HSS 460 PAD & HF (CVD pt. 2)

Stenosis

The narrowing of any hollow vessel, canal, or passageway in the body.

• Leads to ischemia (decreased perfusion/blood flow)

Occlusion

The blockage or obstruction of any hollow vessel, canal, or passageway in the body.

• Leads to ischemia (decreased perfusion/blood flow)

Peripheral artery disease (PAD)

Refers to the blockage of the leg arteries (or any peripheral arteries) by atherosclerotic plaque, leading to gradual narrowing of the arteries in the lower extremities

• Involves stenosis & occlusion → ischemia (decreased perfusion) in the muscles of the legs and hypoxia

• PAD is to the arteries of the lower limbs what CAD is to the coronary arteries of the heart

Peripheral artery disease (PAD) pathophysiology

PAD develops due to atherogenesis in the peripheral arteries: endothelial damage → plaque formation → blood vessel occlusion → ischemia & hypoxia in affected tissues

• The metabolic demands of active muscles cannot be met during even low-intensity exercise

Atherogenesis

1. Circulating LDLc, monocytes, and platelets adhere to and enter the damaged endothelium of the t. intima

2. Activated macrophages…

• Release ROS that oxidize LDLc and then phagocytose LDLc, becoming “foam cells”; toxic, oxidized LDLc further damages the endothelium, allowing blood components like platelets and clotting factors to contact deeper vessel wall layers

• Release growth factors, causing smooth muscle cells (SMCs) and fibroblasts to migrate into the t. intima and secrete collagen & matrix

3. A SMC-rich fibrous cap forms around a necrotic core of lipid/cholesterol, inflammatory “foam cells”, T lymphocytes, and dead cells

Manifestations of PAD

• Most people with PAD are asymptomatic or have “atypical” symptoms (symptoms associated with muscle groups of the lower limbs that present with exertion and are relieved by rest)

• Other symptoms include claudication and/or critical limb ischemia (CLI)

Claudication

Manifestation experienced by 35-40% of individuals with PAD; pain, cramping, or aching in the calves/thighs/buttocks (dependent on vessel(s) experiencing ischemia)

• Muscle cramps that are typically relieved with rest and worsened with activity

• Claudication is to skeletal muscles of the limbs what angina pectoris is to cardiac muscle of the heart

Critical limb ischemia (CLI)

Manifestation experienced by 1-2% of patients with PAD; chronic pain at rest due to ischemia and foot ulcers/gangrene due to occlusive artery disease

• Gangrene — significant necrosis (death) of body tissue due to significant ischemia or serious bacterial infection; 25% of patients require amputation within 1st year

• CLI involves multiple vessels including those of the legs & feet — severe foot pain manifests in the recumbent position (often interrupts sleep) and is relieved by hanging the foot down (e.g., over side of bed)

Diagnostic testing for PAD

• Blood pressure measurements (hemodynamic testing) — provides functional information about disease severity (e.g, ankle-brachial index [ABI])

  • Regular evaluation of lower-limb pulse (femoral, popliteal, dorsalis pedis)

• Imaging studies — provides anatomical information about blood vessel involvement (e.g., CT and MRI angiography using contrast dyes)

Ankle-brachial index (ABI)

Simplest hemodynamic assessment & most widely used screening tool to diagnose PAD; blood pressure measurements are compared between the brachial artery & key arteries at the ankle (posterior tibial & dorsalis pedis arteries)

• Highest measurements from the arm and the ankle are used; ankle measurement is divided by brachial measurement (on L & R sides)

• More severe PAD = lower ABI (e.g., 0.40-0.90 is mild to moderate, while less than 0.40 is severe PAD)

Heart failure (HF)

A failure of the heart to deliver sufficient blood to meet the body’s metabolic demands; may not adequately eject and/or fill with blood

• A “final common pathway” for multiple CVDs

• Results in a clinical syndrome with signs & symptoms involving elevated natriuretic peptide levels in the blood and evidence of pulmonary or systemic congestion

• Etiologies include dyslipidemia, hypertension, poor diet, lack of PA, etc.

