous depolarize/automaticity

3.coupled to each other by gap junctions

Front 74

Myocardial action potential

Which cells

Back 74

Occurs in atrial and ventricular myocytes and Purkinje fibers.

Front 75

Myocardial action potential

Phase 0

Back 75

rapid upstroke––voltage-gated Na+ channels open.

Front 76

Myocardial action potential

Phase 1

Back 76

initial repolarization with inactivation of voltage-gated Na channels. Voltage-gated K+ channels begin to open.

Front 77

Myocardial action potential

Phase 2

Back 77

plateau––Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

Front 78

Myocardial action potential

Phase 3

Back 78

rapid repolarization––massive K+ efflux due to opening of voltage- gated slow K+ channels and closure of voltage-gated Ca2+ channels.

Front 79

Myocardial action potential

Phase 4

Back 79

resting potential––high K+ permeability through K+ channels.

Front 80

Pacemaker action potential

Which cells

Back 80

Occurs in the SA and AV nodes

Front 81

Pacemaker action potential

Phase 0

Back 81

upstroke––opening of voltage-gated Ca2+ 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.

Front 82

Pacemaker action potential

Phase 2

Back 82

plateau is absent.

Front 83

Pacemaker action potential

Phase 3

Back 83

Inactivation of the Ca2+ channels and increase activation of the K+ channels leading to increased K+

Front 84

Pacemaker action potential

Phase 4

Back 84

Phase 4 = slow diastolic depolarization––membrane potential spontaneously depolarize as Na+ conductance ↑ (If different from INa above). Accounts for automaticity of SA and AV nodes.

Front 85

Pacemaker action potential

what determines heart rate

Back 85

The slope of phase 4 in the SA node determines heart rate

Front 86

Pacemaker action potential

effect of neurotransmitters on heart rate

Back 86

ACh ↓ the rate of diastolic depolarization and ↓ heart rate, while catecholamines ↑ epolariza-
tion and ↑ heart rate.

Front 87

Pacemaker action potential

which phase shows effect of neurotransmitters on heart rate

Back 87

Phase 4

Front 88

Pacemaker action potential which phase does not exist

Back 88

Phase 1(initial repolarization) and 2 (plateau)

Front 89

ECG what is represented by the

P wave

Back 89

atrial depolarization.

Front 90

ECG what is represented by the

PR segment

Back 90

conduction delay through AV node (normally < 200 msec).

Front 91

ECG what is represented by the

QRS complex

Back 91

ventricular depolarization (normally < 120 msec).

Front 92

ECG what is represented by the

QT interval

Back 92

mechanical contraction of the ventricles.

Front 93

ECG what is represented by the

masked by QRS complex.

Back 93

Atrial repolarization

Front 94

ECG what is represented by the

T wave

Back 94

ventricular repolarization.

Front 95

ECG what is represented by the

ST segment

Back 95

––isoelectric, ventricles depolarized

Front 96

ECG what is represented by the

U wave

Back 96

––caused by hypokalemia.

Front 97

ECG normal timing of

QRS complex

Back 97

(normally < 120 msec).

Front 98

ECG normal timing of

PR segment

Back 98

(normally < 200 msec).

Front 99

Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.

Back 99

Torsades des pointes

Front 100

describe Torsades des pointes

Back 100

Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.

Front 101

Torsades des pointes complications

Back 101

Can progress to V-fib

Front 102

causes of Torsades des pointes

Back 102

Anything that prolongs the QT interval

Front 103

Anything that prolongs the QT interval can predispose to

Back 103

Torsades des pointes

Front 104

describe Wolff-Parkinson-White syndrome

Back 104

Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node.

Front 105

Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node.

Back 105

Wolff-Parkinson-White syndrome

Front 106

Wolff-Parkinson-White syndrome
name the accesory path

Back 106

bundle of Kent

Front 107

Wolff-Parkinson-White syndrome
on ECG and why

Back 107

characteristic delta wave on ECG

due to ventricles begin to partially depolarize earlier,

Front 108

characteristic delta wave on ECG

Back 108

Wolff-Parkinson-White syndrome

Front 109

Wolff-Parkinson-White syndrome
complications

Back 109

May result in reentry current leading to supraventricular tachycardia.

Front 110

Describe this ECG

Atrial fibrillation

Back 110

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between
irregularly spaced QRS complexes.

Front 111

Describe this ECG

Atrial flutter

Back 111

A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.

Front 112

Describe this ECG

AV block
1st degree

Back 112

The PR interval is prolonged (> 200 msec). Asymptomatic.

Front 113

Describe this ECG

AV block
2nd degree
Mobitz type I

Back 113

Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Usually asymptomatic.

Front 114

Describe this ECG

AV block
2nd degree
Mobitz type II

Back 114

Dropped beats that are not preceded by a change in the length of the PR interval

Front 115

Describe this ECG

AV block
3rd degree

Back 115

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.

Front 116

Describe this ECG

Ventricular fibrillation

Back 116

A completely erratic rhythm with no identifiable waves.

Front 117

ID the ECG

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between
irregularly spaced QRS complexes.

Back 117

Atrial fibrillation

Front 118

ID the ECG

A rapid succession of identical, back-to-back atrial depolarization waves. The identical
appearance accounts for the “sawtooth” appearance of the flutter waves.

Back 118

Atrial flutter

Front 119

ID the ECG

The PR interval is prolonged (> 200 msec). Asymptomatic.

Back 119

AV block
1st degree

Front 120

ID the ECG

Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not
followed by a QRS complex). Usually asymptomatic.

Back 120

2nd degree
Mobitz type I
(Wenckebach)

Front 121

ID the ECG

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.

Back 121

2nd degree
Mobitz type II

Front 122

ID the ECG

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.

Back 122

3rd degree
(complete)

Front 123

ID the ECG

A completely erratic rhythm with no identifiable waves.

Back 123

Ventricular
fibrillation

Front 124

Wenckebach aka

Back 124

2nd degree
Mobitz type I

Front 125

2nd degree Mobitz type I
aka

Back 125

Wenckebach

Front 126

Tx for Atrial fibrillation

Back 126

Anticoagulation

Front 127

Tx for AV node Block 3rd degree

Back 127

Usually treat with pacemaker.

Front 128

Tx for Ventricular fibrillation

Back 128

immediate CPR and defibrillation.

