Cardiology Flashcards
1
Q
3 determinants of arterial pressure
A
- Contractile properties of heart
- Vasculature properties
- Blood volume
2
Q
Parasympathetic activity to heart causes…
A
Decrease in HR by decreasing spontaneous depolarization at SA node
Decreases contractility
3
Q
Sympathetic activity to heart causes…
A
Increase HR and contractility
Increases disatolic filling and volume ejected = Increased SV
4
Q
Baroreceptors
A
Located in aortic arch and carotid sinus
Detect blood pressure and send input to brain for regulation via solitary tract
5
Q
Brain centers for BP regulation
A
Vasoconstrictor center
Cardiac Accelerator center
Cardiac decelerator center
6
Q
Renin Angiotensin Aldosterone System
A
Renin converts Angiotensinogen –> Angiotensin I
ACE converts angiotensin I –> Angiotensin II
Angiotensin II = Vasoconstriction –> Increase TPR –> Increase pressure
Angiotensin II = Aldosterone release –> Na reabsorption –> water reabsorption –> Increase Blood volume and pressure
7
Q
Anti Diuretic Hormone
A
Adds aquaporins to kidney nephron collecting tubule for increased water reabsorption
8
Q
ANP
A
Atrial natiuretic peptide
Secreted in response to increased ECF
Causes vasodilation and sodium/water excretion —> Decrease BP
9
Q
Continuous capillaries
A
Skeletal muscle, lungs, skin, fat, CT, nervous system
Endothelial cells overlap to form clefts
Clefts contain tight junctions for strict regulation of solute transport
10
Q
Fenestrated capillaries
A
Gut mucosa, glomerulus, exocrine glands, ciliary body and choroid plexus
Contain fenestra to allow for more solute/fluid exchange
11
Q
Discontinuous capillaries
A
Liver, spleen, bone marrow
Large openings to facilitate large transport of solutes and fluid and protein
12
Q
Arteriolar Vasodilation and Starling
A
Causes increase in hydrostatic capillary pressure due to reduced pre/post capillary resistance
13
Q
Long term standing/sitting and Starling
A
Increased artial/venous pressure = Increased hydrostatic pressure
14
Q
Liver failure and starling
A
Reduced protein production = Decreased capillary oncotic pressure –> edema
15
Q
Malnutrition and Starling
A
Decreased protein intake –> Decreased oncotic pressure –> edema
16
Q
Late term pregnancy and starling
A
Reduced plasma protein –> decreased oncotic pressure –> edema
17
Q
Functions of lymphatic system
A
Return filtered blood
Disease Defense
Transport absorbed fat
Return filtered protein
18
Q
Venous return and how to increase it
A
Amount of blood that returns to right heart per minute
Increase sympathetic activity to veins (contract) = Increase VR
Muscle contraction pushes blood back through veins = Increase VR
19
Q
Shift VR curve to right
A
Increase blood volume or venous tone
PVP increases –> VR increases
20
Q
Filling phase of cardiac cycle
A
Begins with opening of mitral valve (Pa>Pv)
Begins with rapid filling, then slowed filling
SA node spontaneously depolarizes, atria excitation increases, P wave, adds some more volume to ventricle
21
Q
Isovolumetric contraction phase
A
Pressure in ventricle rises
Pv > Patrium so mitral valve closes –> 1st heart sound
Pv < Paorta so aortic valve is closed
Volume remains the same but excitation has reached ventricles, QRS, so ventricle excitation occurs and pressure increases
22
Q
End of diastole and beginning of systole
A
Closure of mitral valve
23
Q
Ejection phase
A
Pv > Paorta so aortic valve opens and blood is ejected
Ventricular volume rapidly decreases
Decline in force over time = decreased level of active ventricular cells due to repolarization
24
Q
Isovolumetric relaxation phase
A
Pv < Paorta so aortic volve closes –> 2nd heart sound
Pv > Patrium so mitral valve still closed
Ventricular cells decrease in activity with constant volume so pressure decreases
25
Right heart vs left heart cardiac cycle and pressures
Cardiac cycle phases are relatively similar
Pressure gradients are dramatically decreased
26
Tricuspid and mitral valve timing
Tricuspid valve closes after and opens before mitral valve
27
Pulmonary and aortic valve timing
Pulmonary valve opens before and closes after aortic valve
28
Cardiac action potential - Diastole/Rest
High permeability to Potassium so resting potential is negative
K-IR channels
29
Cardiac action potential - Action potential upstroke
Voltage Gated sodium channels open and huge influx of Na depolarizes cell
30
Cardiac action potential - Early repolarization
Fast inactivation of Na channels and increase in K permeability due to VGKC
31
Cardiac action potential - Plateau
Voltage Gated Calcium channels open and Ca influx
K permeability decreases - Mg blocks K-IR channels
Plateau of membrane potential due to combating electric forces
32
Cardiac action potential - Repolarization
Inactivation of Ca channels and voltage activation of K rectifier channels
Cell repolarizes
Channels inactivate as cell repolarizes
33
Purpose of high K permeability
Stabilizes resting membrane potential and requires large excitatory stimulus
Reduces risk of arrhythmias
34
Sympathetic activity and ventricular action potential
NE release --> B-adrenergic receptors --> PKA --> enhance activity of Ca, Kr, Ks ion channels
More calcium = stronger contraction
Shortens AP duration and time between beats
35
Ventricular AP ARP
No propagated action potentials can be elicited
Occurs right after rapid depolarization and ends towards end of repolarization
36
Relative refractory period
Larger than normal stimulus can initiate AP
Closer to end of RRP = stronger AP
37
Supranormal period (SNP)
Slightly smaller than normal stimulus elicits normal response
38
Full recovery time (FRT)
Time after which a normal action potential can be elicited with normal stimulus
39
Long QT syndrome
Repolarization of heart is delayed
Usually genetic with delayed rectifier K channels
MUtations cas delayed activation, reduced open probability, and insensitivity to PKA
Arrhythmias occur at higher heart rates b/c can't shorten AP --> compromised filling
40
Na/K ATPase level in cardiac vs Skeletal muscle
Much more active contributing to higher K gradient
41
K Permeability in cardiac vs skeletal muscle
Much higher in cardiac muscle
42
Na permeability in cardiac vs skeletal muscle
10-50x higher in cardiac
43
Phase 0 permeability
Action potential upstroke
Na influx
44
Phase 1 permeability
Transient increase in K
| Inactivation of Na
45
Phase 2 permeability
Increase in Ca (voltage gated)
Decrease in K because of Mg block
46
Phase 3 permeability
Ca channels close
K rectifier channel
47
Nodal tissue AP vs other parts of heart AP
1. No true resting potential
| 2. Lower AP amplitude and shorter duration
48
Nodal AP - Phase 0
Upstroke
Voltage activated CALCIUM channels
49
Nodal AP - phase 3
Repolarization
Voltage dependent K rectifier channels
Channels inactivate as cell repolarizes
50
Nodal AP - Phase 4
Pacemaker potential
Early portion - Closure of Krectifier (primarily), Ca, K channels (slight depolarization)
I(f) channels open midway through and allow Na, Ca (less) influx --> further depolarization
Late phase 4 - Voltage T type calcium channels
51
B adrenergic stimulation on nodal I channels
PKA activation of channels
Shifts voltage at which channel activates to more positive --> Phase 4 depolarization begins earlier in repolarization phase
Larger depolarizing current
52
B adrenergic stimulation on nodal Ca channels
Both types of channels increased
Upstroke is larger
Ca influx during phase 4 is larger
Transition from phase 4 to 0 occurs earlier in phase 4
Rate of rise and amplitude increased, duration decreased
53
Acetylcholine and nodal AP
ACh at SA and AV nodes
1. Ach gate K channels open
2. Muscarnic receptors activated --> reduces cAMP and negates sympathetic activity
54
Overall pattern of electrical activation of heart
