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N932: Pathophysiology > Cardiac Pathophysiology Week 2 > Flashcards

Cardiac Pathophysiology Week 2 Flashcards

1
Q

What are 7 pathologies that are filling problems?

A
  1. Diastolic HF
  2. Restrictive Cardiomyopathy
  3. Cardiac Tamponade
  4. Constrictive Pericarditis
  5. Restrictive Pericarditis
  6. Tricuspid Valve Stenosis (RV filling problem)
  7. Mitral Valve Stenosis
    (LV filling problem)
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2
Q

What are 5 pathologies that are emptying problems?

A
  1. Systolic HF
  2. Left sided HF
  3. Dilated Cardiomyopathy
  4. Pulmonic Valve Stenosis (RV emptying problem)
  5. Aortic Valve Stenosis (LV emptying problem) - concentric remodeling
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3
Q

What are the 2 pathologies that are filling AND emptying problems?

A
  1. Low-output HF

2. Hypertrophic Cardiomyopathy

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4
Q

What 4 pathologies are volume overload issues?

A
  1. Systolic HF
  2. Tricuspid Valve regurgitation
  3. Mitral Valve Regurgitation
  4. Aortic Valve Regurgitation
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5
Q

What 3 pathologies are pressure overload pathologies?

A
  1. Aortic Stenosis
  2. Pulmonary HTN
  3. Systemic HTN
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6
Q

What 4 pathologies are contracting problems?

A
  1. Angina
  2. Unstable Angina
  3. NSTEMI
  4. STEMI
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7
Q

During muscle contraction, ATP is required to ____ crossbridges.

A

Break

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8
Q

Mechanism of myocardial contraction. 5 steps.

A

Myosin is bound to actin

  1. ATP binds to myosin → energy released → bond broken
  2. Myosin now ‘cocked” and ready to go
  3. Actin binding site is exposed & “cocked” myosin binds
  4. Conformational change in myosin = “powerstroke”
  5. Actin filament is moved along myosin
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9
Q

ATP use is proportional to ____?

A

MVO2

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10
Q

What are 5 factors that modulate MVO2?

A

1 is CARDIOMYOCYTE CONTRACTION

  1. Preload; optimization of tension formation
  2. HR; the more contractile events per minute ↑MVO2
  3. Inotropy; increased Ca2+ release & sensitivity = more cross bridges formed at a faster rate = ↑MVO2
  4. Afterload

CO is WORK

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11
Q

What are 3 factors that can impact afterload?

A
  1. ↑ LV pressure = ↑ afterload
  2. ↑ Chamber radius = ↑ afterload
  3. ↑ ventricular wall thickness = ↓ afterload
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12
Q

How does afterload impact the velocity of contraction or BP?

A

↑ afterload = ↓ velocity of contraction = ↓ time for systole = ↓ volume ejected (SV) = ↓BP

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13
Q

How does concentric hypertrophy impact afterload?

A

↑ wall thickening = ↓ afterload

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14
Q

How does eccentric hypertrophy impact afterload?

A

↑radius / dilation of ventricle = ↑ afterload

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15
Q

How does aortic stenosis impact afterload?

A

requires ↑ ventricular pressure = ↑↑afterload

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16
Q

How does LVOT obstruction impact afterload

A

requires ↑ ventricular pressure = ↑ afterload

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17
Q

What are 4 ways the CRNA can reduce MVO2?

A
  1. Prevent HR increase (aka SNS activation)
  2. Prevent ↑ inotropy (via SNS, Ca2+, Ca2+ sensitivity
  3. Prevent ↑ afterload
  4. Prevent ↑ preload (too high)
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18
Q

MVO2 is increased by what 4 factors?

A
  1. Afterload
  2. HR
  3. Inotropy
  4. Preload
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19
Q

How does ischemic heart disease impact MVO2?

A

↑↑ risk for ischemic event

**make coronary blood flow PRIORITY in the anesthetic plan.

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20
Q

Coronary blood flow is how much of the cardiac output?

A

5%

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21
Q

What is the O2 extraction in the coronary arteries?

A

70-80%

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22
Q

CorrPP = ???

