Cardiac Flashcards
(261 cards)
1
Q
Emptying problems include
A
SHF, dilated cardiomyopathy, aortic stenosis, pulmonic stenosis
2
Q
Considerations for SHF & DCM include:
A
- ) optimize inotropy (balance w/ causing increased MVO2)
- ) decrease afterload (as long as it doesn’t cause drop in BP)
- Maintain NSR to allow for atrial kick
- Don’t fluid overload
3
Q
Systolic heart failure (pathophys)
A
an emptying problem that is triggered by volume overload causing eccentric remodeling
known as heart failure with reduced ejection fraction
4
Q
Systolic heart failure characteristics include
A
decreased LVEF, Increased LV chamber size, volume overload, LV hypertrophy on ECG, S3 gallop, compliant, eccentric remodeling
5
Q
Heart failure is
A
reduce forward flow
6
Q
Causes for the heart to fail include:
A
volume overload, pressure overload (two most common), myocardial contractile impairment d/t ischemia or infarct), restrictive filling (pericarditis, tamponade), idiopathic remodeling of sarcomeric or extracellular matrix proteins, myocardial inflammation
7
Q
Chronic vs. acute heart failure
A
chronic: stable where BP is maintained b/c of physiological compensations
Acute: sudden decrease in CO resulting in hypotension; medical emergency and can turn into flash pulmonary edema
8
Q
Acute heart failure can occur due to
A
worsening chronic HF, new onset HF (i.e. valve or septal wall rupture, MI, or severe HTN crisis)
9
Q
NYHA Class 1
A
no symptoms and no limitation in ordinary physical exercise
10
Q
NYHA Class 2
A
mild symptoms (mild SOB and/or angina) and slight limitation during ordinary activity
11
Q
NYHA Class 3
A
Marked limitation in activity d/t symptoms even during less than ordinary activity; comfortable only at rest
12
Q
NYHA Class 4
A
Severe limitations; experiences symptoms even while at rest; mostly bedbound patients
13
Q
Describe differences between left versus right sided heart failure
A
Left side: pulmonary congestion, dyspnea, increased LVEDP, pulmonary edema, dyspnea
Right side: increased RVEDP, systemic congestion, hepatomegaly
14
Q
Most common causes of left heart failure include
A
HTN, CAD, MI, valvular disease
15
Q
Most common causes of right heart failure include
A
Left-sided heart failure
may also be caused by pulmonary arterial hypertension or MI of right ventricle
16
Q
Describe low output vs. high-output heart failure
A
Both are d/t heart being unable to pump enough blood to meet oxygen demand of tissues
low-output: filling or emptying problem; CO can be normal but only b/c of compensation
High-output: not a filling or emptying problem; problem is metabolic demand and/or SVR; cardiac output can be normal or above normal but CO is insufficient to meet global metabolic demands
17
Q
Causes of low-output HF
A
CAD, chronic HTN, cardiomyopathy, valvular disease, pericardial disease
18
Q
Causes of High-output HF
A
Anemia, septicemia, hyperthyroidism
19
Q
Common causes of HF include:
A
pressure overload, volume overload, MI, idiopathy cardiomyopathy, hypertrophy/cardiac remodeling
20
Q
Increased catecholamines cause cardiotoxicity and promote
A
cardiac remodeling
21
Q
ANP & BNP promote
A
diuresis, natriuresis, inhibition of RAAS and SNS, vasodilation, and INHIBIT REMODELING
22
Q
Concentric remodeling is
A
caused by increased pressure and results in sarcomeres being laid down in parallel; smaller chamber radius and thicker/less compliant chamber wall
Results in a filling problem
associated with DHF
23
Q
Eccentric remodeling is
A
caused by volume overload resulting in sarcomeres being laid down in series; larger chamber radius and more compliant chamber wall
results in an emptying problem
associated with SHF
24
Q
diastolic heart failure is
A
a filling problem (occurs L>R)
triggered by pressure overload
stiff/non-compliant ventricles impair filling
heart failure with preserved EF
25
Diastolic heart failure characteristics include
normal LVEF, decreased chamber size, pressure overload, LV hypertrophy on EKG, S4 gallop, decreased compliance, concentric ventricular remodeling
26
In patients who develop acute heart failure during surgery, the immediate goal is to
increase CO and decrease LVEDP
27
Heart failure responses include
increased SNS, increased RAAS, increased humoral and biochemical, increased remodeling
28
The key difference between SHF & DCM is
etiology!
