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468 Cards in this Set

  • Front
  • Back
Pregnant woman in 3rd trimester
has normal blood pressure when
standing and sitting. When supine,
blood pressure drops to 90/50.
Compression of the IVC.
35-year-old man has high blood
pressure in his arms and low
pressure in his legs.
Coarctation of the aorta.
5-year-old boy presents with
systolic murmur and wide,
fixed split S2.
ASD.
 During a game, a young
football player collapses and
dies immediately.
Hypertrophic cardiomyopathy.
Patient has a stroke after
incurring multiple long bone
fractures in trauma stemming
from a motor vehicle accident.
Fat emboli.
Elderly woman presents with a
headache and jaw pain. Labs
show elevated ESR.
Temporal arteritis.
80-year-old man presents with a
systolic crescendo-decrescendo
murmur.
Aortic stenosis.
Man starts a medication for
hyperlipidemia. He then
develops a rash, pruritus, and
GI upset.
Niacin.
Patient develops a cough and
must discontinue captopril.
name good altenatives
Losartan, an angiotensin II
receptor antagonist, does not ↑
bradykinin as captopril does.
Carotid sheath structures
3 structures inside: VAN.
1. Internal jugular Vein (lateral)
2. Common carotid Artery (medial)
3. Vagus Nerve (posterior)
location of
Internal jugular Vein (lateral)
Common carotid Artery (medial)
Vagus Nerve (posterior)
Carotid sheath
In the majority of cases, the SA
and AV nodes are supplied
by
the RCA.
what supplies
the inferior portion of the
left ventricle
80% of the time the RCA supplies
via the PD
= right dominant).
Coronary artery
names
Acute marginal artery
Left main coronary artery (LCA)
Circumflex artery (CFX)
Left anterior
descending
artery (LAD)
Posterior descending artery (PD)
Right coronary
artery (RCA)
artery (= right dominant).
Coronary artery occlusion
occurs most commonly
in and supplies what?
the LAD, which supplies
the anterior interventricular
septum.
The most posterior part of the
heart is what and implications
left atrium;
enlargement can cause
dysphagia.
Where to listen to the Heart
APTM
aortic: Right 2ndICS
Pulmonic:left 2ndICS
Tricuspid: left 4th ICS
Mitral: left 5th ICS lateral to left midclavicular line
What is heard best at
Aortic area:
Systolic murmur
• Aortic stenosis
• Flow murmur
What is heard best at
Left sternal border:
Diastolic murmur
• Aortic regurgitation
• Pulmonic regurgiation
What is heard best at
Pulmonic area:
Diastolic murmur
• Pulmonic stenosis
• Flow murmur
What is heard best at
Tricuspid area:
Pansystolic murmur
• Tricuspid regurgitation
• Ventricular septal defect
Diastolic murmur
• Tricuspid stenosis
• Atrial septal defect
What is heard best at
Mitral area:
Systolic murmur
• Mitral regurgitation
Diastolic murmur
• Mitrial stenosis
Cardiac output (CO)=
= (stroke volume) × (heart rate).
CO in During exercise, CO ↑
initially as a result of an
↑ in SV. After prolonged
exercise, CO ↑ as a result
of an ↑ in HR.
CO ↑
initially as a result of an
↑ in SV. After prolonged
exercise, CO ↑ as a result
of an ↑ in HR.
fick principle
CO = rate of O2 consumption/
(arterial O2 content-venous O2 content)
Mean arterial pressure =
= (cardiac output) × (total peripheral resistance)
MAP = (co) × (TPR)

MAP = 2/3 diastolic + 1/3 systolic
Pulse pressure =
systolic - diastolic

and is proportional to SV
equation for SV
=CO/HR

also

=EDV-ESV
Stroke Volume affected by
SV CAP.
Stroke Volume affected by Contractility, Afterload,
and Preload. ↑ SV when ↑ preload, ↓ afterload,
or ↑ contractility.
Contractility (and SV) ↑ with:
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.
Contractility (and SV) ↓ with:
1. β1 blockade
2. Heart failure
3. Acidosis
4. Hypoxia/hypercapnea
5. Ca2+ channel blockers
Myocardial O2 demand is ↑ by:
1. ↑ afterload (∝
diastolic BP)
2.↑ contractility
3. ↑ heart rate
4. ↑ heart size (↑ wall
tension)
Preload and
afterload
aka's
Preload = ventricular EDV.
Afterload = diastolic arterial pressure
aka ventricular EDV.
Preload
aka diastolic arterial pressure
Afterload
Preload and afterload
wrt dilators
Venous dilators (e.g., nitroglycerin) ↓ preload.


Vasodilators (e.g., hydralazine) ↓ afterload.
Preload increases with (3 things)
Preload ↑ with exercise
(slightly), ↑ blood volume
(overtransfusion), and
excitement (sympathetics).
Preload pumps up the heart.
Starling curve
Force of contraction is proportional to
initial length of cardiac muscle fiber (preload).
CONTRACTILE STATE OF MYOCARDIUM
+
-Circulating catecholamines

-Digitalis

-Sympathetic stimulation
CONTRACTILE STATE OF MYOCARDIUM
-Pharmacologic depressants


-Loss of myocardium (MI)
Ejection fraction (EF)
equation and description
EF = SV/EDV = (EDV – ESV)/EDV

EF is an index of ventricular contractility.
EF is normally
≥ 55%.
Resistance,
pressure, flow
∆P =
Q × R
Resistance =
P/Q

or

8n(viscosity)(length)/(Pi)(R^4)
Viscosity depends mostly on
hematocrit.
Viscosity ↑ in:
1. Polycythemia
2. Hyperproteinemic states (e.g., multiple myeloma)
3. Hereditary spherocytosis
what vessels account for most of
total peripheral resistance
and how
Arterioles
→ regulate capillary flow.
Phases–left ventricle:
Isovolumetric contraction––
period
between mitral valve closure and
aortic valve opening; period of
highest O2 consumption
Phases–left ventricle:
period of
highest O2 consumption
Isovolumetric contraction––
Phases–left ventricle:
Systolic ejection–
period between
aortic valve opening and closing
Phases–left ventricle:
Isovolumetric relaxation
––period
between aortic valve closing and
mitral valve opening
Phases–left ventricle:
Rapid filling––
period just after
mitral valve opening
Phases–left ventricle:
Slow filling
––period just before
mitral valve closure
Phases–left ventricle: in order
1. Isovolumetric contraction


