Cardiology Flashcards

1
Q

Truncus Arteriosus becomes…

Pathology of TA

A

Ascending Aorta and Pulmonary Trunk
Transposition of the Great Vessels (failure to spiral), Tetralogy of Fallot (skewed AP septum), Persistent TA (partial AP septum development)

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

Bulbus Cordis becomes

A

Smooth part (outflow tract) of L and R Ventricles

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

Primitive Ventricle Becomes

A

Trabeculated Ventricles

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

Primitive Atria become

A

Trabeculated Atria

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

Left Horn of Sinus Venosus becomes

A

Coronary Sinus

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

Right Horn of Sinus Venosus becomes

A

Smooth part of RA

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

Right Common Cardinal Vein and Right Anterior Cardinal Vein become

A

SVC

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

What kind of cells forms the aorticopulmonary septum

A

Neural Crest Cells. Truncal and bulbar ridges spiral and fuse to form AP septum giving rise to the Ascending Aorta and the Pulmonary Trunk

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

Interventricular Septum Development

A
  1. Muscular ventricular septum forms with interventricular foramen
  2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular formane
  3. Growth of endocardial cushions separate atria from ventricles and contributes to both atrial separation and membranous portion of interventricular septum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Membranous septal defect will lead to

A

L-R shunt which later reverses to R-L shunt due to onset of PHTN (Eisenmengers syndrome)

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

Interatrial septum development

A
  1. Foramen primum narrows as septum primum grows towards endocardial cushions
  2. Perforations in septum primum form foramen secundum and FP disappears
  3. FS maintins R-L as suptum secundum begins to grow
  4. Septum Secundum contains FO (permanent opening)
  5. Foramen secundum enlarges and upper part of septum primum degenerates
  6. Remaining portion of septum primum forms valve of FO
  7. Septum secundum and septum primum fuse to form atrial septum
  8. FO closes soon after birth because of increased LA pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PFO caused by

A

Failure of Septum Primum and Septum Secundum to fuse after birth

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

Fetal erythropoiesis occurs in?

A
"Young Livers Synthesize Blood"
Yolk Sac: weeks 3-10
Liver: week 6 - birth
Spleen: 15-30 weeks
Bone Marrow: 22 weeks to adulthood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Blood in umbilical vein
PO2
O2 Sat

A

PO2 = 30mmHg

O2 Sat = 80%

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

Umbilical arteries O2 Sat?

A

Low

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

Fetal Shunts

A
  1. Umbilical vein –> ductus venosus –> IVC to bypass liver
  2. RA –> FO –> LA
  3. Pulmonary Artery –> Ductus Arteriosus –> Aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens to fetal circulation when the infant takes its first breath

A

Decreased resistance in pulmonary vasculature –> increased P in LA –> FO closes
Increased O2 –> decreased prostaglandins –> ductus arteriosus closes