29
DCM risk factors include
African American Men (Dark Dads- DDD)
30
Cardiomyopathy is a
chronic disease of the heart
heart muscle is structurally and functionally abnormal in the absence of CAD, HTN, valvular disease, & congenital heart disease
associated with mechanical and/or electrical abnormality
31
Etiology of cardiomyopathies (in general):
are genetic, genetic/non-genetic (mixed), or acquired
not caused by other CV diseases
Are not congenital diseases
Can include metabolic, inflammatory or toxic
32
Etiology of HCM
Genetic
33
Etiology of DCM & RCM
mixed genetic/non-genetic
34
Causes of DCM include
caused by genetic & non-genetic factors
non-genetic factors include: alcoholism, cocaine, infection, thyroid disease, pheochromocytoma, chemotherapy or radiation
35
Dilated cardiomyopathy pathophysiology
increased cardiomyocyte apoptosis, increased sarcomeric proteins in eccentric pattern resulting in eccentric remodeling of the chamber--> emptying problem
Sarcomeric protein changes that reduce contractile filament senstivity to Ca2+ and decrease force generation
Remodeling can lead to conduction abnormalities
s/s consistent with SHF
36
Signs/symptoms of DCM include
mimic angina pectoris, chamber is hypokinetic and dilated so increased thrombus risk, valve regurgitation possible d/t dilated ventricles, dysrhythmias
37
Diagnosis of DCM is via
Echo or chest XR that shows LV dilation
38
The anesthetic goals for DCM & SHF:
Prevent acute drop in CO and increase in LVEDP
39
Restrictive cardiomyopathy is
rare but lethal
has changes to sarcomeric proteins that impair relaxation and infiltrations/deposits stiffen ventricle
no concentric or eccentric remodeling
a filling problem
40
RCM etiology
caused by genetic and non-genetic factors
| non-genetic causes: infection, chemo or radiation, diseases of infiltration like amyloidosis, sarcoidosis
41
The pathophysiology of RCM includes:
1) ventricular stiffness
2) impaired relaxation d/t altered Ca2+ cycling
3) system diseases that cause ventricular infiltration w/ substances that stiffen the ventricle
Results in high LVEDP, reduced filling, reduced SV, and reduced CO
can progress to DHF
42
Signs and symptoms of RCM include
same as those for DHF- congestion in pulmonary or systemic systems, decreased CO to tissues--> syncope, decreased myocardial contractility
conduction abnormalities d/t deposition of infiltrative substances
43
Diagnosis of RCM
Echo- diastolic dysfunction, atria enlarged not ventricles
44
The quintessential for DHF & restrictive cardiomyopathy:
SV limited: maintain HR in NSR, do not decrease afterload
Need their preload (titrate carefully so as not to fluid overload)
Have inotropy- maintain
Ischemia- avoid hypotension b/c CorrPP is at risk since can't increase SV to compensate
45
Etiology of HCM:
caused in whole or part by genetic abnormality
46
Pathophysiology of HCM:
excessive growth of left ventricular muscle for no apparent reason
usually concentric remodeling which can result in obstruction of LVOT and mitral regurgitation
LVOT is primary cause of HCM clinical manifestations
47
Describe LVOT:
left ventricle hypertrophy w/ unfavorable mitral valve anatomy results in obstruction of the LVOT
decreased forward blood flow d/t:
narrowed tract & leaflet of the mitral valve obstructs LVOT
48
The most common cardiomyopathy is
HCM: 1 in 500
49
S/S of HCM include:
vary widely but similar to SHF (d/t outflow obstruction) and DHF (d/t prolonged relaxation and decreased ventricular compliance)
angina, fatigue, syncope, tachydysrhythmias, HF
50
Positioning is important in this cardiomyopathy:
HCM- supine reduces LVOTO
51
Diagnosis of HCM:
Echo & ECG: looking for LV hypertrophy
| Cardiac cath to measure increased LVEDP
52
Anesthetic considerations for HCM:
Avoid acute HF by minimizing decreased LVOTO
- Avoid increased contractility- makes LVOTO worse
- Avoid decreased afterload- makes LVOTO worse d/t venturi affect
- Avoid tachycardia- does not allow for filling time
- Maintain adequate preload b/c they need filling
53
With regional anesthesia there is a risk for
decreased SVR and venodilation which causes decreases afterload
54
Describe DHF from triggering event to response:
Pressure load--> concentric remodeling--> collagen stiffness--> reduced compliance--> decreased filling--> DHF--> diastolic dysfunction
55
Describe restrictive cardiomyopathy from triggering event to response:
Genetic/acquired--> sarcomeric proteins--> impaired relaxation--> decreased filling--> diastolic dysfunction
56
Describe HCM from triggering event to response:
Genetic--> LVH--> obstruct LVOT--> emptying--> SHF--> systolic dysfunction
Genetic--> collagen, sarcomeric proteins--> decreased compliance and decreased relaxation--> decreased filling--> DHF & RCM--> diastolic dysfunction
57
Describe DCM from triggering event to response:
genetic/acquired--> eccentric--> increased chamber size--> decreased Ca2+ sensitivity--> decreased force--> decreased emptying--> systolic dysfunction
58
Describe systolic HF from triggering event to response:
Volume load--> eccentric--> increased chamber size--> increased L to W ratio--> decreased force--> decreased emptying--> SHF--> systolic dysfunction
59
What is acute pericarditis?
inflammation of the pericardium
60
How much fluid can the pericardial space contain?