Front 129

In AV node block 3rd degree (complete)

which is faster

Back 129

The atrial rate is faster than the ventricular rate. i.e P waves are faster than QRS

Front 130

Control of mean arterial pressure

↑ SYMPATHETIC ACTIVITY at receptors

Back 130

β1 (↑ heart rate, ↑ contractility)— ↑ CO

α1 (venoconstriction: ↑ venous return)—↑ CO

α1 (arteriolar vasoconstriction)— ↑ TPR

Front 131

Control of mean arterial pressure

Medullary vasomotor center senses ↓ baroreceptor firing leads to

Back 131

↑ SYMPATHETIC ACTIVITY

Front 132

Control of mean arterial pressure

JGA senses ↓ MAP leads to

Back 132

↑ RENIN-ANGIOTENSIN SYSTEM

Front 133

Control of mean arterial pressure

↑ RENIN-ANGIOTENSIN SYSTEM leads to

Back 133

Angiotensin II vasoconstriction)— ↑ TPR

Aldosterone (↑ blood volume)—↑ CO

Front 134

Baroreceptors

Aortic arch transmits via ????? to ??????(responds to ????)

Back 134

via vagus nerve

medulla

only to ↑ BP

Front 135

Baroreceptors

Carotid sinus transmits via ????? to ???? (responds to ????)

Back 135

glossopharyngeal nerve

medulla

↓ and ↑ in BP

Front 136

Baroreceptors mech in Hypotension
and when is it important

Back 136

↓ arterial pressure →↓ stretch →↓ afferent baroreceptor firing →↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation →vasoconstriction, ↑ HR, ↑ contractility, ↑ BP. Important in the response to severe hemorrhage.

Front 137

Carotid massage

Back 137

↑ pressure on carotid artery →↑ stretch →↓ HR.

Front 138

peripheral chemoreceptors

where and what they respond to

Back 138

Carotid and aortic bodies respond to ↓ PO2 (< 60 mmHg), ↑ PCO2,
and ↓ pH of blood.

Front 139

Central chemoreceptors

what they respond to

Back 139

Central: Respond to changes in pH and PCO2 of brain interstitial fluid, which in
turn are influenced by arterial CO2. Do not directly respond to PO2.

Front 140

central chemoreceptors

wrt a specific reaction
name it and describe it

Back 140

Cushing reaction:
response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).

Front 141

Cushing reaction

Back 141

response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).

Front 142

response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).

Back 142

Cushing reaction

Front 143

Circulation through organs

Largest share of systemic cardiac output.

Back 143

Liver

Front 144

Circulation through organs

Highest blood flow per gram of tissue.

Back 144

Kidney

Front 145

Circulation through organs

Large arteriovenous O2 difference. ↑ O2 demand is met by ↑ coronary blood flow, not by
↑ extraction of O2.

Back 145

Heart

Front 146

Circulation through organs
features of the Heart

Back 146

Large arteriovenous O2 difference. ↑ O2 demand is met by ↑ coronary blood flow, not by
↑ extraction of O2.

Front 147

Heart ↑ O2 demand is met by

Back 147

↑ coronary blood flow, not by
↑ extraction of O2.

Front 148

PCWP

what and why

Back 148

pulmonary capillary
wedge pressure (in mmHg)
is a good approximation of
left atrial pressure.

Front 149

Swan-Ganz catheter.

Back 149

measures pulmonary capillary
wedge pressure

Front 150

how to measure pulmonary capillary
wedge pressure

Back 150

Swan-Ganz catheter.

Front 151

the pulmonary vasculature is unique in that hypoxia causes

Back 151

vasoconstriction (in other organs hypoxia causes vasodilation).

Front 152

the ????????? is unique in that hypoxia causes vasoconstriction

Back 152

pulmonary vasculature

Front 153

Autoregulation of blood flow

Heart

Back 153

Local metabolites: O2, adenosine, NO

Front 154

Autoregulation of blood flow

Brain

Back 154

Local metabolites: CO2
(pH)

Front 155

Autoregulation of blood flow

Kidneys

Back 155

Myogenic and tubuloglomerular feedback

Front 156

Autoregulation of blood flow

Lungs

Back 156

Hypoxia causes vasoconstriction

Front 157

Autoregulation of blood flow

Skeletal muscle

Back 157

Local metabolites: lactate, adenosine, K+

Front 158

Autoregulation of blood flow

Skin

Back 158

Sympathetic stimulation most important
mechanism––temperature control

Front 159

Name the strucure where blod flow is controlled by

Local metabolites: O2, adenosine, NO

Back 159

Heart

Front 160

Name the strucure where blod flow is controlled by

Local metabolites: CO2
(pH)

Back 160

Brain

Front 161

Name the strucure where blod flow is controlled by

Myogenic and tubuloglomerular feedback

Back 161

Kidneys

Front 162

Name the strucure where blod flow is controlled by

Hypoxia causes vasoconstriction

Back 162

Lungs

Front 163

Name the strucure where blod flow is controlled by

Local metabolites: lactate, adenosine, K+

Back 163

Skeletal muscle

Front 164

Name the strucure where blod flow is controlled by

Sympathetic stimulation most important
mechanism––temperature control

Back 164

Skin

Front 165

4 Starling forces determine fluid movement through capillary membranes:

Back 165

1. Pc = capillary pressure––moves fluid out

2. Pi= interstitial fluid pressure––moves fluid in

3. πc = plasma colloid osmotic pressure––moves fluid in

4. πi = interstitial fluid colloid osmotic Pressure –moves fluid out

Front 166

Thus, net filtration pressure =

Back 166

P = [(Pc − Pi ) − (πc −πi )].

Front 167

Capillary fluid exchange

Kf=

Back 167

filtration constant (capillary permeability).

Front 168

Capillary fluid exchange

Net fluid flow =

Back 168

(Pnet)X(Kf)

Front 169

4 causes of Edema with mechs

Back 169

1. (↑ Pc; heart failure)

2. ↓ plasma proteins (↓πc; nephrotic syndrome, liver failure)

3. ↑ capillary permeability (↑ Kf; toxins, infections, burns)

4. ↑ interstitial fluid colloid osmotic pressure (↑πi lymphatic blockage)

Front 170

early cyanosis

Back 170

Right-to-left shunts “blue babies”

The 3 T’s:
Tetralogy
Transposition
Truncus

Front 171

late cyanosis

Back 171

Left-to-right shunts “blue kids”

1. VSD
2. ASD
3. PDA

Front 172

Freq of Left-to-right shunts

Back 172

VSD > ASD > PDA.

Front 173

Left-to-right shunts
complications

Back 173

↑ pulmonary resistance due
to arteriolar thickening.
→ progressive pulmonary
hypertension; leading to R → L shunt (Eisenmenger’s).