A

(ADBP - LVEDP) / resistance

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23
Q

How does HR effect coronary blood flow?

A

“DOUBLE WHAMMY”

  1. less diastolic time
  2. increased O2 demand
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24
Q

What 5 factors impact coronary artery resistance?

A
  1. cardiac work output
  2. extravascular compressive forces
  3. Neurohumoral & endothelial factors
  4. Blood O2 content impacts cardiac work & metabolic demand of the heart.
  5. **MYOCARDIAL METABOLISM IS THE PREDOMINANT DETERMINANT OF CORONARY VASOMOTOR TONE
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25
Q

4 components of the Neurohumoral regulation of coronary VSMC tone

A
  1. # 1 = metabolic autoregulation
  2. SNS / PSNS (minor role)
  3. Shear forces; dilation
  4. Intraluminal pressure ; constriction
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26
Q

What are the 2 categories of coronary artery disease?

A
  1. atherosclerotic

2. non-atherosclerotic

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27
Q

4 pathologies / results of coronary artery disease

A
  • Angina
  • Unstable angina
  • NSTEMI
  • STEMI
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28
Q

3 pathologies of Acute Coronary Syndrome

A
  • Unstable angina
  • NSTEMI
  • STEMI
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29
Q

Acute coronary syndromes cause considerate ___ & ___

A

considerable immediate morbidity & mortality

HIGH risk of additional injury in the next ONE YEAR

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30
Q

CK-MB

A

creatine kinase, myocardial bound isoenzyme

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31
Q

For angina to be stable it must be unchanged for ___

A

> 2 months

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32
Q

Clinical manifestations of stable angina

A

minimal pain, unchanged for >2 months,

possible EKG changes, ST depression, or T-wave inversion

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33
Q

S/S of stable angina

A

chest pain DURING exertion, pressure, heaviness
-may or may not radiate to arm, shoulder, jaw, neck
epigastric pain

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34
Q

S/S of unstable angina

A

chest pain w/ or w/o exertion
NO cardiac enzymes present in the blood
EKG changes, ST depression or T-wave inversion

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35
Q

Pathological causes of angina

A
  • atherosclerosis
  • inflammation
  • non-occlusive thrombus
  • vasospasm
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36
Q

Anesthetic GOAL in patient with angina

A

decrease MVO2

prevent ischemic event while maintaining CO & BP

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37
Q

6 medications or classes to consider giving for angina

A
  1. O2
  2. analgesia
  3. Beta blocker
  4. Ca channel blocker
  5. sublingual NO
  6. anticoagulation
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38
Q

How long does anticoagulation last if a drug-eluding stent is placed?

A

1 year

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39
Q

How long does anticoagulation last if bare metal stent is placed?

A

6 weeks

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40
Q

If a patient has angina, what 3 things should be avoided in the OR?

A
  1. medications that ↑HR and/or BP
  2. triggering the SNS response
  3. Hypotension [be careful with regional d/t ↓SVR = hypotension]
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41
Q

In LV heart failure, what anesthetic should be avoided?

A

inhaled anesthetics

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42
Q

What volatile anesthetic can cause BAD steal effect in the coronary arteries?

A

Isoflurane

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43
Q

What are 4 post-op considerations for a patient with angina?

A
  1. AVOID ISCHEMIA
  2. monitor for ischemia
  3. treat ischemia
  4. avoid sustained hemodynamic changes
44
Q

Causes of NSTEMI

A

partial blockage of an artery by thrombus, plaque

45
Q

Clinical manifestations of NSTEMI

A

chest pain; may or may not radiate
*elderly may not have pain

anxious, pale, diaphoretic, tachy, hypotension, dyspnea, nausea, vomiting, dizziness, sudden weakness, fatigue

46
Q

When will cardiac enzymes be present in the blood?

A

NSTEMI & STEMI

47
Q

What are 2 main cardiac enzymes?

A

cTroponin

CK-MB

48
Q

What is different in STEMI vs. NSTEMI

A

STEMI is 100% block (full thickness ischemia)

NSTEMI is <100% block

49
Q

An ischemic event is NOT an MI if:

A

troponin is not elevated

50
Q

Clinical manifestations of STEMI (4)

A
  1. physical s/s
  2. significant ST elevation on EKG
  3. cardiac enzymes present
  4. myocardial ischemia
51
Q

Warning sign for STEMI and what does it indicate?