15 to 50 mL
61
How many layers surround the heart?
3 layers:
outermost: fibrous pericardium
middle: parietal pericardium
inner: visceral pericardium
62
Where is the pericardial cavity or pericardial space located?
between the parietal and visceral pericardial layers
63
Common causes of acute pericarditis:
viral infection or MI
| Result: benign unless pericardial effusion occurs
64
S/s of acute pericarditis
no change in cardiac function unless there is an associated pericardial effusion
65
Diagnosis of acute pericarditis:
more often in men commonly between 20-50 years
chest pain
ECG changes d/t inflammation of superficial myocardium
friction rub
66
Tx of acute pericarditis:
Salicylates, NSAIDs, and corticosteroids to treat inflammation
Corticosteroids are second line b/c withdrawal is associated with increased incidence of pericarditis relapse
67
Describe pericardial effusion
collection of fluid in the pericardial space that may occur with or without pericardial inflammation
68
Describe cardiac tamponade
Collection of fluid in the pericardial sac sufficient to cause increased pericardial pressure that results in reduced cardiac filling
69
Describe the pathophysiology of cardiac tamponade:
pressure reduces ventricular dilation, diastolic filling and increases RAP
depends on how rapidly the fluid collection occurs- slow chronic stretch dissipates the pressure
Result: FILLING PROBLEM
70
Filling and emptying problems include:
HCM w/ LVOTO
71
Filling problems include:
cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, DHF, mitral valve stenosis, tricuspid valve stenosis
72
What is the difference between transudative & exudative?
transudative: a filtrate of the blood; it accumulates in tissues outside the blood
Exudative: any fluid that filters from the circulatory system into lesions or areas of inflammation
73
Common causes of pleural effusion/cardiac tamponade include:
fluid in pericardial space d/t disease (cancer, TB, etc.), trauma (implantation of pacemaker or CVC), exposure to radiation
74
Describe the difference between acute and chronic pericardial effusion.
chronic- the effusion develops overtime so the pericardium has time to stretch & no increase in intrapericardial pressure
acute- occurs rapidly and the pericardium is unable to stretch and thus increase intrapericardial pressure and symptoms occur
75
Beck's triad includes:
hypotension, increased JV pressure, distant heart sounds (pericardial fluid muffles)- s/s of cardiac tamponade
76
S/S of cardiac tamponade include
Increased RAP, BP normal if compensated or hypotensive, CVP elevated, compression of adjacent intrathoracic structures leading to anorexia, cough, hoarseness, dyspnea, chest pain, & hiccup
Beck's triad: hypotension, increased JV pressure, distant heart sounds
ultimately decrease in CO
PULSUS PARODOXUS is classic
77
What is pulsus paradoxus?
decrease in systolic BP > 10 mmHg during inspiration (more common if the tamponade is acute rather than chronic)
Inhibition of RV into pericardial space on inspiration and thus it moves toward the LV and impairs filling --> decreased LVEDV--> decreased SV--> decreased SBP
78
Diagnosis of cardiac tamponade:
echo
79
Anesthetic implications of cardiac tamponade:
Goal: relieve pressure before surgery
During: maintain CO & BP
Optimize volume, give catecholamines, avoid decreased HR, decreased SVR, decreased VR
80
An issue when tamponade is relieved is
significant hypertension
81
Quintessential of cardiac tamponade:
```
avoid decreased HR because SV limited
avoid decreased afterload b/c SV limited
Maximize preload to engage F/S & avoid anything that impacts VR (PEEP, coughing)
high risk of ischemia d/t high LVEDP
maintain contractility
```
82
What is constrictive pericarditis?
constriction of the heart due to changes in the pericardial sac
83
What is the difference between chronic constrictive pericarditis & subacute constrictive pericarditis?
Chronic: fibrous scarring and adhesions that create a rigid shell
Subacute: fibroelastic, more common & less serious
84
The pathophysiology of constrictive pericarditis:
pericardium scarring and adhesions--> decreased compliance of sac--> decreased diastolic filling
Thickening of pericardial space---> constricts heart--> increased intrapericardial pressure
FILLING problem
85
Causes of constrictive pericarditis:
usually idiopathic
| can be caused by: radiation, TB, aberrant wound repair of myocardium d/t trauma or surgery
86
The s/s of constrictive pericarditis:
similar to right-sided HF: increased RVP leads to back up of blood, atrial dysrhythmia d/t compression and remodeling of SA node, reduced cardiac filling leads to decreased VR, decreased F/S, decreased SV, and decreased CO
Kussmaul's sign
87
What is Kussmaul's sign?