Front 174

Eisenmenger’s
syndrome

Back 174

Uncorrected VSD, ASD, or PDA leads to progressive
pulmonary hypertension. As pulmonary resistance
↑, the shunt reverses from L → R to R → L, which
causes late cyanosis

Front 175

Tetralogy of Fallot
why do kids squat

Back 175

to ↑ systemic vascular resistance and thereby reduce the R-L shunting

Front 176

Tetralogy of Fallot
4 characteristics

Back 176

1. Pulmonary stenosis

2. RVH

3. Overriding aorta (overrides the VSD)

4. VSD

Front 177

Eisenmenger’s syndrome
2 "other" complications

Back 177

(clubbing and polycythemia).

Front 178

Tetralogy of Fallot most important determinant for prognosis

Back 178

Pulmonary stenosis

Front 179

Tetralogy of Fallot is caused by

Back 179

anterosuperior displacement of the infundibular septum.

Front 180

Tetralogy of Fallot CXR

Back 180

boot-shaped heart due to RVH.

Front 181

Transposition of great vessels
how can they live

Back 181

VSD,
PDA,
patent foramen ovale

Front 182

Transposition of great vessels is due to

Back 182

failure of the aorticopulmonary septum to spiral.

Front 183

Transposition of great vessels
course

Back 183

Without surgical correction, most infants die within the first few months of life.

Front 184

Coarctation of aorta

Infantile type

Back 184

Infantile type: aortic stenosis proximal to insertion
of ductus arteriosus (preductal).

Front 185

Coarctation of aorta

Adult type

Back 185

Adult type: stenosis is distal to ductus arteriosus
(postductal). Associated with notching of the ribs,
hypertension in upper extremities, weak pulses in
lower extremities.

Front 186

Associated with notching of the ribs hypertension in upper extremities, weak pulses in
lower extremities.

Back 186

Coarctation of aorta

Adult type/postductal

Front 187

Coarctation of aorta

who?

Back 187

Male-to-female ratio 3:1.

Front 188

Coarctation of aorta

Dx

Back 188

weak femoral pulses on
physical exam.

Front 189

Coarctation of aorta

mnemonic

Back 189

INfantile: IN close to
the heart.

ADult: Distal to Ductus.

Front 190

??????? is used to close a
PDA. ??????is used to keep a
PDA open, which may be

Back 190

Indomethacin

PGE

Front 191

Patent ductus arteriosus

what keeps it open in the body

Back 191

PGE synthesis and low O2 tension.

Front 192

continuous, “machine-like” murmur

Back 192

PDA

Front 193

Congenital cardiac defect associations

22q11 syndromes

Back 193

Truncus arteriosus, tetralogy
of Fallot

Front 194

Congenital cardiac defect associations

Down syndrome

Back 194

ASD, VSD

Front 195

Congenital cardiac defect associations

Congenital rubella

Back 195

Septal defects, PDA

Front 196

Congenital cardiac defect associations

Turner’s syndrome

Back 196

Coarctation of aorta

Front 197

Congenital cardiac defect associations

Marfan’s syndrome

Back 197

Aortic insufficiency

Front 198

Congenital cardiac defect associations

Offspring of diabetic mother

Back 198

Transposition of great vessels

Front 199

Congenital cardiac defect associations

Truncus arteriosus, tetralogy
of Fallot

Back 199

22q11 syndromes

Front 200

Congenital cardiac defect associations

ASD, VSD

Back 200

Down syndrome

Front 201

Congenital cardiac defect associations

Septal defects, PDA

Back 201

Congenital rubella

Front 202

Congenital cardiac defect associations

Aortic insufficiency

Back 202

Marfan’s syndrome

Front 203

Congenital cardiac defect associations

Coarctation of aorta

Back 203

Turner’s syndrome

Front 204

Congenital cardiac defect associations

Transposition of great vessels

Back 204

Offspring of diabetic mother

Front 205

Hypertension Defined as

Back 205

BP ≥ 140/90.

Front 206

Hypertension
Risk factors

Back 206

↑ age, obesity, diabetes, smoking, genetics, black > white > Asian.

Front 207

Hypertension
types

Back 207

90% of hypertension is 1° (essential) and related to ↑ CO or ↑ TPR; remaining 10%
mostly 2° to renal disease. Malignant hypertension is severe and rapidly progressing

Front 208

Hypertension
Predisposes to

Back 208

Atherosclerosis,
stroke,
CHF,
renal failure,
retinopathy,
aortic dissection.

Front 209

Atheromata

Back 209

Plaques in blood vessel walls.

Front 210

Plaques in blood vessel walls.

Back 210

Atheromata

Front 211

Xanthoma

Back 211

Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the
eyelids.

Front 212

Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the
eyelids.

Back 212

Xanthoma

Front 213

Tendinous xanthoma

Back 213

Lipid deposit in tendon, especially Achilles.

Front 214

Lipid deposit in tendon, especially Achilles.

Back 214

Tendinous xanthoma

Front 215

Corneal arcus

Back 215

Lipid deposit in cornea, nonspecific (arcus senilis).

Front 216

Lipid deposit in cornea, nonspecific (arcus senilis).

Back 216

Corneal arcus

Front 217

Mönckeberg

Back 217

Calcification of the arteries, especially radial or ulnar. Usually benign; "pipestem
arteries."

Front 218

Calcification of the arteries, especially radial or ulnar. Usually benign; "pipestem
arteries."

Back 218

Mönckeberg

Front 219

Arteriolosclerosis

Back 219

Hyaline thickening of small arteries in essential hypertension. Hyperplastic “onion
skinning” in malignant hypertension.

Front 220

Hyaline thickening of small arteries in essential hypertension. Hyperplastic “onion
skinning” in malignant hypertension.

Back 220

Arteriolosclerosis

Front 221

Atherosclerosis

Back 221

Fibrous plaques and atheromas form in intima of arteries.

Front 222

Fibrous plaques and atheromas form in intima of arteries.

Back 222

Atherosclerosis

Front 223

Atherosclerosis
which arteries

Back 223

Disease of elastic arteries and large and medium-sized muscular arteries

Front 224

Atherosclerosis

Risk factors

Back 224

Smoking,
hypertension,
diabetes mellitus, hyperlipidemia,
family history.

Front 225

Atherosclerosis

Progression

Back 225

Fatty streaks → proliferative plaque → complex atheromas.

Front 226

Atherosclerosis

Complications

Back 226

Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.

Front 227

Atherosclerosis

Location

Back 227

Abdominal aorta > coronary artery > popliteal artery > carotid artery.

Front 228

Atherosclerosis

Symptoms

Back 228

Angina, claudication, but can be asymptomatic.

