General, Week 2 Cardio Flashcards
1
Q
what do patients with restrictive cardiomyopathy present with?
A
congestive heart failure or sudden death
decreased filling, back up
2
Q
what do you see in histo of:
viral myocarditis transplant rejection myocarditis hypersensitivity myocarditis fungal/TB myocarditis: bacterial myocarditis:
A
viral myocarditis: lymphocytes
transplant rejection myocarditis: lymphocytes
hypersensitivity myocarditis: eosinophils
fungal/TB myocarditis: giant cells
bacterial myocarditis: neutrophils
3
Q
will the RV hypertrophy in a VSD?
what will happen?
A
no, blood doesn’t stay in for long enough
pulmonary hypertension, L heart dilatation
4
Q
what is natriuretic peptide ? what does it do?
A
a peptide hormones secreted from the atria
promotes salt and water excretion and lowers blood volume, lowers blood pressure
5
Q
Vasopressin
receptor(s)
effect
use
A
Vasopressin 1 (V1) on blood vessels
vasoconstriction –> increase SVR –> increase MAP
can add to NE for septic shock
6
Q
in what congenital heart defects do you see early cyanosis?
general concept specific names (5):
A
R to L shunts
Tetralogy of Fallot Transposition of the great vessels patent Truncus arteriosus Tricuspid atresia Total anomalous pulmonary venous connection (TAPVC)
7
Q
what myopathy has a dilatation of the R ventricle and fatty deposits in the RV?
A
arrythmogenic cardiomyopathy
8
Q
why does the resting HR decrease in an athlete?
A
after training, there is an increase in heart mass (LVH), allowing for increased contractility, HR can decrease
9
Q
what do you see on histology of the L ventricle in hypertrophic cardiomyopathy?
high yield
A
disarrayed myofibers with hypertrophy
10
Q
name the equation for blood flow (Q) to an organ:
A
Q = perfusion pressure/resistance
11
Q
vascular ________ receptors are more sensitive to epinephrine than _______ receptors
thus, at low levels, epi release causes ____________
at high levels, epinephrine release causes __________
A
beta-2, alpha-1
vasodilation
vasoconstriction
12
Q
what is the treatment for an AVSD?
A
fix by 1 year of age
13
Q
what three organs get the greatest blood flow/gram?
A
kidneys, then heart, then brain
14
Q
systemic reduction in tissue perfusion resulting in decreased tissue oxygen delivery
A
shock
15
Q
what problems do you see in dilated cardiomyopathy?
in terms of electrical
valves
output
A
electrical - arrhythmias due to stretching
valves: pull down, tricuspid and mitral regurgitation
output: decrease, can’t contract as strongly
- -> biventricular heart failure
16
Q
Preload = EDV, ______ pressure
A
wedge
17
Q
in tricuspid atresia/single ventricle, what happens to the L ventricle?
A
hypoplastic L ventricle
18
Q
in an organ that shows autoregulation, if the perfusion pressure falls, the vascular resistance must _______ to maintain flow
A
fall
vasodilation
19
Q
what is the murmur in a PDA?
A
continuous, machine-like murmur
20
Q
initial emergent treatment for the transposition of great arteries (2):
long term?
A
- give prostaglandin E (keep PDA)
- balloon atrial septostomy (rip open - make ASD)
switch surgery is long term (including coronary arteries)
21
Q
what are the ABCDEFG’s of reading a radiograph
A
A – airway – should be in midline (trachea)
B – bones
C – cardiac silhouette (heart size, less than half of angle-angle)
D – diaphragm (should have nice curve)
E – edges of heart (pneumonias will obliterate certain edges)
F – lung fields
G – gas bubble (below L diaphragm)
22
Q
coartaction of the aorta is most commonly seen with what other CHD:
A
bicuspid aortic valve
23
Q
benazepril
what is this?
adverse effects
A
ACE-I
cough, angioedema, TERATOGEN, hypotension, hyperkalemia, renal failure
24
Q
sodium nitroprusside
use
mechanism
hemodynamics
side effects
A
hypertensive emergencies
release NO (cGMP - vascular smooth muscle relaxation)
Balanced arteriolar and venous dilation (decrease in preload and SVR)
hypotension, possible cyanic and thiocyanate intoxication
25
myogenic theory:
When blood pressure in arterioles increases, SMCs _________, causing an ___________ in vascular resistance, which decreases the blood flow.