SA node --> Rt atrium before left atrium --> AV node (delay) --> purkinje fiber --> Endocardial ventricle --> Epicardial ventricle
55
Benefit of electrical pattern of heart activation
Delaying ventricle contraction (AV node) relative to atrial = maximize filling
Activating endocardial (surface) cells first and repolarizing last = More efficient contraction
Contracting from apex to base = ejection efficiency
56
Nicotinic cholinergic receptors
Neuromuscular junction of somatic nerves and skeletal muscle
Autonomic ganglia neurons
57
Muscarinic cholinergic receptors
Postganglionic parasympathetic
58
M1 receptor location
Neuron
59
M2 receptor location
Heart and smooth muscle
60
M3 receptor location
Sweat, salivary, lacrimal, GI, bronchial SM, eye
61
Cholinergic crisis
```
Salivation
Lacrimation
Urination
Defecation
Emesis
```
62
Muscarinic antagonist clinical signs
```
Dry mouth
Constipation
Mydriasis
Tachycardia
Decreased lacrimation
Decreased respiratory secretion
```
63
Epinephrine adrenergic targets
A1
A2
B1
B2
64
Norepinephrine adrenergic targets
A1
A2
B1
65
Beta 1 receptor action
Cardiac stimulation
Lipolysis
Renin release
66
Beta 2 receptor action
Bronchodilation
Vasodilation
Skeletal muscle and liver metabolic response
67
Alpha 1 receptor action
Smooth muscle (vessel) constriction
Increase in TPR and thus increase in BP
68
Beta 2 receptors and vessels
Relaxation of vascular smooth muscles in skeletal muscle vascular beds, splanchnic vessels, coronary vessels
Vasodilation --> Decreased TPR --> Decreased BP
Relaxation of bronchial smooth muscle and dilation of airways
69
Norepinephrine effects
Vasoconstriction --> Increase BP (a1)
Increase cardiac rate and contractility (B1)
Compensatory response decreases HR
Net result = Increased BP
70
Epinephrine effects
Vasoconstriction and increased BP (a1)
Vasodilation in skeletal muscle vascular beds and slight offset of vasoconstriction (b2)
Dose plays a role in effects
71
Low dose epinephrine
BP falls because B2 effects on vascular beds
72
Increased dose epinephrine
More vasoconstriction and increased BP
Beta1 increases pulse pressure
73
Phentolamine
Adrenergic antagonist
74
Phenoxybenzamine
Adrenergic antagonist
75
Prazosin
Adrenergic antagonist
76
Doxazosin
Adrenergic antagonist
77
Propanolol
Beta antagonist
78
Timolol
Beta antagonist
79
Metoprolol
Beta 1 antagonist
80
Clonidine
Alpha 2 adrenergic agonist
81
Phenylephrine
Alpha 1 agonist
82
Calcium sources in cardiac muscle
Extracellular space
Sarcoplasmic reticulum
83
Method of bringing in Extracellular Ca into cardiac muscle
Voltage gated Ca channel (L type)
Na-Ca exchange
84
L type Ca channel
Heart depol --> channel open --> triggers SR Ca release channel
85
Na-Ca exchanger
1 Ca for 3 Na
When membrane is more positive (depolarization) exchanger mediates Ca influx
86
Ca efflux of cardiac muscle mechanism
Ca-ATPase in plasma membrane (PMCA)
Na-Ca exchanger
Cell repolarizes --> Na-Ca exchange = Ca efflux.
--> No Ca entry = no activation of SR Ca release
87
Contractility
Change in force production that occurs independently from change in sarcomere length
88
Autonomics and contractility
Downstream effects of B1 receptor agonists --> more Ca into cell and more Ca release from SR --> More Ca available and more cross bridging
89
Contractility and heart rate
HR can affect contractility independent of autonomics
Increased HR --> Decreased time of disatole for Ca to be removed --> more Ca available at next systole
90
Contractility and cardiac glycosides
Cardiac glycosides enhance contractility
Na/K ATPase inhibited --> increase Na in cell --> Increase Na/Ca exchange activity (Ca influx)
91
Homeometric regulation
Regulation of force through changes in contractility
92
Stroke Work
Energy needed for ejection and energy needed to develop tension in IsoVol Contraction
93
Most energy required in cardiac cycle during...
Isovolumetric contraction
94
Factors increasing oxygen consuption
Increased afterload/contractility
Dilation of ventricular chamber
Increased HR
Increased SV
95
Heterometric reserve
Range of volumes over which an increase in volume leads to increased force
Increase in ventricular volume = thick/thin filament overlap enhancement = enhanced contractile force
96
Left ventricle Systolic/Diastolic pressure
120/5-10
97
Aorta systolic/diastolic pressure
120/80
98
Right ventricle systolic/diastolic pressure
25-30/4-6
99
Pulmonary artery systolic/diastolic pressure
25/10
100
Stage 1 HTN
140-159/90-99
101
Stage II HTN
>160/ >100
102
Rationale for treatment of HTN
AntiHTN is associated with reduced CV outcomes
103
First line Diuretics
Chlorthalidone
HCTZ
104
First line ACE inhibitor
Benazepril
105
First line ARB
Losartan
106
First line Ca channel blockers
Amlodipine
| Diltiazem
107
First line Beta blocker
Metoprolol/Propanolol
108
Thiazide MoA
Block Na/Cl cotransporter in DCT of kidney
Produces negative salt/water balance
109
Thiazide hemodynamic response
Drop in BP due to decreased plasma V and CO
EC volume returns to normal due to Renin-Angiotensin-Aldosterone System
110
Adverse effects of thiazide type diuretics
Hypokalemia
111
Ace inhibitor MoA
Inhibit ACE which converst Angiotensin I --> Angiotensin II
112
ACE-I hemodynamic response
Reduction in systemic vascular resistance and preload
Not much change in pulse rate
113
ACE-I adverse effects
Hypotension
Cough due to increased kinin
Renal insufficiency
Hyperkalemia can occur in patients with renal insufficiency, hypoaldosteronism, K sparing diuretic therapy
Teratogen
114
ARB MoA
Block angiotensin II binding
115
ARB Hemodynamic response
Vasodilation with decreased preload/afterload
116
ARB adverse effects
Teratogen
Les frequent cough
117
Ca channel blocker MoA
Bind to and block VGCC so less calcium for heart contraction and vascular smooth muscle contraction
118
Ca channel blocker hemodynamic response
Vasodilation with decrease in systemic vascular resistance
119
Ca Channel blocker Adverse effects
Constipation
Peripheral edema due to precapillary dilation and post capillary constriction
Negative inotropic action
AV node action may cause bradycardia
Headache
120
Beta blocker hemodynamic response
Decrease HR and contractility and CO
Increase SVR
Decrease in Renin --> less Angiotensin II --> less vasoconstriction
121
Beta blocker adverse effects
Dreams/depression
Aggravation of sever/unstable heart failure
122
Effect of increase in preload
Increase preload --> Increase EDV --> heterometric increase in contractility --> ESV stays the same
Result: Increase SW and subsequently CO
123
Effect on increase of contractility
Increase contractility --> more forceful contraction --> decreased ESV --> increased SV and subsequently CO
124
How to change flow of blood to organs
Relaxing or contracting smooth muscle of arterioles
125
Methods of altering organ arteriolar tone
1. Direct autonomic control
2. Local myogenic/metabolic factors
3. Humoral factors
126
Direct autonomic control of organ arteriolar tone
Sympathetic vasoconstriction
B2 vasodilation
127
Local myogenic control
Blood flow autoregulated within certain level of blood pressure
Increase BP = Increased flow --> Increase resistance (vasoconstriction) = Decrease flow
128
Local metabolic control
Metabolites that induce vasodilation (H, K, Lactate, Adenosine, CO2)
Exercise produces metabolites --> metabolites causes vasodilation so more flow to muscles --> Increased flow eventually washes metabolites out --> vasoconstriction
129
Humoral factors
1. Catecholamines - Extreme situations
2. Nitric Oxide
3. Angiotensin II
130
Coronary circulation architecture
Coronary vessels arise from sinuses behind aortic valve
High metabolic demand
131
Coronary exchange vessels
Capillary density of the heart is very high
Cardiac fibers are smaller so highly perfused
132
Cardiac contractility and flow through coronary vessels
