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CardioPulm > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Heart failure

A

Acomplex clinical syndrome that can result from any structural or functional cardiac disorder that results in the inability of the heart to eject blood to meet the demands of the body while maintaining normal pressures in it’s chambers and the lungs.

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2
Q

Compensations with heart failure

A

Neurohormonalmechanisms (SNS & RAAS) to ↑ CO (SV x HR); natriuretic peptides ]

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3
Q

Symptoms of heart failure

A

Shortness of breath, fluid retention, fatigue, orthopnea, paroxysmal nocturnal dyspnea

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4
Q

Complications of heart failure

A

Impaired exercise tolerance, increased risk of ventricular arrhythmias, and shortened life expectancy

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5
Q

Etiology of HF

A
  • Ischemic Heart Disease - (most common in the U.S.)
  • Hypertension*
  • Idiopathic Cardiomyopathy
  • Infections - (e.g., viral myocarditis; Chagas disease)
  • Toxins (e.g., alcohol or cytotoxic drugs)•Valvular Disease
  • Prolonged Arrhythmias (Afib)

*Life time risk for developing HF is greater if BP remains > 160/90 mmHg

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6
Q

Neuro-hormonal effects of HF

A
  • Kidney is not happy with decreased blood flow
  • Increases Na+/H2O retention to increase perfusion pressure
  • Increased epi, renin, endothelin (all vasoconstrictors) and ANP (produced by heart for vasodilation)
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7
Q

Factors that affect cardiac output

A

•Preload is the degree of myocardial distension prior to shortening. - Largely depends on the amount of ventricular filling

  • Afterload- force against which the ventricles must act in order to eject blood; largely dependent on the arterial blood pressure and vascular tone
  • contractile state
  • heart rate
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8
Q

Systolic heart failure

A
  • Impaired contractile function of the heart

* SHF most common etiology is ischemic heart disease, although many patients with DHF have coronary artery disease

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9
Q

diastolic heart failure

A
  • Impaired relaxation of the heart
  • DHF more common in females and HTN is a more common risk factor, although substantial proportion of pts with SHF have HTN
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10
Q

Ejection Fracture

A

EF = EDV-ESV/EDV

normal value 55-75%

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11
Q

NYHA Class 1 heart failure

A

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).

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12
Q

NYHA Class 2 heart failure

A

Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).

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13
Q

NYHA Class 3 heart failure

A

Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea.

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14
Q

NYHA Class 4 heart failure

A

Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest.If any physical activity is undertaken, discomfort increases

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15
Q

ACC/AHA Stage A heart failure

A

Patient at high risk for developing HF with no structural disorder of the heart

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16
Q

ACC/AHA Stage B heart failure

A

Patient with structural disorder without symptoms of HF

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17
Q

ACC/AHA Stage C heart failure

A

Patient with past or current symptoms of HF associated with underlying structural heart disease

18
Q

ACC/AHA Stage D heart failure

A

Patient with end‐stage disease who requires specialized treatment strategies

19
Q

Medical Examination of HF

A
  • Echo- EF, chambers and valves, wall motion
  • Interview
  • Physical exam
  • BNP (B-type natriuretic peptide)
20
Q

Acute HF

A

•Immediately life threatening, in acute pulmonary edema and acute ischemia, medical emergency. End sequela of an MI
•Time - Instant, sudden - Hr to days
•Causal Disease - Acute MI - Pulmonary Embolism - Severe malignant HTN
•Effects - No time to compensate - Acute Pulmonary edema
- Acute Ischemia

21
Q

Chronic HF

A
  • Can exist in compensated failure for many years, cardiac dilation, poor pump quality, chronic peripheral edema and congestion
  • Time - Progressive - Wks to months
  • Causal Disease - Chronic HTN, valve dis - Myocardial fibrosis - Chronic lung disease
  • Effects - Full compensation - Chronic edema, congestion
22
Q

Effects of afterload on HF

A
  • In normal heart, not much decrease in SV with increased afterload
  • However the effects are much more significant in patients with HF.
  • Which is why vasodilator therapy though a bit counter intuitive is effective for patients with HF
23
Q

Exercise Testing HF

A
  • Cardiopulmonary stress test (gold standard)
  • Six Minute Walk Test (6MWT)
    • Alternative to CPXT to assess functional capacity
    • Used extensively in HF studies 1
    • Predicts morbidity and mortality in patients with HF 2 (6MWD <300 m)
24
Q

Implications of an abnormal hemodynamic response to exercise

A
  • Associated pulmonary disorders impair breathing
  • Reduced gas diffusion in the lungs
  • Increased work of breathing
  • Contribute to dyspnea and fatigue
  • Exaggerated redistribution of blood flow away from the periphery and to the respiratory muscles during Exercise - May contribute to the enhance perception of fatigue in HF patients
25
Q