2. Systolic ejection

3. Isovolumetric relaxation


4. Rapid filling

5. Slow filling
heart sound events
S1
S2
S3
S4
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.
S3 is associated with
dilated CHF.
Heart sound associated with dilated CHF.
S3
Heart sound associated with (“atrial kick”)
S4 (“atrial kick”)
S4 (“atrial kick”)
is associated with
a hypertrophic ventricle
Heart sound associated with
hypertrophic ventricle.
S4 (“atrial kick”)
a wave=
a wave––atrial contraction.
c wave=
c wave––RV contraction (tricuspid valve
bulging into atrium).
v wave=
v wave–– ↑ atrial pressure due to
filling against closed tricuspid valve.
Normal S2 spliting
S2 splitting: aortic valve closes before
pulmonic;
S1...A2.P2
inspiration ↑ this
difference.
s1...A2..P2
Wide splitting (associated with
Pulmonic stenosis
S1....A2(more time)P2
Fixed splitting (associated with
ASD

no change on inspiration
Paradoxical splitting (associated with
Aortic stenosis
S1...P2...A2 on expire
S1...P2.A2
Cardiac muscle contraction is dependent on what Ion
extracellular calcium,
Cardiac muscle contraction is dependent on ?????? which enters the
cells during ?????? action potential and stimulates ???????from the cardiac
muscle ??????(?????????).
extracellular calcium,

plateau of

calcium release

sarcoplasmic reticulum

calcium-induced calcium release
Cardiac myocyte physiology in contrast to skeletal muscle

WRT Plateau
Cardiac muscle action potential has a plateau, which is due to Ca2+ influx
Cardiac myocyte physiology in contrast to skeletal muscle

WRT sponienaity
Cardiac nodal cells spontaneously depolarize, resulting in automaticity
Cardiac myocyte physiology in contrast to skeletal muscle

WRT coupling
Cardiac myocytes are electrically coupled to each other by gap junctions
Name 3 features of Cardiac myocyte physiology that contrast skeletal muscle
1. has a plateau

2. spontaneous depolarize/automaticity

3.coupled to each other by gap junctions
Myocardial action potential

Which cells
Occurs in atrial and ventricular myocytes and Purkinje fibers.
Myocardial action potential

Phase 0
rapid upstroke––voltage-gated Na+ channels open.
Myocardial action potential

Phase 1
initial repolarization with inactivation of voltage-gated Na channels. Voltage-gated K+ channels begin to open.
Myocardial action potential

Phase 2
plateau––Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.
Myocardial action potential

Phase 3
rapid repolarization––massive K+ efflux due to opening of voltage- gated slow K+ channels and closure of voltage-gated Ca2+ channels.
Myocardial action potential

Phase 4
resting potential––high K+ permeability through K+ channels.
Pacemaker action potential

Which cells
Occurs in the SA and AV nodes
Pacemaker action potential

Phase 0
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.
Pacemaker action potential

Phase 2
plateau is absent.
Pacemaker action potential

Phase 3
Inactivation of the Ca2+ channels and increase activation of the K+ channels leading to increased K+
Pacemaker action potential

Phase 4
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.
Pacemaker action potential

what determines heart rate
The slope of phase 4 in the SA node determines heart rate
Pacemaker action potential

effect of neurotransmitters on heart rate
ACh ↓ the rate of diastolic depolarization and ↓ heart rate, while catecholamines ↑ epolariza-
tion and ↑ heart rate.
Pacemaker action potential

which phase shows effect of neurotransmitters on heart rate
Phase 4
Pacemaker action potential which phase does not exist
Phase 1(initial repolarization) and 2 (plateau)
ECG what is represented by the

P wave
atrial depolarization.
ECG what is represented by the

PR segment
conduction delay through AV node (normally < 200 msec).
ECG what is represented by the

QRS complex
ventricular depolarization (normally < 120 msec).
ECG what is represented by the

QT interval
mechanical contraction of the ventricles.
ECG what is represented by the

masked by QRS complex.
Atrial repolarization
ECG what is represented by the

T wave
ventricular repolarization.
ECG what is represented by the

ST segment
––isoelectric, ventricles depolarized
ECG what is represented by the

U wave
––caused by hypokalemia.
ECG normal timing of

QRS complex
(normally < 120 msec).
ECG normal timing of

PR segment
(normally < 200 msec).
Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.
Torsades des pointes
describe Torsades des pointes
Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.
Torsades des pointes complications
Can progress to V-fib
causes of Torsades des pointes
Anything that prolongs the QT interval
Anything that prolongs the QT interval can predispose to
Torsades des pointes
describe Wolff-Parkinson-White syndrome
Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node.
Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node.
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome
name the accesory path
bundle of Kent
Wolff-Parkinson-White syndrome
on ECG and why
characteristic delta wave on ECG

due to ventricles begin to partially depolarize earlier,
characteristic delta wave on ECG
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White syndrome
complications
May result in reentry current leading to supraventricular tachycardia.
Describe this ECG

Atrial fibrillation
Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between
irregularly spaced QRS complexes.
Describe this ECG

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

AV block
1st degree
The PR interval is prolonged (> 200 msec). Asymptomatic.
Describe this ECG

AV block
2nd degree
Mobitz type I
Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Usually asymptomatic.
Describe this ECG

AV block
2nd degree
Mobitz type II
Dropped beats that are not preceded by a change in the length of the PR interval
Describe this ECG

AV block
3rd degree
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.
Describe this ECG