When blood pressure in arterioles decreases, SMCs _______, causing a ________ in vascular resistance, and increase in blood flow
contract, increase
relax, decrease
26
what explains the phenomenon flow induced vasodilation?
shear stress activating endothelial cells to release NO, relaxation/dilation
27
in isolated aortic valve stenosis (CHD) what do you see in the heart structure?
LVH
mitral regurgitation
LA dilitation
28
Filling pressure (volume) = wedge pressure = pre-load estimation of ____
EDV
29
major side effects (2) of the diuretics (chlorthalidone):
drug-disease effect:
drug-drug interaction:
1. hypokalemia
2. electrolyte imbalance
increases risk of gout
NSAIDs
30
why is there cyanosis in tricuspid atresia/single ventricle?
because there is one pump for the whole body, the RA must give deoxy blood to LA, and LV.
in the common ventricle, all of the blood mixes
31
drugs that end in "-pril" are -
ACE inhibitors
32
what is the most important factor in pulmonary vascular smooth muscle tone?
local metabolic control (intrinsic)
33
in aortic valve atresia with intact ventricular septum, what do you see in the heart?
PDA needed to live
mitral valve, ascending aorta, LV all hypoplastic
34
how do patients with myocarditis present?
with arrhythmia, heart failure, fever, dyspnea, fatigue
35
during exercise, what is the most important factor in vascular smooth muscle tone?
local metabolic control
36
when a left to right shunt shifts to right to left because of pulmonary hypertension, this is called _________ syndrome. What do you note about the color of the patient?
Eisenmenger
turns acyanotic to cyanotic
37
what is the most common ASD?
esteem secundum type
38
list the 5 classes of 1st line antihypertensives:
1. Thiazide type diuretics
2. ACE-I
3. Angiotensin receptor block
4. Calcium channel blocker
5. Beta blocker
39
in an organ that shows autoregulation, if the perfusion pressure increases, the vascular resistance must _______ to maintain flow
increase
vasoconstrict
(think about equation)
40
a MAP < _______ means hypotension
[MAP] <65 mmHg
41
what are the features of a partial AVSD?
primum type ASD, mitral valve cleft (mitral regurgitation)
42
drugs that end in "-olol" are:
beta blockers
43
amlodipine
```
use/class
mechanism
hemodynamic effect
```
antihypertensive, dihydropyridine calcium channel blocker
Bind to L-type Ca++ channel, decrease amount of calcium available for vascular smooth muscle and cardiac muscle contraction.
vasodilation, decrease SVR, increase BP
44
the net result of direct sympathetic input to the heart results in what tone of the coronaries? why?
vasodilation
the alpha and beta counteract, the local metabolites due to the increased rate and force of the heart (sympathetic input) predominate
45
IMAGING: a term that you lose a portion of the anatomy or visualization of the normal structure since there is an adjacent disease
silhouette sign
46
Phenylephrine
receptor?
function?
alpha-1 purely.
vasoconstriction, increase SVR, increase BP
47
what is the most common comorbidity (of CHD) in people with a coarcted aorta?
bicuspid aortic valve
48
to regulate how much blood flow an organ gets, what is changed at the organ level?
vascular resistance (at arteriolar level)
49
what do you see on microscopic examination of hypertensive heart disease?
grossly?
increased myocyte diameter with increase in nuclear size nuclei often appear "squared off" or "box-car" shaped
L ventricular hypertrophy
50
what is the characteristic primary physiologic derangement of disruptive shock
afterload increase
51
in hypertrophic cardiomyopathy, what is the main finding grossly?
is the problem systolic or diastolic? why?
massive hypertrophy of LV ventricular septum
diastolic - decreased LV compliance, decreased filling, decreased CO
52
when first line antihypertensive drugs fail or can't be used, __________ is used
hydralazine
53
what are some examples of metabolites that locally affect blood vessel diameter?