Increase in JV distension during inspiration
| RV unable to expand normally during inspiration so increased VR d/t abdominal compression on inspiration goes to JV
88
How is constrictive pericarditis diagnosed?
increased CVP w/ other signs of heart disease
pericardial thickening on ECHO
ECG may or may not display minor abnormalities
89
Anesthetic implications of constrictive pericarditis?
Avoid decrease in VR as this reduces cardiac filling
Avoid increased HR as this reduces cardiac filling
avoid decreased SVR since heart cannot compensate (SV LIMITED)
Optimize preload
90
Common themes with filling disorders:
Stroke volume limited so maintain HR and do not decrease afterload; careful titration of preload b/c need volume to fill but do not overload
91
What factors increase MVO2?
Preload, HR, inotropy, afterload
| CO is work and works is proportional to MVO2
92
What factor increases MVO2 the least?
preload
93
The afterload equation:
Afterload= (LVP x chamber radius )/Wall thickness
94
What factors cause an increase in LVEDP?
increased volume--> increases LVEDV and thus LVEDP
| Increased elastance of ventricle or poor relaxation
95
What type of hypertrophy reduces afterload?
concentric hypertrophy
96
When we say heart rate is a double whammy we are referring to the idea that
heart rate affects both supply and demand- increased heart rate increases the MVO2 demand and decreases the supply (less time in diastole= less coronary perfusion time)
97
Coronary perfusion pressure is equal to
CorrPP=aortic DP-LVEDP
98
Coronary perfusion pressure is
diastolic dependent
depends on time in diastole (HR)
Diastolic BP (hypotension)
LV pressures during diastole (diastolic dysfunction)
99
Any kind of internal or external pressures squeezes the arteries which means
resistance goes up and supply goes down
100
Factors that affect coronary vascular resistance include:
Cardiac work output, cardiac extravascular compressive forces, neurohumoral and endothelial factors
101
Supply is affected by
coronary blood flow and O2 carrying capacity
102
Neurohumoral regulation of coronary VSMC tone:
vasodilation: adenosine, hypoxia, nitric oxide, PSNS stimulation, SNS stimulation (B2)
Vasoconstriction: SNS stimulation (a1), Ang II, endothelin (also PSNS acts on endothelin receptors)
103
Coronary blood flow is directly proportional to
CorrPP/coronary resistance
104
Blood flow to the coronaries occurs mainly during
diastole
105
Myocardial ischemia occurs when
O2 supply cannot keep pace with O2 demand
106
Ischemic heart disease is
insufficient coronary blood flow to meet the metabolic demands of the cardiomyocytes
107
The two major components of cardiac ischemia are
metabolism in cardiomyocytes (demand) & delivery of O2 and nutrients to cardiomyocytes (supply)
108
Most ischemic heart disease results from
coronary artery disease which can be atherosclerotic or non-atherosclerotic
109
Atherosclerosis is
abnormal deposition of a plaque in the artery wall--> arterial narrowing--> increased resistance--> decreased blood flow
110
Non-atherosclerotic decreased coronary blood flow can result from
coronary artery dissection, coronary artery spasm, coronary artery embolism and congenital abnormalities of the heart
111
CAD is a problem at
the level of the coronary arteries
112
The two most common reasons for myocardial ischemia:
coronary artery narrowing (atherosclerosis) & occlusion (thrombus)
113
Coronary microvascular disease affects
women more than men and it affects the tiny arteries in the heart muscle (can occur with or without CAD)
114
Risks associated with ischemic heart disease include:
increased risk for periop CV events including MI, HF, and death
recent UA or MI further increase the risk
115
What is stable angina?