Ventricular fibrillation
A completely erratic rhythm with no identifiable waves.
ID the ECG

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between
irregularly spaced QRS complexes.
Atrial fibrillation
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.
Atrial flutter
ID the ECG

The PR interval is prolonged (> 200 msec). Asymptomatic.
AV block
1st degree
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.
2nd degree
Mobitz type I
(Wenckebach)
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.
2nd degree
Mobitz type II
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.
3rd degree
(complete)
ID the ECG

A completely erratic rhythm with no identifiable waves.
Ventricular
fibrillation
Wenckebach aka
2nd degree
Mobitz type I
2nd degree Mobitz type I
aka
Wenckebach
Tx for Atrial fibrillation
Anticoagulation
Tx for AV node Block 3rd degree
Usually treat with pacemaker.
Tx for Ventricular fibrillation
immediate CPR and defibrillation.
In AV node block 3rd degree (complete)

which is faster
The atrial rate is faster than the ventricular rate. i.e P waves are faster than QRS
Control of mean arterial pressure

↑ SYMPATHETIC ACTIVITY at receptors
β1 (↑ heart rate, ↑ contractility)— ↑ CO

α1 (venoconstriction: ↑ venous return)—↑ CO

α1 (arteriolar vasoconstriction)— ↑ TPR
Control of mean arterial pressure

Medullary vasomotor center senses ↓ baroreceptor firing leads to
↑ SYMPATHETIC ACTIVITY
Control of mean arterial pressure

JGA senses ↓ MAP leads to
↑ RENIN-ANGIOTENSIN SYSTEM
Control of mean arterial pressure

↑ RENIN-ANGIOTENSIN SYSTEM leads to
Angiotensin II vasoconstriction)— ↑ TPR

Aldosterone (↑ blood volume)—↑ CO
Baroreceptors

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

medulla

only to ↑ BP
Baroreceptors

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

medulla

↓ and ↑ in BP
Baroreceptors mech in Hypotension
and when is it important
↓ arterial pressure →↓ stretch →↓ afferent baroreceptor firing →↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation →vasoconstriction, ↑ HR, ↑ contractility, ↑ BP. Important in the response to severe hemorrhage.
Carotid massage
↑ pressure on carotid artery →↑ stretch →↓ HR.
peripheral chemoreceptors

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

what they respond to
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.
central chemoreceptors

wrt a specific reaction
name it and describe it
Cushing reaction:
response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).
Cushing reaction
response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).
response to cerebral ischemia, due to ↑ intracranial
pressure:

hypertension (sympathetic response via peripheral vasoconstriction) and bradycardia (parasympathetic
response via vaso-vagal response).
Cushing reaction
Circulation through organs

Largest share of systemic cardiac output.
Liver
Circulation through organs

Highest blood flow per gram of tissue.
Kidney
Circulation through organs

Large arteriovenous O2 difference. ↑ O2 demand is met by ↑ coronary blood flow, not by
↑ extraction of O2.
Heart
Circulation through organs
features of the Heart
Large arteriovenous O2 difference. ↑ O2 demand is met by ↑ coronary blood flow, not by
↑ extraction of O2.
Heart ↑ O2 demand is met by
↑ coronary blood flow, not by
↑ extraction of O2.
PCWP

what and why
pulmonary capillary
wedge pressure (in mmHg)
is a good approximation of
left atrial pressure.
Swan-Ganz catheter.
measures pulmonary capillary
wedge pressure
how to measure pulmonary capillary
wedge pressure
Swan-Ganz catheter.
the pulmonary vasculature is unique in that hypoxia causes
vasoconstriction (in other organs hypoxia causes vasodilation).
the ????????? is unique in that hypoxia causes vasoconstriction
pulmonary vasculature
Autoregulation of blood flow

Heart
Local metabolites: O2, adenosine, NO
Autoregulation of blood flow

Brain
Local metabolites: CO2
(pH)
Autoregulation of blood flow

Kidneys
Myogenic and tubuloglomerular feedback
Autoregulation of blood flow

Lungs
Hypoxia causes vasoconstriction
Autoregulation of blood flow

Skeletal muscle
Local metabolites: lactate, adenosine, K+
Autoregulation of blood flow

Skin
Sympathetic stimulation most important
mechanism––temperature control
Name the strucure where blod flow is controlled by

Local metabolites: O2, adenosine, NO
Heart
Name the strucure where blod flow is controlled by

Local metabolites: CO2
(pH)
Brain
Name the strucure where blod flow is controlled by

Myogenic and tubuloglomerular feedback
Kidneys
Name the strucure where blod flow is controlled by

Hypoxia causes vasoconstriction
Lungs
Name the strucure where blod flow is controlled by

Local metabolites: lactate, adenosine, K+
Skeletal muscle
Name the strucure where blod flow is controlled by

Sympathetic stimulation most important
mechanism––temperature control
Skin
4 Starling forces determine fluid movement through capillary membranes:
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
Thus, net filtration pressure =
P = [(Pc − Pi ) − (πc −πi )].
Capillary fluid exchange

Kf=
filtration constant (capillary permeability).
Capillary fluid exchange

Net fluid flow =
(Pnet)X(Kf)
4 causes of Edema with mechs
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)
early cyanosis
Right-to-left shunts “blue babies”

The 3 T’s:
Tetralogy
Transposition
Truncus
late cyanosis
Left-to-right shunts “blue kids”

1. VSD
2. ASD
3. PDA
Freq of Left-to-right shunts
VSD > ASD > PDA.
Left-to-right shunts
complications
↑ pulmonary resistance due
to arteriolar thickening.
→ progressive pulmonary
hypertension; leading to R → L shunt (Eisenmenger’s).
Eisenmenger’s
syndrome
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
Tetralogy of Fallot
why do kids squat
to ↑ systemic vascular resistance and thereby reduce the R-L shunting
Tetralogy of Fallot
4 characteristics
1. Pulmonary stenosis