A

worsening angina

2/3 of patients had MI within 30d of worsening angina

52
Q

Anesthetic Implications of STEMI

A
  1. give thrombolytic

* bleeding risk ↑ with history of GI bleed, surgery, intracranial hemorrhage, >75 years old

53
Q

When does a perioperative MI occur?

A

within 24-48 hours after surgery

54
Q

What factors increase the risk of a perioperative MI?

A

Hx ischemic heart disease
emergency surgery
highly vascular surgery

55
Q

what is the mortality of perioperative MI?

A

20%

56
Q

What is a perioperative MI preceded by?

A

Tachycardia & ST depression

57
Q

Most perioperative MIs are what kind?

A

NSTEMI

58
Q

Why is diagnosis of a perioperative MI difficult?

A
  • post-op hemodynamic instability is common
  • post-op analgesia may mask chest pain
  • ECG changes alone are not diagnostic
  • Cardiac enzyme levels are not indicative of duration of ischemia
59
Q

Percutaneous Cardiac Intervention (PCI) is AKA

A

angioplasty

60
Q

How long should a patient wait after PCI to have surgery?

A

90 days

61
Q

What are anesthetic considerations of PCI?

A 
if PCI was recent, patient likely on anti-platelet therapy
     - weigh bleeding risk vs thrombus
monitor closely for MI or infarct
     - continuous ECG w/ST analysis
     - TEE for ventricular wall function
62
Q

What is intraoperative hypotension?

A

SBP <90mmHg

63
Q

What are 5 causes of intraoperative hypotension?

A
  1. drug side effects (sympatholytic)
  2. decreased stimulation
  3. Neuraxial anesthesia (↓SNS = ↓SVR = hypotension, bradycardia)
  4. MI / congestive HF
  5. HTN patients are at much higher risk of intraoperative hypotension
64
Q

Clinical implications of a ↓DBP

A
  • ↓coronary artery perfusion = cardiac ischemia or infarct
  • ↓ cerebral perfusion
  • ASSOCIATED WITH ANESTHESIA RELATED DEATH
65
Q

patients with uncontrolled HTN at baseline may develop hypotensive effects, when?

A

at a “normal” BP

66
Q

What are 5 mechanisms that cause ↓DBP?

A
  1. Arterial vasodilation
  2. myocardial depression
  3. venodilation
  4. bradycardia
  5. decreased volume (↓F/S)
67
Q

What are the CV effects/mechanisms of arterial vasodilation? (5)

A 
↓SNS
↑metabolites
↓SVR
↓CO
↓BP
68
Q

What are the CV effects/mechanisms of myocardial depression?

A 
drugs
↓SNS
↓inotropy
↓SVR
↓CO
↓BP
69
Q

What are the CV effects/mechanisms of venodilation?

A

↓VR
↓SV
↓CO
↓BP

70
Q

What are the CV effects of bradycardia?

A

↓HR
↓CP
↓BP

71
Q

Treatments for intra-operative Hypotension

A
  • modest fluid loading
  • smaller initial drug dose
  • re-introduce RAAS (hold ACEi / ARBs)
  • monitor for intraop MI
  • Small doses of short acting vasoactive meds
  • small short acting vasoactive gtt
72
Q

What is considered acute post-op hypotension?

A

SBP <90
MAP <65
OR >20% drop from baseline

73
Q

What are causes of acute post-op hypotension?

A
  • administration of anti-hypertensive meds
  • inadequate fluid replacement
  • blood loss
  • residual anesthetic effects
  • allergic rxn
  • adrenal insufficiency
  • myocardial ischemia / CHF
74
Q

What is considered perioperative hypertension?

A

USA BP > 130/80

Europe BP >140/90

75
Q

Clinical implications of hypertension?