Front 229

Ischemic heart disease
Possible manifestations:

Back 229

1. Angina
2. Myocardial infarction
3. Sudden cardiac death
4. Chronic ischemic heart disease

Front 230

when does Angina occur

Back 230

(CAD narrowing > 75%):

Front 231

Angina
types and features

Back 231

a. Stable –mostly 2° to atherosclerosis (retrosternal chest pain with exertion)

b. Prinzmetal’s variant –occurs at rest 2° to coronary artery spasm

c.Unstable/crescendo –thrombosis but no necrosis (worsening chest pain)

Front 232

which Angina
occurs at rest 2° to coronary artery spasm

Back 232

Prinzmetal’s varian

Front 233

which Angina
mostly 2° to atherosclerosis

Back 233

Stable

Front 234

which Angina
thrombosis but no necrosis

Back 234

Unstable/crescendo

Front 235

most often cause of MI

Back 235

most often acute thrombosis from coronary artery atherosclerosis.

Front 236

Sudden cardiac death most common cause

Back 236

lethal arrhythmia

Front 237

What is Sudden cardiac death

Back 237

death from cardiac causes within 1 hour of onset of
symptoms

Front 238

what is Chronic ischemic heart disease

Back 238

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

Front 239

Red (hemorrhagic) infarcts occur in

Back 239

loose tissues with collaterals, such as lungs, liver, intestine, or following reperfusion.

Front 240

Pale infarcts occur in

Back 240

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

Front 241

Coronary artery occlusion frequency

Back 241

LAD > RCA > circumflex.

Front 242

MI symptoms

Back 242

Diaphoresis,
nausea and vomiting,
severe retrosternal pain,
pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms

Front 243

MI markers

Cardiac troponin I rises

Back 243

after 4 hours
peaks at 24
and is elevated
for 7–10 days;

Front 244

MI markers

more specific than other protein
markers.

Back 244

Cardiac troponin I

Front 245

MI markers

rises after 4 hours and is elevate
for 7–10 days;

Back 245

Cardiac troponin I

Front 246

MI markers

CK-MB rises

Back 246

4-8 hours
peaks at 24
gone in 2-3 days

Front 247

MI markers

predominantly found in myocardium but
can also be released from skeletal muscle

Back 247

CK-MB

Front 248

MI markers

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

Back 248

AST

Front 249

MI markers

AST rises

Back 249

by 18 hours
peaks at
1.5 days

Front 250

MI markers

LDH rises

Back 250

in 10 hours

peaks at 2-3 days

gone in 7

Front 251

Diagnosis of MI In the first 6 hours, ?????? is the gold standard.

Back 251

ECG i

Front 252

Diagnosis of MI wrt ECG

Back 252

changes can include:
ST elevation (transmural
infarct),

ST depression (subendocardial infarct),

pathological Q waves (transmural infarct).

Front 253

MI complications

Cardiac arrhythmia

Back 253

important cause of death before reaching hospital; common in
first few days

Front 254

MI complications

Aneurysm formation

Back 254

↓ CO, risk of arrhythmia, embolus from mural thrombus

Front 255

MI complications

Fibrinous pericarditis

Back 255

friction rub (3–5 days post-MI)

Front 256

Dressler’s syndrome

Back 256

autoimmune phenomenon resulting in fibrinous pericarditis
(several weeks post-MI)

Front 257

autoimmune phenomenon resulting in fibrinous pericarditis
(several weeks post-MI)

Back 257

Dressler’s syndrome

Front 258

friction rub (3–5 days post-MI)

Back 258

Fibrinous pericarditi

Front 259

4–10 days post–MI; can lead to cardiac tamponade.

Back 259

Rupture

Front 260

Most common cardiomyopathy (90% of cases).

Back 260

Dilated (congestive)
cardiomyopathy

Front 261

Dilated cardiomyopathy
causes

Back 261

chronic Alcohol abuse,
Beriberi,
Coxsackie B virus myocarditis, chronic Cocaine use,
Chagas’ disease,
Doxorubicin toxicity, peripartum cardiomyopathy.

Front 262

Dilated cardiomyopathy CXR

Back 262

Heart dilates and looks like a balloon on
chest x-ray.

Front 263

Dilated cardiomyopathy what type of dysfunction

Back 263

Systolic dysfunction ensues.

Front 264

Hypertrophic cardiomyopathy what type of dysfunction

Back 264

Diastolic dysfunction ensues.

Front 265

Cause of sudden death in young athletes.

Back 265

Hypertrophic cardiomyopathy

Front 266

Hypertrophy often asymmetric and involving the intraventricular septum. Normal heart size.

Back 266

Hypertrophic cardiomyopathy

Front 267

describe Hypertrophic cardiomyopathy

Back 267

Hypertrophy often asymmetric and involving the intraventricular septum. Normal heart size.

Front 268

Hypertrophic cardiomyopathy CXR

Back 268

Normal heart size.

Front 269

Hypertrophic cardiomyopathy causes

Back 269

50% of cases are familial, autosomal dominant.

Front 270

Hypertrophic cardiomyopathy
Dx

Back 270

Findings: loud S4, apical impulses, systolic
murmur.

Front 271

Hypertrophic cardiomyopathy
Tx

Back 271

Treat with β-blocker. and/or Surgical septal myectomy

Front 272

causes of Restrictive/obliterative
cardiomyopathy

Back 272

sarcoidosis,
amyloidosis,
postradiation fibrosis, endocardial fibroelastosis,
endomyocardial fibrosis (Löffler’s),
hemochromatosis (dilated cardiomyopathy can also occur).

Front 273

Heart sounds

Holosystolic high-pitched “blowing murmur.” Loudest at apex.

Back 273

Mitral regurgitation

Front 274

Heart sounds

Mitral regurgitation

Back 274

Holosystolic high-pitched “blowing murmur.” Loudest at apex.

Front 275

Heart sounds

Crescendo-decrescendo systolic ejection murmur

Back 275

Aortic stenosis

Front 276

Heart sounds

LV >> aortic pressure during systole

Back 276

Aortic stenosis

Front 277

Heart sounds

“Pulsus parvus et tardus”

Back 277

pulses weak compared
to heart sounds.
aortic stenosis

Front 278

Heart sounds

Holosystolic murmur.

Back 278

VSD

Front 279

Heart sounds

Late systolic murmur with midsystolic click.

Back 279

Mitral prolapse

Front 280

Heart sounds

Most frequent valvular lesion.

Back 280

Mitral prolapse

Front 281

Heart sounds

Immediate high-pitched “blowing” diastolic murmur. Wide pulse
pressure.

Back 281

Aortic regurgitation

Front 282

Heart sounds

Follows opening snap. Delayed rumbling late diastolic murmur.

Back 282

Mitral stenosis

Front 283

Heart sounds

LA >> LV pressure during diastole.

Back 283

Mitral stenosis

Front 284

Heart sounds

Mitral vs Tricuspid stenosis

Back 284

Tricuspid stenosis differs because
it gets louder with inspiration.