K+, H+, lactate, adenosine, CO2
54
metropolol
```
use/class
mechanism
hemodynamic effect
```
antihypertensive (first line only in special cases)
cardioselective beta blocker
decrease cardiac output (HR and contractility), decrease renin secretion, decrease in BP
55
what organs show autoregulation of vessel tone?
brain, kidneys, heart, skeletal muscle
56
what are the three things to look for when determining a chest x-ray quality? how do you check them?
R - rotation (is the spinner process between the clavicular heads?)
I - inspiration (5-6 anterior ribs)
P - penetration (should perceive spine behind the heart, and descending aorta)
57
Turner syndrome is associated with what two congenital heart defects?
coarctation of the aorta
| bicuspid aortic valve
58
tricuspid atresia/single ventricle what do you need in order to live?
ASD/VSD or PDA
59
chlorthalidone
```
use/class
mechanism
hemodynamic effect
```
antihypertensive
thiazide type diuretic
Blocks the Na+/Cl- cotransporter of the distal convoluted tubule of the kidney. Increased secretion of water.
Over time, lower TPR for the long term hypotensive effect
60
compelling indications for beta blockers
Heart failure with reduced EF mortality After myocardial infarction
61
the Swan-Ganz catheter measures _____ _____ pressure. This is the "wedge pressure". Wedge pressure = __________ pressure
left atrial
filling
62
what are the two most important factors in local control of the coronary artery vascular tone?
adenosine, hypoxia (decreased O2)
63
why does metabolic acidosis occur in shock?
with hypoxia, can't get sufficient ATP from aerobic respiration
produce lactate through the utilization of anaerobic respiration
64
what organ gets the most cardiac output?
liver, then kidneys
65
how do you diagnose myocarditis?
RV sample (biopsy)
66
what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in HYPOVOLEMIC SHOCK
preload decreases
cardiac output decreases
afterload increases (increased SVR as a reflex)
67
what septal defect is most commonly found in patients with Down syndrome?
AVSD
68
what factors dominates vascular tone in skeletal muscle at rest?
the sympathetic input - tends to vasocsontrict
69
what do histamine and bradykin do?
to arteries/veins
permeability
arteriolar vasodilation, venous constriction
increase in permeability
70
define a cardiomyopathy:
myocardial disease leading to cardiac dysfunction
| abnormality of cardiac muscle cells
71
list some humeral factors? (4)
circulating catecholamines (indirect from the ANS)
Nitric Oxide
Vasopressin
Angiotensin 2
72
what is the most important factor in skin vascular smooth muscle tone?
sympathetics - ANS (extrinsic)
73
what is the main feature of restrictive cardiomyopathy grossly? secondary problems?
what does this mean hemodynamically? diastolic or systolic?
increased wall stiffness, biatrial dilation
limits ventricular stretch - causes decreased filling
DIASTOLIC dysfunction
74
explain the basis of the myogenic theory: what happens when a vessel is stretched?
when vascular smooth muscle is stretched, it contracts
75
Norepinephrine
receptor(s)?
function?
most commonly used to treat:
alpha-1 and beta-1 adrenergic receptors
potent vasoconstriction as well as an increase in cardiac output (HR, force)
septic shock
76
what is the most common finding in the sudden death of a young athlete?
what would you find on autopsy? grossly, histo
hypertrophic cardiomyopathy (genetic)
hypertrophy LV septum
disarray of muscle fibers on autopsy pathology
77
what are the two key findings in a NORMAL lateral CXR
1. The clear triangles (should be clear in a normal patient)
Retrosternal
Retrotracheal
Retrocardiac
2. The spine should become more visible towards the diaphragm
78
what happens to the heart anatomy with an ASD over time?
lungs?
RV hypertrophy, RV/RA dilatation (right heart enlargement)
could cause pulmonary vascular occlusive disease
79
what could cause blunting of the costophrenic angles seen on chest x-ray?
PLEURAL EFFUSIONS
80
why does cardiac output increase during exercise?
HR and SV increased significantly
81
the formation of NO is stimulated by two things, what are they?