chest pain or discomfort due to CAD
Stable means frequency and severity of symptoms consistent for >2 months
usually occur on exertion so demand is what is changing
116
S/S of stable angina include
chest pain, pressure, or heaviness; may or may not radiate to neck, arms, shoulder or jaw
epigastric discomfort
pain characterized by crescendo-decrescendo
lasts several minutes
117
Diagnosis of stable angina:
induced by physical exertion, emotional tension, or cold
| ECG changes coincide with chest pain- ST segment depression or T wave inversion
118
Acute coronary syndrome includes:
unstable angina, NSTEMI, and STEMI
SA is NOT an ACS
occurs when atherosclerotic coronary plaque becomes unstable, leading to a series of events that eventually results in partial or total thrombotic occlusion of a coronary artery
119
STEMI definition
MI caused by complete blockage of coronary artery
120
Pathophysiology of STEMI
ischemia--> injury--> death
121
S/S of STEMI include:
same as for NSTEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, sudden weakness, fatigue
122
STEMI is characterized by
ST elevation on more than one EKG
Cardiac biomarkers
imaging may show abnormal ventricular wall motion
123
STEMI is treated with
TPA because it can get at fibrin to break it down
| may need PCI or CABG
124
NSTEMI definition:
MI caused by a partially blocked coronary artery
125
NSTEMI is characterized by
ECG showing absence of elevated ST segment (transient ST elevation, T wave inversion, ST depression), elevated cardiac biomarkers
126
S/S of NSTEMI:
same as those for STEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, fatigue
127
Definition of unstable angina:
chest pain or discomfort due to coronary artery disease that occurs randomly and unpredictably without any of the obvious triggers (physical exertion, emotional stress, or cold)
128
Causes of unstable angina include:
decreased myocardial oxygen supply (vasospasm, worse narrowing, inflammation) or increased myocardial oxygen demand
129
Descriptive pathology of unstable angina:
angina at rest, angina of new onset, increase in the severity or frequency of previously stable angina, no elevation of cardiac biomarkers
130
Unstable angina treatment
still needs to be treated like a medical emergency
Reduce myocardial O2 consumption
Rest, increased FIO2, analgesia, BB, Ca2+ inhibitor, NO, anticoagulant
131
Diagnosis of unstable angina:
no elevation of ST segment (other EKG changes)
| no elevation of cardiac biomarkers
132
Management of patients with IHD:
take a thorough cardiac history of patients with suspected
avoid triggering SNS elevation during intubation or laryngoscopy (increased SNS increases demand)
monitor for ischemia- continuous ECG w/ ST analysis, cardiac biomarkers, TEE monitoring
133
The goals for patients with IHD are
avoid ischemia, monitor ischemia, treat ischemia
134
Perioperative MI has a ____ risk of death
20% which occurs 24-48 hours post surgery
135
Risk of periop MI is increased if:
history of IHD, high-risk vascular surgery, emergency surgery
136
Diagnosis of periop MI is difficult because
hemodynamic instability is common post-op, post-op analgesia may mask MI pain, measure cardiac troponin to understand duration of ischemia
137
For patients getting a PCI and stents:
if PCI was recent then patient will be on anti-platelet therapy
monitor patient closely for MI or infarct
138
Volume overload problems include:
AVR & MVR
139
High ischemia risks patients include:
HCM-LVOTO, Cardiac tamponade, AS, AVR
140
Patients with baseline elevated afterload include
AS, SHF
141
Patients with elevated inotropy include:
Constrictive pericarditis, cardiac tamponade, Tricuspid valve stenosis, aortic stenosis, pulmonic stenosis
142
Any of the diastolic/filling problems can advance
to DHF
143
Any of the emptying problems can advance to
SHF
144
Regional anesthesia will decrease
SVR
145
Hypotension is defined as
systolic blood pressure < 90 mmHg
146
Neuraxial anesthesia can lead to
hypotension and bradycardia d/t anesthesia of spinal sympathetic nerve fibers
147
Patients with preexisting hypertension are at higher risk for
intraoperative hypotension
| & increased risk of mortality and/or MI
148
The duration of hypotension
increases risk
149
Hypotensive effects may occur at
normal BP in patients with uncontrolled hypertension (autoregulatory adaptation to higher pressures)
150
Hypotension can result from:
arterial vasodilation, myocardial depression, venodilation, bradycardia, volume: hemorrhage or third space (starling forces)
151
Causes of intra-operative hypotension includes:
hypovolemia, induction of general anesthesia, sympathectomy due to neuraxial block, inhibition of RAAS, periop MI or acute HF causing hypotension
152
For severe or refractory hypotension (treatment):
infusion of a short-acting vasopressor/inotropic agent, aggressive treatment
153
Acute post-operative hypotension is defined by
systolic BP <90 mmHg, mean BP <65 mmHg, or relative decrease in BP 20% below baseline
154
