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AP III > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

A complex pathophysiologic state characterized by the heart’s inability to fill with or eject blood to meet tissue requirements

A

Heart Failure

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2
Q

What are the two most common symptoms of HF no matter which type?

A

Dyspnea and Fatigue

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3
Q

List different etiologies of Heart Failure.

A

-Impaired contractility due to ischemic heart disease or cardiomyopathy (CM)
-Valve abnormalities
-Systemic hypertension
-Pericardial disease
-Pulmonary hypertension

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4
Q

What is the most common cause of RV Failure?

A

LV Failure

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5
Q

What are the causes of Systolic Heart Failure?

A

-CAD
-Dilated CM
-Chronic Pressure overload (AS, HTN)
-Chronic Volume overload (regurgitant valves, high output failure)

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6
Q

How do you diagnose Systolic HF?

A

ECHO, ventriculography

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7
Q

What are the S/Sx of Systolic HF?

A

-Hallmark Sign = Decreased EF
-Ventricular dysrhythmias common (risk of sudden death)
-Third Heart Sound (S3)
-More common in men d/t CAD

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8
Q

What are the causes of Diastolic HF?

A

-Ischemic Heart Disease
-Chronic HTN
-Progressive AS

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9
Q

What are the S/Sx of Diastolic HF?

A

-Normal EF
-Classic Sign: Increased LVEDP
-Inability of heart to “fill” LV due to fibrosis, hypertrophy, aging (age dependent), or pressure overload
-Fourth Heart Sound (S4)
-Women > Men
-May coexist with systolic HF

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10
Q

Which type of HF requires emergency therapy, is characterized by the presence of systemic hypotension, and is associated with sudden decreased CO, HoTN, and NO edema?

A

Acute

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11
Q

What are the causes of Acute HF?

A

1) Worsening of chronic HF
2) New onset: Valve rupture, HTN crisis, large MI
3) Terminal HF: refractory to therapy (Death)

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12
Q

Describe Chronic HF

A

-Long-standing disease
-Typically venous congestion (edema)
-Usually adequate BP
-Heart undergoes adaptive responses (dilation and hypertrophy)

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13
Q

What are the S/Sx of Left-sided HF?

A

-Increased LVEDP
-Pulmonary venous congestion
-Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
-Pulmonary edema eventually results

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14
Q

What are the S/Sx of Right-sided HF?

A

-Systemic venous congestion
-Peripheral edema and congestive hepatomegaly
-May be caused by pulmonary htn or RV infarct
-Usually caused by left sided failure

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15
Q

What is the mechanism responsible for fluid retention in heart failure?

A

Decreased tissue perfusion = activation of the RAAS

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16
Q

Which HF?
-Ascites
-Impaired liver function
-Anorexia, GI distress, weight loss

A

Right HF

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17
Q

Which HF?
-Orthopnea
-Activity intolerance
-Cough with frothy sputum
-Paroxysmal nocturnal dyspnea

A

Left HF

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18
Q

What are the effects of inotropes on a PV loop?

A

Increase SV, decrease ESV

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19
Q

What are the effects of diuretics and vasodilators on a PV Loop?

A

Reduce LVEDP

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20
Q

What are the effects of vasopressors on a PV Loop?

A

Raise Systolic pressure

21
Q

What are the 3 basic strategies of interventions for acute LV failure?

A

1) Augmentation of preload by volume infusion
2) Use of inotropic, vasodilator or inodilator drugs
3) Use of mechanical interventions (IABP) or physiologic pacing along with pharmacologics

22
Q

What is Low Output Failure?

A

-What we classically think of as HF
-Systolic and/or Diastolic
-May have normal CI at rest, but inadequate responses to stress or exercise

23
Q

What are the causes of Low output HF?

A

CAD, CM, hypertension, valve disease, pericardial disease

24
Q

What are the causes of High Output HF?

A

1) Increased HD burden: Pregnancy, AV fistulas, sepsis
2) Direct myocardial toxicity: Thyrotoxicosis, Beriberi (b1 def)
3) Myocardial Hypoxia: severe, prolonged anemia leading to MSOF due to not enough Hgb and heart tries to compensate

25
Q

What is Cardiogenic Shock?

A

An acute form of HF.
-Inadequate pumping of the heart leads to cell death throughout the body and in the heart muscle
-Survival is <15%
-May require emergency surgery or catheterization to remove blockage
-Streptokinase or tPA to remove clot
-Think ACLS algorithm

26
Q

What are the causes of cardiogenic shock?