Front 285

Heart sounds

PDA

Back 285

Continuous machine-like murmur. Loudest at time of S2.

Front 286

Heart sounds

Continuous machine-like murmur. Loudest at time of S2.

Back 286

PDA

Front 287

CHF what is the cause of

Dyspnea on exertion

Back 287

Failure of LV output to ↑
during exercise.

Front 288

CHF what is the cause of

Cardiac dilation

Back 288

Greater ventricular end-diastolic
volume.

Front 289

CHF what is the cause of

Pulmonary edema, paroxysmal
nocturnal dyspnea

Back 289

LV failure →↑ pulmonary
venous pressure → pulmonary venous distention and transudation of fluid.

Front 290

CHF what is the cause of

Orthopnea

Back 290

↑ venous return in supine
position exacerbates pulmonary
vascular congestion.

Front 291

CHF what is the cause of

Hepatomegaly
(nutmeg liver)

Back 291

↑ central venous pressure
→↑ resistance to portal flow.
Rarely, leads to “cardiac
cirrhosis.”

Front 292

CHF what is the cause of

Ankle, sacral edema

Back 292

RV failure →↑ venous pressure
→ fluid transudation.

Front 293

CHF what is the cause of

Jugular venous
distention

Back 293

R heart failure →↑ venous pressure.

Front 294

hemosiderin-laden
macrophages (“heart failure”
cells).

Back 294

(“heart failure”
cells).

Front 295

“heart failure” cells

Back 295

hemosiderin-laden
macrophages

Front 296

Embolus types

Back 296

An embolus moves like a FAT
BAT.
Fat,
Air,
Thrombus,
Bacteria,
Amniotic fluid,
Tumor.

Front 297

Fat emboli are associated with

Back 297

acute long bone fractures and liposuction.

Front 298

Amniotic fluid emboli can lead to

Back 298

DIC,

Front 299

Pulmonary embolus clinical findings

Back 299

chest pain, tachypnea,
dyspnea.

Front 300

Virchow’s triad:

Back 300

1. Stasis
2. Hypercoagulability
3. Endothelial damage

Front 301

Cardiac tamponade

Back 301

Compression of heart by fluid (i.e., blood) in pericardium, leading to ↓ CO.

Front 302

Compression of heart by fluid (i.e., blood) in pericardium, leading to ↓ CO.

Back 302

Cardiac tamponade

Front 303

Cardiac tamponade and pressure changes

Back 303

Equilibration of diastolic pressures in all 4 chambers of the heart with intrapericardial pressure

Front 304

Cardiac tamponade
clinical findings

Back 304

hypotension,
↑ venous pressure (JVD),
distant heart sounds,
↑ HR,
pulsus paradoxus;

Front 305

pulsus paradoxus

Back 305

is an exaggeration of the normal variation in the pulse during the inspiratory phase of respiration, in which the pulse becomes weaker as one inhales and stronger as one exhales

Front 306

Cardiac tamponade
ECG findings

Back 306

ECG shows electrical alternans (beat-to-beat alterations of QRS
complex height).

Front 307

what are ECG electrical alternans and what do they mean

Back 307

beat-to-beat alterations of QRS
complex height

Cardiac tamponade

Front 308

Osler’s nodes

Back 308

Osler's nodes are painful, red, raised lesions on the finger pulps, indicative of the heart disease subacute Infective endocarditis. They are caused by immune complex deposition.

Front 309

Osler's nodes are painful, red, raised lesions on the finger pulps, indicative of the heart disease subacute Infective endocarditis. They are caused by immune complex deposition.

Back 309

Osler’s nodes

Front 310

Bacterial endocarditis
clinical findings

Back 310

Bacteria FROM JANE
Fever
Roth’s spots
Osler’s nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli

Front 311

Roth's spots

Back 311

retinal hemorrhages with white or pale centers composed of coagulated fibrin. immune complex mediated vasculitis often resulting from bacterial endocarditis

Front 312

retinal hemorrhages with white or pale centers composed of coagulated fibrin immune complex mediated vasculitis often resulting from bacterial endocarditis

Back 312

Roth's spots

Front 313

Janeway lesions
what
who
mech

Back 313

non-tender, small erythematous or haemorrhagic macules or nodules in the palms or soles,

are pathognomonic of infective endocarditis.

The pathology is due to a type III hypersensitivity reaction.

Front 314

non-tender, small erythematous or haemorrhagic macules or nodules in the palms or soles, which are pathognomonic of infective endocarditis. The pathology is due to a type III hypersensitivity reaction.

Back 314

Janeway lesions

Front 315

Bacterial endocarditis

most common valve

Back 315

Mitral

Front 316

Bacterial endocarditis

most common valve in IVDA

Back 316

Tricuspid

Front 317

Bacterial endocarditis

acute

Back 317

1. Acute––S. aureus (high virulence). Large
vegetations on previously normal valves.
Rapid onset.

Front 318

Bacterial endocarditis

subacute

Back 318

2. Subacute––viridans streptococcus (low virulence). Smaller vegetations on congenitally abnormal or diseased valves.

Front 319

Bacterial endocarditis

Sequela of dental procedures

Back 319

subacute - viridans streptococcus

Front 320

Bacterial endocarditis

complications

Back 320

chordae rupture,
glomerulonephritis,
suppurative pericarditis,
emboli.

Front 321

Endocarditis may also be nonbacterial 2° to

Back 321

metastasis or renal failure (marantic/thrombotic endocarditis).

Front 322

Libman-Sacks
endocarditis

Back 322

Vegetations develop on both sides of valve (→ mitral valve stenosis) but do not embolize. Seen in lupus.

Front 323

Vegetations develop on both sides of valve (→ mitral valve stenosis) but do not embolize. Seen in lupus.

Back 323

Libman-Sacks
endocarditis

Front 324

endocarditis seen in Lupus

Back 324

Libman-Sacks
-- SLE causes LSE.

Front 325

Rheumatic fever is a consequence of

Back 325

pharyngeal infection with group A β-hemolytic strep

Front 326

Rheumatic fever
early cause of death

Back 326

Early deaths due to myocarditis.

Front 327

rheumatic heart disease
affects which heart valves

Back 327

––mitral > aortic >>
tricuspid (high-pressure valves affected most).

