Ischemic cardiovascular conditions and other vascular pathologies

Two basic rules of fluid dynamics

- pressure gradient

- path of least resistance

Major determinants of myocardial blood flow

- DBP = driving force of blood into myocardial tissue

- VMT (vasomotor tone) = determine the volume of blood passed along to the tissue

- Resistance (R) to flow commonly results from atheroclerosis

- Left ventricular end diastolic pressure (LVEDP) = pressure within ventricle at end of diastole

flow of blood to myocardium equation

DBP + VMT - R - LVEDP

CAD (coronary artery disease)

presence of an obstruction that limits coronary artery blood flow, but does not significantly inhibit heart muscle function

CHD (coronary heart disease)

obstruction + permanent damage to heart mm fibers downstream (limits function)

CVD

includes CHD, HTN, HF and cerebrovascular disease (major CVDs)

- common CVDs linked to atherosclerosis include HTN, stroke, PAD, and other vascular disorders

What can occur with advanced atherosclerosis?

Vasospastic Angina (Prinzmetal or Variant Angina)

- ST segment elevation at rest

- not associated with any preceding increase in myocardial oxygen demand

8 recommendations for atherosclerosis

- eat better

- be more active

- quit tobaco

- get healthy sleep

- manage weight

- control cholesterol

- manage Blood sugar

- manage blood pressure

Contributing risk factors for coronary heart disease (CHD)

- family Hx

- inc age

- gender (males>females until menopause)

- stress - risk to CV disease

Emerging risk factors for cardiovascular disease

- lipid related biomarkers: lipoprotein(a) and high lipoprotein associated phospholipase A2 (LP-PLA2)

- inflammatory markers: IL-6, CRP

- kidney biomarkers (microalbuminuria)

- pollution

- mediastinal radiation

- HIV

- elevated homocysteine

- abnormal sleep

Typical clinical course

1. sudden cardiac death

2. chronic stable angina

3. Acute coronary syndrome

4. cardiac muscle dysfunction

acute coronary syndrome (ACS)

- unstable angina

- STEMI ST segment elevation + MI

- nonstemi

Clinical Course: Sudden Cardiac Death

- abrupt, unexpected loss of conciousness and heart function

- no signs of circulation

- usual cause of death: ventricular tachy and VFib --> no CO

- survival: cardiopulmonary resuscitiation with AED --> ER

Clinical Course: Chronic Stable Angina

substernal pressure anywhere from epigastric area to jaw

- squeezeing, tightness, crushing

- imbalance supply and demand of myocardial O2

- well established onset

- not enough blood supply to meet demands

- controlled by reducing intensity of exercise or sublingual nitroglycerin

Heart attack symptoms: men

- nausea/vomiting

- jaw, neck, back pain

- squeezing chest pressure/pain

-SOB

Heart attack symptoms: women

- nausea/vomiting

- jaw, neck, upper back pain

- chest pain, not always

- pain/pressure in lower chest and upper abdomen

- SOB

- fainting

- indigestion

- extreme fatigue

Clinical Course: Acute Coronary Syndrome

chest discomfort for >20min

- unstable angina

- acute MI

Unstable angina

signs or symptoms of inadequate blood supply to myocardium without demands that usually provoke imbalance (e.g., in a person at rest)

- alert physician for signs

- at rest >20min

- pt typical angina occurs at lower exercise

- deterioration of prev stable pattern

- loss of myocardial reserve (drop in BP or inc HR)

Acute myocardial infarction

- STEMI: Q wave on ECG in 24-48hrs

- Non-STEMI: Q wave not developed

STEMI

1) ST elevation

2) Develop Q wave on ECG in

subsequent 24 hours

3) Transmural (full or near full

thickness infarction)

4) Elevated troponin

Non-STEMI

1. No ST Elevation

2. No Q wave

3. Can still have elevated troponin levels

4. partial thickness infarction

how can you prevent necrosis from MI?

Reperfusion (arterial) of myocardium within 15 to 20 mins of MI

other causes of MI

1. Embolization

2. Spontaneous coronary artery dissection (esp. in women <50 years

of age)

3. Arteritis (e.g., Kawasaki syndrome)

4. Trauma

5. Metabolic disease (e.g., amyloidosis)

6. Hematologic disorders

7. Cocaine abuse

8. Other (e.g., vasospasm)

Other general treatment measures for MI

1. Aspirin

2. Anticoagulant therapy

3. Control of cardiac pain

- Use of nitrates

- Use of morphine

- Use of β blockers

4. Improve oxygenation - Use of oxygen

5. Limitation of infarct size

- Early reperfusion—consider the need for PCI

6. Treatment of arrhythmias if needed for hemodynamic stability

7. Control of other complications

- Treatment of left ventricular dysfunction

Complications associated with acute MI

- >15% LV is involved = dec SV (EF)