Flow through coronary vessels decreases during ejection b/c heart is contracted
Flow deficit greatest in subendocardium b/c thats where contractions come from
133
Control of coronary flow
Local metabolic control - Hypoxia and adenosine
Nitric oxide
Net sympathetic activity is vasodilatory
134
Pulmonary circulation
Blood flow through lungs is much higher than metabolic need
Blood shunts away from poorly ventilated areas
135
Pulmonary edema natural prevention
Starling forces favor reabsorption - continuous capillaries
Lymph system drains and removes foreign bodies
136
Skeletal muscle capillaries
Oxidative fibers have more capillary anastamoses
137
Skeletal muscle starling during exercise
Starling forces favor filtration
Vasodilation = increased hydrostatic pressure
Metabolites released into interstitium --> Increased tissue oncotic pressure
138
HR immediate response to exercise
Anticipatory response via sympathetic system
139
SV immediate response to exercise
SV increases as intensity increases
Increased contractility
Increased preload
140
CO response to exercise
HR and SV increase
141
Blood flow response to exercise
Blood distributed to tissues with greatest demand: Heart, lungs, muscles
142
Blood pressure response to exercise
Increased contraction = increased BP (systolic, not diastolic)
143
Blood response to exercise
VO2 difference increases
More oxygen released from Hb
144
Heart size and rate adaptation to training
Increased heart mass, esp left ventricle
Resting heart rate decreases due to increased contractile properties
Range of heart rates increases
145
SV response to training
Increase due to increased preload
146
CO in response to training
CO increases during exercise but stays same at rest
147
Blood flow response to training
Skeletal muscle receives large % during training
Increased capillary growth and blood volume
148
BP in response to training
Systolic and diastolic BP decrease at rest and submaximal exercise
Increased compliance of large vessels
149
Blood volume in response to training
Endurance training increased BV and decreased HCT
150
Myocarditis definition
Inflammatory disease of heart
Inflammatory infiltrates in myocardium
151
Clinical features of myocarditis
Arryhythmias
EKG changes
Heart failure
Fatigue
Dyspnrea
152
Etiology of myocarditis
1. Infectious - Particularly viral but can be bacterial/fungal/parasitic
2. Hypersensitivity/autoimmune
3. Rejection of cardiac transplant
4. Idiopathic
153
Gross pathology of myocarditis
May appear normal or with dilated ventricles
154
Microscopic path of myocarditis
Necrosis of myocytes, inflammatory infiltrates
155
Outcome of myocarditis
Most recover
Supportive therapy
156
Cardiomyopathy definition
Abnormality or disease of cardiac muscle cells occurring in absence of other known mechanisms of myocardial injury
157
Primary cardiomyopathy
Primary involvement is myocardial and no known etiology
158
Secondary cardiomyopathy
Associated with another cardiac disease such as myocarditis
159
Dilated cardiomyopathy
60% are primary idiopathic
40% are secondary cardiomyopathies: Alcoholism, prev myocarditis, pregnancy, drug/toxin exposure
160
Physiologic consequences of dilated cardiomyopathy
Systolic disorder - Decreased contractility and decreased EF
LV hypertrophy and dilatation, arrhythmias
161
Hypertrophic cardiomyopathy
Hypertrophy of ventricular septum
Gene mutation in gene that encode cardia sarcomeric proteins
162
Physiologic consequences of hypertrophic cardiomyopathy
Diastolic disorder - Decreased LV compliance and decreased LV filling
Sudden death at young age esp in young athletes
163
Restrictive cardiomyopathy
Cardiac wall stiffness (decreased compliance) --> decreased cardiac filling
50% amyloidosis
35% Eosinophilia which causes endocardial fibrosis and stiffening of ventricles
164
Physiological consequences of restrictive cardiomyopathy
Diastolic disorder
Decreased ventricular compliance and decreased cardiac filling
Biatrial dilatation
Normal systolic function
Can result in heart failure and sudden death
165
Arrhythmogenic cardiomyopathy
Fibrosis and fatty replacement of ventricles, esp right
RV dilatation
166
Physiological consequence of arrythmogenic cardiomyopathy
Systolic disorder
Decreased contractility of ventricles and decreased EF, esp right
Arrhythmias
Sudden death at young age
167
Criteria for diagnosing hypertensive heart disease
Cardiac enlargement (LV hypertrophy without dilatation)
Absence of other etiologic factors that would produce LV hypertrophy
History of hypertension
168
Vascular changes in HTN heart disease
Systemic arterioles narrow --> Increased TPR --> Increased afterload --> LV hypertrophy
169
Mild myocardial hypoxia in HTN heart disease
Increased myocyte size = larger diffusion distances from capillaries to individual myocytes --> mild hypoxia
170
Additional factors of HT heart disease
Hypertrophies myocytes dont contract effectively
Interstitial collagen increases --> reduced compliance
Atherosclerosis of coronary arteries decreases myocardial blood supply and exacerbates myocardial hypoxia
171
Microscopic pathology of HTN heart disease
Increased myocyte diameter with increased size nucleus
Nuclei :squared off" or box car shaped
172
Complications and causes of death in HTN heart disease
Congestive heart failure (40%)
Coronary atherosclerosis
Strokes
Nephrosclerosis --> kidney failure
173
Most common CV anomaly
Bicuspid aortic valve
174
Second most common CV anomaly
Ventricular septal defect
175
Pathogenesis of congenital cardiac abnormalities
Sporadic genetic abnormalities
Chromosomal abnormalities
Viral infection during pregnancy (rubella)
Drugs/teratogens
Radiation
176
Cyanosis
Blue discoloration of mucous membranes caused by >2.5gms/dl of deoxyHb in blood
177
Pulmonary HTN and congenital defects
Pulmonary HTN can arise if shunts are present
Left to Right shunts increase blood to lungs and cause hypertrophy of pulmonary arteries
178
Plexogenic pulmonary HTN
Severe form of pulmonary artery hypertrophy
Cannot be corrected by surgery except total lung transplant
Common with VSD
Severe = Eisenmenger syndrom
179
Eisenmenger Syndrome
Reversal of Lt to Rt shunt
Caused by increased pulmonary HTN and shunt reversal
Acyanotic --> cyanotic
180
Lt to Rt shunts
Develop late cyanosis via Eismenger syndrome
181
Rt to Lt shunts
Early cyanosis
182
Congenital obstructions
No cyanosis
183
Congenital regurgitation
No cyanosis
184
Atrial septal defect
Abnormal opening between atria
L --> R
May be asymptomatic until adulthood
RV hypertrophy and dilatation, RA/LA dilatation
Pulmonary HTN infrequent
185
Types of atrial deptal defects
1. Fossa ovalis (most common)
2. Primum type - Low on septum and adjacent to AV valves
Sinus venosus type - High on septum, near SVC
186
Ventricular septal defect
Abnormal opening between ventricles
L --> R
Can cause pulmonary HTN if large --> Shunt reversal --> Eismengers
Small VSD's spontaneously close, no surgery and no pulmHTN
187
Types of VSD
Membranous - Membranous septum, most common, large
Muscular VSD - muscular septum, multiple, small
188
Atrioventricular septal defect (AVSD)
Deficient AV septum associated with mitral and tricuspid valve anomalies
Endocardial cushion defect
Associated with Downs
189
Types of AVSD
1. Partial - Primum ASD with cleft mitral anterior leaflet
| 2. Complete AVSD - Primum ASD and Membranous VSD. Large hole in center of heard and a common AV valve
190
Patent Ductus Arteriosus
Persistence of normal fetal structure that connects aorta and pulmonary artery
Pulmonary HTN
May be required for survival in complex cyanotic congenital heart diseases
191
Tetralogy of Fallot
1. Large and subarotic VSD
2. Subpulmonary stenosis
3. Overriding aorta
4. RV hypertrophy
Most common cyanotic congenital disease
Usually NO pulmHTN because lung vessels protected by subpulmonary stenosis