Systolic HF (HFrEF)

Heart failure with reduced ejection fraction due to systolic dysfunction

• Defined by an ejection fraction <40% (normal ventricle ejects 55-70% of the end diastolic volume [EDV])

Diastolic HF (HFpEF)

Heart failure with preserved ejection fraction; accounts for >50% cases of HF after age 75 (and <10% cases under age 60) — highly associated with aging & loss of elasticity

• Abnormal resistance to filling of the ventricle; stiff or less compliant ventricle that is partially unable to relax and expand as blood flows in during diastole

• Ultimately, stroke volume and cardiac output will be impaired

Heart failure (HF) pathophysiology

The syndrome of HF reflects physiological adaptations and compensation strategies that, over time, are detrimental and lead to decompensation (“failure”)

• Edema or fluid retention — can be a direct result of HF or compensatory activation of the RAAS

• Compensatory activation of the sympathetic nervous system

• Compensatory hormone & chemical changes (e.g., increased epinephrine & norepinephrine)

• Remodeling of the ventricles → shape changes that further diminish systolic functions

Edema due to HF

Associated with a “back up” of fluid resulting in congestion due to activation of the RAAS

• Left-sided HF will lead to pulmonary edema that manifests as central cyanosis, dyspnea, frothy sputum, & respiratory failure

• Right-sided HF will lead to systemic edema that manifests as peripheral cyanosis due to impaired venous return, portal hypertension, and ascites (due to edema in liver/GI tract)

Compensatory hormone & chemical changes due to HF

• Increased release of natriuretic peptides (ANP & BNP) — the heart’s “distress signals” that inhibit the RAAS, increase natriuresis & GFR (to reduce edema), increase vasodilation (to reduce BP)

• Decreased production of nitric oxide (NO) — leads to vasoconstriction & decreased BP

• Increased cytokines (e.g., tumor necrosis factor-alpha)

Additional manifestations of HF due to pulmonary edema/congestion

• Dyspnea on exertion (DOE) — leads to exercise/activity intolerance

• Orthopnea — difficulty breathing when lying down (blood returns to the heart and already congested lungs)

• Paroxysmal nocturnal dyspnea — sudden attack of dyspnea at night while sleeping; resolves by sitting upright

Additional manifestations of HF due to compensatory vasoconstriction in the kidneys

• Nocturia (early stages) — retention of urine during day (when upright); frequent urination after lying down at night

• Oliguria (late stages) — decreased urination; sign of reduced cardiac output and/or renal failure

Diagnosis of HF

• Echocardiogram — allows measurement of EF

• Diagnostic cardiac catheterization (evaluation only)

• Abnormal heart sounds

• Abnormal breathing sounds (pulmonary congestion, evidenced by rales)

What is the key cardiac biomarker used to diagnose and mark progression of HF?

Brain derived natriuretic peptide (BNP)

Mechanical Left Ventricular Assist Device (LVAD)

Treatment for HF that replaces the function of the failing left ventricle; continuous flow LVADs provide circulation to support underperfused organs and partially reverse/slow the progression of HF

• Acts as a bridge to transplant or destination treatment

• Extends survival 70%+ at 2-years post diagnosis

• Challenges: required anticoagulation medication; increase risk of stroke, bleeding, and infection; requires wearing external device at all times (risk of damaging it)

Cardiac transplantation

Surgical therapeutic intervention for end-stage HF patients (~4,200/year)

• Median survival of ~14 years for those who survive 1-year post transplant

• Challenges: donated heart is “decentralized” — PNS postganglionic fibers are left intact, other cardiac autonomic fibers (PNS preganglionic and all SNS fibers) are severed

  • No SNS effect on the heart and lessened PNS control

  • Heart wholly reliant on catecholamines to increase HR & contractility (slower response than SNS innervation)

Determinants of exercise capacity in patients with HF

HF patients are largely limited in their ability to improve central components of exercise capacity (Q), however, peripheral components (A-VO2 diff) will adapt to exercise