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

Medication for PDA

A

Indomethacin closes the PDA

PGE keeps in open

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

Umbilical vein becomes

A

Ligamentum teres hepatis contained in the falciform ligament

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

Umbilical arteries become

A

Medial umbilical ligaments

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

Ductus arteriosus becomes

A

Ligamentum arteriosum

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

Ductus venosus becomes

A

Ligamentum venosum

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

Foramen Ovale becomes

A

Fossa Ovalis

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

Allantois becomes

A

Urachus - median umbilical ligament. The Urachus is part of the allantoic duct between bladder and the umbilicus
Urachal cyst or sinus is a remnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Notochord becomes
Nucleus pulposus of IV disc
26
What vessels supplies the SA and AV nodes?
RCA
27
What percentage of individuals are Right Dominant? Left Dominant? Codominant?
PDA arises from RCA in 85% of individuals From LCX in 8% Both in 7%
28
Most commonly occluded coronary arteries?
LAD > RCA > CFX
29
Coronary arteries fill during
Diastole
30
Branches of RCA
Acute Marginal, PDA (80%)
31
Branches of LCA
CFX, LAD
32
If LA enlarged | How to diagnose?
Dysphagia (compression of esophagus) + Hoarseness (compression recurrent laryngeal nerve) Transesophageal Echocardiography
33
What can transesophageal echocardiography be used to diagnose?
LA Enlargement, Aortic Dissection, Thoracic Aortic Aneurysm
34
What does LAD supply?
Ant 2/3 of IV septum, anterior papillary muscles, anterior surface of LV
35
What does LCX supply?
Lateral and Posterior walls of LV
36
What does PDA supply?
Posterior 1/3 of IV septum and posterior walls of ventricles
37
Cardiac Output Equation (2)?
CO = SV x HR Fick Principle CO = (Rate of O2 consumption)/(arterial O2 - venous O2)
38
Mean Arterial Pressure Equation? (2)
``` MAP = CO x TPR MAP = 2/3 Diastole + 1/3 Systole ```
39
Pulse Pressure Equation? | What is PP proportional to?
PP = Systolic - Diastolic | PP α SV
40
Stroke Volume Equation?
EDV - ESV
41
During exercise, how is CO maintained? Early? Late
Early: Increases in HR and SV Late: HR only, SV plateaus
42
What happens if HR is too high?
Diastolic filling is incomplete and CO decreases resulting in ventricular tachycardia
43
What variables affect SV?
SV CAP | Contractility, Afterload, Preload
44
What decreases Contractility?
BACH β Blockers (decreased cAMP), Acidosis, Ca Channel Blockers (non-dihydropyridine), Hypoxia/Hypercapnea, Systolic Heart Failure
45
What Chemicals Increase Contractility?
Catecholamines (increase activity of Ca pump in SR). Digitalis (Increased intracellular Na --> increased intracellular Ca)
46
SV increases in what states?
Pregnancy, Exercise, Anxiety
47
Myocardial O2 demands increase with
CARS | Increased Contractility, Afterload, Rate, Size (wall tension)
48
Preload is equal to?
EDV
49
Afterload is equal to?
MAP | Proportional to peripheral resistance
50
What kind of drugs reduce preload?
Venodilators like Nitroglycerin
51
What kind of drug reduce afterload?
Vasodilators like Hydralazine
52
Preload increases with
Exercise, Volume, Excitement
53
Force of contraction proportional to?
Preload
54
``` Ejection Fraction Formula Index for? Normal value Decreases in? ```
EF = SV/EDV Index for ventricular contractility Normally ≥ 55% Decreases in Systolic HF
55
Pressure formula
P = Q x R
56
Resistance formula (2)
R = P/Q = (8 x viscosity x length)/π(r^4)
57
Viscosity depends on... | Increases with...
Hct | Increases with Polycythemia, Hyperproteinemic state (multiple myeloma), Hereditary spherocytosis
58
Viscosity decreases with
Anemia
59
Most of the total peripheral resistance due to
Arterioles
60
S1 | Loudest at
Mitral and Tricuspid valves close | Loudest in Mitral area
61
S2 | Loudest at
Aortic and Pulmonary valves close | Loudest at L sternal border
62
``` S3 When Associated with Sign of Normal in ```
``` In early diastole Associated with increased filling pressures MR, CHF Sign of dilated ventricles Normal in Pregnants and Children ```
63
S4 When Caused by Associated with
Atrial Kick in late diastole Caused by high atrial pressure Associated with ventricular hypertrophy
64
JVP wave
a: atrial contraction c: RV contraction (tricuspid valve bulges into atrium) x: atrial relaxation v: RA filling y: blood flow from RA to RV
65
Normal Splitting Physiology
S1 - A2-P2 Inspiration --> drop in intrathoracic pressure --> increased venous return to RV --> increased RV SV --> increased RV ejection time --> delayed closure of pulmonic valve Inspiration also leads to increased capacity of pulmonary circulation which also delays P closing
66
Wide Splitting Pathology Seen in conditions with
Due to delayed RV emptying | Pulmonic stenosis, R bundle branch block
67
Fixed Splitting Seen in Pathophysiology
ASD. L-R shunt --> ⇑ RA and RV volumes --> ⇑ flow through pulmonic valves such that regardless of breath, valve closure greatly delayed
68
Paradoxical Splitting PathoPhys Seen in what conditions
Seen in conditions that delay LV emptying (Aortic Stenosis, Left Bundle Branch Block). Reversal of A2 and P2
69
What can be heard in aortic area?
Systolic murmors: AS, Flow Murmur, Aortic Valve Sclerosis.
70
What can be heard over Left Sternal Border
Diastolic murmurs: AR, PR | Systolic murmurs: HOCM
71
What can be heard in Pulmonic Area?
Systolic ejection murmur: Pulmonic stenosis, Flow murmur from ASD or PDA.
72
What can be heard in the tricuspid area?
Pansystolic murmurs: Tricuspid Regurg, VSD | Diastolic murmurs: Tricuspid stenosis, ASD
73
What can be heard over Mitral area?
Systolic: MR Diastolic: MS
74
ASD Early presentation PathoPhys Later presentation
"Drs press forward" Diastolic rumble and pulmonary flow murmur Blood flow across ASD does not cause the murmur because there is no pressure gradient The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery
75
Where is the best place to hear a PDA? What does it sound like? Due to
Left infraclavicular region. Continuous machine like murmur. Loudest at S2 Often due to congenital rubella or prematurity
76
Bedside Maneuver: Inspiration
Increased intensity of R heart sounds
77
Bedside Maneuver: Expiration
Increased intensity of L heart sounds
78
Bedside Maneuver: Hand Grip | What does it do physiologically
⇑systemic vascualr resistance. ⇑ intensity of MR, AR, VSD, MVP ⇓ intensity of AS, HOCM
79
Bedside Maneuver: Valsala | What does it do physiologically
⇓ venous return Bedside Maneuver: Valsala ⇑ MVP and HOCM
80
Bedside Maneuver: Rapid Squatting | What does it do physiologically?
⇑ venous return, ⇑ preload, ⇑ afterload (if prolonged) | ⇓ MVP and HOCM
81
``` Sound of MR Loudest at? Radiates? Enhanced by? Often due to? ```
Holosystolic high pitched blowing murmur. Loudest at apex and radiates towards axilla Enhanced by maneuvers that ↑ TPR (squatting, hand grip) and ↑ LA return (expiration) Most often due to Ischemic heart disease, MVP, LV dilation, RF, infective endocarditis
82
``` Sound of TR Loudest at? Radiates? Enhanced by? Often due to? ```
Holosystolic high pitched blowing murmur. Loudest at tricuspid area and radiates to R sternal border Enhanced by maneuvers ↑ RA return (inspiration) Most often due to RV dilation, RF, infective endocarditis
83
``` Aortic Stenosis Sound and Radiation Pressures Presentation Caused by ```
Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets) that radiates towards carotids and loudest at heart base P in LV > P in Aorta "SAD" --> Syncope, Angina, Dyspnea Pulsus Parvus et Tardus Age related calcification or bicuspid valve
84
VSD Sound Location Maneuvers
Holosystolic, harsh sounding murmur loudest at tricuspid area and ↑ by handgrip (increased afterload)
85
``` MVP Sound Location? When? Predisposes pts to Caused by Enhanced by ```
Late systolic crescendo murmur with midsystolic click (from sudden tensing of chordae tendineae) Best heard over apex during S2 Predisposes to infective endocarditis Caused by myxomatous degeneration, RF, chordae rupture. Enhanced by maneuvers that ↓ venous return (standing, valsala)
86
Most frequent valvular lesion
MVP
87
``` Aortic Regurgitation Sound Presentation Due to Affected by ```
Immediate high pitched blowing diastolic decrescendo murmur. Wide pulse pressure, bounding pulse, head bobbing. Due to aortic root dilation, bicuspid endocarditis, RF. ↓ by vasodilators ↑ by hand grip
88
``` Mitral Stenosis Sound Pressures Due to Can lead to Enhanced by ```
Delayed rumble in late diastole with opening snap (abrupt halting of leaflets due to fusion) P in LA (measured by PCWP) > P in LV Due to RF and can lead to LA dilation Enhanced by maneuvers that ↑ LA return (expiration)
89
Ventricular AP also occurs in
Bundles of His and Purkinje fibers
90
Phases of Ventricular AP
0: INa 1: Na channels inactivated, K channels open 2: Plateau. Ca channels open 3: Repolarization. K channels open. Ca channels close 4: Resting Potential. High K permeability
91
Ca enters cardiac myocytes by
Ca induced Ca release
92
Pacemaker AP Phases
0: Ca mediated upstroke 2: no plateau 3: Inactivation of Ca channels, Opening of K 4: Slow diastolic depolarization because of Na funny channels
93
What affects Slope of Phase 4 in pacemaker cells?
ACh and Adenosine --> ↓ Slope --> ↓ HR | Catecholamines --> ↑ Slope --> ↑ HR
94
P wave on EKG
Atrial depolarization
95
Speed of conduction of parts of heart
Purkinje > atra > ventricles > AV node
96
Speed of conduction of pacemaker cells
SA > AV > Bundle of His/Purkinje/Ventricles
97
PR interval represents | Normal value
Conduction delay through AV node | Normally < 200 msec
98
QRS Complex represents | Normally
Ventricular depolarization | Normally < 120 msec
99
QT interval represents
Mechanical contraction of the ventricles
100
T wave represents | Inversion may indicate
Ventricular repolarization | T wave inversion may indicate recent MI
101
ST segment
Isoelectric | Ventricles Depolarize
102
U Wave causes
HypoK, Bradycardia
103
Conduction pathway in heart
SA --> Atria --> AV --> Common Bundle --> Bundle Branches --> Purkinje Fibers --> Ventricles
104
Atrioventricular delay? | Allows for?
100 msec delay allows for ventricular filling
105
V Tach Can progress to What predisposes towards it Treatment
Can progress to Vfib Long QT interval predisposes towards it Treatment is Magnesium Sulfate
106
Congenital Long QT syndrome Defect in Can present as
Defect in cardiac Na or K channels | Can present with congenitcal sensorineural deafness (Jervell and Lang Nielsen Syndrome)
107
Afib ECG Can lead to Treatment
Irregularly irregular with no discrete P wave between irregularly spaced QRS Can result in atrial stasis which leads to stroke Treatment: anticoagulants, β Blockers, cardioversion, Ca Channel Blockers, Digoxin
108
Atrial Flutter EKG Treatment
Back to back P waves (sawtooth) | IA, IC, II, III, IV
109
V fib EKG Treatment
Erratic rhythm with no identifiable waves | Fatal without CPR and Defib
110
1st Degree AV Block
PR interval prolonged (>200 msec) | Asymptomatic
111
2nd Degree AV Block | Mobitz Type I
Wenckenbach Progressive lengthening of PR interval until a beat is dropped Usually asymptomatic
112
2nd Degree AV Block Mobitz Type II Treatment Risk
Extra P waves Treat with pacemaker Can progress to 3rd degree black
113
3rd Degree AV Block Treat with Can be caused by
A and V beat independently Treat with pacemaker Can be caused by Lyme Disease
114
ANP Released by In response to Leads to
Released by atrial myocytes in response to ↑ vol and atrial pressure. Leads to vascular relaxation and ↓ Na reabsorption in medullary collecting tubule. Constricts EA and dilates AA (via cGMP)
115
Aortic arch receptors | Transmit via ... to ... responds to ...
Transmit via Vagus nerve to NTS in medulla and respond to ↑ BP only
116
Carotid Sinus | Transmits via ... to ... and responds to ...
Transmits via glossopharyngeal nerve to NTS and responds to any change in BP
117
Baroreceptors | Course of signals