2. RVH

3. Overriding aorta (overrides the VSD)

4. VSD
Eisenmenger’s syndrome
2 "other" complications
(clubbing and polycythemia).
Tetralogy of Fallot most important determinant for prognosis
Pulmonary stenosis
Tetralogy of Fallot is caused by
anterosuperior displacement of the infundibular septum.
Tetralogy of Fallot CXR
boot-shaped heart due to RVH.
Transposition of great vessels
how can they live
VSD,
PDA,
patent foramen ovale
Transposition of great vessels is due to
failure of the aorticopulmonary septum to spiral.
Transposition of great vessels
course
Without surgical correction, most infants die within the first few months of life.
Coarctation of aorta

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

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

Adult type/postductal
Coarctation of aorta

who?
Male-to-female ratio 3:1.
Coarctation of aorta

Dx
weak femoral pulses on
physical exam.
Coarctation of aorta

mnemonic
INfantile: IN close to
the heart.

ADult: Distal to Ductus.
??????? is used to close a
PDA. ??????is used to keep a
PDA open, which may be
Indomethacin

PGE
Patent ductus arteriosus

what keeps it open in the body
PGE synthesis and low O2 tension.
continuous, “machine-like” murmur
PDA
Congenital cardiac defect associations

22q11 syndromes
Truncus arteriosus, tetralogy
of Fallot
Congenital cardiac defect associations

Down syndrome
ASD, VSD
Congenital cardiac defect associations

Congenital rubella
Septal defects, PDA
Congenital cardiac defect associations

Turner’s syndrome
Coarctation of aorta
Congenital cardiac defect associations

Marfan’s syndrome
Aortic insufficiency
Congenital cardiac defect associations

Offspring of diabetic mother
Transposition of great vessels
Congenital cardiac defect associations

Truncus arteriosus, tetralogy
of Fallot
22q11 syndromes
Congenital cardiac defect associations

ASD, VSD
Down syndrome
Congenital cardiac defect associations

Septal defects, PDA
Congenital rubella
Congenital cardiac defect associations

Aortic insufficiency
Marfan’s syndrome
Congenital cardiac defect associations

Coarctation of aorta
Turner’s syndrome
Congenital cardiac defect associations

Transposition of great vessels
Offspring of diabetic mother
Hypertension Defined as
BP ≥ 140/90.
Hypertension
Risk factors
↑ age, obesity, diabetes, smoking, genetics, black > white > Asian.
Hypertension
types
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
Hypertension
Predisposes to
Atherosclerosis,
stroke,
CHF,
renal failure,
retinopathy,
aortic dissection.
Atheromata
Plaques in blood vessel walls.
Plaques in blood vessel walls.
Atheromata
Xanthoma
Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the
eyelids.
Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the
eyelids.
Xanthoma
Tendinous xanthoma
Lipid deposit in tendon, especially Achilles.
Lipid deposit in tendon, especially Achilles.
Tendinous xanthoma
Corneal arcus
Lipid deposit in cornea, nonspecific (arcus senilis).
Lipid deposit in cornea, nonspecific (arcus senilis).
Corneal arcus
Mönckeberg
Calcification of the arteries, especially radial or ulnar. Usually benign; "pipestem
arteries."
Calcification of the arteries, especially radial or ulnar. Usually benign; "pipestem
arteries."
Mönckeberg
Arteriolosclerosis
Hyaline thickening of small arteries in essential hypertension. Hyperplastic “onion
skinning” in malignant hypertension.
Hyaline thickening of small arteries in essential hypertension. Hyperplastic “onion
skinning” in malignant hypertension.
Arteriolosclerosis
Atherosclerosis
Fibrous plaques and atheromas form in intima of arteries.
Fibrous plaques and atheromas form in intima of arteries.
Atherosclerosis
Atherosclerosis
which arteries
Disease of elastic arteries and large and medium-sized muscular arteries
Atherosclerosis

Risk factors
Smoking,
hypertension,
diabetes mellitus, hyperlipidemia,
family history.
Atherosclerosis

Progression
Fatty streaks → proliferative plaque → complex atheromas.
Atherosclerosis

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

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

Symptoms
Angina, claudication, but can be asymptomatic.
Ischemic heart disease
Possible manifestations:
1. Angina
2. Myocardial infarction
3. Sudden cardiac death
4. Chronic ischemic heart disease
when does Angina occur
(CAD narrowing > 75%):
Angina
types and features
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)
which Angina
occurs at rest 2° to coronary artery spasm
Prinzmetal’s varian
which Angina
mostly 2° to atherosclerosis
Stable
which Angina
thrombosis but no necrosis
Unstable/crescendo
most often cause of MI
most often acute thrombosis from coronary artery atherosclerosis.
Sudden cardiac death most common cause
lethal arrhythmia
What is Sudden cardiac death
death from cardiac causes within 1 hour of onset of
symptoms
what is Chronic ischemic heart disease
progressive onset of CHF over many years due to chronic ischemic myocardial damage
Red (hemorrhagic) infarcts occur in
loose tissues with collaterals, such as lungs, liver, intestine, or following reperfusion.
Pale infarcts occur in
solid tissues with single blood
supply, such as brain, heart, kidney, and spleen.
Coronary artery occlusion frequency
LAD > RCA > circumflex.
MI symptoms
Diaphoresis,
nausea and vomiting,
severe retrosternal pain,
pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms
MI markers

Cardiac troponin I rises
after 4 hours
peaks at 24
and is elevated
for 7–10 days;
MI markers

more specific than other protein
markers.
Cardiac troponin I
MI markers

rises after 4 hours and is elevate
for 7–10 days;
Cardiac troponin I
MI markers

CK-MB rises
4-8 hours
peaks at 24
gone in 2-3 days
MI markers

predominantly found in myocardium but
can also be released from skeletal muscle
CK-MB
MI markers

