Cardiac Pathophysiology Week 1 Flashcards
1
Q
Types of HF
A
- Diasotlic HF
- Systolic HF
- Low Output vs High Output
- Left-sided vs Right-sided HF
- Chronic vs Acute HF
2
Q
heart failure
A
inability of the heart to FILL WITH or EJECT blood at a flow rate sufficient to meet GLOBAL metabolic demands
3
Q
2 most important mechanisms of HF
A
- Volume overload
2. Pressure overload
4
Q
Volume overload causes:
A
- Mitral regurgitation
- Aortic regurgitation
5
Q
Pressure overload causes:
A
- aortic stenosis
- chronic systemic HTN
- chronic pulmonary HTN
6
Q
ischemia or infarct → myocardial contractile impairment
A
- angina
- STEMI
- N-STEMI
- unstable angina
7
Q
restrictive filling causes
A
- constrictive pericarditis
- cardiac tamponade
- restrictive myocarditis
8
Q
idiopathic remodeling of sarcomeric or extracellular matric (ECM) causes:
A
- dilated cardiomyopathy
- hypertrophic cardiomyopathy
- restrictive cardiomyopathy
9
Q
myocardial inflammation → HF progression causes
A
unknown?
10
Q
the 2 problems of heart failure
A
- filling problem
2. emptying problem
11
Q
Acute HF
aka “decompensating HF”
A
-sudden decrease in CO
12
Q
Acute HF precipitated by
A
worsening chronic HF
new onset HF [valve or septal wall rupture, MI, severe HTN crisis]
13
Q
pulmonary edema or cardiogenic shock observed in
A
new onset HF
14
Q
______ characterized by pulmonary or systemic edema
A
chronic HF
15
Q
New York Heart Association Functional Classification of Breathlessness
Class I
A
no symptoms
no limitations to ordinary activity
16
Q
New York Heart Association Functional Classification of Breathlessness
Class II
A
mild symptoms [mild angina, SOB]
slight limitation during ordinary activity
17
Q
New York Heart Association Functional Classification of Breathlessness
Class III
A
marked limitation in activity d/t symptoms [SOB walking short distances]
ONLY comfortable at rest
18
Q
New York Heart Association Functional Classification of Breathlessness
Class IV
A
severe limitations
experiences symptoms at rest
*BEDBOUND PATIENTS
19
Q
Left-sided HF s/s
A
↑ LVEDP
- pulmonary venous congestion
- ↑ Pulmonary BP
- ↑ Pulmonary ISF edema
- *Pulmonary edema
20
Q
Right-sided HF s/s
A
↑ RVEDP
- systemic venous congestion
- ↑ systemic edema
- hepatomegaly
- nausea / anorexia
21
Q
Causes of right sided HF
A
1 left-sided HF
- pulmonary HTN
- MI of right ventricle
22
Q
Low Output vs High Output
A
good pump [FILLING or EMPTYING problem]
vs
bad pump [METABOLIC DEMAND or SVR problem
23
Q
hypertrophy vs hyperplasia
A
hypertrophy: enlarged cardiomyocytes (↑ sarcomere proteins)
hyperplasia: growth of new cells (not possible)
24
Q
immediate response to HF
A
↑ inotropy
↑ chronotropy
25
long term response to HF
cardiac hypertrophy
26
physiological responses to ↓ CO
& lead to...
1. SNS response
2. Renal response (RAAS)
3. Humoral & Biochemical response [Local sensors *at ONE CELL* & Neural sensors]
lead to CARDIAC REMODELING
27
SNS response to ↓ CO (5)
arterial baroreceptors sense ↓ BP →
DISINHIBIT SNS signal →
1. art VSMC constriction (a1) →
↑ SVR (↑afterload)
*note: heart/brain will have ↑autoregulation = ↓ resistance so more blood is shunted to heart/brain with ↑SVR
2. venous VSMC ( ) →
↑ venomotor tone, ↑Psf, ↑VR, ↑ F/S mechanism = ↑SV
3. SA node →
↑ firing = ↑ HR
*HELPS in SHF, HINDERS in DHF
4. ↑ myocardium inotropy
(↓ sensitivity to catecholamines?)