↓ BP --> ↓ stretch --> ↓ afferent baroreceptor firing --> ↑ efferent sympathetic firing and ↓ efferent parasympathetic firing --> vasoconstriction, ↑ HR, ↑ contractility, ↑ BP
118
Carotid Massage
↑ pressure on carotid artery --> increase stretch --> ↑ afferent firing --> ↓ HR
119
Cushings Rxn Presentation PathoPhys
HTN, Bradycardia, Respiratory Depression ↑ ICP constricts arterioles --> cerebral ischemia --> reflex HTN --> ↑ stretch --> Reflex baroreceptor induced bradycardia
120
Peripheral Chemoreceptors
Carotid and Aortic bodies stimulated by ↓ PO2 (< 60mmHg), ↑ PCO2, and ↓ pH
121
Central Chemoreceptors
Stimulated by change in pH and PCO2 of brain interstitial fluid Do not directly respond to PO2
122
Organ with largest share of systemic CO
Liver
123
Organ with highest blood flow per gram of tissue
Kidney
124
Organ with largest O2 extraction
Heart | ~80%. ↑ O2 demand must be met with ↑ blood flow
125
Pressures in the Heart
``` RA: less than 5 RV: 5-25 PA: 25-10 LA: less than 12 LV: 130-10 Aorta: 130-90 ```
126
Approximation of P in LA | Measured with...
PCWP measured with Swan-Ganz catheter
127
Autoregulation of blood flow to heat mediated by
Local metabolites - CO2, Adenosine, NO
128
Autoregulation of blood flow to Brain mediated by
Local metabolites - CO2, pH
129
Autoregulation of blood flow to Kidneys mediated by
Myogenic and tubuloglomerular feedback
130
Autoregulation of blood flow to Lungs mediated by
Hypoxia vasoconstriction
131
Autoregulation of blood flow to Skeletal Muscle mediated by
Local metabolites - lactate, adenosine, K
132
Autoregulation of blood flow to Skin mediated by
Sympathetic stimulation for temperature control
133
Starling Equation
J = K[(Pc-Pi)-(πc-πi)]
134
Edema from Heart Failure in terms of Starling Equation
↑ Pc pushes fluid out of capillaries
135
Edema from ↓ plasma proteins in terms of Starling Equation
↓ πc
136
Edema from ↑ capillary permeability in terms of Starling Equation What causes a change in capillary permeability?
↑ K | Toxins, Infections, Burns
137
Edema from ↑ interstitial fluid colloid osmotic pressure in terms of Starling Equation Caused by
πi | Caused by lymphatic blockage
138
Blue Baby PathoPhys Causes
``` R-L shunt Tetralogy of Fallot (most common) Transposition of the great vessels Persistent Truncus arteriosus (with PDA) Tricuspid atresia Total Anomalous Pulmonary Venous Return ```
139
What usually accompanies a persistent truncus arteriosus?
PDA
140
What accompanies TAPVR?
ASD and sometimes PDA to allow for R-L shunt to maintain CO
141
Blue Kids PathoPhys Causes Frequency of causes
L-R shunt | VSD > ASD > PDA
142
Eisenmengers Syndrome PathyPhys Presents as
Uncorrected VSD, ASD, PDA causes compensatory pulmonary vascular hypertrophy --> PHTN As pulmonary resistance ↑, the shunt reverses and becomes R-L Presents as Cyanosis, Clubbing, Polycythemia
143
``` Tetralogy of Fallot Caused by Characteristics Shunting? XR Treatment ```
Caused by anterosuperior displacement of infundibular septum PROV Pul stenosis, RVH, Overriding Aorta (overrides VSD), VSD R-L shunting --> cyanosis Boot-shaped heart on XR Surgery
144
What do pts with ToF do to relieve symptoms
Squatting --> ↓ blood flow to legs --> ↑ Resistance --> ↓ R-L shunt across VSD
145
Transposition of the Great Vessels Only compatible with life if there is a Due to Treatment
Only compatible with life if there is a VSD, PDA, or PFO Due to failure of the aorticopulmonary septum to spiral Surgery
146
Coarctation of the aorta | Results in
Aortic Regurgitation
147
Coarctation of the aorta: Infantile Type Location of stenosis? Associated with? On physical exam remember to check...
Stenosis proximal to ductus arteriosus Associated with Turners Syndrome Check femoral pulses
148
Coarctation of the aorta: Adult Type Location of stenosis? Associated with? On physical exam remember to check...
Stenosis distal to ligamentum arteriosum Associated with bicuspid aortic valve On Physical Exam: Notching of the ribs due to collateral circulation, HTN in upper extremities, Weak pulses in lower extremities
149
Presentation of uncorrected PDA
Cyanosis in the lower extremities (differential cyanosis)
150
Consequences of PDA on the heart?
L-R shunt --> RVH and/or LVH and failure
151
Cardiac defect associated with 22q11 syndrome (DiGeorge syndrome)
Truncus arteriosus and ToF
152
Cardiac defect associated with Down Syndrome
ASD, VSD, AVSD (endocardial cushion defect)
153
Cardiac defect associated with Congenital Rubella?
Septal defects, PDA, Pulmonary artery stenosis
154
Cardiac defect associated with Turners Syndrome
Preductal coarctation of the aorta
155
Cardiac defect associated with Marfan's Syndrome
Aortic insufficiency and dissection (late)
156
Cardiac defect associated with diabetic mother
Transposition of the great vessels
157
TAPVR pathophys?
Pulmonary veins drain into R heart
158
Definition of HTN?
> 140/90
159
Risk factors for HTN
Age, diabetes, obesity, smoking, genetics
160
Risk of HTN in different races?
Black > White > Asian
161
Primary vs Secondary HTN
90% primary. 10% Secondary
162
Primary HTN
Related to ↑ CO and TPR
163
Secondary HTN usually caused by
Renal disease
164
Malignant HTN definition and prognosis
> 180/120 and rapidly progressing
165
HTN predisposes pts to
Aterosclerosis, LVH, Stroke, CHF, Renal Failure, Retinopathy, Aortic Dissection
166
Atheroma definition
Lipid plaques in blood vessel walls
167
Xanthomas definition. Where are they found?
Plaques or nodules composed of lipid laden histiocytes in the skin. Found on eyelids (xanthelasma), tendons (Tendinous Xanthomas) (esp Achilles tendon)
168
Corneal arcus definition. | Sign of?
Lipid deposits in cornea. | Nonspecific (arcus senilis)
169
``` Monckeberg PathoPhys Usually affects Problem? Layers involved? ```
Calcification of media of arteries. Especially radial or ulnar. Usually benign and does not obstruct blood flow. Only involves media, not intima
170
Arteriolosclerosis Types Where is each type present?
Hyaline: Thickening of small arteries seen in essential HTN and DM Hyperplastic: "onion skinning" seen in MHTN
171
Atherosclerosis Definition What kind of arteries Where in the artery?