• Fick Eq: VO2 = Q x A-VO2 diff

• A-VO2 diff improved by increased skeletal muscle mass, increased percentage of type I oxidative fibers, and increase in mitochondiral enzymes/volume density

Exercise impact on HF

Exercise training has favorable impact on many clinical outcomes

• HF-ACTION trial (HFrEF only): compared the effects of exercise training plus usual care with usual care alone — showed an exercise training-related 10-25% reduction in the adjusted risk for all-cause mortality or hospitilization

• Mainly leads to peripheral adaptations to increase exercise tolerance and peak VO2

Specific adaptations to exercise training in HF patients

• No change or modest increase in peak cardiac output

• Improved ability to dilate small blood vessels — increased levels of endothelium-derived relaxing factor & flow-mediated improvement in endothelial function

• Downregulation of SNS — decrease in plasma norepinephrine & increase in PNS activity

• Changes within skeletal muscle — volume density of mitochondria & enzymes improved; skeletal muscle strength & endurance improved

• Exercise training partially normalizes autonomic, immune, & hormonal function in patients with HF

COT

Claudication onset time — time of onset of pain during activity

PWT

Peak walking time — time of exercise termination due to pain

Exercise impact on PAD

Excellent improvements in walking distances with both low- & high-intensity training improving claudication onset (COT) and peak walking time (PWT); mechanisms for improvement of walking distance include…

• Improved biomechanics of walking → decreased metabolic demands

• Improved blood flow & endothelial function

• Reduction in blood viscosity & decreased RBC aggregation

• Attenuation of atherosclerosis

• Increased extraction of oxygen & metabolic substrates resulting from improvements in skeletal muscle oxidative metabolism

• Increased pain tolerance

What must be added to a preexercise evaluation before a patient with HF can be cleared for exercise?

Preexercise evaluation should consider the following signs & symptoms:

• Fluid retention

• Exercise intolerance (DOE — dyspnea on exertion)

• Paroxysmal nocturnal dyspnea

• Orthopnea

Exercise testing for HF

Use cardiopulmonary exercise test (GXT) with measured gas exchange; determines VO2 peak and/or ventilatory derived lactate threshold (aka ventilatory threshold)

• Patients with stable HF routinely and safely undergo symptom-limited maximum cardiopulmonary exercise testing to evaluate cardiorespiratory function

• Contraindications: instability of disease (signs & symptoms) → 6-minute walk or another submaximal/functional test can be used

Focus of exercise prescription and testing for PAD

Walking ability (when claudication is worst)

Exercise testing for PAD

• Treadmill testing is useful for assessing claudication onset time (COT) or distance and peak walking time (PWT) or distance

• GXTs can be used (e.g., Naughton, Balke)

• Functional tests considered gold standard — the 6-minute walk test is useful in predicting the patient’s functional capacity based on the distance that can be completed; other valid & reliable tests include incremental- and constant-speed shuttle walking tests

Which disease scale is primarily used in the assessment of ACS (CAD & MI)?

The angina scale

Which disease scale is primarily used in the assessment of HF?

The dyspnea scale

Which disease scale is primarily used in the assessment of PAD?

The peripheral vascular disease scale for assessment of intermittent claudication

Overview of exercise prescription for CVD (ACS, HF, & PAD)

Supervised, ECG-monitored exercise should be used first within an inpatient then cardiac rehab setting; after demonstrating tolerance of supervised training 3x per week, patients can begin a home-based exercise program

• Cardiorespiratory endurance is an obvious focus & strategy for improvement in all CVD populations

• Muscular strength, muscular endurance, and flexibility training can also improve functional capacity & foster independence (and impact disease progression for some patients)

Cardiorespiratory exercise recommendations for CVD

• Frequency: 3-7 d/wk

• Intensity: RPE 11-16; 40-80% of exercise capacity (use intensity below ischemic threshold)

• Time: 20-60 min.

• Type: aalking, jogging, arm-leg ergometer, etc.