5. adrenal gland →
↑ circulating catecholamines & ↑ RAAS
*catecholamines stimulate all above
28
in HF the F/S curve shifts ____ b/c ____
DOWN
↓ cardiac contractility
↓ (reduced) cross bridges formed for a given length & Ca concentration of cardiomyocyte
*slope is less due to ↓ sensitivity to calcium
29
RAAS response to ↓ CO
* *SNS stimulation = RAAS
* *↓ renal blood flow = ↑RAAS
1. ↑ activity of Na/K ATP pump on renal tubular epithelial cells to increase Na REABSORPTION & K EXCRETION →
H2O is retained with the Na →
increased body fluid volume →
↑Psf, ↑VR, ↑F/S, ↑SV
2. ↑ salt appetite & thirst →
increased body fluid volume
3. ↑SVR via ANGII-mediated peripheral vasoconstriction
****ANGII triggers cardiomyocyte REMODELING
30
Humoral & Biochemical response to ↓ CO:
NEURAL SENSORS
* hormone released from neurons, glands or inflammatory cells (locally)
* biochemical occurs within a cell
- atrial baroreceptors
- arterial baroreceptors
(trigger sympathoadrenal release of catecholamines)
31
Humoral &Biochemical response to ↓ CO:
LOCAL SENSORS
* hormone released from neurons, glands or inflammatory cells (locally)
* biochemical occurs within a cell
- macula densa cells
- cardiomyocytes
- endothelial cells
- atrial cells
- ventricular cells
32
biochemical changes within a cardiomyocyte
change to growth factors
change to enzymes [fuel utilization enzymes can be altered to ↓ hearts ability to use fuel = FURTHER IMPAIRING CARDIAC FUNCTION
33
high levels of circulating catecholamines
CARDIOTOXIC [apoptosis, necrosis]
- promotes CARDIAC REMODELING
- ↑ Vasopressin leads to ↑SVR & ↑renal water retention
34
Promoters of cardiac remodeling
- high circulating catecholamines
- RAAS [circulating catecholamines - cardiotoxic & ANGIOTENSIN II - promotes collagen deposition]
- ENDOTHELIN released from ischemic cells
- INFLAMMATORY MEDIATORS released from ischemic cardiomyocytes
35
ANP / BNP
```
promote diuresis
natriuresis
inhibit RAAS & SNS
vasodilation
anti-inflammatory
```
** INHIBITS REMODELING
36
2 locations of cardiac remodeling
1. sarcomeric proteins
| 2. proteins of the extracellular matrix (ECM)
37
"fibrosis"
release of excess collagen or other extracellular matrix (ECM) protein
38
fibrocytes & myofibrocytes
cells that release collagen & other ECM proteins in response to:
- stretch
- injury
- hormones
- inflammatory mediators
39
cardiac remodeling changes (3)
& examples (6)
size
shape
function of the heart [ventricles]
Myocardial:
- fibrosis
- dilation
- hypertrophy
- wall thinning
- wall thickening
- cell death
40
sarcomeres added in SERIES
eccentric hypertrophy
* Volume overload*
- walls & chamber INCREASE in OVERALL size & volume
**SHF/dysfunction
41
sarcomeres added in PARALLEL
concentric hypertrophy
*Pressure overload*
- walls thicken; DECREASE in chamber VOLUME
results in ↓ wall stress
**DHF/dysfunction
42
systolic HF
type of problem
trigger
AKA
- emptying problem [↓ contractile force generation]
- triggered by volume overload, cardiomyopathy-induced structural abnormalities, cardiac ischemia
AKA: HFrEF
heart failure with reduced ejection fraction
43
diastolic HF
type of problem
trigger
AKA
- filling problem
- triggered by pressure overload, ↓ ventricular relaxation, compression of ventricles, systemic HTN, aortic stenosis, cardiac ischemia
* STIFF ventricles relax slowly = impaired filling in early diastole