Good results with surgical repair
192
Types of Tetralogy of Fallot
Types based on pulmonary stenosis severity
1. Pink: Mild stenosis, no cyanosis
2. Classic: Moderate-severe stenosis, Cyanosis
3. PA-VSD - Complete absence of pulmonary valve and main pulmonary artery, with cyanosis
193
Transposition of Great Arteries
Pulmonary artery comes off LV and aorta comes off RV
Two separate circulations, not compatible with life unless shunt present
194
Types of TGA
1. TGA + no VSD = 65%, rare pulmHTN
| 2. TGA + VSD = 35%. Severe pulmHTN
195
How to treat TGA
Give PGE so DA remains
Create shunt
196
Truncus arteriosus
One common trunk the gets blood from RV and LV
Early cyanosis because deoxygenated blood can travel through aorta
Severe PulmonaryHTN
DiGeorge Syndrome
197
First heart sound: Occurs during what part of cardiac cycle and why
Isovolumetric contraction
Closure of mitral/tricuspid valves
198
Second heart sound: Occurs during what part of cardiac cycle and why
Isovolumetric relaxation
Closure of aortic/pulmonic valves
199
Third heart sound: Occurs during what part of cardiac cycle and why
Early ventricular filling
Normal in children, abnormal in adults
Rapid ventricular filling or dilated ventricle
200
Fourth heart sound: Occurs during what part of cardiac cycle and why
Atrial contraction
Blood hitting stiffened ventricle
Ventricular hypertrophy/ischemic ventricle
201
Pulmonary stenosis
Pulmonary valve obstruction
202
Types of pulmonary stenosis
Based on severity of obstruction
1. Isolated PV stenosis: RV hypertrophy, tricuspid regurg, RA/PA dilatation
2. PV atresia with intact ventricular septum: PDA required for survival. Hypoplastic RV and tricuspid valve
203
Congenital Aortic stenosis
Aortic valve obstruction
204
Types of congenital aortic stenosis
Severity based on level of obstruction
1. Isolated AV stenosis: LV hypertrophy, mitral regurgitation, LA dilatation
2. AV atresia with intact ventricular septum: PDA required for survival
205
Coarctation of aorta
Ridge like indentation or narrowing of distal aortic arch
50% have congenitally bicuspid AV
Hypertension in arms, hypotension in legs
Shunting around narrowing through enlarged collateral arteries
206
Types of coarctation of aorta
With (infants) and without (adults) PDA
207
Ebstein anomaly
Tricuspid valve malformation - septal and posterior leaflets point downwards and allow blood to flow back into RA
Torrential tricuspic regurgitation
Massive RA/RV dilatation
208
Congenital heart disease patients and endocarditis
Increased risk
209
Survival of children with Congenital HD
85% survive to adulthood
210
Fetal Circulation Overall
Oxygenated blood from placenta returns via umbilical vein --> into IVC vis Ductus venosus --> LA via foramen ovale --> systemic circulation --> RA --> RV --> pulmonary artery --> through ductus arteriosus --> umbilical artery
211
Pathophysiology and consequences of PDA
Pediatric congestive heart failure
Pulmonary vascular occlusive disease
Excessive blood return to left heart
Endarteritis risk
212
Pediatric Congestive Heart failure
Pulmonary edema and decreased efficiency of gas exchange = tachypnea
CO increases because more work needed to push out blood
Inability to eat well b/c feeding requires work and energy --> impaired weight gain
213
Pulmonary vascular occlusive disease
Pulmonary arterioles respond to increased pressure and flow by constricting
Arterioles can lose ability to relax and are fixed at high pressure --> increase in pulmonary pressure and subsequent Rt to Lt shunting (Eisenmenger syndrome)
214
Excessive blood return to left heart
LV dilatation and increased ED-pressure
215
Endarteritis risk
1%/yr risk of PDA infection due to turbulent flow
216
Type of murmur in VSD
Holosystolic murmur
LV pressure is higher than RV for entire systole
217
Most common mumur heard in AVSD
Systolic ejection murmur at PV
Excessive flow across PV
218
Pathyphys of AVSD
Left to right shunting at atrial and ventricular level
High flow to pulmonary arteries and increased blood return to left heart
219
Pathophys changes seen in pulmonary artery stenosis - neonates and older
Neonates - Hyperplasia which produces more efficient work, can handle pressure load
Neonates/older children - hypertrophy
220
Pathophysiology of aortic stenosis - neonates
LV in utero deals with low afterload so it doesn't work as hard as RV
Aortic stenosis can cause LV to work hard and after birth, LV may not be able to handle increased pressure load
Diastolic LV dysfunction --> Increased LV EDP --> Increased LA pressure --> Increased pulmonary venous presurre --> Increased PA/RV pressure
221
Pathophysiology of aortic stenosis - Older children
Rarely symptomatic, diagnosed after being evaluated for murmur
Able to maintain LV systolic performance through hypertrophy
222
Intervention for PDA
Indomethacin to close PDA
Catheter based closure of PDA
223
ASD intervention
Surgical closure but need to asses pulmonary arterial resistance first
224
VSD interventions
Medication - diuretics, ACE-I to reduce pulm overcirculation
Surgical closure
225
AVSD intervention
Medication to reduce pulmonary overcirculation
Surgical closure
226
Pulmonary stenosis intervention
Neonates - need intervention
Catheter balloon based vavluloplasty
227
Aortic stenosis intervention
Catheter based balloon valvuloplasty
228
Intervention for coarctation of aorta
Neonates/young children - surgical reconstruction
Catheter based balloon angioplasty
229
Intervention for ToF
BTT shunt - surgical PDA
Complete repair
230
TGA intervention
Balloon atrial septostomy to create large atrial communication and maximize mixing
231
Total anomalous pulmonary venous return (TAPVR)
Problem with connection of pulmonary venous confluence to primitive LA --> veins have nowhere to drain
Pop off vessel develops which can go
1. Superiorly to innominate vein
2. Inferiorly through diaphragm to IVC/hepatic veins
3. Infracardiac to coronary sinus
Oxygenated pulmonary venous blood goes back to RA
Infants will be cyanotic but not in distress (if vein isnt obstructed)
232
TAPVR intervention
Surgical
Emergency if vein is obstructed
233
Tricuspid atresia
Failure of tricupsid valve formation, no right ventricle - single ventricle
234
Intervention for single ventricle
Ultimate goal is to separate systemic and pulmonary circulation
Stage 1 surgery: BTT shunt for pulmonary flow, cut atrial septum
Stage 2: Glenn procedure. SVC detached from RA and sewn to right PA (bypass right heart completely)
Stage 3: Fontan procedure. IVC detached from RA and connected to pulmonary arteries
All systemic blood flows to pulmonary arteries, bypassing right heart
235
Hypovolemic shock classification
Results from decreased preload
Hemorrhage or fluid loss
236
Cardiogenic shock classification
Pump failure
Decreased systolic function and CO
237
Distributive shock classification
Vasodilatory shock
Severe decrease in SVR and increase in CO
Septic, anaphylaxis, neurogenic shock
238
Hypovolemic shock: CVP, CO, SVR
CVP - Decreased
CO - Decreased
SVR - Increased (sympathetic reflex)
239
Cardiogenic shock: CVP, CO, SVR
CVP - Increased (can't pump out preload)
CO - Decreased
SVR - Increased
240
Distributive shock: CVP, CO, SVR
CVR - Same or decreased
CO - Increased
SVR - Huge decrease (vasodilation)
241
Truncus arteriosus adult structure
Aorta and pulmonary trunk
242
Bulbus cordis adult structure
Smooth L/R ventricle
243
Ventricle adult structures
Trabeculated L/R ventricle
244
Sinus venosus adult structure
Coronary sinus and smooth RA
245
Ductus arteriosus adult structure
Ligamentum arteriosum
246
P wave signifies
SA conduction and atrial depolarization
247
P-R interval
AV node
248
QRS signifies
Ventricular depolarization
249
ST interval
Isoelectric segment
250
T wave signifies
Ventricular repolarization
251
Long P-R =?