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

AST rises
by 18 hours
peaks at
1.5 days
MI markers

LDH rises
in 10 hours

peaks at 2-3 days

gone in 7
Diagnosis of MI In the first 6 hours, ?????? is the gold standard.
ECG i
Diagnosis of MI wrt ECG
changes can include:
ST elevation (transmural
infarct),

ST depression (subendocardial infarct),

pathological Q waves (transmural infarct).
MI complications

Cardiac arrhythmia
important cause of death before reaching hospital; common in
first few days
MI complications

Aneurysm formation
↓ CO, risk of arrhythmia, embolus from mural thrombus
MI complications

Fibrinous pericarditis
friction rub (3–5 days post-MI)
Dressler’s syndrome
autoimmune phenomenon resulting in fibrinous pericarditis
(several weeks post-MI)
autoimmune phenomenon resulting in fibrinous pericarditis
(several weeks post-MI)
Dressler’s syndrome
friction rub (3–5 days post-MI)
Fibrinous pericarditi
4–10 days post–MI; can lead to cardiac tamponade.
Rupture
Most common cardiomyopathy (90% of cases).
Dilated (congestive)
cardiomyopathy
Dilated cardiomyopathy
causes
chronic Alcohol abuse,
Beriberi,
Coxsackie B virus myocarditis, chronic Cocaine use,
Chagas’ disease,
Doxorubicin toxicity, peripartum cardiomyopathy.
Dilated cardiomyopathy CXR
Heart dilates and looks like a balloon on
chest x-ray.
Dilated cardiomyopathy what type of dysfunction
Systolic dysfunction ensues.
Hypertrophic cardiomyopathy what type of dysfunction
Diastolic dysfunction ensues.
Cause of sudden death in young athletes.
Hypertrophic cardiomyopathy
Hypertrophy often asymmetric and involving the intraventricular septum. Normal heart size.
Hypertrophic cardiomyopathy
describe Hypertrophic cardiomyopathy
Hypertrophy often asymmetric and involving the intraventricular septum. Normal heart size.
Hypertrophic cardiomyopathy CXR
Normal heart size.
Hypertrophic cardiomyopathy causes
50% of cases are familial, autosomal dominant.
Hypertrophic cardiomyopathy
Dx
Findings: loud S4, apical impulses, systolic
murmur.
Hypertrophic cardiomyopathy
Tx
Treat with β-blocker. and/or Surgical septal myectomy
causes of Restrictive/obliterative
cardiomyopathy
sarcoidosis,
amyloidosis,
postradiation fibrosis, endocardial fibroelastosis,
endomyocardial fibrosis (Löffler’s),
hemochromatosis (dilated cardiomyopathy can also occur).
Heart sounds

Holosystolic high-pitched “blowing murmur.” Loudest at apex.
Mitral regurgitation
Heart sounds

Mitral regurgitation
Holosystolic high-pitched “blowing murmur.” Loudest at apex.
Heart sounds

Crescendo-decrescendo systolic ejection murmur
Aortic stenosis
Heart sounds

LV >> aortic pressure during systole
Aortic stenosis
Heart sounds

“Pulsus parvus et tardus”
pulses weak compared
to heart sounds.
aortic stenosis
Heart sounds

Holosystolic murmur.
VSD
Heart sounds

Late systolic murmur with midsystolic click.
Mitral prolapse
Heart sounds

Most frequent valvular lesion.
Mitral prolapse
Heart sounds

Immediate high-pitched “blowing” diastolic murmur. Wide pulse
pressure.
Aortic regurgitation
Heart sounds

Follows opening snap. Delayed rumbling late diastolic murmur.
Mitral stenosis
Heart sounds

LA >> LV pressure during diastole.
Mitral stenosis
Heart sounds

Mitral vs Tricuspid stenosis
Tricuspid stenosis differs because
it gets louder with inspiration.
Heart sounds

PDA
Continuous machine-like murmur. Loudest at time of S2.
Heart sounds

Continuous machine-like murmur. Loudest at time of S2.
PDA
CHF what is the cause of

Dyspnea on exertion
Failure of LV output to ↑
during exercise.
CHF what is the cause of

Cardiac dilation
Greater ventricular end-diastolic
volume.
CHF what is the cause of

Pulmonary edema, paroxysmal
nocturnal dyspnea
LV failure →↑ pulmonary
venous pressure → pulmonary venous distention and transudation of fluid.
CHF what is the cause of

Orthopnea
↑ venous return in supine
position exacerbates pulmonary
vascular congestion.
CHF what is the cause of

Hepatomegaly
(nutmeg liver)
↑ central venous pressure
→↑ resistance to portal flow.
Rarely, leads to “cardiac
cirrhosis.”
CHF what is the cause of

Ankle, sacral edema
RV failure →↑ venous pressure
→ fluid transudation.
CHF what is the cause of

Jugular venous
distention
R heart failure →↑ venous pressure.
hemosiderin-laden
macrophages (“heart failure”
cells).
(“heart failure”
cells).
“heart failure” cells
hemosiderin-laden
macrophages
Embolus types
An embolus moves like a FAT
BAT.
Fat,
Air,
Thrombus,
Bacteria,
Amniotic fluid,
Tumor.
Fat emboli are associated with
acute long bone fractures and liposuction.
Amniotic fluid emboli can lead to
DIC,
Pulmonary embolus clinical findings
chest pain, tachypnea,
dyspnea.
Virchow’s triad:
1. Stasis
2. Hypercoagulability
3. Endothelial damage
Cardiac tamponade
Compression of heart by fluid (i.e., blood) in pericardium, leading to ↓ CO.
Compression of heart by fluid (i.e., blood) in pericardium, leading to ↓ CO.
Cardiac tamponade
Cardiac tamponade and pressure changes
Equilibration of diastolic pressures in all 4 chambers of the heart with intrapericardial pressure
Cardiac tamponade
clinical findings
hypotension,
↑ venous pressure (JVD),
distant heart sounds,
↑ HR,
pulsus paradoxus;
pulsus paradoxus
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
Cardiac tamponade
ECG findings
ECG shows electrical alternans (beat-to-beat alterations of QRS
complex height).
what are ECG electrical alternans and what do they mean
beat-to-beat alterations of QRS
complex height