A

1) LV or RV infarct
2) PE
3) Cardiac Tamponade
4) Endocarditis leading to MV Prolapse
5) Ventricular tachycardia refractory to tx

27
Q

What are the different causes of HF?

A

1) Pressure Overload: AS or systemic HTN
2) Volume Overload: Mitral or Aortic regurg
3) Myocardial ischemia or infarction
4) Myocarditis
5) Restricted diastolic filling: constrictive pericarditis or restrictive CM

28
Q

What are the different mechanisms of compensation to HF?

A

1) Utilization of Frank-Starling mechanism – RAAS increases preload to heart
2) SNS stimulation
3) Alterations in CO/HR/SVR
4) Humoral mediation (ANP, BNP)
5) Myocardial hypertrophy- Remodeling

29
Q

What is the Frank-Starling Law?

A

Represents the relationship between stroke volume and end diastolic volume.
-SV increases in response to an increase in volume
-Increased volume in the ventricle = blood stretches the cardiac muscle fibers leading to increased force of contraction (length-tension relationship)
-With Heart failure, reduced compliance = inadequate filling = decreased EDV, leading to decreased SV.

30
Q

How does activation of the SNS compensate with HF?

A

SNS activation = arteriolar and venous constriction.
-Arteriolar constriction to maintain SBP
-Venous constriction to shift blood to central compartment, increasing PL, maintaining CO via Frank-Starling Law

Arterial constriction redistributes blood away from kidneys, splanchnic, and skeletal circulation.
-Activates RAAS
-Na and water retention increases blood volume = increased CO
-Increases AL and causes some remodeling

31
Q

Why does activation of the SNS lead to worsening HF?

A

Fluid retention, increased venous return, and increased SVR lead to increased workload of heart, increased O2 use and leads to decreased CO and decreased tissue perfusion… (a vicious cycle)

Down regulation of beta receptors is seen with increased circulating catechols. Associated with worse outcomes, cardiotoxic. Beta Blockers decrease these deleterious effects.

32
Q

Why is Stroke Volume fixed in Systolic HF?

A

-The sarcomeres are maximally stretched. Increasing PL will not increase SV.
-Only way to increase CO is by increasing HR
-CO is HR dependent!
-Mild tachycardia is helpful in systolic HF

33
Q

Is tachycardia good or bad for diastolic HF?

A

In diastolic HF, tachycardia can produce decreases in CO due to inadequate relaxation and filling time (bad).

34
Q

How do humoral responses and biochemical pathways help maintain CO in HF?

A

Generalized vasoconstriction via:
-SNS & RAAS activation
-Parasympathetic withdrawal (higher resting HR)
-High levels of vasopressin, inflammatory mediators
-Secretion of ANP and BNP leads to diuresis, natriuresis, vasodilation, anti-inflammatory effects, and inhibition of the SNS and RAAS

35
Q

What is ANP?

A

“Atrial Natriuretic Peptide”
-Stored in Atrial Muscle
-Released in response to increased atrial pressure
-Protects the CV system by decreasing RAAS and SNS
-Protects from effects of volume & pressure overload
-Overtime, the response to ANP is blunted.

36
Q

What is BNP?

A

“B-Type Natriuretic Peptide”
-Secreted by Atrial & Ventricular cells in response to stretch
-Protects from effects of volume & pressure overload

37
Q

How does myocardial remodeling occur?

A

-Adaptive measures have failed, leading to changes in LV size, shape, and function
-Myocardial hypertrophy (thick muscle) (pressure overload), cardiac dilation (volume overload), thinning, collagen deposition, fibrosis, scar formation (d/t myocardial death), etc.
-Hypertrophy increases MVO2 requirements (inc risk for ischemia)
-Can be reversed by ACE-inhibitors and these drugs are 1st line therapy for HF
-Cardiac Resynchronization therapy has beneficial reverse remodeling effects

38
Q

What S/Sx of HF should you ask about in preop?