* ↑ LVEDP = reduced filling in late diastole
AKA: HFpEF
heart failure with preserved ejection fraction
- adaptation is to add more mass to overcome pressure = concentric hypertrophy
44
Brain s/s hypoperfusion
lightheaded, dizzy, near syncope/syncope, insomnia, anxiety, memory deficit, confusion
45
Heart s/s hypoperfusion
↓ myocardial contractility, MI, dysrhythmia 2ndary to ischemia, fatigue, exercise intolerance
46
Kidney s/s hypoperfusion
activation of RAAS, volume saving, ISF edema, oliguria, prerenal azotemia (excess BUN & creat)
47
HF anesthetic implications
- pts will be taking multiple medications [B-blockers, ACEi, AIIRB, diuretics, vasodilators, -statins, mineralocorticoid receptor antagonists]
- implanted devices [pacer/defib]
- may be heavily anti-coagulated
- hx CAD
- valve prosthetics
- on transplant list
- VAD as palliation or bridge to transplant [electical, electromagnetic, thromboembolic, no pulse, chest compression dislodgement, ATBx prophylaxis]
48
Acute HF DURING surgery
GOAL: ↑ CO & ↓ LVEDP
Tools: inotropes, vasodilators, diuretics, Ca2+ sensitizers, BNP, NO inhibitors, mechanical devices
49
Chronic HF during surgery
prevent acute episode; keep patient stable
*PRE-OP: renal, liver, electrolyte panels*
Recent EKG, ECHO
Intra-op:
PEEP can ↓ pulmonary congestion
* use TEE to monitor LVEDV & LVEDP
- avoid fluid overload
- NSR - filling time very important in DHF
*Regional anesthesia acceptable but avoid hypotension (↓ coronary perfusion)
POST-OP
- avoid pain (d/t ↑ SNS)
- if acute HF = ICU ADMISSION d/t risk for death
50
underlying mechanism of dilated cardiomyopathy
changes in the #, size, and function of sarcomere proteins
*↑apoptosis = ↓ force generation
*eccentric pattern =
thinning of ventricular wall → enlarged chamber size
- ↓ sensitivity to Ca (contractile filaments)
51
dilated cardiomyopathy chamber size
size ↑ = cardiac EMPTYING problems.
similar to SHF
52
dilated cardiomyopathy (DCM) can lead to:
1. systolic heart failure
| 2. conduction abnormalities
53
s/s of DCM
diagnosis image
- chest pain on exertion
- hypokinetic / dilated chamber
- ↑ thrombus risk
- valve regurgitation possible
- dysrhythmias
diagnosis by ECHO or LV dilation on chest xray
54
DCM treatment
- many medications
- FLUID RESTRICTION
- implanted devices [pacer / defib]
- heavily anti-coagulated
- on transplant list
55
DCM anesthetic implications
same as SHF
- goal is to prevent acute ↑ LVEDP or ↓CO
- do not fluid overload!
56
restrictive cardiomyopathy (RCM)
- NO concentric or eccentric remodeling
- ventricular wall size is normal, changes to sarcomere protein Ca2+ cycling & cross-bridge formation impairs relaxation; infiltrations/collagen deposits stiffen ventricle [some systemic diseases can ↑ ventricular infiltration = stiff]
- FILLING PROBLEM
diastolic dysfunction is primary cause of s/s
LVEDP will be ↑, ↓ filling, ↓SV, ↓CO
*can lead to diastolic heart failure
57
s/s of RCM
diagnosis imaging
same as DHF w/o cardiomegaly
- congestion in pulmonary or systemic systems
- ↓ CO [syncope, coronary ischemia, ↓ myocardial contractility, activation of volume saving mechanisms
*conduction anomalies d/t deposition of infiltrative substances and/or cardiac ischemia = sudden death
Diagnosis: ECHO normal systolic fx, abnormal diastolic fx
ATRIA enlarged, not ventricles
58
restrictive cardiomyopathy anesthetic implications
GOAL: prevent acute ↑LVEDP or ↓CO