Cardiac tamponade
Osler’s nodes
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.
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.
Osler’s nodes
Bacterial endocarditis
clinical findings
Bacteria FROM JANE
Fever
Roth’s spots
Osler’s nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli
Roth's spots
retinal hemorrhages with white or pale centers composed of coagulated fibrin. immune complex mediated vasculitis often resulting from bacterial endocarditis
retinal hemorrhages with white or pale centers composed of coagulated fibrin immune complex mediated vasculitis often resulting from bacterial endocarditis
Roth's spots
Janeway lesions
what
who
mech
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.
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.
Janeway lesions
Bacterial endocarditis

most common valve
Mitral
Bacterial endocarditis

most common valve in IVDA
Tricuspid
Bacterial endocarditis

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

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

Sequela of dental procedures
subacute - viridans streptococcus
Bacterial endocarditis

complications
chordae rupture,
glomerulonephritis,
suppurative pericarditis,
emboli.
Endocarditis may also be nonbacterial 2° to
metastasis or renal failure (marantic/thrombotic endocarditis).
Libman-Sacks
endocarditis
Vegetations develop on both sides of valve (→ mitral valve stenosis) but do not embolize. Seen in lupus.
Vegetations develop on both sides of valve (→ mitral valve stenosis) but do not embolize. Seen in lupus.
Libman-Sacks
endocarditis
endocarditis seen in Lupus
Libman-Sacks
-- SLE causes LSE.
Rheumatic fever is a consequence of
pharyngeal infection with group A β-hemolytic strep
Rheumatic fever
early cause of death
Early deaths due to myocarditis.
rheumatic heart disease
affects which heart valves
––mitral > aortic >>
tricuspid (high-pressure valves affected most).
Rheumatic heart disease
Micro
Associated with Aschoff bodies (granuloma with giant cells),

Anitschkow's cells (activated
histiocytes),
What are Aschoff bodies
granuloma with giant cells
What are Anitschkow's cells
activated histiocytes
Jones criteria
diagnosis of rheumatic fever

# Joints (Migratory polyarthritis):

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


# Erythema marginatum

# Sydenham's chorea (St. Vitus' dance)
diagnosis of rheumatic fever
Jones criteria

# Joints (Migratory polyarthritis):

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


# Erythema marginatum

# Sydenham's chorea (St. Vitus' dance)
diagnosis of rheumatic fever
lab test
ESR ↑

elevated ASO titers.
diagnosis of rheumatic fever
Jones criteria
J
Joints (Migratory polyarthritis): a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
diagnosis of rheumatic fever
Jones criteria
O
O [imagine heart-shaped O] (carditis): inflammation of the heart muscle which can manifest as congestive heart failure
diagnosis of rheumatic fever
Jones criteria
N
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.
diagnosis of rheumatic fever
Jones criteria
E
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.
diagnosis of rheumatic fever
Jones criteria
S
Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms.
cause of Serous Pericarditis
SLE, rheumatoid arthritis, infection, uremia.
cause of Fibrinous Pericarditis
Uremia, MI (Dressler's syndrome), rheumatic fever.
cause of Hemorrhagic Pericarditis
TB, malignancy (e.g., melanoma).
Pericarditis
Clinical findings
Findings: pericardial pain, friction rub, pulsus paradoxus, distant heart sounds.
Pericarditis
ECG findings
ECG changes (diffuse ST elevations in all leads),
Pericarditis
course
Can resolve without scarring or lead to chronic adhesive or chronic constrictive
pericarditis.
Syphilitic heart
disease
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.
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.
3° syphilis
Syphilitic heart disease
can result in
aneurysm of the ascending aorta or aortic arch and aortic valve
incompetence.
Syphilitic heart disease
wrt visualization
May see calcification of the aortic root and ascending
aortic arch.
Syphilitic heart disease
which stage of syphilis
3° syphilis
most common 1° cardiac tumor in adults
Myxomas
Myxomas
where are they and imps
90% occur in the atria
(mostly LA). Myxomas are usually described as a “ball-valve” obstruction in the LA.
“ball-valve” obstruction in the LA.
Myxomas
most frequent 1° cardiac tumor in children
Rhabdomyomas
Rhabdomyoma association
associated with
tuberous sclerosis
heart tumor associated with
tuberous sclerosis
Rhabdomyomas
most common heart tumor
Metastases
Kussmaul's sign
observation of a jugular venous pressure (JVP, the filling of the jugular vein) that rises with inspiration
Cardiac tumors
wrt special sign
Kussmaul's sign
observation of a jugular venous pressure (JVP, the filling of the jugular vein) that rises with inspiration
Kussmaul's sign
Adverse effects of
Antihypertensive drugs

Hydrochlorothiazide
Hypokalemia,
hyperlipidemia,
hyperuricemia,
lassitude,
hypercalcemia,
hyperglycemia
Adverse effects of
Antihypertensive drugs

Loop diuretics
Potassium wasting,
metabolic alkalosis,
hypotension,
ototoxicity
Adverse effects of
Antihypertensive drugs

Clonidine
Dry mouth,
sedation,
severe rebound hypertension
Adverse effects of
Antihypertensive drugs

Methyldopa
Sedation,
positive Coombs’ test
Adverse effects of
Antihypertensive drugs

Hexamethonium
Severe orthostatic hypotension, blurred vision,
constipation,
sexual dysfunction
Adverse effects of
Antihypertensive drugs

Reserpine
Sedation,
depression,
nasal stuffiness,
diarrhea
Adverse effects of
Antihypertensive drugs

Guanethidine
Orthostatic and exercise hypotension,
sexual dysfunction,
diarrhea
Adverse effects of
Antihypertensive drugs

Prazosin
1st-dose orthostatic hypotension, dizziness,
headache
Adverse effects of
Antihypertensive drugs