Fibrous plaques and atheromas for in the intima of elastic arteries and large/medium muscular arteries.
172
Modifiable risk factors of Atherosclerosis
Smoking, HTN, Hyperlipidemia, Diabetes
173
Non-modifiable risk factors for Atherosclerosis
Age, Male, Postmenopausal women, family history
174
Progression of Atherosclerosis
Endothelial cell dysfunction --> macs and LDL accumulation --> Foam cells --> Fatty streaks --> SM migration (PDGF and FGF), proliferation, and ECM deposition --> Fibrous plaque
175
Complications of Atherosclerosis
Aneurysm, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
176
Common locations of Atherosclerosis
Abdominal Aorta > coronary arteries > Popliteal arteries > carotid arteries
177
Atherosclerosis presentation
angina, claudication, but may be asymptomatic
178
Abdominal Aortic Aneurysm | Classic pt?
Atherosclerosis in Male smoker >50 with HTN
179
Thoracic Aortic Aneurysm associations
HTN, Marfan's (Cystic Medial Necrosis), and Tertiary Syphilis
180
``` Aortic Dissection Definition Associations Presentation CXR Can result in... ```
Longitudinal tear forms false lumen Associated with HTN, Bicuspid Aortic Valve, Cystic Medial Necrosis, Connective Tissue Disorder (i.e. Marfan's) Presents with tearing chest pain radiating to the back CXR shows mediastinal widening with false lumen larger than true lumen Can result in pericardial tamponade, aortic rupture
181
How narrow must the coronary artery be to produce angina?
> 75% but this does not produce myocyte necrosis
182
Stable Angina Definition Mostly due to EKG
Retrosternal chest pain with exertion Mostly secondary to atherosclerosis ST depression on ECK
183
Prinzmetals Angina Due to EKG
Secondary to coronary artery vasospasms | ST elevation on EKG
184
Unstable Angina Definition Caused by EKG
Worsening chest pain at rest or with minimal exertion. Caused by thrombosis with incomplete coronary artery occlusion. ST depression on ECK
185
Coronary Steal Syndrome
Vasodilators aggravate ischemia by shunting blood from affected area to region of higher perfusion
186
Myocardial infarction Definition Most often due to... ECK
Complete occulsion of coronary artery producing myocyte necrosis. Most often due to thrombosis ST depression progressing to ST elevation
187
ST depression means
Subendocardial wall damage
188
ST elevation means
Transumarl wall damage
189
Sudden Cardiac Death Definition Most commonly due to Associated with
Death from cardiac cause within 1 hour of symptom onset Most commonly due to lethal arrhythmia (Vfib) Associated with CAD
190
Chronic Ischemic Heart Disease Definition Progresses to
Chronic ischemic myocardial damage. Progresses to CHF
191
MI presentation
Diaphoresis, naseau, vomiting, retrosternal pain, pain in left arm and/or jaw, dyspnea, fatigue
192
0-4 hours after MI Gross LM Risk
Gross: none LM: none Risk: Arrhythmias, CHF exacerbation, shock
193
4-12 hours after MI Gross LM Risk
Gross: Dark mottling. Pale with tetrazolium stain LM: Early coagulative necrosis, edema, hemorrhave, wavy fibers Risk: Arrhythmias
194
12-24 hours after MI Gross LM Risk
Gross: Dark mottling. Pale with tetrazolium stain LM: Contraction bands from reperfusion injury, Release of necrotic cell contents into blood, Beginning of neutrophil migration Risk: Arrhythmias
195
1-3 days after MI Gross LM Risk
Gross: hyperemia LM: Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation. Neutrophil migration Risk: Fibrinous pericarditis
196
2-14 days after MI Gross LM Risk
Gross: Hyperemic border with centrally yellow-brown softening (maximally yellow at day 10) LM: Macs. Granulation tissue at margins Risk: Free wall rupture --> tamponade, Papillary muscle rupture, Aneurysm, IV septal rupture
197
2-Several weeks after MI Gross Risk
Gross: Gray-white tissue | Dresslers syndrome
198
Diagnosis of MI | EKG and blood tests
EKG is gold standard in the first 6 hours. Troponin I rises after 4 hours and is elevated for 7-10 days (specific). CKMB predominantly found in myocardium but also skeletal muscle. Useful in diagnosing reinfarction because returns to normal after 48 hours
199
Transmural infarct: EKG
ST elevation. Pathological Q wave
200
Subendocardial infarcts EKG Necrosis?
ST depression. Necrosis of <50% of ventricle wall
201
EKG diagnosis of Anterior wall infarct based on leads showing Q waves?
"SAL" Anteroseptal: V1-V2 (LAD) Anterior: V1-V4 (LAD Anterolateral: V4-V6 (LCX)
202
EKG diagnosis of Lateral or Inferior wall infarct based on leads showing Q waves?
"Love Is Incredible. Nothing Like It" Lateral: I, aVL (LCX) Inferior: II, III, aVF
203
Dresslers Syndrome | PathoPhys
Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI
204
Causes of Dilated Cardiomyopathies
Most common cause = idiopathic (>50%) "A Bold, Devout Christian Crusader Charged Petrified Hindus" Alcohol, wet Beriberi, Doxorubicin, Chagas, Coxackie B, Cocaine, Postpartum, Hemochromatosis
205
``` Dilated Cardiomyopathy Common? Sound, US, CXR What kind of hypertrophy? What kind of dysfunction? Treatment ```
Most common cardiomyopathy (90%) S3, US = dilated heart, CXR = balloon Eccentric hypertrophy w/ sarcomeres added in series --> systolic dysfunction? Treat w/ Na restriction, ACEI, diuretics, digoxin, transplant
206
HOCM: PathoPhys Genetics Association
Hypertrophied IV septum is too close to mitral valve and obstructs aortic outflow 60-70% are caused by autosomal dominant mutation in β myosin heavy chain --> disorganized, tangled myocardial fibers Associated with Friedreich's Ataxia
207
HOCM Classic Pt Size, Sound, Murmur, Impulses Treatment
Cause of death in young athletes Normal sized heart, S4, Systolic murmur, apical impulses Treat with II or nonDHP IV
208
HOCM Hypertrophy Kind of dysfunction? May produce?
Concentric hypertrophy with sarcomeres added in parallel Diastolic dysfunction ensues May produce syncopal episodes.
209
Causes of Restrictive Cardiomyopathies
"A SHELF" Amyloidosis, Sarcoidosis, Hemochromatosis, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffers Syndrome (endomyocardial fibrosis with eosinophils), Fibrosis (post radiation)