Resistance training recommendations for CVD

• Frequency: 2-3 d/wk

• Intensity: RPE 11-14, 30-80% of 1RM

• Time: 8-10 exercises; 1-4 sets of 8-10 slow reps

• Type: free weights, machines, bands, stability ball, etc.

Flexibility/ROM recommendations for CVD

• Frequency: daily

• Intensity: hold to point of mild discomfort

• Time: 5-15 min.

• Type: static stretching

CV exercise recommendations for ACS patients (special considerations)

• Frequency: daily is ideal but at least 3-4 d wk

• Intensity: if symptomatic use ischemic threshold from GXT & if asymptomatic use %HRR (HIIT: 85-95%) or RPE (HIIT: 14-17)

• Time: intermittent to continuous 30 min as tolerance allows OR progress to HIIT

  • 4 x 4-minutes with 3-minute recovery

  • Avoid in patients with arrhythmias or abnormal BP during exercise

• Type: any traditional modes – ideally those with high levels of muscle utilization

  • Avoid surgery-induced discomfort: chest and groin regions

RT & flexibility exercise recommendations for ACS patients (special considerations)

• Intensity: 4-weeks post-hospitalization = ROM/stretching only; 5-weeks+ = 1-3 lb or resistance bands only to rep ranges that allow for completion without breath holding or Valsalva

• Type:

  • Avoid surgery-induced discomfort: chest and groin regions

  • Exercises that focus on ADLs, especially muscles involved in lifting, carrying, standing, and climbing stairs

  • Rational mode progression: bands → hand weights → free weights → machines

**Frequency & duration follow general recommendations

What key questions should be asked of HF patients every session?

1. How did you sleep? How many pillows? (Paroxysmal nocturnal dyspnea & orthopnea)

2. How has your body weight been over the last three days? (Edema)

3. Have you had increased difficulty breathing (DOE & orthopnea)

4. Have you noticed ankle swelling? (Edema)

Special exercise considerations for HF

• Many patients with HF are inactive & possess low tolerance for activity

  • Emphasis on warm-up & cool down to illicit proper CV responses to exercise

  • Interval training may be necessary to include recover & build tolerance

  • Exercise should be progressively increased in an indivdiual manner

• %HRR can be used for some but RPE to guide intensity is recommended for most

• Resistance training programs play an important role — consider orthopnea issues when selecting exercises (impact of changes in position & posture)

Special exercise considerations for patients with LVAD

• For patients with an LVAD and a pacemaker, guide exercise intensity by RPE alone

• Avoid all exercises that would increase intra-abdominal pressure or cause physical trauma

  • Upper-body RT = resistance bands & light weights

  • Lower-body RT examples = ¼ wall sit or ¼ bilateral squat (avoid any compression of abdomen!)

Special exercise considerations for patients with cardiac transplantation

• Marked increases in body fat leading to obesity sometimes occur in cardiac transplant patients (due to prednisone prescription)

• Because of the sternotomy, postoperative ROM in thorax and upper limbs may be limited for several weeks

• Patients with a cardiac transplant present with a decentralized heart:

  • Resting HR = lower

  • HR little to no increase early in exercise, and slow HR increases later in exercise

  • Peak HR, SV, and Q are lower than normal

  • HR recovery very slow, but SBP normal recovery

CV exercise recommendations for PAD patients (special considerations)

Intermittent exercise recommended, with time limited by onset of moderate to moderately severe claudication

• Intensity: guided by claudication symptoms appears to be most recommended (COT)

  • Exercise until 3 or 4 ranking followed by rest or a decreased workload until leg pain subsides

• As patients exercise at higher intensities, attention should be focused on potential CVD symptoms because of a high incidence of CAD

• Mode: walking always preferred – can use recumbent cycling/NuStep for extreme pain

• Duration: accumulate 30-45 min of exercise during a 60 min session (5–10-minute work intervals)

RT & flexibility exercise recommendations for PAD patients (special considerations)

• Can use the same guidelines as ACS or healthy adult if symptoms are mild

• Only additional recommendation = use only machine & free weights