*fluid volume: diuretics for congestion but ↓volume = impaired ventricular filling
- NSR (atrial kick helps)
- prevent ↑ HR (filling & coronary perfusion times)
- prevent ↓ HR (↓↓CO b/c ↓↓SV)
- TEE to monitor ventricular volume
- treat pain, return to baseline meds
59
Hypertrophic Cardiomyopathy
*excessive growth of left ventricular muscle for no apparent reason; symmetric or asymmetric
* usually concentric
* *can result in LEFT VENTRICULAR OUTFLOW TRACT obstruction [narrow tract; leaflet of M.valve obstructs LVOT- VENTURI effect] & MITRAL valve regurgitation = ↓ forward blood flow
- can have diastolic dysfunction
**FILLING and EMPTYING PROBLEM
***↓SVR will WORSEN obstruction
60
hypertrophic cardiomyopathy filling/emptying
Impaired FILLING
- altered sarcomeric proteins = slower relaxation = ↓coronary perfusion
- collagen deposits = stiff ventricles = ↓compliance
Impaired EMPTYING
- thickening of ventricular wall [occludes LV outflow & systolic anterior movement of mitral valve AKA mitral regurgitation]
- scaring = dysrhythmia
61
HCM can progress to ____
restrictive cardiomyopathy (RCM)
62
s/s of HCM
will vary widely
- similar to SHF & DHF
1. ↓ outflow
2. prolonged relaxation
3. ↓ decreased ventricular compliance
[angina, fatigue, syncope, tachydysrhythmias, heart failure]
- supine position often ↓ obstruction and ↓ regurgitation
↑ risk of cardiac ischemia & sudden death
63
HCM anesthetic implications
GOAL: ↑ diastolic filling, ↓ LVOT obstruction, ↓ myocardial ischemia
- many meds
- implanted device?
- surgery to remove small part of septum
1. AVOID increased squeeze
↑ intrathoracic pressure
↑ cardiac contractility
2. reduced preload
normovolemia, NO venodilation, avoid ↑ HR
3. reduced afterload
AVOID ↓BP, vasodilators
4. ↑ risk of tachydysrhythmias & arrest; have dfib
5. AVOID SNS activation; anxiolytics, beta-blockers, careful intubation
6. Regional anesthsia = ↑ risk of ↓ SVR & venodilation
[↓SVR = ↓afterload, ↓LVEDP, ↓outflow]
[venodilation = ↓VR = ↓CO]
64
primary issue in hypertrophic cardiomyopathy
**obstruction of outflow tract
EMPTYING problem
65
murmurs present in HCM
1. mitral regurgitation
| 2. turbulent flow d/t LVOT obstruction (mid-systole)
66
3 pericardial diseases
1. acute pericarditis
2. cardiac tamponade
3. constrictive pericarditis
67
acute pericarditis definition
inflammation of the pericardium
68
pericardial layers
1. fibrous pericardium
2. serous pericardium
a. parietal layer
(pericardial space = 15=50mL of plasma ultrafiltrate from visceral pericardium)
b. visceral layer
69
causes of acute pericarditis
- vital infection
- MI [takes 1-3d to become inflamed from cytosolic contents of necrotic cardiomyocytes]
*benign unless pericardial effusion occurs
70
Dressler's syndrome
autoimmunity to circulating necrotic cardiomyocytes (presents months after MI)
71
anesthetic implications of acute pericarditis
- can occur after pericardiotomy
- more common in pediatric patients
- less common if pt is immunosuppressed
72
pericardial effusion definition
collection of fluid in the pericardial space w/ or w/o inflammation
73
cardiac tamponade
collection in the pericardial sac sufficient to cause increased pericardial pressure that results in
reduced cardiac filling
↑intrapericardial pressure = ↓ ventricular dilation, ↓ diastolic filling, ↑ RAP
74
what kind of "problem" is cardiac tamponade?