210
What kind of dysfunction ensues in restrictive cardiomyopathies?
diastolic
211
Treatment for CHF Mortality reducers? Symptom relief? Both?
Mortality reducers: ACEI, II (except in acute decompensated HF), ATII antagonists, Spironolactone Symptom relief: Thiazide and Loop Diuretics Both: Hydralazine and Nitrates
212
CHF presentation
Dyspnea, fatigue, edema, rales
213
What produces Cardiac Dilation?
Greater EDV
214
Why do Pts experience dyspnea on exertion
Failure of CO to Increase
215
Results of LHF?
Pul Edema: transudation of fluid into alveoli. Hemosiderin laden Macs in lung Paroxysmal Nocturnal Dyspnea and Orthopnea: Increased venous return --> pulmonary vascular congestion
216
Results of RHF?
Hepatomegaly (nutmeg liver), Peripheral edema, JVD
217
Bacterial Endocarditis Presentation
"FROM JANE" | Fever, Roth Spots, Osler's Nodes, Murmur, Janeway Lesions, Anemia, Nail-bed hemorrhages, Emboli
218
Roth Spots
Round, white spots on retina surrounded by hemorrhage
219
Osler's Nodes
Tender raised lesions on finger and toe pads caused by IC deposition
220
Janeway Lesions
Small, painless, erythematous lesions on palm or sole. Hemorrhagic
221
Complications of Bacterial Endocarditis
Chordae rupture, Glomerulonephritis, Suppurative pericarditis, emboli
222
Site of infection in Bacterial endocarditis?
Usually Mitral Valve | Tricuspid in IV drug users
223
Main Causes of Bacterial Endocarditis
Acute: S aureus (large vegetations on normal valve) Subacute: S. viridans (small vegetations on abnormal or diseased valve) Common after dental procedures
224
Organisms Causing Tricuspid Bacterial Endocarditis
S aureus, Pseudomonas, Candida
225
Causes of non bacterial endocarditis
Malignancy, Hypercoagulable state, SLE
226
Bacterial endocarditis in colon cancer caused by
S bovis
227
Bacterial endocarditis with a prosthetic valve caused by...
S epidermidis
228
Rheumatic Fever Presentation
"FEVERSS" Fever, Erythema marginatum, Valve damage, ESR ↑, Red-Hot Joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus dance (Sydenham's Chorea)
229
``` RF Organisms causing it Valves affected Early vs Late Type of Disease? ```
GAS (β hemolytic strep) mitral > aortic >>> tricuspid Early MR, late MS Type II Hypersensitivity Rxn with Abs against bacterial M protein
230
RF Histology Blood titers
Aschoff Bodies (granuloma with giant cells), Antischkow cells (activated histiocytes), Elevated ASO
231
Acute Pericarditis Presentation PE findings EKG
Sharp pleuritic pain relieved by sitting up and leaning forward. Friction rub Widespread ST elevation and/or PR depression
232
Fibrinous Pericarditis Causes Findings
Dressler's, Uremia, Radiation | Loud Friction Rub
233
Causes of Serous Pericarditis
Viral (often resolves spontaneously), noninfectious inflammatory disease (SLE, RA)
234
Causes of SuppurativePurulent Pericarditis
``` Bacterial infection (Pneumococcus Streptococcus) Rare now with antibiotics ```
235
Cardiac Tamponade What happens to diastolic pressures? HR? Sounds? BP? PE findings?
Diastolic pressures equalize in all 4 chambers. HR↑, Distant heart sounds, hypotension and Pulsus Paradoxus, JVD
236
Pulsus Paradoxus Definition Seen in what diseases?
↓ in systolic P by >10mmHg during inspiration | Seen in pericarditis, tamponade, asthma, obstructive sleep apnea, croup
237
Syphilitic Hearth Disease Causative agent MoA Risk for
Tertiary Syphilis disrupts vasa vasorum of the aorta and vessel wall atrophys and dilates. Risk for aortic aneurysm (ascending and arch) and aortic insufficiency (dilation of aorta and valve ring)
238
In Syphilitic Hearth Disease, what happens to the aortic root and ascending aortic arch? How does the aorta appear?
Calcification | Tree bark appearance
239
``` Cardiac Myxoma Common? Usually described as Location Present with ```
Most common primary cardiac tumor in adults. "ball valve" obstruction of LA presents with multiple syncopal episodes
240
Rhabdomyomas Common? Associated with?
Most common primary cardiac tumor in children. Associated with Tuberous Sclerosis
241
Most common cardiac tumor?
Metastatic (melanoma, lymphoma)
242
Kussmaul's Sign Definition Seen in
↑ in JVP during inspiration because negative intrathoracic pressure not transmitted to the heart Constrictive Pericarditis, Restrictive Cardiomyopathy, RA or RV tumors, Cardiac Tamponade
243
``` Raynaud's Phenomenon PathoPhys Location Disease Syndrome Presentation ```
↓ blood flow to skin due to arteriolar constriction in response to cold or stress Fingers and toes Disease if primary (idiopathic) Syndrome if secondary to connective tissue disease, SLE, CREST Cyanosis of fingertips and toes
244
``` Temporal Giant Cell Arteritis Kind of vasculitis? Classic Pt Presentation Risk of Associated with Affects which vessels? Histo Blood Treatment ```
Large vessel Old female with unilateral temporal headache and jaw claudication Risk of blindness due to ophthalmic artery occlusion Associated with Polymyalgia Rheumatica Branches of Carotid artery.Focal Granulomatous inflammation, ↑ESR, Treat with corticosteroids
245
``` Takayasu's Arteritis Kind of vasculitis? Classic Pt Presentation Affects which vessels? Histo Blood Treatment ```
"FAN My Skin On Wed" Large vessel Asian female < 40 with weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances Granulomatous thickening of aortic arch and proximal great vessels, ↑ESR Treat with corticosteroids
246
``` Polyarteritis Nodosa Kind of vasculitis? Classic Pt Presentation Affects which vessels? Histo What mediates the disease? Ages of lesions? Arteriogram Treatment ```
"Scalded My Right Hand on the PAN" Medium vessels Young Adult with HepB with fever, wt loss, malaise, headache, abdominal pain, melena, HTN, Neuro dysfunction (wrist drop), Cutaneous eruptions, renal damage Renal and Visceral vessels Transmural inflammation with fibrinoid necrosis IC mediated Typically of different ages Arteriogram shows many aneurysms and constrictions Corticosteroid and cyclophosphamide
247
``` Kawasaki Disease Kind of vasculitis? Classic Pt Presentation Affects which vessels? Risk of Treatment ```