Post-op hypotension may occur due to:
chronic or recent administration of hypertensive agents, inadequate intraoperative fluid replacement, blood loss, residual anesthetic effects, allergic drug reactions, adrenal insufficiency, myocardial ischemia or acute congestive heart failure
155
Hypertension is defined by
BP >130/80 mmHg or higher
| 1/3rd of non-cardiac patients will be hypertensive & 2/3rds of cardiac patients will be hypertensive
156
Patients with chronic HTN are at significant risk for
IHD, HF, CVA, arterial aneurysm, and ESRD
157
Even short durations of MAP <65 was associated with
increased overall mortality, AKI, myocardial injury and stroke
158
Anesthetic implications for hypertensive patients:
prevent end-organ damage, reduce periop risk of adverse events (vessel injury)
159
Isolated systolic hypertension is primarily a result of
stiffening of the arteries
| suspect in patients >65 years
160
Widening pulse pressure is better than
SBP alone as diagnostic for intraoperative hemodynamic instability and adverse postoperative outcomes
161
Distinguish hypertensive urgency from emergency:
presence of end organ damage: emergency
162
Hypertensive crisis is defined as
BP >180/120 mmHg
163
The cause of hypertensive emergency is
pheochromocytoma
164
S/S of hypertensive urgency:
HA, epistaxis, anxiety
165
Chronic HTN patients are more likely to experience a hypertensive
urgency than emergency
166
S/S of hypertensive emergency:
acute CV emergency (ACS, acute decomp. HF, pulm edema, dissecting aortic aneurysm), acute RF, postop complications exacerbated by the elevated BP (hemorrhage, increased ICP), neurologic s/s
167
Treatment of hypertensive emergency includes:
using short-acting vasodilators such as nitroprusside (need to bring SVR down)
168
Pheochromocytoma is
adrenal gland chromaffin cell tumor that has NE release greater than Epi release
169
S/S of pheochromocytoma:
tachycardia, diaphoresis, HA, paroxysmal HTN, HTN, hyperglycemia
170
For patients diagnosed with pheochromocytoma
pre-treat to inhibit alpha 1 adrenergic
| 2 in 1 million patients have undiagnosed pheochromocytoma
171
Define stenosis:
abnormal narrowing of a passage or orifice
| valve stenosis thickens and stiffens the valve and increases resistance to blood flow through the orifice
172
Mitral valve stenosis is
a narrowing of the mitral valve resulting in a LV filling problem
173
Pathology of mitral valve stenosis:
increased resistance to blood flow through the mitral valve--> reduced LV filling--> decreased SV--> decreased CO
back up of blood in the LA results in increased LAP
when LAP >25 mmHg then blood is backed up into pulmonary circulation
174
S/S of mitral valve stenosis begin when
orifice narrowing is >50%
| heart murmur, pulm arterial HTN, 1/3rd of patients have afib
175
Diagnosis of mitral valve stenosis:
Echo, increased transvalvular pressure gradient, LA hypertrophy
176
Treatment of mitral valve stenosis:
goal is to decrease LAP
| diuretics, control a-fib (thrombus risk), surgery to repair leaflet
177
Anesthetic implications of mitral valve stenosis:
Goal: avoid pulm edema or decreased CO
avoid increased HR- causes reduced LV filling time and ultimately decreased CO
Careful fluid balance to avoid hypotension but prevent fluid overload
Avoid increased pulmonary vascular resistance--> may lead to RHF
178
Causes of aortic valve stenosis:
calcification of aortic valve leaflet occurs with increasing age
infective endocarditis
rheumatic fever
risk factors: HTN, hypercholesterolemia
179
Aortic valve stenosis is:
a narrowing of the aortic valve resulting in an obstruction to the flow of blood from the left ventricle to the aorta
results in an LV emptying problem
180
In advanced stages of aortic valve stenosis,
concentric remodeling may occur resulting in a LV filling problem
181
Pathology of aortic valve stenosis
Myocardial oxygen demand problem: increased LVSP, increased LVEDP, increased afterload
Myocardial oxygen supply problem: increased afterload: emptying is not complete and increased LVEDV and LVEDP leads to compression of coronary arteries
182
S/S of aortic valve stenosis:
systolic murmur, exercise intolerance, syncope, LV hypertrophy, can lead to LH failure
183
Diagnosis of aortic valve stenosis:
ECG LV hypertrophy, Echo/doppler shows decreased aortic valve area, increased transvalvular pressure gradient increases
184
Treatment of aortic valve stenosis:
surgical valve replacement
185
Anesthetic implications of aortic valve stenosis:
goal is to maintain CO and decrease risk of myocardial ischemia/infarct
AVOID HYPOTENSION AND KEEP HR NORMAL
avoid hypotension b/c decreased coronary perfusion
keep NS b/c need atrial kick to improve SV via F/S
186
Tricuspid valve stenosis is
a narrowing of the tricuspid valve opening resulting in an obstruction to the flow of blood from the RA to the RV
results in a RV filling problem
187
Tricuspid valve stenosis the the result of
rheumatic fever
188
S/S of tricuspid valve stenosis include:
systemic venous congestion with JVD, ascites, and peripheral edema; decreased CO, abdominal discomfort d/t hepatomegaly, Kussmaul's sign, NO pulmonary congestion unless have mitral valve stenosis
189
Diagnosis of tricuspid valve stenosis:
echo
| differential diagnosis: r/o other causes of systemic venous HTN
190
Treatment of tricuspid valve stenosis includes:
diuretics to avoid congestion
191
Anesthetic implications of tricuspid valve stenosis:
balance fluids so that decreased CO is avoided but that systemic congestion is not exacerbated
192
Normal HR for infants:
113-145 bpm
193
Normal HR for child:
75-113 bpm
194
Normal HR for adult:
60-90 bpm
195
MHR declines with
age- normal MHR for older adult ~73 bpm
196
Cardiac dysrhythmia is a
cardiac rhythm that displays abnormal rate, interval length or conduction path
197
Tachydysrhythmias can result in
HTN increased CO & IHD (decreased supply/ increased demand)
198
Sinus tachycardia is defined as
HR: 100-160
| tolerable unless history of cardiac disease
199
Supraventricular tachycardia is defined as
HR 160-180 initiated at or sustained by tissue at or above the AV node
more common Young>old, women>men
200
Ventricular tachycardia is defined as
HR>170 + 3 or more PVCs
| common after MI, cardiac infection
201
Atrial fibrillation is defined as
no ECG P wave
| multiple areas of the atrium continuously depolarize, quivering atrial wall
202
Big risk with atrial fibrillation is
blood clots
203
Atrial flutter differs from atrial fibrillation because
atrial to ventricular beat rate is 1:2
204
Ventricular fibrillation is defined by
no pulse or BP
most common cause of sudden cardiac death
common in IHD, risk declines with statins, ACEi, beta-blockers
205
Sinus bradycardia is defined by
HR <60 (athletes, sleeping)
206
Premature ventricular contractions
arise from single or multiple foci below the AV node
s/s: palpitations, syncope, near syncope
management: keep defib handy, rule out acid-base or electrolyte triggers
207
Heart blocks can be precipitated by:
MI, myocarditis, lyme disease, rheumatic fever, infiltrative disease, mononucleosis, overdose of beta blockers or Ca2+ channel blockers
208
1st degree AV block is defined by
PR interval >200msec (slow conduction through AV node)
| inconsequential except increased risk for a-fib
209
2nd degree heart block is defined by
impaired conduction in "conduction fibers" (MI, fibrosis, calcification, infiltration, inflammation)
P wave and no corresponding QRS
may require atropine or pacing
210
3rd degree heart block is defined by
"complete heart block" atrial electrical system disconnected from ventricular
MI, aged, or diseased heart
treatment: pace, beta-agonists
211
Bundle branch blocks are defined as
conduction error in conducting fibers
RBBB- ASD, IHD, valve disease, DCM
LBBB- IHD, valve disease, HTN, cardiomyopathy
212
The goal of cardioversion is to
re-coordinate the electrical pathways
213
Defibrillation creates
a fire risk in the OR b/c it arcs electricity
| electrical discharge to correct dysrhythmias when cardioversion is not possible (no R wave or no pulse)
214
Aneurysm is
dilation of all three layers of the artery wall (intima, media, and adventitia)
rupture is a medical emergency
215
Dissection is
when blood enters the medial wall layer d/t intimal layer tear
216
Risk factors for aortic aneurysm:
HTN, family history, smoking, atherosclerosis, male, older age, Marfan's syndrome (dissecting aneurysm, atherosclerosis
217
Factors that precipitate dissection:
deceleration injuries, crack cocaine, pregnancy, aortic cannulation/clamping, aortic valve replacement
218
S/S of thoracic aortic aneurysm:
usually asymptomatic, stridor, hoarseness, dysphagia, superior vena cava edema, aortic valve incompetence--> aortic regurgitation--> HF
219
S/S of aneurysm dissection:
severe sharp pain in chest, neck, shoulder blades, progress to high SVR, shock, absence of peripheral pulses, myocardial ischemia, ischemic stroke
220
When the thoracic aortic is cross-clamped-->
there is an increased blood flow to the brain and reduced blood flow to the spinal cord
release of the clamp can result in hypotension (severe)
221
Surgical considerations for aortic aneurysm:
increased risk for: high blood loss, hypoperfusion of end organs
222
Peripheral arterial disease is defined by
atherosclortic plaque deposition in peripheral artery, narrowed artery, reduced blood flow (chronic); embolism (acute); or vasculitis (inflammation)- rare
223
Risk factors for peripheral arterial disease include
smoking, age, family history, DM, HTN, obesity, dyslipidemia
224
Diagnosis of PAD includes:
ankle to brachial index <0.9
| SBP is reduced at ankle in PAD
225
S/S of PAD include:
intermittent claudication (muscle pain/cramps), leg coolness, pallor, atrophy, hair loss, leg symptoms worse when supine, absent or decreased peripheral arterial pulse
226
Anesthetic considerations for PAD
similar to that for surgical repair of AAA b/c aortic clamping occurs
issues revolve around hypotension with unclamping
227
PVD formation is promoted by
