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N932: Pathophysiology > Cardiac Pathophysiology Week 1 > Flashcards

Cardiac Pathophysiology Week 1 Flashcards

1
Q

Types of HF

A
  1. Diasotlic HF
  2. Systolic HF
  3. Low Output vs High Output
  4. Left-sided vs Right-sided HF
  5. Chronic vs Acute HF
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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

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3
Q

2 most important mechanisms of HF

A
  1. Volume overload

2. Pressure overload

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4
Q

Volume overload causes:

A
  • Mitral regurgitation

- Aortic regurgitation

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5
Q

Pressure overload causes:

A
  • aortic stenosis
  • chronic systemic HTN
  • chronic pulmonary HTN
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6
Q

ischemia or infarct → myocardial contractile impairment

A
  • angina
  • STEMI
  • N-STEMI
  • unstable angina
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7
Q

restrictive filling causes

A
  • constrictive pericarditis
  • cardiac tamponade
  • restrictive myocarditis
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8
Q

idiopathic remodeling of sarcomeric or extracellular matric (ECM) causes:

A
  • dilated cardiomyopathy
  • hypertrophic cardiomyopathy
  • restrictive cardiomyopathy
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9
Q

myocardial inflammation → HF progression causes

A

unknown?

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10
Q

the 2 problems of heart failure

A
  1. filling problem

2. emptying problem

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11
Q

Acute HF

aka “decompensating HF”

A

-sudden decrease in CO

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12
Q

Acute HF precipitated by

A

worsening chronic HF

new onset HF [valve or septal wall rupture, MI, severe HTN crisis]

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13
Q

pulmonary edema or cardiogenic shock observed in

A

new onset HF

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14
Q

______ characterized by pulmonary or systemic edema

A

chronic HF

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15
Q

New York Heart Association Functional Classification of Breathlessness
Class I

A

no symptoms

no limitations to ordinary activity

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16
Q

New York Heart Association Functional Classification of Breathlessness
Class II

A

mild symptoms [mild angina, SOB]

slight limitation during ordinary activity

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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

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18
Q

New York Heart Association Functional Classification of Breathlessness
Class IV

A

severe limitations
experiences symptoms at rest

*BEDBOUND PATIENTS

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19
Q

Left-sided HF s/s

A

↑ LVEDP

  • pulmonary venous congestion
  • ↑ Pulmonary BP
  • ↑ Pulmonary ISF edema
  • *Pulmonary edema
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20
Q

Right-sided HF s/s

A

↑ RVEDP

  • systemic venous congestion
  • ↑ systemic edema
  • hepatomegaly
  • nausea / anorexia
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21
Q

Causes of right sided HF

A

1 left-sided HF

  • pulmonary HTN
  • MI of right ventricle
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22
Q

Low Output vs High Output

A

good pump [FILLING or EMPTYING problem]

vs

bad pump [METABOLIC DEMAND or SVR problem

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23
Q

hypertrophy vs hyperplasia

A

hypertrophy: enlarged cardiomyocytes (↑ sarcomere proteins)
hyperplasia: growth of new cells (not possible)

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24
Q

immediate response to HF

A

↑ inotropy

↑ chronotropy

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25
Q

long term response to HF

A

cardiac hypertrophy

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26
Q

physiological responses to ↓ CO

& lead to…

A
  1. SNS response
  2. Renal response (RAAS)
  3. Humoral & Biochemical response [Local sensors at ONE CELL & Neural sensors]

lead to CARDIAC REMODELING

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27
Q

SNS response to ↓ CO (5)

A

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
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28
Q

in HF the F/S curve shifts ____ b/c ____

A

DOWN

↓ cardiac contractility
↓ (reduced) cross bridges formed for a given length & Ca concentration of cardiomyocyte

*slope is less due to ↓ sensitivity to calcium

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29
Q

RAAS response to ↓ CO

A
  • *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

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30
Q

Humoral & Biochemical response to ↓ CO:
NEURAL SENSORS

  • hormone released from neurons, glands or inflammatory cells (locally)
  • biochemical occurs within a cell
A
  • atrial baroreceptors
  • arterial baroreceptors

(trigger sympathoadrenal release of catecholamines)