Medium vessels "FEAR ME" Asian child < 4 with Fever, conjunctival infection (Eye), cervical lymphAdenitis, desquamating Rash, Mouth and Extremity erythema Coronary vessels Risk of coronary aneurysm --> MI, Rupture Treat with IV Igs and Aspirin
248
Buerger's Disease (Thromboangiitis Obliterans) Kind of vasculitis? Classic Pt Presentation Treatment
Medium vessels "SCRAPS" Male < 40 with Segmenting Thrombosing vasculitis, Claudication (may lead to gangrene and auto-amputation), Raynaud's, Smoker, Painful, Superficial Nodular Phlebitis Treat with smoking cessation
249
``` Microscopic Polyangiitis Kind of vasculitis? Histo Organs involved w/ manifestation? Blood Treatment ```
``` Small vessels Necrotizing vasculitis w/ No Granulomas Lungs, Kidney (Pauci Immune Glomerulonephritis), and Skin (Palpable Purpura) P-ANCA Cyclophosphamide and Corticosteroids ```
250
``` Wegener's Granulomatosis (Granulomatosis with Polyangiitis) Kind of vasculitis? Presentation Histo Blood CXR Treatment ```
``` Small vessels Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis Lower RT: Hemoptysis, Cough, Dyspnea Renal: Hematuria, RBC Casts Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis c-ANCA Large Nodular Densities Cyclophosphamide and corticosteroids ```
251
``` Churg Strauss Syndrome Kind of vasculitis? Classic Presentation But can also affect Histo Blood ```
Small vessels "BEAN SAP? No, Go to Hell" Blood Eosinophils, Asthma, Neuropathy (food/wrist drop), Sinusitis, Allergies, Palpable Purpura, glomeruloNephritis (pauci immune), GI, Heart Granulomatous, necrotizing vasculitis w/ eosinophilia p-ANCA + ↑ IgE
252
``` Henoch-Schonlein Purpura Kind of vasculitis? Most common vasculitis in... Classic Presentation Disease Mediated by Associated with Age of lesions? ```
``` Small vessels Most common vasculitis in children "NAPA" Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia Mediated by IgA complex deposition Associated with IgA nephropathy Multiple lesions of same age ```
253
Essential HTN therapy
ACEI, ARB, Diuretics, IV
254
When are II contraindicated?
Cardiogenic shock and must be used with caution in decompensated CHF
255
Treatment for Diabetes Mellitus?
ACEI, ARB, Diuretics, II, α blockers, IV
256
``` Ca Channel Blockers Names MoA Used to treat Tox ```
Verapamil, Diltiazem, Nifedipine, Amlodipine --/ Voltage gated L-type Ca channel in plasma membrane Used to treat HTN, Angina, Arrhythmias (not N), Prinzmetals Angina, Raynaud's Cardiac depression, AV block, Peripheral edema, Flushing, Dizziness, Constipation
257
``` Hydralazine MoA Used to treat First line therapy for Coadministration Tox Contraindicated in ```
↑cGMP --> Smooth Muscle relaxation. Vasodilates arterioles > veins --> ↓ afterload Used to treat HTN, CHF First line therapy for HTN in pregnancy with methyldopa Coadministered with II to --/ reflex tachycardia Compensatory tachycardia, fluid retention, nausea, headache, angina, Lupus. Contraindicated in Angina/CAD
258
Treatment for MHTN
Nitroprusside (short acting) --> Release of NO --> ↑cGMP --> Smooth Muscle relaxation. Can cause cyanide poisoning Fenoldopam = D1 agonist --> coronary, peripheral, renal, and splanchnic vasodilation. ↓ BP and ↑ Natriuresis
259
``` Nitric Oxide (NO) Releasing Drugs Names MoA Use Tox ```
Nitroglycerin, Isosorbide, Dinitrate NO --> ↑cGMP --> Smooth Muscle relaxation. Dilates veins > arteries --> ↓ preload Used to treat angina and Pul Edema Reflex tachycardia, Hypotension, Flushing, Headache, Monday disease (industrial exposure)
260
Goal of Antianginal therapy
Reduce O2 demand of myocardium | Reduces Contractility, Afterload, Rate, Size (wall tension = Preload)
261
``` Nitrates as Antianginal EDV BP Contractility HR Ejection time MVO2 ```
``` EDV ↓ BP ↓ Contractility ↑ (response) HR ↑ (response) Ejection time ↓ (response) MVO2 ↓ ```
262
``` II as Antianginal EDV BP Contractility HR Ejection time MVO2 ```
``` EDV ↑ BP ↓ Contractility ↓ HR: ↓ Ejection time: ↑ MVO2: ↓ ```
263
``` Nitrates + II as Antianginal EDV BP Contractility HR Ejection time MVO2 ```
``` EDV: No change or ↓ BP: ↓ Contractility: NC HR: ↓ Ejection time: NC MVO2: ↓↓ ```
264
Which IV are similar to Nitrates? | Which IV are similar to II?
Nitrates: Nifedipine II: Verapamil
265
Partial β blockers contraindicated in angina
Pindolol, Acebutolol
266
``` Strawberry Hemangioma Benign or malignant? What kind of vessels? Time and frequency Course ```
Benign capillary hemangioma of infancy Appears in first few weeks of life 1/200 births Grows rapidly and regresses spontaneously at ages 5-8
267
``` Cherry Hemangioma Benign or malignant? What kind of vessels? Time and frequency Course ```
Benign capillary hemangioma of the elderly Does not regress Frequency increase with age
268
Cystic Hygroma What kind of growth? Where on body? Associated with?
Cavernous lymphangioma of the neck. Associated with Turners Syndrome
269
Pyogenic Granuloma What kind of tumor? What can it do? Associations?
Polyploid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy
270
``` Glomus Tumor Benign or malignant Painful or not? Color? Location? Arises from? ```
Benign, painful, red-blue, tumor of fingernails. Arises from modified smooth muscle cells of glomus body
271
``` Bacillary Angiomatosis Benign or malignant Which vessels? Location? What kind of Pts? Cause? Frequently confused with ```
Benign capillary skin papules found in AIDS pts. Caused by Bartonella henselae infection. Frequently mistaken for Kaposi Sarcoma
272
``` Angiosarcoma Frequency? Kind of malignancy? Location on body? Associated with what kind of pts? Prognosis? ```
Rare blood vessel malignancy typically occuring in head, neck and breast areas. Associated with pts recieving radiation therapy (breast cancer, Hodgkin's lymphoma). Very aggressive and difficult to resect due to delayed diagnosis
273
Lymphangiosarcoma What kind of malignancy? Associated with?
Lymphatic malignancy associated with persistent lymphedema (post-radical masectomy)
274
``` Kaposi Sarcoma What kind of malignancy Location on body Associated with Frequently mistaken for... ```