Virchow's triad: venous stasis (immobility), hypercoagulability, and injury to vascular endothelium
228
Congenital heart disease is
a defective heart structure
gene-environmental interactions account for 90% of cardiac congenital abnormalities
single or multi-gene abnormalities account for 10%
229
Atrial septal defect results in
RH and pulm circulatory volume overload
septal wall between right and left atria is defective
allows blood flow through the septum
decreased systemic blood flow because LA kick is reduced
230
Atrial septal defect accounts for
1/3rd of all cardiac congenital defects
| more likely in females
231
With septal defects the goal is to avoid
increased shunt volume or right to left shunt (can lead to hypoxemia)
Decreased SVR will increase right to left shunt and increased PVR will increase right to left shunt
232
Ventricular septal defect is
the most common cardiac congenital defect
| pulm circulation and left heart volume overload (volume overload in pulm circulation transmitted to left heart)
233
Pulmonic valve stenosis is
a narrowing of the pulmonic valve resulting in an obstruction to the flow of blood from the right ventricle to the pulmonary artery
234
Prevalence of pulmonic valve stenosis:
accounts for 10% of all congenital heart disease; acquired is rare, PVS usually discovered in childhood
235
Cause of pulmonic valve stenosis:
congenital>>> rheumatic heart disease, infective endocarditis, carcinoid heart disease, iatrogenic causes (radiation or chemo)
236
Pulmonic valve stenosis results in
a RV emptying problem, increased MVO2
237
With pulmonic valve stenosis, right ventricle
outflow tract can also be obstructed
238
In pulmonic valve stenosis, RV pressures become elevated d/t increased
pulmonic valve resistance and RVOT obstruction--> RV hypertrophy--> RV diastolic dysfunction occurs
239
S/S of pulmonic valve stenosis include
Mild disease: asymptomatic, good long term survival
Severe disease: present during childhood--> RV failure and cyanosis
adult: exertional dyspnea, fatigue RV hypertrophy, RV failure
240
Diagnosis of pulmonic valve stenosis:
echo
| a systolic ejection murmur
241
Treatment of aortic valve stenosis:
valve surgery
| balloon pulmonary valvuloplasty
242
Anesthetic implications of pulmonic valve stenosis:
goal is to maintain CO & avoid RV decompensation
volume needs to be sufficient but don't overload
inotropes may be necessary
243
Aortic valve regurgitation is defined by:
during diastole a portion of the SV moves backwards from aorta into the LV
results: decreased CO, LV volume overload, Increased LVEDV & LVEDP, and decreased coronary perfusion
244
Aortic valve regurgitation is a
volume overload and ischemia problem
245
Chronic aortic regurgitation is due to
rheumatic fever, idiopathic, Marphan's syndrome, Rheumatoid arthritis
246
Acute aortic regurgitation is due to
infective endocarditis, aortic dissection
247
Rapid deterioration in LV function results in (aortic valve regurgitation)
LHF; coronary ischemia
248
S/S of aortic valve regurgitation
patients may be asymptomatic for decades; initial symptoms are exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea
249
Descriptive pathology of aortic valve regurgitation:
regurgitant flow increased LVEDV, LV remodeling--> eventually LHF
250
With aortic valve regurgitation, volume regurgitated is
directly proportional to duration of diastole, directly proportional to the pressure across the valve, directly proportional to size of aortic valve orifice
251
Diagnosis of aortic valve regurgitation
diastolic murmur, decrease DBP d/t backflow, enlarged LV on ECHo
acute s/s include CV collapse
252
Treatment of aortic valve regurgitation:
surgically replace valve
253
Anesthetic management of aortic valve regurgitation:
Maintain LV forward flow & CO
Summary: desire slight increase in HR and slight decrease in SVR, adequate volume
Heart rate- Increase >80 bpm; decreased duration in diastole and increased CO
Preload: need preload for F/S and SV/CO
Afterload: decreased afterload favors forward flow; avoid increased SVR
254
Mitral valve regurgitation is
during systole a portion of the SV moves backwards from LV into the LA
255
Mitral valve regurgitation is a
Volume overload problem
256
Causes of chronic mitral regurgitation include
rheumatic fever, incompetent valve
257
Causes acute mitral regurgiation include
myocardial ischemia/infarct, infective endocarditis, chest trauma
258
Descriptive pathology of mitral valve regurgitation:
decreased forward flow, regurgitation into LA, increased LAP, pulmonary congestion
259
Diagnosis of mitral valve regurgiation:
murmur, echo, ECG atrial or ventricular hypertophy
260
Treatment of mitral valve regurgitation
surgery
261
Anesthetic management of mitral valve regurgitation:
avoid increased CO
HR- normal or slight increase
preload: need preload for F/S and SV but overload increases pulmonary congestion
use inotropes to improve forward flow and decrease LV volume
Summary: inotropes increase SV, vasodilators decrease SVR, titrate volume