Conduction problem through AV node/bundle branches/Purkinje
252
Wide QRS = ?
Bundle branch or purkinje problem
253
Unipolar leads
```
V1
V2
V3
V4
V5
V6
aVF
aVL
aVR
```
254
Bipolar leads
Vector combination of aVF/aVR/aVL
255
Lead I looks at what part of heart
High lateral
256
Lead II/III look at what part of heart
Inferior
257
aVF looks at what part of heart
Inferior
258
V1 lead looks at what part of heart
Septal
259
V2/V3/V4 looks at what part of heart
Anterior
260
V5/V6 looks at what part of heart
Lateral
261
Arteriosclerosis encompasses ?
Atherosclerosis
Arteriolosclerosis
Monckeberg medial calcific sclerosis
262
Atherosclerosis definition
Atheromatous plaque formation within large/medium sized arteries and elastic arteries
263
Pathogenesis of atherosclerosis
1. Endothelial cell dysfunction
2. Smooth muscle proliferation and migration into intima
3. Macrophage proliferation and migration into intima
4. Hyperlipidemia
264
Endothelial cell dysfunction
May stimulate smooth muscle proliferation with synthesis of collagen, elastic fibers, proteoglycans
Can induce macrophage proliferation
265
Smooth muscle proliferation
Synthesize ECM and accumulate lipids
266
Macrophage proliferation
Increased phagocytosis and accumulation of lipids within macrophages (foam cells)
Inflammatory cell recruitment
Oxidation of LDL
267
Hyperlipidemia
Promotes endothelial and smooth muscle cell injury
Increase penetration of lipids into plaque, increase formation of lipid laden foam cells in plaque
268
Complications of atheroma formation
Narrowing of lumen
Calcification and ulceration of plaque
Hemorrhage into plaque
Weakening of vessel wall with formation of aneurysms
269
Arteriolosclerosis
Disease of arterioles
1. Hyaline arteriolosclerosis (hyaline accumulation)
2. Hyperplastic arteriolosclerosis - Lumen narrowing by proliferating fibroblasts and smooth muscle cells in onionskin pattern
Elderly patients or young HTN/diabetic patients
270
Monckberg Medial Calcific Sclerosis
Disease of medium to small sized arteries
Calcification of media
>50yrs old
Calcification of tunica media without inflammation
271
Hemostasis sequence of events
Vascular injury --> Responsive vasoconstriction --> subendothelial tissue exposure leads to platelet aggregation --> TF exposure begins coagulation cascade --> --> fibrin accumulation and permanent hemostatic plug
272
Platelet aggregation
vWF = platelet aggregation
Platelet receptors for ADP/thrombin --> Activate COX-1 and fibrinogen binding protein
273
Intrinsic pathway of coagulation cascade
Factor VIII, IX, XI, XII --> Factor V
274
Extrinsic pathway of coagulation cascade
TF + Factor VII --> Factor X
275
Antithrombin
Blocks Factor IX, X, XI, Thrombin
276
Protein C
Activated protein C (with protein S cofactor) blocks V and VIII
277
TPA
Activates plasminogen --> plasmin --> fibrinolysis
278
PT monitoring
Prothrombin time
Assesses extrinsic pathway
279
aPTT
Activated partial thromboplastic time
Assesses intrinsic pathway
280
LMWH vs UFH
Both are efficacious and safe but LMWH needs no monitoring
281
Enoxaparin
Prototype LMWH
282
Fondaparinux
Pentasaccharide analog
283
Heparin MoA
Binds to antithrombin and causes conformational change --> mediates binding to Factor X to prevent clotting
284
UFH vs LMWH vs Fondaparinux MoA
UFH can mediate both antithrombin-Factor X binding AND antithrombin-thrombin binding
LMWH and Fondaparinux can only block Factor X, not long enough to mediate thrombin-antithrombin connection
285
Heparin pharmacodynamics
UFH can bind to no coagulation proteins and needs to be monitored
LMWH and fondaparinux do not bind to other proteins
286
Heparain monitoring
aPTT
287
Reversal of UFH
Protamine sulfate
Binds heparin so no anticoagulant activity
288
Heparin Induced thrombocytopenia
Heparin molecules cross react with patient IgG and can cause a thrombotic response and thrombocytopenia
289
Highest risk of HIT when using?
Unfractioned Heparin
After major surgery
290
HIT diagnosis
Decreased platelets >50% or thrombosis 5-10 days after heparin treatment
291
Treatment of HIT
Stop Heparin and use alternate anticoagulant
Argatroban - Direct thrombin inhibitor
292
Warfarin
Oral anticoagulant
Vitamin K antagonist - Prevents synthesis of clotting factors that require Vit K: II, VII, IX, X, protein C/S
Monitor with PT
293
Rifampin and Warfarin
Decrease Warfarin activity
294
Antimicrobials and Warfarin
Increase Warfarin activity via enzymes and by decreased Vit K absorption in gut
295
Alcohol and Warfarin
Acute use - Increased activity
Chronic use - Decreased activity
296
Metronidazole and Warfarin
Increased activity
297
Amiodarone and Warfarin
Large increase in activity
298
Dabigatran
Direct thrombin inhibitor
No monitoring required but can use aPTT
Use for stroke prevention or systemic embolism
299
Idarucizumab
Antidote for Dabigatran
Use if life threatening bleeding/uncontrolled hemorrhage
300
Rivaroxaban (Xarelto)
Factor Xa inhibitor
Reduce stroke and systemic embolism risk
DVT/PE phrophylaxis
CYP450
301
Apixaban (Eliquis)
Factor Xa inhibitor
Reduce stroke and systemic embolism risk
CYP3A4
302
Edoxaban
Latest factor Xa inhibitor
Stroke and systemic embolism prevention
PE/DVT treatment in patients who have been treated with parenteral anti-coagulant for 5-10 days
303
Bivalirudin
Parenteral direct thrombin inhibitor
Used in percutaneous coronary interventions after acute infarction and stent placement
304
Argotroban
Used in PCI and HIT management
305
Clopidogrel
Block platelet ADP receptor that activates fibronogen binding protein
Decrease platelet aggregation and clotting
306
Abiciximab
GpIIa/IIIa receptor antibody
Inhibits platelet aggregation
307
TPA
Tissue plasminogen activator = Clot breakdown
Ischemic symptoms ST elevation MI <12hr
PCI while stenting
Acute ischemic stroke within 3-4.5hrs of symptom onset
Use in PE management with associated shock
308
Physiological roles of cholesterol
Lipid component of membranes
Precursor o steroid hormones and Vit D
Source of bile acids which help in lipid digestion and absorption
309
Most abundant saturated fatty acid
Palmitic acid
310
Trans fatty acids
Lower HDL and raise LDL
Decrease membrane fluidity
311
Monounsaturated Fatty acids
Oleic Acid (18:1)
Mediterranean Diet
Lower LDL and Raise HDL
312
Polyunsaturated fatty acids
Omega 3 and omega 6
Lower LDL and raise HDL
313
Cholesterol biosynthesis
Fatty acid beta oxidation in mitochondria --> acetyl coA --> Citrate and exits mitochondria into cytoplasm --> Lyase splits citrate to Acetyl CoA --> Acetoacetyl CoA --> HMG CoA --> Mevalonate --> --> cholesterol
314
Rate limiting step of cholesterol biosynthesis
HMG CoA reductase
Rxn occurs in SER
315
HMG CoA reductase
Rate determining step of cholesterol biosynthesis
Cholesterol activates proteolytic degradation
Amount of enzyme controlled by induction/repression
Require NADPH
316
Stage 2 cholesterol biosynthesis
Mevalonate --> 5 carbon chain --> Combine to make 30 C chain Squalene
Require NADPH
317
Stage 3 cholesterol biosynthesis
Cyclization
Use NADPH
318
Stage 4 cholesterol biosynthesis
19 steps
Use NADPH and Oxygen
Cholesterol formation
319
Normal/high free cholesterol and HMG CoA reductase
SCAP-SREBP complex remains in ER membrane
No involvement with promoter region so no transcription/translation of HMG CoA reductase
320
Low free cholesterol and HMG CoA Reductase