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31
Q

Humoral &Biochemical response to ↓ CO:
LOCAL SENSORS

  • hormone released from neurons, glands or inflammatory cells (locally)
  • biochemical occurs within a cell
A
  • macula densa cells
  • cardiomyocytes
  • endothelial cells
  • atrial cells
  • ventricular cells
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32
Q

biochemical changes within a cardiomyocyte

A

change to growth factors

change to enzymes [fuel utilization enzymes can be altered to ↓ hearts ability to use fuel = FURTHER IMPAIRING CARDIAC FUNCTION

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33
Q

high levels of circulating catecholamines

A

CARDIOTOXIC [apoptosis, necrosis]
- promotes CARDIAC REMODELING

  • ↑ Vasopressin leads to ↑SVR & ↑renal water retention
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34
Q

Promoters of cardiac remodeling

A
  • high circulating catecholamines
  • RAAS [circulating catecholamines - cardiotoxic & ANGIOTENSIN II - promotes collagen deposition]
  • ENDOTHELIN released from ischemic cells
  • INFLAMMATORY MEDIATORS released from ischemic cardiomyocytes
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35
Q

ANP / BNP

A 
promote diuresis
natriuresis
inhibit RAAS & SNS
vasodilation
anti-inflammatory

** INHIBITS REMODELING

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36
Q

2 locations of cardiac remodeling

A
  1. sarcomeric proteins

2. proteins of the extracellular matrix (ECM)

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37
Q

“fibrosis”

A

release of excess collagen or other extracellular matrix (ECM) protein

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38
Q

fibrocytes & myofibrocytes

A

cells that release collagen & other ECM proteins in response to:

  • stretch
  • injury
  • hormones
  • inflammatory mediators
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39
Q

cardiac remodeling changes (3)

& examples (6)

A

size
shape
function of the heart [ventricles]

Myocardial:

  • fibrosis
  • dilation
  • hypertrophy
  • wall thinning
  • wall thickening
  • cell death
40
Q

sarcomeres added in SERIES

A

eccentric hypertrophy

  • Volume overload*
  • walls & chamber INCREASE in OVERALL size & volume

**SHF/dysfunction

41
Q

sarcomeres added in PARALLEL

A

concentric hypertrophy

Pressure overload

  • walls thicken; DECREASE in chamber VOLUME
    results in ↓ wall stress

**DHF/dysfunction

42
Q

systolic HF

type of problem
trigger
AKA

A
  • emptying problem [↓ contractile force generation]
  • triggered by volume overload, cardiomyopathy-induced structural abnormalities, cardiac ischemia

AKA: HFrEF
heart failure with reduced ejection fraction

43
Q

diastolic HF

type of problem
trigger
AKA

A
  • 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
Q

Brain s/s hypoperfusion

A

lightheaded, dizzy, near syncope/syncope, insomnia, anxiety, memory deficit, confusion

45
Q

Heart s/s hypoperfusion

A

↓ myocardial contractility, MI, dysrhythmia 2ndary to ischemia, fatigue, exercise intolerance

46
Q

Kidney s/s hypoperfusion

A

activation of RAAS, volume saving, ISF edema, oliguria, prerenal azotemia (excess BUN & creat)

47
Q

HF anesthetic implications

A
  • 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
Q

Acute HF DURING surgery

A

GOAL: ↑ CO & ↓ LVEDP

Tools: inotropes, vasodilators, diuretics, Ca2+ sensitizers, BNP, NO inhibitors, mechanical devices

49
Q

Chronic HF during surgery

A

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
Q

underlying mechanism of dilated cardiomyopathy

A

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
Q

dilated cardiomyopathy chamber size

A

size ↑ = cardiac EMPTYING problems.

similar to SHF

52
Q

dilated cardiomyopathy (DCM) can lead to:

A
  1. systolic heart failure

2. conduction abnormalities

53
Q

s/s of DCM

diagnosis image

A
  • chest pain on exertion
  • hypokinetic / dilated chamber
  • ↑ thrombus risk
  • valve regurgitation possible
  • dysrhythmias

diagnosis by ECHO or LV dilation on chest xray

54
Q

DCM treatment

A
  • many medications
  • FLUID RESTRICTION
  • implanted devices [pacer / defib]
  • heavily anti-coagulated
  • on transplant list
55
Q

DCM anesthetic implications

A

same as SHF

  • goal is to prevent acute ↑ LVEDP or ↓CO
  • do not fluid overload!
56
Q

restrictive cardiomyopathy (RCM)