A

1) Dyspnea - due to interstitial pulmonary edema
-The earliest subjective sign of HF
2) “How many flights of stairs can you climb?”
-early finding and a helpful estimate (MET’s)
3) Orthopnea
-LV can’t handle the increased venous return in the supine position (usually dry, non-productive cough)
4) PND (paraoxysmal nocternal dyspnea) – this is SOB that awakens from sleep
5) Hallmarks of decreased reserve = fatigue at rest
6) Liver Congestion:
-Anorexia, nausea, abdominal pain
7) Decreased cerebral blood flow
-Confusion, difficulty concentrating, insomnia, anxiety, memory loss
8) Anemia
9) Narrow pulse pressure with high diastolic pressure reflects decreased SV
10) Cardiac cachexia -“body wasting”
11) Right heart failure signs: JVD, liver engorgement, pleural effusion, pitting edema

39
Q

Describe clinical diagnostic criteria of HF

A

-#1 most useful test is Echocardiography: detects abnormal pericardium, valves, RV/LV structure, EF, any hypertrophy, etc.
-Plasma BNP levels >500 pg (pico)/mL
-EKG: low predictive value for HF, but may show CAD, hypertrophy, etc
-CXR: Not good for diagnosis of HF, but shows pulm disease, cardiomegaly, pulm venous congestion/edema
-Also obtain full metabolic and electrolyte panel due to RAAS activation

40
Q

What is the NYHA Classification based on?

A

Functional Status
-Class I: Ordinary activity does not cause symptoms
-Class II: Symptoms with ordinary exertion
-Class III: Symptoms with less than normal exertion
-Class IV: Symptoms at rest

41
Q

Describe the AHA Stages of HF

A

-Stage A: patients at high risk of HF but without structural heart disease or symptoms
-Stage B: patients with structural HD but without symptoms of HF
-Stage C: patients with structural HD with previous or current symptoms of HF
-Stage D: patients with refractory HF requiring special interventions

42
Q

Describe medical management of Systolic HF

A

-Beta Blockers: Dec SNS stimulation, inc EF, dec remodeling
-RAAS inhibitors (ACE-Is, ARBs, Aldosterone antagonists)
-Statins: Anti-inflammatory, lipid-lowering
-Diuretics: dec LVEDP, Dec LV wall stress
-Vasodilators: Inc SV, dec AL, dec ventricular filling pressures

43
Q

Describe medical management of Diastolic HF

A

-#1 tx is prevention!
-Maintain NSR and HR control: need adequate filling time! Dependent on atrial kick
-PL Dependent: cautious use of diuretics (relieve pulmonary congestion without decreasing PL)
-Correct precipitating factors (Acute MI or systemic HTN)

44
Q

Describe anesthetic management of VADs.

A

-Antibiotics are very important
-Have rhythm devices available (pads)
-Use Bipolar (!) cautery
-May have non-pulsatile flow, monitor MAP
-Arterial line useful, may not be able to use non-invasive cuff.
-Use of chest compressions is facility dependent
-Drugs: Low, Slow, Neo (low doses, administer slowly, neo is pressor of choice)

45
Q

What are causes of Hypotension with an LVAD?

A

1) Decreased Preload:
-Can lead to LV “suck down”
2) RV Failure:
-Avoid increases in PVR: Avoid hypercarbia (use controlled ventilation), have nitric available
3) Increased afterload:
-Small doses of pressors

46
Q

Describe management of acute HF.

A

-Diuretics/vasodilators – lasix, nitroglycerin
-Inotropic support- current favorites are dopamine (for small problems) epinephrine (big problems), add milrinone for more impact
-Calcium sensitizers – levosimenden (inodilator)
-B-type natriuretic peptide – inhibits RAAS, pesky side effects
-Nitric oxide synthase inhibitors- (L-NAME)
-Mechanical device- IABP, percutaneous VADs (Tandem Heart and impella )

47
Q

What is the prognosis of HF?

A

-HF continues to increase in the USA, despite advances in therapy
-Mortality in first 4 years after diagnosis is 40%
-If correctable cause of HF can be identified, prognosis improves

48
Q

Describe overall management of anesthesia in a HF patient

A

-Optimize patient and continue meds: Continue BB and dig, D/C diuretics, Ace-I
-Opioids are beneficial: Temper the SNS
-Monitoring based on complexity of surgery: TEE is very helpful, Art line (consider vigileo), defibrillator pads, ICD mgmt (magnet)
-ICU postop may be necessary

49
Q

Describe anesthetic management of the transplanted heart

A

Strict aseptic technique

Transplanted heart is Denervated:
-Indirect acting drugs will have blunted effect
-Use direct acting drugs like epinephrine and isuprel
-Atropine/panc will not produce a change in HR

Preload dependent: The transplanted heart increases CO by increasing SV, not HR

AP III (20 decks)

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