β-blockers
Impotence,
asthma,
cardiovascular effects (bradycardia, CHF, AV block), CNS effects
(sedation, sleep alterations)
Adverse effects of
Antihypertensive drugs

Hydralazine
Nausea, headache,
lupus-like syndrome,
reflex tachycardia,
angina,
salt retention
Adverse effects of
Antihypertensive drugs

Minoxidil
Hypertrichosis,
pericardial effusion,
reflex tachycardia,
angina,
salt retention
Adverse effects of
Antihypertensive drugs

Nifedipine,
Dizziness,
flushing,
nausea
Adverse effects of
Antihypertensive drugs

verapamil
constipation
Dizziness,
flushing,
nausea
Adverse effects of
Antihypertensive drugs

Nitroprusside
Cyanide toxicity (releases CN)
Adverse effects of
Antihypertensive drugs

ACE inhibitors
Hyperkalemia,
Cough,
Angioedema,
Proteinuria,
Taste changes,
hypOtension,
Pregnancy problems (fetal renal damage),
Rash,
Increased renin, Lower
angiotensin II
Adverse effects of
Antihypertensive drugs

Angiotensin II receptor Inhibitors
Fetal renal toxicity, hyperkalemia
Which Antihypertensive drug has this adverse effect

Hypokalemia
Hydrochlorothiazide
and
Loop diuretics
Which Antihypertensive drug has this adverse effect

ototoxicity
Loop diuretics
Which Antihypertensive drug has this adverse effect

Dry mouth, sedation, severe rebound hypertension
Clonidine
Which Antihypertensive drug has this adverse effect

positive Coombs’ test
Methyldopa
Which Antihypertensive drug has this adverse effect

Severe orthostatic hypotension, blurred vision
Hexamethonium
Which Antihypertensive drug has this adverse effect

Sedation, depression, nasal stuffiness
Reserpine
Which Antihypertensive drug has this adverse effect

lupus-like syndrome
Hydralazine
Which Antihypertensive drug has this adverse effect

Cyanide toxicity (releases CN)
Nitroprusside
Which Antihypertensive drug has this adverse effect

pericardial effusion
Minoxidil
Which Antihypertensive drug has this adverse effect

Pregnancy problems (fetal renal damage)
ACE inhibitors
and
ARB's
Which Antihypertensive drug has this adverse effect

Hyperkalemia, Cough
ACE inhibitors
Which Antihypertensive drug has this adverse effect

Increased renin, Lower
angiotensin II
ACE inhibitors
Which Antihypertensive drug has this adverse effect

hyperkalemia
ACE inhibitors
and
ARB's
Which Antihypertensive drug has this adverse effect

Taste changes
ACE inhibitors
Which antihypertensive agent

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

Minoxidil
special considerations for using

Hydralazine
or
Minoxidil
Use with β-blockers to prevent reflex tachycardia, diuretic to block salt retention.
Antihypertensive drugs
name the

Sympathoplegics
Clonidine
Methyldopa
Hexamethonium
Reserpine
Guanethidine
Prazosin
β-blockers
Antihypertensive drugs
name the

Vasodilators
Hydralazine
Minoxidil
Nifedipine,
verapamil
Nitroprusside
Antihypertensive drugs
name the

ACE inhibitors
-pril's
Antihypertensive drugs
name the

Angiotensin II receptor inhibitors
-sartan's
Hydralazine
Mechanism
↑ cGMP →smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.
Hydralazine
Clinical use
Severe hypertension, CHF. First-line for HTN in pregnancy, with methyldopa.
Hydralazine
Toxicity
Compensatory tachycardia, fluid/salt retention. Lupus-like syndrome.
Calcium channel blockers
names
Nifedipine, verapamil, diltiazem.
Calcium channel blockers
Mechanism
Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.
Calcium channel blockers
Clinical use
Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.
Calcium channel blockers
Toxicity
Cardiac depression, peripheral edema, flushing, dizziness, and constipation.
Calcium channel blockers
which one not to use for arrhythmias
nifedipine
Calcium channel blockers
relative effects on
Vascular smooth muscle
vs
Heart
Vascular smooth muscle nifedipine > diltiazem > verapamil.

Heart– verapamil > diltiazem > nifedipine.
Nitroglycerin, isosorbide dinitrate

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

Clinical use
Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer.
Nitroglycerin, isosorbide dinitrate

Toxicity
Tachycardia,
hypotension, flushing,
headache,
“Monday disease” in industrial exposure/ development of tolerance
“Monday disease”
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.
Antianginal therapy
goals
reduction of myocardial O2 consumption by decreasing 1 or more of the
determinants: end diastolic volume, blood pressure, heart rate, contractility,
ejection time.
Calcium channel blocker
wrt
Antiangianl effects
Nifedipine is similar to Nitrates in effect;

verapamil is
similar to β-blockers in effect.
Cardiac glycosides
names
Digoxin, ...
Digoxin
pharmacokinetics
75% bioavailability,
20–40% protein bound,
t1/2 = 40 hours, urinary excretion.
Cardiac glycosides
Mechanism
Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/
antiport. ↑ intracellular [Ca2+] → + ionotropy.
Cardiac glycosides
Clinical use
and reasons
CHF (↑ contractility);

atrial fibrillation (↓ conduction at AV node and depression of
SA node).
Cardiac glycosides
Toxicity
May cause ↑ PR, ↓ QT, scooping of ST segment, T-wave inversion of ECG. Also
↑ parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision ,
Arrhythmias
Cardiac glycosides
Antidote
Slowly normalize K+,
lidocaine,
cardiac pacer,
anti-dig Fab fragments.
Digoxin
factors that affect its toxicities
Toxicity of digoxin are ↑ by: renal failure (↓ excretion)
hypokalemia (potentiates drug’s effects),
quinidine (↓ digoxin clearance by displacing digoxin from tissue binding sites).
Antiarrhythmics
Class I
mech and features
Slow or block (↓) conduction (especially in depolarized cells). ↓ slope of phase 4 depolarization and ↑ threshold for firing in abnormal pacemaker cells.
Antiarrhythmics
Class I
selectivity
Are state dependent (selectively depress tissue that is frequently depolarized,
e.g., fast tachycardia).
Antiarrhythmics
Class IA
names
“Queen Amy Proclaims
Dis o' pyramid.”