A
  • 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
Q

s/s of RCM

diagnosis imaging

A

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
Q

restrictive cardiomyopathy anesthetic implications

A

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
Q

Hypertrophic Cardiomyopathy

A

*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
Q

hypertrophic cardiomyopathy filling/emptying

A

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
Q

HCM can progress to ____

A

restrictive cardiomyopathy (RCM)

62
Q

s/s of HCM

A

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
Q

HCM anesthetic implications

A

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
Q

primary issue in hypertrophic cardiomyopathy

A

**obstruction of outflow tract

EMPTYING problem

65
Q

murmurs present in HCM

A
  1. mitral regurgitation

2. turbulent flow d/t LVOT obstruction (mid-systole)

66
Q

3 pericardial diseases

A
  1. acute pericarditis
  2. cardiac tamponade
  3. constrictive pericarditis
67
Q

acute pericarditis definition

A

inflammation of the pericardium

68
Q

pericardial layers

A
  1. fibrous pericardium
  2. serous pericardium
    a. parietal layer
    (pericardial space = 15=50mL of plasma ultrafiltrate from visceral pericardium)
    b. visceral layer
69
Q

causes of acute pericarditis

A
  • vital infection
  • MI [takes 1-3d to become inflamed from cytosolic contents of necrotic cardiomyocytes]

*benign unless pericardial effusion occurs

70
Q

Dressler’s syndrome

A

autoimmunity to circulating necrotic cardiomyocytes (presents months after MI)

71
Q

anesthetic implications of acute pericarditis

A
  • can occur after pericardiotomy
  • more common in pediatric patients
  • less common if pt is immunosuppressed
72
Q

pericardial effusion definition

A

collection of fluid in the pericardial space w/ or w/o inflammation

73
Q

cardiac tamponade

A

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
Q

what kind of “problem” is cardiac tamponade?

A

FILLING problem (impaired diastolic filling)

75
Q

causes of cardiac tamponade

A

[fluid in the pericardial space]

  • disease (cancer, TB)
  • trauma (pacemaker, CVC)
  • exposure to radiation
76
Q

pericardial fluid can be _______ or ______

A

transudative or exudative

77
Q

transudative fluid

A

filtrate of blood.

- accumulates in tissues outside of the blood

78
Q

exudative fluid

A

fluid that filters from the circulatory system into lesions or areas of inflammation

79
Q

s/s of pericardial effusion

A

only if ↑ pericardial pressure occurs:

↑LVEDP = ↓ CO & ↓ blood supply through coronaries

80
Q

s/s cardiac tamponade

A
  • ↑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
Q

Beck’s triad

A
  1. hypotension
  2. increased JV pressure
  3. distant heart sounds

**occurs in cardiac tamponade

82
Q

pulsus paradoxus

A

**CLASSIC sign of cardiac tamponade

DECREASE in systolic BP >10mmHg during inspiration

83
Q

Kussmaul’s sign and Pulsus paradoxus

A

represent desynchrony of L & R ventricular filling

84
Q

anesthetic implications in cardiac tamponade

A

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
Q

chronic constrictive pericarditis

A

fibrous scarring & adhesions of the pericardium that obliterate the pericardial space. RIGID shell is created around heart

→ may advance to calcification

86
Q

subacute constrictive pericarditis

A

fibroelastic constriction of the pericardium that ↓ pericardial space and ↑ pericardial pressure

87
Q

constrictive pericarditis

A

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
Q

constrictive pericarditis is a _____ problem

A

FILLING (impaired diastolic filling)

89
Q

constrictive pericarditis presents with

A

diastolic HF with PRESERVED GLOBAL systolic function

90
Q

causes of constrictive pericarditis

A
  • usually idiopathic
  • radiation to the heart
  • wound repair to pericardium d/t trauma or surgery
  • TB
91
Q

s/s constrictive pericarditis

A
  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
Q

Kussmaul’s sign

A

↑ 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
Q

pericardiectomy

A

removal of adherent constricting region of pericardial sac

94
Q

difference between constrictive pericarditis & cardiac tamponade treatment response

A

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
Q

anesthetic implications of constrictive pericarditis

A

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
Q

Pericardiectomy surgery considerations

A
  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

N932: Pathophysiology (5 decks)

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