Front 328

Rheumatic heart disease
Micro

Back 328

Associated with Aschoff bodies (granuloma with giant cells),

Anitschkow's cells (activated
histiocytes),

Front 329

What are Aschoff bodies

Back 329

granuloma with giant cells

Front 330

What are Anitschkow's cells

Back 330

activated histiocytes

Front 331

Jones criteria

Back 331

diagnosis of rheumatic fever

# Joints (Migratory polyarthritis):

# O [imagine heart-shaped O] (carditis):


# Erythema marginatum

# Sydenham's chorea (St. Vitus' dance)

Front 332

diagnosis of rheumatic fever

Back 332

Jones criteria

# Joints (Migratory polyarthritis):

# O [imagine heart-shaped O] (carditis):


# Erythema marginatum

# Sydenham's chorea (St. Vitus' dance)

Front 333

diagnosis of rheumatic fever
lab test

Back 333

ESR ↑

elevated ASO titers.

Front 334

diagnosis of rheumatic fever
Jones criteria
J

Back 334

Joints (Migratory polyarthritis): a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.

Front 335

diagnosis of rheumatic fever
Jones criteria
O

Back 335

O [imagine heart-shaped O] (carditis): inflammation of the heart muscle which can manifest as congestive heart failure

Front 336

diagnosis of rheumatic fever
Jones criteria
N

Back 336

Nodules (subcutaneous nodules - a form of Aschoff bodies): painless, firm collections of collagen fibers on the back of the wrist, the outside elbow, and the front of the knees.

Front 337

diagnosis of rheumatic fever
Jones criteria
E

Back 337

Erythema marginatum: a long lasting rash that begins on the trunk or arms as macules and spreads outward to form a snakelike ring while clearing in the middle. This rash never starts on the face and is made worse with heat.

Front 338

diagnosis of rheumatic fever
Jones criteria
S

Back 338

Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms.

Front 339

cause of Serous Pericarditis

Back 339

SLE, rheumatoid arthritis, infection, uremia.

Front 340

cause of Fibrinous Pericarditis

Back 340

Uremia, MI (Dressler's syndrome), rheumatic fever.

Front 341

cause of Hemorrhagic Pericarditis

Back 341

TB, malignancy (e.g., melanoma).

Front 342

Pericarditis
Clinical findings

Back 342

Findings: pericardial pain, friction rub, pulsus paradoxus, distant heart sounds.

Front 343

Pericarditis
ECG findings

Back 343

ECG changes (diffuse ST elevations in all leads),

Front 344

Pericarditis
course

Back 344

Can resolve without scarring or lead to chronic adhesive or chronic constrictive
pericarditis.

Front 345

Syphilitic heart
disease

Back 345

3° syphilis disrupts the vasa vasora of the aorta
with consequent dilation of the aorta and valve ring
Often affects the aortic root and calcification of
ascending arch of the aorta.

Front 346

disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring Often affects the aortic root and calcification of ascending arch of the aorta.

Back 346

3° syphilis

Front 347

Syphilitic heart disease
can result in

Back 347

aneurysm of the ascending aorta or aortic arch and aortic valve
incompetence.

Front 348

Syphilitic heart disease
wrt visualization

Back 348

May see calcification of the aortic root and ascending
aortic arch.

Front 349

Syphilitic heart disease
which stage of syphilis

Back 349

3° syphilis

Front 350

most common 1° cardiac tumor in adults

Back 350

Myxomas

Front 351

Myxomas
where are they and imps

Back 351

90% occur in the atria
(mostly LA). Myxomas are usually described as a “ball-valve” obstruction in the LA.

Front 352

“ball-valve” obstruction in the LA.

Back 352

Myxomas

Front 353

most frequent 1° cardiac tumor in children

Back 353

Rhabdomyomas

Front 354

Rhabdomyoma association

Back 354

associated with
tuberous sclerosis

Front 355

heart tumor associated with
tuberous sclerosis

Back 355

Rhabdomyomas

Front 356

most common heart tumor

Back 356

Metastases

Front 357

Kussmaul's sign

Back 357

observation of a jugular venous pressure (JVP, the filling of the jugular vein) that rises with inspiration

Front 358

Cardiac tumors
wrt special sign

Back 358

Kussmaul's sign

Front 359

observation of a jugular venous pressure (JVP, the filling of the jugular vein) that rises with inspiration

Back 359

Kussmaul's sign

Front 360

Adverse effects of
Antihypertensive drugs

Hydrochlorothiazide

Back 360

Hypokalemia,
hyperlipidemia,
hyperuricemia,
lassitude,
hypercalcemia,
hyperglycemia

Front 361

Adverse effects of
Antihypertensive drugs

Loop diuretics

Back 361

Potassium wasting,
metabolic alkalosis,
hypotension,
ototoxicity

Front 362

Adverse effects of
Antihypertensive drugs

Clonidine

Back 362

Dry mouth,
sedation,
severe rebound hypertension

Front 363

Adverse effects of
Antihypertensive drugs

Methyldopa

Back 363

Sedation,
positive Coombs’ test

Front 364

Adverse effects of
Antihypertensive drugs

Hexamethonium

Back 364

Severe orthostatic hypotension, blurred vision,
constipation,
sexual dysfunction

Front 365

Adverse effects of
Antihypertensive drugs

Reserpine

Back 365

Sedation,
depression,
nasal stuffiness,
diarrhea

Front 366

Adverse effects of
Antihypertensive drugs

Guanethidine

Back 366

Orthostatic and exercise hypotension,
sexual dysfunction,
diarrhea

Front 367

Adverse effects of
Antihypertensive drugs

Prazosin

Back 367

1st-dose orthostatic hypotension, dizziness,
headache

Front 368

Adverse effects of
Antihypertensive drugs

β-blockers

Back 368

Impotence,
asthma,
cardiovascular effects (bradycardia, CHF, AV block), CNS effects
(sedation, sleep alterations)

Front 369

Adverse effects of
Antihypertensive drugs

Hydralazine

Back 369

Nausea, headache,
lupus-like syndrome,
reflex tachycardia,
angina,
salt retention

Front 370

Adverse effects of
Antihypertensive drugs

Minoxidil

Back 370

Hypertrichosis,
pericardial effusion,
reflex tachycardia,
angina,
salt retention

Front 371

Adverse effects of
Antihypertensive drugs

Nifedipine,

Back 371

Dizziness,
flushing,
nausea

Front 372

Adverse effects of
Antihypertensive drugs

verapamil

Back 372

constipation
Dizziness,
flushing,
nausea

Front 373

Adverse effects of
Antihypertensive drugs

Nitroprusside

Back 373

Cyanide toxicity (releases CN)

Front 374

Adverse effects of
Antihypertensive drugs

ACE inhibitors

Back 374

Hyperkalemia,
Cough,
Angioedema,
Proteinuria,
Taste changes,
hypOtension,
Pregnancy problems (fetal renal damage),
Rash,
Increased renin, Lower
angiotensin II