A
  • leads to 57% of stroke deaths
  • 24% of CVD deaths
  • BP lability
  • High risk of hypotension INTRA-OP
  • High risk of HTN POST-OP

*even short duration of MAP <65 mmHg can have deleterious effects = increased mortality, AKI, MI, Stroke

76
Q

Goal when a patient has Hx HTN

A

maintain BP within 20% of baseline & keep MAP >65mmHg

77
Q

treatment of HTN

A

vasoactive medications; short acting, monitor frequently, do not overdose

78
Q

Patients that are candidates for intra-op arterial BP monitoring

A

CAD
cerebral ischemic disease
bleeding and/or fluid shifts

79
Q

Goal when caring for a patient with HTN

A

prevent end organ damage

80
Q

Proceed with surgery if a patient’s BP is

A

DBP <110mmHg

SBP <180mmHg

81
Q

Factors that can ↑SNS perioperatively

A 
anxiety
pain
DL/intubation
surgical stimulation
hypoxemia/hypercarbia
hypervolemia
vasoactive meds [must be short acting and SMALL doses]
82
Q

What is isolated systolic hypertension?

A

SBP >140

DBP <90 (normal)

83
Q

What causes isolated systolic hypertension?

A

stiffening of blood vessels; primarily in elderly

Suspect if patient is >65yr old

84
Q

Patients with isolated systolic hypertension are at significantly increased risk of?
(7)

A

CAD, ischemic heart disease, left ventricular hypertrophy, CVA, perioperative morbidity & mortality

85
Q

In a patient with isolated systolic hypertension, aggressive attempts to lower the SBP may result in

A

PROFOUND diastolic hypotension & compromised end organ perfusion

86
Q

What is worse, elevated SBP or widening pulse pressure?

A

widening pulse pressure

87
Q

What are the 2 types of hypertensive crisis?

A
  1. hypertensive urgency

2. hypertensive emergency

88
Q

What is hypertensive urgency?

A

BP >180/120mmHg

89
Q

What are the s/s of hypertensive urgency?

A

headache, epistaxis, anxiety

90
Q

What is a hypertensive emergency?

A

BP > 180/120 & EVIDENCE OF END ORGAN DAMAGE

91
Q

Hypertensive emergency is especially dangerous in who?

A

women about to give birth

92
Q

What pathologies can cause hypertensive emergency? (4)

A
  1. acute coronary syndrome
  2. acute decompensating HF
  3. acute LV failure with pulmonary edema
  4. dissecting aortic aneurysm
  5. Pheochromocytoma
93
Q

What are post-op complications of hypertensive emergency?

A

hemorrhage & increased ICP

94
Q

What are the neurological s/s of hypertensive emergency?

A

agitation, delirium, stupor, visual disturbances, seizures, stroke, encephalopathy

95
Q

What is the treatment of hypertensive emergency?

A
  1. IV antihypertensive
  2. short acting vasodilators (SNP)
  3. AVOID precipitous decline to normo-tension, may cause cerebral or coronary ischemia
96
Q

Pheochromocytoma

A

Adrenal gland chromaffin cell tumor

97
Q

What is released from a pheochromocytoma?

A

NE > Epi

opposite of normal

98
Q

S/S of pheochromocytoma?

A 
Tachycardia
diaphoresis
headache
paroxysmal HTN
hyperglycemia
99
Q

What can worsen the catecholamine effects of pheochromocytoma?

A

anesthesia

100
Q

What medication should you give with pheochromocytoma?

A

Phentolamine

101
Q

What does phentolamine do?

A

inhibits A1 receptors = vasodilation

102
Q

What are the 4 pathological outcomes of pheochromocytoma

A
  1. CVH
  2. HF
  3. arrhythmias
  4. MI
103
Q

What do you give pheochromocytoma patients in preop?

A

PO phenoxybenzamine and/or IV phentolamine

104
Q

What do you give pheochromocytoma patients post-op?

A

administration of inotropic agents to correct hypotension resulting from catecholamine withdrawal

105
Q

What are the 3 take aways from HTN/Hypotension?

A
  1. hypotension = high risk morbidity & mortality
  2. the most at risk patients are HTN patients
  3. HTN patients are the lowest risk for HTN emergency

N932: Pathophysiology (5 decks)

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