1. Agonists (Ach, bradykinin, thrombin, substance P)
| 2. Shear stress
82
what are the (2) methods to help prevent formation of pulmonary edema?
1) starling forces favor fluid resorption in lung (oncotic pressure high)
2) significant lymphatic system
83
what is the largest problem in the persistent truncus arteriosus after the baby is born?
since the circulations are mixed, the decreasing pulmonary resistance in the lungs after birth makes all the blood flow there
early CHF
84
what are the findings grossly of arrhythmogenic cardiomyopathy?
is it a systolic or diastolic finding?
fibrosis and fatty replacement of ventricles, especially the R ventricle! R ventricular dilatation
systolic - decreased contractility with arrhythmias, can result in sudden death at a young age
85
what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in CARDIOGENIC SHOCK
```
preload increases (backup of blood)
cardiac output decreased (impaired heart function)
afterload increases (SVR increased as a reflex)
```
86
list the 5 common features of shock:
1. hypotension
2. cold/clammy skin
3. oliguria
4. change in mental status
5. metabolic acidosis
87
vasopressin (ADH) does what (2)?
what releases it?
released by posterior pituitary
acts on collecting ducts to decrease secretion water, also a potent vasoconstrictor
88
how does a child compensate for coarctation of the aorta if they survived infancy (2)?
what physical findings (3)?
LV hypertrophy
collateral flow
hypertension in arms, decreased femoral pulses, rib notching
89
K+, H+, lactate, adenosine, CO2
tend to cause:
smooth muscle relaxation - vasodilation
90
calcium channel blockers
adverse side effects
DDI
hypotension, headache (vasodilation), constipation, heart failure, AV block
DDI - with drugs acting on AV node (do not take diltiazem and a beta blocker or digoxin for example)
91
what is the primary way by which the coronary blood flow is regulated?
local metabolic control
92
when severe, pulmonary hypertension can cause _____________ syndrome
Eisenmenger
93
what would you find in terms of preload (central venous pressure measurement), pump function (cardiac output) and after lad (SVR) in DISTRIBUTIVE SHOCK
```
preload (less or equal)
cardiac output (increases to try to make up for decreased SVR)
afterload decreases (SVR decreased significantly)
```
94
the __________ (diastolic, systolic) cardiomyopathies generally result in arrhythmias
systolic
dilatation!
95
in dilated cardiomyopathy, what is the main finding grossly?
is the problem systolic or diastolic? why?
massive dilation of all 4 chambers (BIG HEART)
systolic - unable to contract as strongly, biventricular heart failure
96
in TAPVR - total anomalous pulmonary venous return, what is the problem?
there is no connection between pulmonary veins and L atrium
atrium does not get oxygenated blood (obligate R to L shunt - CYANOSIS)
97
what are the most common causes/associations of restrictive cardiomyopathy?
```
amyloidosis (50%) - lodge in myocardium - stiff
blood eosinophilia (35%)
sarcoidosis
```
NOT necessarily familial
98
what are the features of a complete AVSD?
ASD, VSD, and a COMMON AV valve (batman logo)
99
what is the most important factor in cerebral vascular smooth muscle tone?
local metabolic control (intrinsic)
100
what is the most important factor in coronary vascular smooth muscle tone?
local metabolites (intrinsic)
101
what are the main cause(s) of arrhythmogenic cardiomyopathy?
familial
102
why does stroke volume increase during exercise?
sympathetic input to beta-1, increased contractility, decreased ESV
increased venous return (many mechanisms), increased EDV
103
what are the most common causes of hypertrophic cardiomyopathy?
GENETIC (100%) in cardiac sarcomeric proteins
104
what is the most important factor in renal vascular smooth muscle tone?
local metabolic control (intrinsic)
105
what is the characteristic primary physiologic derangement of cariogenic shock
decrease in pump function
106
what is the murmur in pulmonary valve stenosis?
harsh, systolic ejection murmur
107
Dobutamine
receptor(s)
effect
beta-1 agonist (selective)
increase HR and force
108
what determines the prognosis in tetralogy of fallot?
degree of sub-pulmonic stenosis
109
what are the two key findings in a NORMAL lateral CXR
1. The clear triangles (should be clear in a normal patient)
Retrosternal
Retrotracheal
Retrocardiac
2. The spine should become more visible towards the diaphragm
110
what is the incidence of Eisenmengers syndrome in atrial septal defects?