Front 375

Adverse effects of
Antihypertensive drugs

Angiotensin II receptor Inhibitors

Back 375

Fetal renal toxicity, hyperkalemia

Front 376

Which Antihypertensive drug has this adverse effect

Hypokalemia

Back 376

Hydrochlorothiazide
and
Loop diuretics

Front 377

Which Antihypertensive drug has this adverse effect

ototoxicity

Back 377

Loop diuretics

Front 378

Which Antihypertensive drug has this adverse effect

Dry mouth, sedation, severe rebound hypertension

Back 378

Clonidine

Front 379

Which Antihypertensive drug has this adverse effect

positive Coombs’ test

Back 379

Methyldopa

Front 380

Which Antihypertensive drug has this adverse effect

Severe orthostatic hypotension, blurred vision

Back 380

Hexamethonium

Front 381

Which Antihypertensive drug has this adverse effect

Sedation, depression, nasal stuffiness

Back 381

Reserpine

Front 382

Which Antihypertensive drug has this adverse effect

lupus-like syndrome

Back 382

Hydralazine

Front 383

Which Antihypertensive drug has this adverse effect

Cyanide toxicity (releases CN)

Back 383

Nitroprusside

Front 384

Which Antihypertensive drug has this adverse effect

pericardial effusion

Back 384

Minoxidil

Front 385

Which Antihypertensive drug has this adverse effect

Pregnancy problems (fetal renal damage)

Back 385

ACE inhibitors
and
ARB's

Front 386

Which Antihypertensive drug has this adverse effect

Hyperkalemia, Cough

Back 386

ACE inhibitors

Front 387

Which Antihypertensive drug has this adverse effect

Increased renin, Lower
angiotensin II

Back 387

ACE inhibitors

Front 388

Which Antihypertensive drug has this adverse effect

hyperkalemia

Back 388

ACE inhibitors
and
ARB's

Front 389

Which Antihypertensive drug has this adverse effect

Taste changes

Back 389

ACE inhibitors

Front 390

Which antihypertensive agent

Use with β-blockers to prevent reflex tachycardia, diuretic to block salt retention.

Back 390

Hydralazine

Minoxidil

Front 391

special considerations for using

Hydralazine
or
Minoxidil

Back 391

Use with β-blockers to prevent reflex tachycardia, diuretic to block salt retention.

Front 392

Antihypertensive drugs
name the

Sympathoplegics

Back 392

Clonidine
Methyldopa
Hexamethonium
Reserpine
Guanethidine
Prazosin
β-blockers

Front 393

Antihypertensive drugs
name the

Vasodilators

Back 393

Hydralazine
Minoxidil
Nifedipine,
verapamil
Nitroprusside

Front 394

Antihypertensive drugs
name the

ACE inhibitors

Back 394

-pril's

Front 395

Antihypertensive drugs
name the

Angiotensin II receptor inhibitors

Back 395

-sartan's

Front 396

Hydralazine
Mechanism

Back 396

↑ cGMP →smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.

Front 397

Hydralazine
Clinical use

Back 397

Severe hypertension, CHF. First-line for HTN in pregnancy, with methyldopa.

Front 398

Hydralazine
Toxicity

Back 398

Compensatory tachycardia, fluid/salt retention. Lupus-like syndrome.

Front 399

Calcium channel blockers
names

Back 399

Nifedipine, verapamil, diltiazem.

Front 400

Calcium channel blockers
Mechanism

Back 400

Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Front 401

Calcium channel blockers
Clinical use

Back 401

Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.

Front 402

Calcium channel blockers
Toxicity

Back 402

Cardiac depression, peripheral edema, flushing, dizziness, and constipation.

Front 403

Calcium channel blockers
which one not to use for arrhythmias

Back 403

nifedipine

Front 404

Calcium channel blockers
relative effects on
Vascular smooth muscle
vs
Heart

Back 404

Vascular smooth muscle nifedipine > diltiazem > verapamil.

Heart– verapamil > diltiazem > nifedipine.

Front 405

Nitroglycerin, isosorbide dinitrate

Mechanism

Back 405

Vasodilate by releasing nitric oxide in smooth muscle, causing ↑ in cGMP and smooth
muscle relaxation. Dilate veins >> arteries. ↓ preload.

Front 406

Nitroglycerin, isosorbide dinitrate

Clinical use

Back 406

Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer.

Front 407

Nitroglycerin, isosorbide dinitrate

Toxicity

Back 407

Tachycardia,
hypotension, flushing,
headache,
“Monday disease” in industrial exposure/ development of tolerance

Front 408

“Monday disease”

Back 408

in industrial exposure,
development of tolerance for the vasodilating action during the work week and loss of
tolerance over the weekend, resulting in tachycardia, dizziness, and headache.

Front 409

Antianginal therapy
goals

Back 409

reduction of myocardial O2 consumption by decreasing 1 or more of the
determinants: end diastolic volume, blood pressure, heart rate, contractility,
ejection time.

Front 410

Calcium channel blocker
wrt
Antiangianl effects

Back 410

Nifedipine is similar to Nitrates in effect;

verapamil is
similar to β-blockers in effect.

Front 411

Cardiac glycosides
names

Back 411

Digoxin, ...

Front 412

Digoxin
pharmacokinetics

Back 412

75% bioavailability,
20–40% protein bound,
t1/2 = 40 hours, urinary excretion.

Front 413

Cardiac glycosides
Mechanism

Back 413

Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/
antiport. ↑ intracellular [Ca2+] → + ionotropy.

Front 414

Cardiac glycosides
Clinical use
and reasons

Back 414

CHF (↑ contractility);

atrial fibrillation (↓ conduction at AV node and depression of
SA node).

Front 415

Cardiac glycosides
Toxicity

Back 415

May cause ↑ PR, ↓ QT, scooping of ST segment, T-wave inversion of ECG. Also
↑ parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision ,
Arrhythmias

Front 416

Cardiac glycosides
Antidote

Back 416

Slowly normalize K+,
lidocaine,
cardiac pacer,
anti-dig Fab fragments.

Front 417

Digoxin
factors that affect its toxicities

Back 417

Toxicity of digoxin are ↑ by: renal failure (↓ excretion)
hypokalemia (potentiates drug’s effects),
quinidine (↓ digoxin clearance by displacing digoxin from tissue binding sites).

Front 418

Antiarrhythmics
Class I
mech and features

Back 418

Slow or block (↓) conduction (especially in depolarized cells). ↓ slope of phase 4 depolarization and ↑ threshold for firing in abnormal pacemaker cells.

Front 419

Antiarrhythmics
Class I
selectivity

Back 419

Are state dependent (selectively depress tissue that is frequently depolarized,
e.g., fast tachycardia).

Front 420

Antiarrhythmics
Class IA
names

Back 420

“Queen Amy Proclaims
Dis o' pyramid.”