Endothelial malignancy found on skin, mouth, GI tract, respiratory tract. Associated with HHV8 and HIV. Frequently mistaken for bacillary angiomatosis
275
Sturge Weber Disease What kind of disease? Vessels affected? Manifestation?
Congenital Capillary sized blood vessels Port-Wine stain (nevus flammeus) on face, Ipsilateral leptomeningeal angiomatosis (intracerebral arteriovenous malformation), Seizures, early onset Glaucoma
276
``` HMG CoA Reductase Inhibitors (Statins) LDL HDL Tri MoA Tox ```
``` LDL ↓↓↓ HDL ↑ Tri ↓ MoA --/ conversion of HMG-CoA to mevalonate (a cholesterol precursor) Hepatotoxic (↑LFTs), Rhabdomyolysis ```
277
``` Niacin (Vit B3) LDL HDL Tri MoA Tox ```
LDL ↓↓ HDL ↑↑ Tri ↓ MoA Inhibits lipolysis in adipose tissue. Reduced hepatic VLDL secretion Red, flushed face (↓ by aspirin). Hyperglycemia (acanthosis nigricans), Hyperuricemia (exacerbates gout)
278
``` Bile Acid Resins Names LDL HDL Tri MoA Tox ```
Cholestyramine, Colestipol, Colesevelam LDL: ↓↓ HDL: Slightly ↑ Tri: Slightly ↑ Prevents intestinal reabsorption of bile acids forcing liver to use cholesterol to make Bile Bad taste, GI discomfort, ↓ absorption of soluble vitamins, Cholesterol Gallstones
279
``` Cholesterol Absorption Blockers Names LDL HDL Tri MoA Tox ```
``` Ezetimibe LDL: ↓↓ HDL: - Tri: - MoA: Prevents cholesterol reabsorption in small intestine brush border Rare ↑ in LFTs, Diarrhea ```
280
``` Fibrates Names LDL HDL Tri MoA Tox ```
Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate LDL ↓ HDL ↑ Tri ↓↓↓ Upregulate LPL --> ↑ TG clearance Myositis, hepatotoxic (↑ LFTs), cholesterol gallstones
281
``` Cardiac Glycosides Names Bioavailability Protein bound? T1/2 Excretion ```
``` Digoxin 75% bioavailability 20-40% protein bound T1/2 40h Urinary excretion ```
282
Digoxin MoA Use
--/ Na/K ATPase. ↑ Na --/ Na/Ca exchanger --> ↑ Ca --> ↑ contractility --> Vagus Nerve --> ↓ HR Used to treat CHF (↑ contractility), Afib (↓ conduction at AV node, depression at SA node)
283
Digoxin Tox EKG Factors predisposing to toxicity
Cholinergic --> nausea, vomiting, diarrhea, blurry yellow vision AV block, Hyperkalemia, ↑ PR, ↓QT ST scooping, T wave inversion, arrhythmias Predisposition: renal failure (↓ excretion), Hypokalemia (permissive binding of Na/K pump), Quinidine (↓ clearance. displaces digoxin from tissue binding sites)
284
Digoxin OD antidote
Slowly normalize K, Lidocaine, Cardiac Pacer, Anti Digoxin Fab Fragment, Mg
285
``` Class I antiarrhythmics What kind of molecules What do they do? Dependence? Toxicity is aggravated by... ```
Local anesthetics ↓ conduction in depolarized cells. ↓ slope of phase 0. ↑ threshold for firing in abnormal pacemaker cells Are state dependent (selective depress frequently depolarized tissues) Hyperkalemia ↑ toxicity
286
``` Class IA antiarrhythmics Name Action on AP? Action on EKG? Regions of heart? Especially useful in treating ```
``` Procainamide, Disopyramide, Quinidine ↑ AP duration. ↑ effective refractory period ↑ QT Affect both Atria and Ventricles Reentrant and Ectopic SVT and Vtach ```
287
Class IA antiarrhythmics | Toxicity
Thrombocytopenia, torsades de pointes Q --> cinchonism (headache + tinnitus) P --> SLE D--> heart failure
288
``` Class IB antiarrhythmics Names Affect on AP? Preferentially affects Useful in Tox ```
Lidocaine, Mexiletine, Tocainide, (Phenytoin) ↓ AP duration Preferentially affects ischemic or depolarize Purkinje and ventricular tissue Useful in acute ventricular (Is Best Post MI) + digitalis induced arrhythmias. Local anesthetic, CNS↑↓, CV depression
289
``` Class IC antiarrhythmics Name Affect on AP? Useful in Usually only used as Affect on AV node Toxicity Contraindicated ```
Flecainide, Propafenone No affect on AP duration Useful in Vtach that progresses to Vfib + intractable SVT Usually used only as a last resort for refractory tachyarrhythmias Prolongs refractory period in AV node Tox: Proarrhythmic Contraindicated Post MI and structural heart disease
290
``` Class II antiarrhythmics Names MoA Affect on AP Area particularly sensitive? Use ```
Metoprolol, propanolol, esmolol (very short acting), atenolol, timolol Decrease SA and AV nodal activity by ↓ cAMP --> ↓ Ca currents Decreases phase 4 slope in pacemaker cells AV node particularly sensitive (↑ PR interval) VTach, SVT, Slows ventricular rate during Afib + Aflutter
291
Class II antiarrhythmics | Tox
BBC Loses Viewers in Houston Bradycardia (AV block, CHF), Bronchoconstriction (aggravates asthma), Claudication, CNS effects (sedation), Lipids (metoprolol), Vivid dreams, Hypoglycemia masked
292
Propanolol can exacerbate
Vasospasms in Prinzmetal's angina
293
Beta Blocker OD treatment
Glucagon
294
``` Class III antiarrhythmics Names MoA Effect on AP Used when EKG effects ```
``` "AIDS" Amiodarone, Ibutilide, Dofetilide, Sotalol --/ K channels ↑AP duration, ↑ERP, Used when other antiarrhythmics fail ↑QT interval ```
295
Class III | Toxicity
Sotolol: TdP, excessive β Block Ibutilide: TdP, Amiodarone: Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism
296
Amiodarone Toxicity | Real Classification
Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism (40% I by weight), Corneal deposits, Skin deposits (blue/gray) --> photodermatitis, neurological effects, constipation, AV affects (bradycardia, heart block, CHF) Affects lipid membranes so has I, II, III, and IV activity
297
``` Class IV antiarrhythmics Names Affects on AP Used to Tox ```
Verapamil, Diltiazem ↓ conduction velocity, ↑ERP, ↑PR Used to prevent nodal arrhythmias (SVT) Constipation, Flushing, Edema, CV (CHF, AV block, Sinus node depression
298
``` Adenosine MoA Drug of choice for Speed Toxicity Affects blocked by ```
↑K out of cells --> hyperpolarization and ↓ Ca current. Drug of choice for SVT (diagnosis and treatment) Very short acting (15 sec) Flushing, hypotension, angina Blocked by caffeine and theophylline
299
Mg used to treat
TdP and Digoxin toxicity
300
Names of β1 selective β Blockers
Start with A-N
301
Names of non-selective β Blockers (β1 and β2)
Start with O-Z
302
Breathing in a pt with CHF
Cheyne Stokes Breathing