Large VSDs? Small VSDs?
10% - ASD
100% - large VSD
0% small VSD
111
who should you NOT give beta blockers to? (6)
5 - conditions
1 - drug adverse reaction
people with asthma, COPD, AV block, severe unstable heart failure, occlusive peripheral vascular disease
OR anyone that is taking drugs that impair AV conduction (digoxin, some Ca channel blockers)
112
what blood vessel has the most amount of vascular basal tone?
skeletal muscle
113
hydrazine
use
mechanism
hemodynamics
adverse effects
antihypertensive - second line
Mechanism: Direct relaxation of smooth muscle by actions that are not well understood.
Hemodynamics: Decrease in SVR.
Adverse effect: Reflex tachycardia lupus-like syndrome.
114
how is the microcirculation of the heart designed to most efficiently extract O2 from blood? (2)
the capillary density of the heart is much greater
the cardiac muscle cells are smaller
decreased travel distance --> increased efficiency
115
in what types of shock is administration of fluids the initial treatment needed?
next line?
hypovolemic and distributive shock
vasopressors (sympathomimetics)
116
what are the main problems and outcomes of hypertrophic cardiomyopathy?
decreasing filling because of decreased LV compliance, ventricular arrhythmias can cause sudden death at a young age
ALSO can block outflow track (syncope with exercise)
117
pulmonary hypertension is seen most common with what congenital heart defect?
what histo changes can be seen due to the increased blood pressure in lungs?
ventricular septal defects
hypertrophy, plexiform lesions
118
Blood flow in coronary arteries ________ during heart contraction. why? (2)
1. the arteries are compressed (increased resistance, decreased flow)
2. the aortic valve flaps up against the openings
119
what kind of murmur would you hear with a AVSD?
a systolic ejection murmur at the pulmonic valve
| increased flow
120
drug for hypertensive emergencies:
sodium nitroprusside
121
which has a higher basal tone? kidney or skeletal muscle?
why?
skeletal muscle, there is a greater vasodilatory reserve
122
what is the ebstein anomaly?
displacement of tricuspid valve leaflets downward into RV
Associated with tricuspid regurgitation and right HF.
123
what is the initial problem in embryology leading to transposition of the great arteries??
the conotruncal septum does not spiral. it divides but does not spiral
124
define the blood pressures for hypertension
systolic > 140, diastolic > 90
125
name three general mechanisms in which to change the basal tone of a vessel:
1. direct autonomic control (sympathetics)
2. humeral factors
3. local myogenic and metabolic factors
126
on histology, you find inflammatory cells in the myocardium, causing myocyte damage. What is this disease?
myocarditis
127
how does NO (once formed) cause vasodilation?
produces cGMP, activating the phosphatase to dephosphorylate myosin, relaxation
128
what are causes of myocarditis? (4)
1. infectious (viral, bacterial, etc)
2. autoimmune reactions (SLE, drug reactions)
3. rejection of heart transplant
4. idiopathic (i.e. sarcoidosis)
129
what is the treatment for a patent ductus arteriosus?
indomethacin - decreases prostaglandin E, which closes the shunt
130
diltiazem
```
use/class
mechanism
hemodynamic effect
```
antihypertensive, non-dihydropyridine calcium channel blocker
Bind to L-type Ca++ channel, decrease amount of calcium available for vascular smooth muscle and cardiac muscle contraction.
ALSO decreases AV node and contractility.
vasodilation, decrease SVR, increase BP
131
what is the prevalence of Eisenmengers in PDA? what does it cause?