- dec SV = dec aortic pressure, dec coronary perfusion pressure, inc MI

- >25% LV = S/S of HF

- >40% LV = death

- persistant angina and arrhythmias

Factors related to prognosis post-MI

1. Any complications

2. Infarction size

3. Presence of disease in other coronary aa

4. LV function

HTN and exercise

ex capacity reduced 15-30%

- SV inc & Peak HR lower = dec CO

- aerobic - reduces BP

- resistance - lacking evidence

HTN: ex testing

Resting BP > 200 sys or > 100 diastolic - need physician clearance

HTN: ex training

Rest: Uncontrolled: >180 sys or >110 dia - need clearance

HTN: side effects for meds

Beta blockers block hemodynamic response

Antihistamines

ACE Inhibitors

Anti-hypertensive meds

Long term standing

watch for signs of hypotension with:

- Change of position

- Post-exercise - possible secondary to anti-HTN meds (gradual cool down)

- Long-term standing

- Warm environments

HTN: endurace trainging

mod intensity

- avoid valsalva

- low weights/high reps in deconditioned/high risk

Cerebrovascular Accident

results from ischemia (restricted or reduced blood flow); a smaller percentage results from hemorrhage

- TIA if symptoms resolve completely within 24hrs

- stroke deficit results after 24hrs

Treatment for stroke prevention

- Early recognition, risk factor reduction, medical management

- Reducing BP more

important than the medications used

to achieve reduction

- Optimal regimen includes combo of:

-- aspirin

-- lipid-lowering medication

-- glycemic control

-- antihypertensive medication

-- risk factor modification

Implications for physical therapy intervention

- For patients with carotid or vertebral disease, monitor vital signs (especially blood pressure) at rest and with all new activities.

- Educate patients about primary and secondary prevention, as well as: symptoms of instability (signs of TIAs); importance of urgent medical treatment to reduce risk of permanent brain injury

Peripheral Arterial Disease

narrowing of peripheral arteries, resulting in a decreased supply of blood

- result of same atherosclerotic process for CAD (in LE)

- appear when atheroma becomes enlarged that BF to distal tissues is blocked

- pallor

Peripheral Arterial Disease & Exercise

- unable to prod regular inc in peripheral BF

- inadequate O2 supply --> ischemia --> lactic acid --> pain and SOB

- intermittent claudation --> moderate to severe impairment in walking ability

- structured exercise training --> improve symptoms

- treadmill training and arm ergometru = improvements

PAD: as a PT we should:

- assess vital signs

- expect steep rise in BP during exercise (8-10 mmHg/MET)

- know how to perform and interpret ABI (ankle brachial index)

- value of 0.9 or less is considered abnormal

- assess for other clinical signs

PAD symptoms

- pain (intermittent claudation or other atypical symptoms

- pallor

- pulses

- paresthesia

- paresis

- + signs of trophic changes; dry, shiny skin, hair loss, thick toenails, wounds

pallor

lighter skin, more while in color, dark skin more ashen or gray, brown skin more yellowish or brown

pulses

decreased or absent with an extremity cool to touch

paresthesia

impaired sensation, esp more distally

paresis

weakness; muscle atrophy

Does PAD only present in lower legs?

NO

- subclavian artery stenosis:SBP can be 15-20mmHg lower in parm

- aortoiliac arterial disease: thigh, hip, butt claudation

BP measurements with subclavian artery stenosis is taken in which arm?

higher value arm

other vascular disorders

- renal artery disease

- aortic aneurysm

- abnormal aortic aneurisms (AAA)

aortic aneurysm

- permanent pathological dilation of aortic wall at least 50% greater than normal (>3cm)

- described as location, size, morphological appearance, origin

abdominal aortic aneurysms (AAA)

sig risk for rupture

- PT: during initial assessment - ID risk factors (>60y/o and fam Hx)

- asses vitals with rest and ex

- high BP during ex --> stress on already weakended area

venous disease

- venous insufficiency

- venous stasis ulcers

- venous thromboembolism (VTE)

Venous insufficiency

results from inadequate muscle action, incompetent venous valves, or venous obstruction

Venous stasis ulcers

chronic venous insufficiency leads to skin changes, swelling, and wounds

Venous thromboembolism (VTE)

includes both deep venous thrombosis (DVT) and pulmonary embolism PE)

DVT

development of a clot in a deep vein of the lower extremity or pelvis (or less often, in the arm)

Interventions for VTE:

mechanical compression, early monitored mobility, and anticoagulation medication

Interventions for venous insufficiency and venous ulcers

• Exercise

• Extremity elevation

• Avoiding long periods of sitting or standing

• Compression

• Aggressive wound management

• Education to prevent further progression

Physical Therapy Implications for Venous Disease

- consider risk factors with history, S/S for venous insufficiency and VTE

- wels prediction model for LE DVT

- conditions that can mimic DVT (muscle injury, baker's cyst)

- assess vital signs and monitor S/S for PE