Quinidine, Amiodarone, Procainamide, Disopyramide.

Front 421

Antiarrhythmics
Class IA
what they affect

Back 421

↑ AP duration, ↑ effective refractory period (ERP),
↑ QT interval.

Front 422

Antiarrhythmics
Class IA
used for

Back 422

Affect both atrial and ventricular arrhythmias especially reentrant and ectopic supraventricular and ventricular tachycardia.

Front 423

Antiarrhythmics
Class IA
toxicities
Quinidine

Back 423

cinchonism––headache,
tinnitus;
thrombocytopenia;
torsades de pointes due to ↑
QT interval)

Front 424

Antiarrhythmics
Class IA
toxicities
Procainamide

Back 424

reversible SLE-like
syndrome

Front 425

Cinchonism

Back 425

or quinism is a pathological condition in humans caused by an overdose of quinine or its natural source, cinchona bark

Front 426

a pathological condition in humans caused by an overdose of quinine or its natural source, cinchona bark

Back 426

cinchonism or quinism

Front 427

Which antiarrhythmic toxicity has

cinchonism––headache, tinnitus;
thrombocytopenia;

Back 427

Quinidine

Front 428

Which antiarrhythmic toxicity has

reversible SLE-like
syndrome

Back 428

Procainamide

Front 429

Antiarrhythmics
Class IB
names

Back 429

Lidy's Mexican Tacos

Lidocaine, mexiletine, tocainide

Front 430

Antiarrhythmics
Class IB
effect

Back 430

↓ AP duration.
Affect ischemic or depolarized Purkinje and
ventricular tissue.

Front 431

Antiarrhythmics
Class IB
uses

Back 431

Useful in acute ventricular
arrhythmias (especially post-MI) and in digitalis induced arrhythmias.

Front 432

Antiarrhythmics
Class IB
Toxicity

Back 432

local anesthetic.
CNS stimulation/depression,
cardiovascular depression.

Front 433

Antiarrhythmics
Class IC
Toxicity

Back 433

proarrhythmic, especially post-MI
(contraindicated).
Significantly prolongs
refractory period in AV node.

Front 434

Antiarrhythmics
Class IC
names

Back 434

Flecainide, encainide, propafenone.

Front 435

Antiarrhythmics
Class IC
effect

Back 435

No effect on
AP duration.

Front 436

Antiarrhythmics
Class IC
uses

Back 436

Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias.

Front 437

Antiarrhythmics
Class II
names

Back 437

β-blockers

Front 438

Antiarrhythmics
Class II
effects

Back 438

↓ cAMP, ↓ Ca2+ currents. Suppress abnormal pacemakers by ↓ slope of phase 4.
AV node particularly sensitive––↑ PR interval.

Front 439

Antiarrhythmics
Class II
Which is very short acting

Back 439

Esmolol

Front 440

Antiarrhythmics
Class II
toxicity in general

Back 440

Impotence, exacerbation of asthma, cardiovascular effects (bradycardia,
AV block,
CHF),
CNS effects (sedation, sleep alterations).
May mask the signs of hypoglycemia.

Front 441

Antiarrhythmics
Class II
toxicity of metoprolol

Back 441

can cause dyslipidemia.

Front 442

Antiarrhythmics
Class II
can cause dyslipidemia.

Back 442

metoprolol

Front 443

Antiarrhythmics
Class III
name them

Back 443

K+ channel blockers

Sotalol,
ibutilide,
bretylium,
amiodarone.

Front 444

Antiarrhythmics
Class III
mech

Back 444

↑ AP duration, ↑ ERP. Used when other
antiarrhythmics fail. ↑ QT interval.

Front 445

Antiarrhythmics
Class III
Toxicity
Sotalol

Back 445

Sotalol––torsades de pointes, excessive β block;

Front 446

Sotalol
which class of Antiarrhythmics

Back 446

Class III

Front 447

Antiarrhythmics
Class III
Toxicity
torsades de pointes

Back 447

Sotalol
and
ibutilide

Front 448

Antiarrhythmics
Class III
Toxicity
ibutilide

Back 448

torsades;

Front 449

Antiarrhythmics
Class III
Toxicity
bretylium

Back 449

hypotension
and
new arrhythmias

Front 450

Antiarrhythmics
Class III
Toxicity
hypotension and new arrhythmias

Back 450

bretylium

Front 451

Antiarrhythmics
Class III
Toxicity
pulmonary fibrosis

Back 451

amiodarone

Front 452

Antiarrhythmics
Class III
Toxicity
amiodarone

Back 452

pulmonary fibrosis,
corneal deposits, hepatotoxicity,
skin deposits resulting in photodermatitis, neurologic effects,
constipation, cardiovascular effects (bradycardia,
heart block, CHF), hypothyroidism/
hyperthyroidism.

Front 453

Antiarrhythmics
Class III
Toxicity
hypothyroidism/
hyperthyroidism.

Back 453

amiodarone

Front 454

Antiarrhythmics
Class III
Toxicity
corneal deposits

Back 454

amiodarone

Front 455

Antiarrhythmics
Class III
Toxicity
skin deposits

Back 455

amiodarone

Front 456

What to check when using amiodarone

Back 456

P(pulmonary)FTs,
LFTs, and TFTs when

Front 457

Amiodarone is safe to use in
????? syndrome.

Back 457

Wolff-Parkinson-White

Front 458

??????is safe to use in
Wolff-Parkinson-White
syndrome.

Back 458

Amiodarone

Front 459

Antiarrhythmics
Class IV
names

Back 459

Verapamil, diltiazem. bepridil

Front 460

Antiarrhythmics
Class IV
Mechanism

Back 460

Primarily affect AV nodal cells. ↓ conduction velocity, ↑ ERP, ↑ PR interval.

Front 461

Antiarrhythmics
Class IV
uses

Back 461

prevention of nodal arrhythmias (e.g., SVT).

Front 462

Antiarrhythmics
Class IV
toxicity

Back 462

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression);

torsades de pointes (bepridil).

Front 463

Antiarrhythmics
misc
names

Back 463

Adenosine
K+
Mg+
Digoxin

Front 464

misc antiarrhythmics
Adenosine

Back 464

Drug of choice in diagnosing/abolishing AV nodal arrhythmias.

Front 465

misc antiarrhythmics
K+

Back 465

Depresses ectopic pacemakers, especially in digoxin toxicity.

Front 466

misc antiarrhythmics
Mg+

Back 466

Effective in torsades de pointes and digoxin toxicity.

Front 467

Effective in torsades de pointes and digoxin toxicity.

Back 467

Mg+sulfate

Front 468

Drug of choice in diagnosing and abolishing AV nodal arrhythmias.

Back 468

Adenosine