80%, causes lower extremity cyanosis
132
losartan:
```
use/class
mechanism
hemodynamic effect
```
antihypertensive
angiotensin receptor blocker
decreases SVR (heart rate and output unchanged), decreasing BP
133
do not take a calcium channel blocker (L-type Ca channels) and a medication that decreases _________ firing, such as:
AV node firing
a beta blocker, digoxin
134
what happens to blood pressure in a trained individual? why?
it decreases due to more compliant large arteries
135
what are the 4 things you see in tetralogy of fallot?
1. Sub-pulmonic valve stenosis
2. R ventricular hypertrophy
3. VSD
4. overriding aorta
136
benazepril
```
use/class
mechanism
hemodynamic effect
```
antihypertensive, ACE-I
inhibits angiotensin converting enzyme (ACE) to reduce formation of angiotensin 2 and aldosterone, also inhibits lysis of bradykinin
decreases SVR, decreasing BP
137
what is the main goal of surgery in tricuspid atresia/single ventricle
separate the pulmonary and systemic circulations
138
Dopamine
low dose
medium dose
high dose
Low dose: dopamine-1 receptors in the renal, mesenteric, cerebral, and coronary beds, resulting in selective vasodilation
Moderate dose: beta-1 adrenergic receptors and increases cardiac output (HR, force)
High doses, alpha-1 receptors --> vasoconstriction with an increased SVR.
Dopamine may be used in hypotension due to sepsis or cardiac failure, but is not a first line drug for either
139
NO is released by __________ cells and promotes ________
endothelial cells
vasorelaxation
140
what does bradykinin do?
what breaks it down?
vasodilator - releases NO
ACE
141
metropolol
what is it
adverse effects
cardioselective beta blocker
aggravation of severe HF, aggravation occlusive arterial disease, slows AV conduction
142
what are the most common causes of dilated cardiomyopathy?
what is the treatment?
familial (60%)
alcoholism
pregnancy
previous myocarditis
transplant
143
why is the baby cyanotic in persistent truncus arteriosus?
the oxygenated and deoxygenated blood are mixed in the common trunk before getting to their circulations
144
what do patients do in response to cyanotic spells (tet spells) when they have tetralogy of fallot?
they squat
| kink femoral arteries, increase SVR, decrease the R to L degree of shunting
145
what is the characteristic primary physiologic derangement of hypovolemic shock
decreased preload
146
sympathetic direct innervation will cause vasoconstriction at the ______ receptors and vasodilation of vessels that have ______ receptors
alpha-1 - vasoconstriction
beta-2 (skeletal muscle)
147
in pulmonary valve atresia with an intact ventricular septum, what do you need? what do you find in the heart secondarily?
need intact PDA
hypoplasic tricuspid valve and RV
148
what cardiomyopathy is unique in mainly affecting the Right Ventricle?
arrythmogenic cardiomyopathy
fibrosis, fatty replacement, and dilatation of RV
149
in a sedentary person vs an athlete, what is the difference in CO? why?
there is no difference in CO
the HR decreases and SV increases in an athlete
150
in isolated pulmonary valve stenosis (CHD), what are the secondary cardiac findings?
RVH
tricuspid regurgitation
dilatation pulmonary artery RA
151
Epinephrine
```
receptor(s)
function (low dose/high dose)
```
uses
beta-1, beta-2, alpha-1
Low doses: increase CO (beta-1), vasoconstriction (alpha-1) is offset by the vasodilation (beta-2).
Higher doses, the alpha-1 effect predominates beta-2 producing an increase in SVR in addition to an increase in CO.
anaphylaxis
152
drugs that end in "-sartan" are:
angiotensin receptor blockers
153
losartan
what is it?
adverse drug effects
a angiotensin receptor blocker
TERATOGEN, renal failure, hyperkalemia
*less of a cough and less angioedema than ACEI
154
is the ability of the organ to maintain its blood supply in the face of changing perfusion pressure
(without even help from innervation - an extrinsic factor)
autoregulation
155
the difference between what two things is vascular tone?
basal flow to maximal flow
156
how (molecularly) is NO activated?
shear stress or an agonist opens calcium channels on the surface of endothelial cells
calcium --> nitric oxide synthase --> NO formed --> smooth muscle
157
what is the initial problem in embryology leading to tetralogy of fallot?
the conotruncal septum deviating anteriorly