SCAP-SREBP complex unstable and dissociates and goes to golgi to get cleaved --> SREBP binds to promoter region and induce HMG CoA reductase transcription/translation
321
Fates of cholesterol
Membrane structure
Precursor for steroid hormones and Vit D
Esterification for storage/elimination
Precursor to bile salts
322
LCAT esterification
For HDL transport to liver
323
ACAT esterification
Esterifies cholesterol making it hydrophobic
Clumps together in cytoplasm/vacuoles
Cell storage
324
Esterified cholesterol in liver
Can be made into bile acids
7-a-hydroxylase
Requires NADPH, Vit C
325
7 alpha hydroxylase regulation
Enzyme induction by cholesterol binding to liver LXR receptor --> --> enzyme production
Enzyme repression by bile acids
326
How to increase cellular cholesterol
Increase uptake
Increase biosynthesis
Cholesterol esterase
327
How to decrease cholesterol in cel
Esterification
Cholesterol metabolism to bile acids/steroids
Cholesterol release for transport to liver
328
Release of cholesterol from cell
Golgi directed trafficking to plasma membrane --> pumped to exterior surface by CERP --> Transfer to HDL
329
Statins
Compettive inhibitors of HMG CoA reductase
Act at low concentrations
Decreased cholesterol synthesis:
Liver = decreased VLDL output and decreased LDL production
Tissues = LDL induction and increased LDL uptake
Increase HDL
Need to monitor liver enzymes and CK for myopathies
330
Bile acid sequestering Resins
Reduced recycling lowers bile salt concentration --> Lowers feedback repression of 7a hydroxylase --> Increased cholesterol conversion to bile acids --> Lower cholesterol --> More LDL receptors --> Increased LDL uptake --> Lower plasma cholesterol
331
Nicotinic acid
Decrease release by adipose tissues of fatty acids to lower availability to making TAGs and cholesterol for VLDL
332
Fibrates
Lower curculating TG's
Improve HDL
333
Ezetimibe
Lowers intestinal absorption of dietary cholesterol
Binds to NPC1L1 protein on epithelial cells
334
Aneurysm definition
Abnormal localize dilatation of a tubular structure
335
Aneurysm etiology
Atherosclerosis
Congenital
Infection
Structural abnormalities
Vasculitis
336
Atherosclerotic aneurysm - Which vessel and complications?
Usually involve abdominal aorta
Complications:
1. Rupture with massive hemorrhage --> sudden death
2. Compression of adjacent structures
3. Occlusion of arterial branches
4. Embolism from mural thrombus with ischemia or infarction of distal extremities
337
Syphylitic aneurysms - vessel involved and complications
Usually ascending aorta
Can extend proximally to produce aortic valve annular dilatation and regurg
Clinical symptoms due to compression of adjacent structures
Lymphocytic/plasma cell infiltration
338
Dissecting aneurysms
Dissection of blood along a plane of cleavage through media of aortic wall, hematoma formation
HTN, bicuspid aortic valve, medial degeneration, aortic weakness, Marfans/EDS
339
Mechanism of dissecting aneurysm
Weakened media allows intima to buckle into lumen
Pressure wave of blood impacts on bulging intima to produce tear
Blood dissects through intima tear into media, BP promotes dissection along weakened media
340
Clinical features of dissecting aneurysm
Chest pain
Occlusion of arterial branches of aorta
Aortic valve regurg
Rupture with hemorrhage --> death
341
Vasculitis
Inflammation of vessel causing medial injury
Autoimmune
342
Giant cell arteritis
Chronic inflammatory disease of large sized arteries
Granulomatous, giant cells
Often cranial vessels
343
Clinical signs of giant cell arteritis
Headache
Tenderness of artery
Visual disturbances
344
Diagnostic testing for giant cell arteritis
ESR elevated
Temporal artery biopsy
345
Polyarteritis nodosa
Fibrinoid necrosis and acute inflammation of medium sized muscular arteries
346
Clinical signs and diagnosis of polyarteritis nodosa
Young adult-middle age
Symptoms vary by organs affected
Biopsy of affected organ for diagnosis
347
Granulomatosis with polyangitis
Granulomatous vasculitis of small arteries, arterioles, capillaries
348
GPA histo triad
Acute necrotizing granulomas of nose, sinuses, upper airways
Granulomatous arteritis or capillaritis of lung
Glomerulonephritis
349
Clinical signs of GPA
Middle aged
Male > Female
Infiltrate/mass in lung
Sinusitis
Renal abnormalities
Nasopharyngeal ulceration
350
Diagnostic studies for GPA
Nasal/sinus biopsy
Lung biopsy
Renal biopsy
ANCA (anti neutrophil cytoplasmic antibodies)
351
Cause of increase in CHD?
Longer life span
Smoking
Diet
Activity
352
Framingham study factors
Elevated cholesterol
HTN
Smoking
353
Seven countries study
Link between diet and heart disease
LDL as risk factor
354
Two main functional consequences of valvular disease
Stenosis - Failure of valve to open completely
Regurgitation - Failure of valve to close completely
355
Functional regurgitation
Regurgitation cause by dilatation of valvular annulus in setting of ventricular dilatation
356
Murmur
Abnormal heart sounds, caused by abnormal blood flow
357
Causes of aortic stenosis
Degenerative fibrocalcific aortic valve disease
Congenitally bicuspid aortic valve with degeneration
Postinflammatory valve disease
358
Causes of aortic regurgitation
Diseases that dilate aorta
Bicuspid aortic valve
Postinflammatory valve disease
Infective endocarditis
359
Causes of mitral stenosis
Postinflammatory valve disease (99%)
Radiation valulopathy
Rare diseases
360
Causes of mitral regurgitation
Myxomatous mitral valve degen (floppy), with mitral prolapse
Postinflammatory
Infective endocarditis
Papillary muscle rupture (MI)
Annular dilatation (ischemic heart disease with secondary LV dilatation)
Annular calcification
361
Degenerative fibrocalcific aortic valve disease
Age related - eldery
Dystrophic calcification on sinus side of aortic valve
Mitral valve normal or shows annular calcification
362
Physiological consequences of Senile aortic valve disease
Stenosis, with or without regurg
Increased pressure gradient across valve, LV hypertrophy without dilatation due to pressure overload
CHF or sudden cardiac death
363
Congenital bicuspid aortic valve
1-2% of population, silent until adulthood
Two unequal sided cusps
Dystrophic calcification on sinus side of valve at accelerated rate
Congenital ascending aortopathy - prone to developing aneurysms and dissections
Stenosis and LV hypertrophy
364
Mitral valve prolapse
Redundant leaflet tissue balloons back into LA during systole
Myxomatous degeneration of leaflet tissue
365
Mitral valve prolapse complications
Infective endocarditis
Mitral regurg
Stroke or systemic infarct from thrombi on leaflets
366
Physiological consequences of mitral valve prolapse
Regurgitation
LV hypertrophy and dilatation due to volume overload
LA dilatation
Increased risk for atrial and ventricular arrhythmias
367
Mitral annular calcification
Elderly women
No inflammation, valve leaflets mildly affected
Mitral regurgitation
Calcified particles may break loose and embolize
368
Rheumatic fever
Systemic autoimmune disease following Strep infection
Autoimmune rxn after bacterial antibodies cross react with normal tissue
Fever, migratory polyarthritis
Disease reactivated by new strep infections
Heart failure occurs after decades
369
Acute rheumatic heart disease - pancarditis
Myocarditis - Aschoff bodies
Pericarditis - fibrinous
Endocarditis - small non infectious vegetations
370
Aschoff body
Pathognomonic of rheumatic heart disease
Giant cells (Aschoff giant cells)