Medical management of HF

A
  • exercise
  • pharmacologic
  • surgical
26
Q

Special exercise considerations for heart failure

A
  • Avoid exercise after eating and vasodilator medications
  • Use VO2maxrather that HRmax
  • Initial exercise intensity should be 10 beats below significant symptoms
  • Signs of cardiac decompensation - Pulse Narrowing, Arrhythmia, Fluid Changes 3lbs in 24hrs, 5lbs in a week
  • Goal writing: -Increased intensity/duration -Functional activities and independence
27
Q

Aerobic Training

A
  • AT is considered the gold standard exercise intervention patients with HF
  • Most often performed at “Moderate Intensities” (60-70% VO2Max).
  • Most studies have used walking (treadmill/over-ground), or a recumbent bike/stepper (NuStep)
  • Easier for monitoring and allows for an objective method for progression
  • Improvements - VO2max, 6MWD, MLHFQ, LVEF, capillary density and peripheral artery diameter.
28
Q

Resistance Training

A

•Resistance training was once considered unsafe for even less severe cases.
•RT has become accepted as more evidence has emerged supporting it.
•Most often prescribed in the form of a PRE (progressive resistance exercise) -
- 60-80% 1RM.
•Machines, free weights, body weight
•Most protocols emphasized lower extremity muscles.

•Improvements
“Muscle Hypothesis” Attenuated the loss of muscle mass, improved functional mobility and ADLS, 6MWD and QoL(SF-36)

29
Q

Should you do just AT or RT?

A

a combination of both

30
Q

High Intensiity Interv

A

Periods of high-level exercise training (ET) are interspersed with periods of lower-intensity ET that permit enough recovery such that the individual is able to reengage in high-intensity ET bouts, or ‘‘intervals.

31
Q

Basic format of HIIT

A
  • 10-min warm-up at 40–50 % of peak VO2 (& 60–70 % of peak heart rate)
  • 3-min interval at 80–90 % of peak VO2 (& 85–95 % of peak heart rate)
  • 3-min active recovery at & 40–50 % of peak VO2 (& 60–70 % of peak heart rate)
  • Repeat intervals 4–6 times
  • 5 min cool-down at 30–40 % of peak VO2 (50–60 % of peak heart rate)
32
Q

HIIT limitations

A
  • May not be tolerated by all patients even if appropriate.
  • Requires close and skilled supervision.
  • As on 2013 out of all studies published only 100 subjects total.
  • Some patients may benefit from beginning with conventional therapies before initiating HIIT.
33
Q

HIIT contraindications

A

severely deconditioned patients or those susceptible to arrhythmias

34
Q

Noninvasive positive-pressure ventilation

A
  • Commonly delivered as CPAP or BiPAP.
  • Provides patients with a higher fraction of inspired oxygen and increases inter-thoracic pressure; which decreases dyspnea, and improves cardiac function.
  • Improvements: - LVEF, FVC, FEV1, Plasma NorEp, 6MWD.
  • Beneficial effects have been elicited with both nocturnal and acute delivery.
35
Q

NMES

A
  • Not typically considered for patients with HF but within the past 10 years its usage has been researched more extensively.
  • Patients with severe HF can at times be too incapacitated to move volitionally. NMES can be used to help the muscles remain/become more active, attenuate some of the atrophy resulting from inactivity and provide low level strengthening.
36
Q

NMES basic protocol

A

10-25Hz, biphasic, variable “on and off” times totaling 20min-60min, 5-7days/week.
•Targeted Muscles: Quadriceps, Soleus and Gluteals.

37
Q

pharmacotherapy

A

•Angiotensin-converting enzyme inhibitors OR Angiotensin antagonists - Vasodilate,
decreases Remodeling
•Beta Blockers - decreases HR, remodeling (blockSNS), anti-arrhythmic
•Diuretic - decreases Fluid volume, relieves dyspnea
•Aldosterone - decreases Fibrosis,Na retention, Antagonists remodeling, aldosterone release
•Digoxin or Dobutamine or PD3 - Positive inotrope

38
Q

Ventricular Assist Device for HF

A
  • Limited organ availability
  • Short term solution*
  • Ability to sense preload
  • Need Doppler to take pressure, may not have a true HR either (use RPE)
  • Progressive exercise training is indicated
39
Q

Heart transplantation

A
  • Native SA Node
  • No longer innervated
  • Different mechanisms for CO regulation during exercise
40
Q

Immunosuppressive agents after transplant

A
  • Prevent rejection
  • Cyclosporine or Tacrolimus
  • Prednisone
  • Side effects: HTN, osteoporosis, muscle weakness, liver damage

CardioPulm (14 decks)

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