Quinidine, Amiodarone, Procainamide, Disopyramide.
Antiarrhythmics
Class IA
what they affect
↑ AP duration, ↑ effective refractory period (ERP),
↑ QT interval.
Antiarrhythmics
Class IA
used for
Affect both atrial and ventricular arrhythmias especially reentrant and ectopic supraventricular and ventricular tachycardia.
Antiarrhythmics
Class IA
toxicities
Quinidine
cinchonism––headache,
tinnitus;
thrombocytopenia;
torsades de pointes due to ↑
QT interval)
Antiarrhythmics
Class IA
toxicities
Procainamide
reversible SLE-like
syndrome
Cinchonism
or quinism is a pathological condition in humans caused by an overdose of quinine or its natural source, cinchona bark
a pathological condition in humans caused by an overdose of quinine or its natural source, cinchona bark
cinchonism or quinism
Which antiarrhythmic toxicity has

cinchonism––headache, tinnitus;
thrombocytopenia;
Quinidine
Which antiarrhythmic toxicity has

reversible SLE-like
syndrome
Procainamide
Antiarrhythmics
Class IB
names
Lidy's Mexican Tacos

Lidocaine, mexiletine, tocainide
Antiarrhythmics
Class IB
effect
↓ AP duration.
Affect ischemic or depolarized Purkinje and
ventricular tissue.
Antiarrhythmics
Class IB
uses
Useful in acute ventricular
arrhythmias (especially post-MI) and in digitalis induced arrhythmias.
Antiarrhythmics
Class IB
Toxicity
local anesthetic.
CNS stimulation/depression,
cardiovascular depression.
Antiarrhythmics
Class IC
Toxicity
proarrhythmic, especially post-MI
(contraindicated).
Significantly prolongs
refractory period in AV node.
Antiarrhythmics
Class IC
names
Flecainide, encainide, propafenone.
Antiarrhythmics
Class IC
effect
No effect on
AP duration.
Antiarrhythmics
Class IC
uses
Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias.
Antiarrhythmics
Class II
names
β-blockers
Antiarrhythmics
Class II
effects
↓ cAMP, ↓ Ca2+ currents. Suppress abnormal pacemakers by ↓ slope of phase 4.
AV node particularly sensitive––↑ PR interval.
Antiarrhythmics
Class II
Which is very short acting
Esmolol
Antiarrhythmics
Class II
toxicity in general
Impotence, exacerbation of asthma, cardiovascular effects (bradycardia,
AV block,
CHF),
CNS effects (sedation, sleep alterations).
May mask the signs of hypoglycemia.
Antiarrhythmics
Class II
toxicity of metoprolol
can cause dyslipidemia.
Antiarrhythmics
Class II
can cause dyslipidemia.
metoprolol
Antiarrhythmics
Class III
name them
K+ channel blockers

Sotalol,
ibutilide,
bretylium,
amiodarone.
Antiarrhythmics
Class III
mech
↑ AP duration, ↑ ERP. Used when other
antiarrhythmics fail. ↑ QT interval.
Antiarrhythmics
Class III
Toxicity
Sotalol
Sotalol––torsades de pointes, excessive β block;
Sotalol
which class of Antiarrhythmics
Class III
Antiarrhythmics
Class III
Toxicity
torsades de pointes
Sotalol
and
ibutilide
Antiarrhythmics
Class III
Toxicity
ibutilide
torsades;
Antiarrhythmics
Class III
Toxicity
bretylium
hypotension
and
new arrhythmias
Antiarrhythmics
Class III
Toxicity
hypotension and new arrhythmias
bretylium
Antiarrhythmics
Class III
Toxicity
pulmonary fibrosis
amiodarone
Antiarrhythmics
Class III
Toxicity
amiodarone
pulmonary fibrosis,
corneal deposits, hepatotoxicity,
skin deposits resulting in photodermatitis, neurologic effects,
constipation, cardiovascular effects (bradycardia,
heart block, CHF), hypothyroidism/
hyperthyroidism.
Antiarrhythmics
Class III
Toxicity
hypothyroidism/
hyperthyroidism.
amiodarone
Antiarrhythmics
Class III
Toxicity
corneal deposits
amiodarone
Antiarrhythmics
Class III
Toxicity
skin deposits
amiodarone
What to check when using amiodarone
P(pulmonary)FTs,
LFTs, and TFTs when
Amiodarone is safe to use in
????? syndrome.
Wolff-Parkinson-White
??????is safe to use in
Wolff-Parkinson-White
syndrome.
Amiodarone
Antiarrhythmics
Class IV
names
Verapamil, diltiazem. bepridil
Antiarrhythmics
Class IV
Mechanism
Primarily affect AV nodal cells. ↓ conduction velocity, ↑ ERP, ↑ PR interval.
Antiarrhythmics
Class IV
uses
prevention of nodal arrhythmias (e.g., SVT).
Antiarrhythmics
Class IV
toxicity
Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression);

torsades de pointes (bepridil).
Antiarrhythmics
misc
names
Adenosine
K+
Mg+
Digoxin
misc antiarrhythmics
Adenosine
Drug of choice in diagnosing/abolishing AV nodal arrhythmias.
misc antiarrhythmics
K+
Depresses ectopic pacemakers, especially in digoxin toxicity.
misc antiarrhythmics
Mg+
Effective in torsades de pointes and digoxin toxicity.
Effective in torsades de pointes and digoxin toxicity.
Mg+sulfate
Drug of choice in diagnosing and abolishing AV nodal arrhythmias.
Adenosine