Histiocytes
Lymphocytes
Plasma cells
Surrounds a focus of
371
Chronic rheumatic heart disease
Deforming fibrosis of valves
Mitral valve almost always involved
Isolated mitral valve - 75%
Combined mitral/aortic valve - 25%
Tricuspid valve uncommon, PV rare
372
Pathology of rheumatic mitral valve disease
Diffuse fibrosis of mitral valve, calcification
Commissural and chordal fusion
373
Physiological consequences of rehumatic mitral valve disease
Usually stenosis but sometimes regurg or both
Severely dilated RA, no LV changes
Atrial arrhythmias
increased risk for left atrial thrombus and embolism
374
Infective endocarditis definition
Colonization or invasion of heart valves by microorganism
375
Predisposing factors of infective endocarditis
Preexisting valve disease
Congenital heart disease
Immunodeficiency
Any endocardial injury
376
Most commonly affected valves in infective endocarditis
Normal people - left sided valves
IV drug users - Right sided valves
377
Complications of infective endocarditis
Valve dysfunction - Regurgitation to due leaflet perforations or chordal rupture
Annular or myocardial abscess
Systemic/pulmonary emboli
Glomerulonephritis
378
Non bacterial thrombotic endocarditis
Formation of small vegetations on the endocardial surface due to an underlying hypercoagulable state - ABSENCE OF MICROBE INFECTION
1. Usually debilitated patients
2. Cancer patients esp mucinous carcinomas that produce circulating mucin --> can cause formation of small thrombi
379
Main causes of aortic stenosis
Bicuspid aortic valve
Aortic sclerosis
380
Bicuspid aortic valve
More susceptible to calcification
Often collagen disorder and dilation of ascending aorta
Symptoms only occur with stenosis
381
Aortic Sclerosis
Thickening/calcification of leaflets
Similar pathophys to atherosclerosis
382
Physical Findings of Aortic sclerosis but not severe stenosis
Systolic ejection murmur heard early in systole
Low grade murmur
383
Physical findings of aortic sclerosis w/ more severe stenosis
Systolic ejection murmur heard later in systole
Higher grade murmur
May lose S2
Decrescendo murmur @AV due to aortic insufficiency
Carotid pulses have delayed upstroke and decreased amplitude
384
Symptoms of severe aortic stenosis
1. Angina
2. Syncope
3. Dyspnea on exertion
385
Chest XR findings for Aortic stenosis
Subtle findings
Prominent LV
Calcification of AV
386
EKG findings in aortic stenosis
LV hypertrophy so increased QRS amplitude
387
Echocardiography for aortic stenosis
Identify # of leaflets
Identify calcification of valves
Measure pressure gradient and vavlular area
Measures velocity of blood through valve: Increased stenosis = increased velocity
>4m/s is severe stenosis
388
Valve pressure gradient and area in aortic stenosis
>40mm Hg
<1cm squared area
Consistent with severe aortic stenosis
389
Cardiac catheterization
Performed when echo indicates severe aortic stenosis and valve replacement is planned
Measures pressure gradient and valvular area
390
Length of time to death with aortic stenosis symptoms
Angina - 5 yrs
Syncope - 3 years
Dyspnea on exertion - 2 years
391
Aortic stenosis therapy
No treatment, valve replacement needed
392
Mechanical valve replacement
Durable and long lasting but are susceptible to thrombosis
Pt on anticoagulants for life
393
Bioprosthetic valve replacement
Use synthetic material or animal
No need for anticoagulants but not as durable as mechanical valve
394
VTE prophylaxis
1. Early ambulation
2. Sequential compression devices
3. Anticoagulation
395
2 most common symptoms of chest pain
Dyspnea
Chest pain
396
Acute cor pulmonale
Large PE
RV failure caused by primary disorder of respiratory system
Symptoms: Shock, collapse, syncope
Exam: Hypotension, distended neck veins
CXR: Normal
ABG's: Decrease pO2, decreased CO2
EKG: S1Q3T3
397
Acute unexplained dyspnea
Medium sized PE
SOB without syncope and no chest pain
Elevated RR
Normal ECG, CXR
Differential: CHF, hyperventilation
398
Pulmonary infarction
Occlusion of small vessel with no collateral circulation --> infarction
Acute pleuritic pain
Dyspnea +/- hemoptysis
Tachypnea
Crackles/wheezes/rub in lungs
CXR: Consolidation in lung periphery, possible effusion
Ddx: Pneumonia
399
Wells Criteria
Probability score based on symptoms/history
400
D dimer
Sensitive test for PE
Not specific
D dimer = clotting is occurring
401
Chest CT for PE
Sensitive and specific
402
Ventilation Perfusion scan
Substitute for Chest CT
Pregnant women/women of child bearing age
Pts with normal/near normal CXR
Abnormal renal function so risk with contrast
403
Prophylactic PE treatment
Anticoagulation - decrease further clotting and allowing fibrinolytic system to activate
IVC interruption
404
Definitive PE treatment
Thrombolytic therapy - bleeding risk
Pulmonary embolectomy
405
Left main coronary artery branches
Left anterior descending
Circumflex (lateral)
406
Right main coronary artery
Descends as posterior descending artery
407
Most common sites for grade 4 atherosclerotic lesions
Proximal 1/3 of LAD and LCX and most of RCA
408
Angina Pectoris definition
Ischemic heart pain
Can be Stable, Unstable, Variant
409
Stable angina
Poor blood flow through atherosclerotic lesions
Exacerbated with exercise
Resolves with nitroglycerin
410
Unstable angina
Highly occluded artery - thrombus and possible embolus
Pain at rest and gets worse over time
411
Prinzmetal angina
Variant
Due to vasospasm
412
Acute myocardial Infarction
Ischemic necrosis of portion of myocardium
413
Transmural infarction
Entire or nearly entire ventricular wall thickness
414
Subendocardial infarction
Less than 1/3 of inner wall
415
Complications of myocardial infarction
Sudden death
Cardiogenic shock
Transmural infarct --> ventricular aneurysms or mural thrombi (embolization)
Cardiac rupture
416
Sudden cardiac death
Death when not expected, usually due to coronary artery disease
417
End stage ischemic heart disease
Progressive CHF due to ischemic heart disease
Most common indication for heart transplant
418
Determinants of myocardial oxygen demand
Heart rate
Afterload
Preload
Contractility
419
Myocardial oxygen supply
Coronary blood flow
Coronary perfusion pressure (aortic diastolic pressure)
420
Organic nitrates
Nitroglycerin & Isosorbide dinitrate
MoA: Prodrug for Nitric oxide --> venous decrease in vascular resistance --> decrease preload --> Reduce myocardial oxygen demand
421
Nitroglycerin
Used for treatment and prophylaxis
Sublingual to bypass liver
Side effects - Tolerance, headache, syncope, interaction with PDE5 inhibitors
422
Isosorbide dinitrate
Slow acting so only use for prophylaxis
Headache, tolerance, PDE5 inhibitor interaction
423
Beta blocker MoA
Decrease heart rate, contractility, BP during exercise
Contraindications - bradyarrythmias, HF, AV block, asthma
424
Ca Channel blocker MoA
Block L type calcium channels --> vasodilation, decreased contractility, decreased AV conduction
Decrease demand and increase supply (coronary artery vasodilation)
AE: Hypotension, constipation, HF, AV block, edema
425
Ranolazine
Inhibits inward Na channels
Unknown angina mechanism
Use when other drugs don't work
Long QT
426
Atrial flutter ECG characteristics
Rapid atrial activity (~300bpm)
Reentrant circuit around Tricuspid valve
Saw toothed pattern
427
Atrial fibrillation ECG characteristics
Chaos
Multiple reentry circuits
Numerous atrial depolarizations and only some become QRS