FILLING problem (impaired diastolic filling)
75
causes of cardiac tamponade
[fluid in the pericardial space]
- disease (cancer, TB)
- trauma (pacemaker, CVC)
- exposure to radiation
76
pericardial fluid can be _______ or ______
transudative or exudative
77
transudative fluid
filtrate of blood.
| - accumulates in tissues outside of the blood
78
exudative fluid
fluid that filters from the circulatory system into lesions or areas of inflammation
79
s/s of pericardial effusion
only if ↑ pericardial pressure occurs:
↑LVEDP = ↓ CO & ↓ blood supply through coronaries
80
s/s cardiac tamponade
- ↑RAP & CVP
- systemic congestion [ascites, hepatomegaly]
[if compensated] ↑SNS, ↑HR, ↑SVR
[uncompensated] ↓ventricular diastolic filling, ↓stretch ↓F/S, ↓SV, ↓CO, ↓BP
- compression of adjacent structures
esophagus → anorexia
trachea → cough, hoarseness
lungs → dyspnea, chest pain, hiccup
Beck's triad
Kussmaul's sign
**Pulsus paradoxus** CLASSIC
81
Beck's triad
1. hypotension
2. increased JV pressure
3. distant heart sounds
**occurs in cardiac tamponade
82
pulsus paradoxus
**CLASSIC sign of cardiac tamponade
DECREASE in systolic BP >10mmHg during inspiration
83
Kussmaul's sign and Pulsus paradoxus
represent desynchrony of L & R ventricular filling
84
anesthetic implications in cardiac tamponade
GOAL: relieve pressure before general surgery via percutaneous pericardiocentesis (use local anesthesia)
1. ***maintain CO and BP***
- optimize intravascular volume
- give catecholamines
- correct metabolic acidosis
2. AVOID:
vasodilation
myocardial depression
↓ HR
3. consider positive pressure ventilation will ↓ venous return
4. Monitor: ABP & CVP
****BEWARE OF HTN after tamponade is relieved****
d/t ↑ preload
85
chronic constrictive pericarditis
fibrous scarring & adhesions of the pericardium that obliterate the pericardial space. RIGID shell is created around heart
→ may advance to calcification
86
subacute constrictive pericarditis
fibroelastic constriction of the pericardium that ↓ pericardial space and ↑ pericardial pressure
87
constrictive pericarditis
scarring & adhesions = ↓ compliance of sac = ↓ diastolic filling
visceral & parietal pericardia thickened and adhere to each other = ↓ pericardial space = constricted heart & ↑ intrapericardial pressure = ↑ R ventricular pressure & ↓ diastolic filling
***pericardium can become fibrotic or calcified
88
constrictive pericarditis is a _____ problem
FILLING (impaired diastolic filling)
89
constrictive pericarditis presents with
diastolic HF with PRESERVED GLOBAL systolic function
90
causes of constrictive pericarditis
- usually idiopathic
- radiation to the heart
- wound repair to pericardium d/t trauma or surgery
- TB
91
s/s constrictive pericarditis
1. ↑RVP → ↑RAP → ↑CVP
2. atrial dysrhythmia d/t compression & remodeling of SA NODE
3. changed heart sounds??
*Reduced cardiac filling leads to:
↓VR, ↓stretch / F/S, ↓SV, ↓CO
*****KUSSMAUL'S SIGN IS CLASSIC
92
Kussmaul's sign
↑ JVD during inspiration.
on inspiration the ♥ does not "receive" negative intrapleural pressure = the ♥ does NOT "suction" blood into it from the venous system = ↑ blood back up into jugular venous system
93
pericardiectomy
removal of adherent constricting region of pericardial sac
94
difference between constrictive pericarditis & cardiac tamponade treatment response
Constrictive Pericarditis: may have disuse atrophy; months of recovery before CO, BP, CVP, RAP return to baseline
Cardiac Tamponade: HTN once fluid is removed and pressure relieved.
95
anesthetic implications of constrictive pericarditis
GOAL: maintain end organ perfusion with adequate CO
AVOID:
- ↓SVR [heart cannot compensate]
- ↓VR [further ↓filling, ↓SV, ↓CO]
- ↑HR [will ↓ cardiac filling time & coronary artery perfusion]
CHOOSE: muscle relaxant with minimal circulatory effects
Pre-op optimization of intravascular fluid
96
Pericardiectomy surgery considerations
1. significant blood loss is likely
2. dysrhythmia is common d/t mechanical irritation
3. LONG / tedious surgery [invasive ABP, CVP monitoring]
4. monitor for post-op ventilatory insufficiency, dysrhythmias, low CO