Irregularly irregular
428
Class I anti arrhythmia drugs
Sodium channel blockers
429
Class II anti arrhythmia
Beta blocker
430
Class III anti arrhythmia
K channel block
431
Class IV anti arrhytmia
Calcium channel blocker
432
Lidocaine
Na channel blocker
Greatest affinity for inactivated channels
Decreases automaticity
Decrease phase 4 slope
433
Lidocaine uses
V tach
V fib
434
Lidocaine adverse effects
CNS stimulation
435
Amiodarone
Class III
Block Na, K, Ca channels
Alpha/Beta blocker
436
Amiodarone effect on: AP duration
Refractory period
Conduction velocity
PR, QRS, QT intervals
AP duration - Prolonged
Refractory period - Prolonged
Conduction velocity - Slowed
Intervals - prolonged
437
Amiodarone uses
V tach
V fib
Atrial fib when structural disease present
438
Amiodarone toxicities
Cutaneous
Eye - Corneal deposits, optic neuritis
Lung - fibrosis
Cardiac - VT/VF
Liver - hepatitis
Thyroid - Hypo/hyper
439
Amiodarone drug interactions - pharmacokinetic
Warfarin b/c inhibits CYP450
Digoxin - P-gp inhibition
440
Beta blocker effect on:
SA/AV automaticity
AV nodal conduction
AV nodal refractory period
Net effect
Automaticity in SA/AV - Decreased
Nodal conduction - Slowed
Nodal refractory period - Prolonged
Net effect - Cardiac slowing
441
A fib drug indication
Metoprolol
442
Beta blockers and arrhythmias
A fib with RVR
A flutter
PSVT
Tachycardias
443
Beta blocker AE
CV - aggravation of severe CHF, slow AV conduction
Pulmonary - Bronchospasm in severe asthmatics
444
Beta blocker drug interactions
Drugs that impair Av conduction (Digoxin, Ca channel blocker)
445
Calcium channel blockers
Blocks activated/inactivated CA channel
Slow AV conduction
446
Indications for Ca channel blockers
SVT - slows ventricular rate
A fib - slow ventricular rate
447
a wave
atrial contraction
448
c wave
RV contraction
TV bulging into RA
449
v wave
Increased RA pressure due to fill against closed TV
450
Fixed splitting
Heard in ASD
Increased flow through RV so pulmonary valve closure is delayed
451
Aortic area - systolic murmur
Aortic stenosis
Aortic valve sclerosis
Flow murmur
452
Pulmonic area - systolic ejection murmur
Pulmonic stenosis
Flow murmur
453
Tricuspid area - holosystolic murmur
Tricuspid regurgitation
VSD
454
Tricuspid area - diastolic murmur
Tricuspid stenosis
ASD
455
Mitral area - holosystolic murmur
Mitral regurgitation
456
Mitral area - systolic murmur
Mitral valve prolapse
457
Mitral area - diastolic murmur
Mitral stenosis
458
ACCF/AHA Stage A
At risk for HF but no symptoms or structural disease
459
ACCF/AHA Stage B
Structural disease but without signs/symptoms of HF
460
ACCF/AHA Stage C
Structural heart disease with prior/current symptoms of HF
461
ACCF/AHA Stage D
Refractory HF
Require special intervantion
462
NYHA I
No limitation of physical activity
463
NYHA II
Slight limitation of physical activity
Comfortable at rest but normal physical activity = HF symptoms
464
NYHA III
Marked limitation of physical activity
Comfortable at rest but less than ordinary activity = HF symptoms
465
NYHA IV
Unable to carry on any physical activity without HF symptoms
HF symptoms at rest
466
Leading causes of HF
Ischemic heart disease
Cardiomyopathy
467
Alcoholic cardiomyopathy
Dilated cardiomyopathy
468
Cocaine cardiomyopathy
Long term use
Dilated cardiomyopathy without CAD, vasculitis, or MI
469
Heart failure pathogenesis
Index event (MI etc) that decreases pumping capacity of heart --> compensatory mechanisms activated, restore CV functions so patient asymptomatic --> Long term compensatory mechanisms lead to secondary end organ damage within ventricle --> LV remodeling and cardiac decompensation
470
Compensatory mechanism long term effects - Sympathetic system
Renin release
Can lead to:
Desensitization of Beta receptors
Myocyte hypertrophy, necrosis, apoptosis, fibrosis
Vasoconstriction in kidneys
471
Compensatory mechanism long term effects - RAS
Can lead to:
Increase salt/water retention --> increased preload
472
Aldosterone actions in compensatory response
Increase Na absorption and K excretion
Stimulation of collagen synthesis --> fibrosis (remodeling)
473
ADH actions
Thirst stimulation
Water reabsorption
Vasoconstriction with increased SVR
474
Long term effects of Salt/water retention
Caused by RAS, sympathetic, and ADH release
Pulmonary congestion and peripheral edema
475
Long term effects of vasoconstriction
Caused by sympathetic and RAS
Increased cardiac afterload --> more energy needed from LV and further dysfunction
476
Long term effects from sympathetic stimulation
Increased energy expenditure of heart --> can cause arrhythmias
477
Short term effect of cardiac remodeling due to RAS/Sympathetic
Adaptive remodeling
Increased sarcomere number with increased CO
478
Long term effect of cardiac remodeling due to RAS/sympathetic
Maladaptive
Accelerated cell death, arrhythmias, pathologic remodeling
479
Platelets COX enzyme and PG activity
COX-1
Thromboxane
Vasoconstriction, platelet aggregation
Thrombosis
480
Gastric mucosa COX enzyme and action
COX 1
Gastric protection (less acid)
481
Joints COX enzyme and action
COX 2
Pain
Inflammation
482
Endothelial cells COX enzyme and action
COX 2 mainly (slight COX1)
Vasodilation
Decreased platelet aggrefation
483
Celecoxib
Selective COX-2 inhibitor
484
Aspirin
Covalently modifies COX-1/2
Irreversible binding
485
NSAIDs
Reversible block of COX enzymes
486
How to limit Acetaminophen toxicity
N-acetylcysteine
Detoxifies NAPQI
487
NSAIDs and pregos
NO!!!
488
ACEH
Acid cholesterol ester hydrolase
Hydrolysis of cholesterol esters to form FFA and free cholesterol
489
What increases LDL receptor formation?
Low INTRACELLULAR cholesterol concentration
SREBP mechanism induces transcription/translation of LDL
490
VLDL: Source, ApoProteins, function
Source: Liver
ApoProteins: CII, E, B100
Function: FFA to adipose/muscle
CE --> LDL
491
IDL: Source, apoProteins, function
Blood
E, B100
CE --> Liver via ApoE R
492
LDL: Source, ApoProteins, Function
Blood
B100
CE --> peripheral cells via B100
493
HDL: Source, apoP, function
Liver
A1, CII, E
Supply CII and E to VLDL
Reverse cholesterol transport
494
LPL: Site of action, activator, function
Capillary walls
ApoCII
Excise FFA from TG in VLDL for use by adipose and muscle
495
ACAT: Site of action, activator, function
Inside cells
Free cholesterol
Esterify cholesterol for storage
496
LCAT: Site of action, activator, function
Blood
ApoA1
Esterifies free cholesterol and adds to HDL for transport to liver
497
CERP: Site of action, activator, function
Plasma membrane
ApoA1
Flips Cholesterol and Lecithin to outer layer of membrane for LCAT action
498
MTP: Site of action, activator, function
Intestine/liver/smooth ER
Loads TAG onto B100
499
ApoA1: Site of action, function
Blood/plasma membrane
Activates LCAT/CERP. Binds ApoA1 receptor on cells for cholesterol extraction
500
ApoB100: Site of action, function
Liver, cells
Ligand for LDL receptor, export/packaging of VLDL from liver into blood
501
ApoCII: Site of action, function
Capillary walls
Activate LPL
502
ApoE: Site of action, function
Liver
Return of IDL/LDL to liver after LPL activity
503
Adenosine
Antiarrhythmic
Slow HR by decreasing K conductance
Bronchoconstriction
504
Isoproterenol
B1 B2 direct agonist
Bronchodilator
Treat for heart block/arrest, shock
AE: HR increase, BP decrease
505
Dobutamine
B1 direct agonist
Heart failure, cardiogenic shock
AE: Tachycardia, arrhythmias
