Perfusion Part 2 Notes
HYPERTENSION
Epidemiology:
50 million individuals in the U.S.
1 billion worldwide.
75% are using antihypertensive medication.
Risk factors include age, gender, race, and socioeconomic status.
Major risk factor for atherosclerotic cardiovascular disease, heart failure (HF), stroke, and kidney failure; common and manageable chronic condition.
Types of Hypertension:
Essential or Primary Hypertension:
Accounts for 90% to 95% of cases in the adult population.
Has no identifiable medical cause; appears to be multifactorial.
Heredity is a predisposing factor, but the exact mechanism is unclear; tends to be familial.
Risk Factors: Smoking, hyperlipidemia, age over 60, overweight, physical inactivity, excessive alcohol intake, excessive and continuous stress.
Secondary Hypertension:
Elevations in BP due to a specific cause.
Renal parenchymal disease (affecting the renal medulla and cortex) is the most common cause, excluding obesity and alcohol abuse.
Responsible for 2% to 5% of all cases of secondary hypertension.
Risk Factors: Medications (estrogen, glucocorticoids, mineralocorticoids), pregnancy, brain tumors, Cushing’s disease.
Malignant Hypertension:
BP is 200/130 or greater.
Symptoms: Morning headache, blurred vision, dyspnea, and/or symptoms of uremia.
If not treated promptly, can cause kidney failure, left ventricular heart failure, or stroke.
Mostly seen in patients in their 30s-50s.
Pathophysiology:
BP is the result of cardiac output (CO) multiplied by total peripheral vascular resistance (PVR): BP = CO \times PVR
Pathogenic mechanisms involve increased CO, increased PVR, or both.
Clinical Manifestations:
Evident only after long-term increased BP has resulted in target organ damage (TOD).
Some symptoms of chronic uncontrolled hypertension are headaches, chest pain, vision changes, shortness of breath, renal dysfunction, dizziness, fatigue, or nosebleeds.
Management:
Diagnosis, treatment, and medications.
Lifestyle modifications: weight management, diet (DASH diet), alcohol consumption, and exercise.
DASH Diet (Dietary Approaches to Stop Hypertension):
Emphasizes intake of vegetables, fruits, and whole grains.
Consume low-fat dairy, poultry, fish, legumes, non-tropical vegetable oils, and nuts.
Limit intake of sweets, sugar-sweetened beverages, and red meats.
Engage in aerobic physical activity three or four times a week, with each session at least 40 minutes in length at moderate to vigorous intensity.
Complications of Hypertension:
Stroke: Sudden loss of function resulting from a disruption of blood supply to the brain.
Aneurysm: Dilation of the walls of a cerebral artery due to weakness in the arterial wall.
“Silent killer” because it can cause damage to the heart, brain, and kidneys (target organs) before symptoms are apparent.
Hypertensive Crisis:
Umbrella term for acute, severe elevations in BP.
Can lead to dyspnea, severe headaches, blurred vision, dizziness, epistaxis (nosebleed), severe anxiety, possible vascular damage to eyes.
Comprises two conditions: hypertensive urgency and hypertensive emergency.
Hypertensive Urgency: Severely elevated BP (diastolic BP \geq 120 mm Hg) with no obvious, acute TOD.
Hypertensive Emergency: Differentiated from hypertensive urgency by evidence of TOD, such as signs of stroke, papilledema, HF, or aortic dissection.
Assessment and Interventions for Hypertensive Crisis:
Severe headache: Place patient in semi-Fowler’s position.
Extremely high blood pressure (BP): Administer oxygen.
Dizziness, blurred vision: Administer IV drug (such as nitroprusside) as ordered; when stable, switch to oral antihypertensive drug.
Shortness of breath: Monitor BP every 5 to 15 minutes until the diastolic pressure is below 90 and not less than 75; then monitor BP every 30 minutes to ensure that BP is not lowered too quickly.
Epistaxis (nosebleed), severe anxiety: Observe for neurologic or cardiovascular complications, such as seizures; numbness, weakness, or tingling of extremities; dysrhythmias; or chest pain (possible indicators of target organ damage).
Hypertension Medications by Class:
ACE Inhibitors (lisinopril)
ARBs (valsartan)
Calcium Channel Blockers (amlodipine)
β-Blockers (β1 and β2) (metoprolol)
Combined α and β blockers (carvedilol)
Central Agonist (clonidine)
Vessel Dilators (apresoline)
Loop Diuretic (furosemide)
Thiazide Diuretic (hydrochlorothiazide; HCTZ)
Potassium-sparing Diuretics (spironolactone)
CORONARY ARTERY DISEASE (CAD)
Epidemiology:
Prevalent in 15.4 million people over age 20.
Most common cause of heart disease.
Incidence increases with age.
Racial and gender differences exist; higher prevalence in white males compared to African American and Mexican American males. Among females, African American women had the highest prevalence rate.
Pathophysiology:
Characterized by the obstruction of blood flow within the coronary arteries.
Atherosclerosis is the principal cause of obstruction to blood flow.
The arterial wall is made up of 3 layers.
Silent until the artery is approximately 40% blocked by plaque.
Ischemia Developments
Angina Clinical Manifestations
Radiographical diagnostic tests
Percutaneous transluminal coronary angioplasty Management
Ischemia develops when there is an imbalance between supply and demand of oxygen-rich blood to the heart tissue resulting in insufficient oxygen to meet the demands of the myocardial tissue.
Infarction, or cell death, occurs when that imbalance is severe or prolonged, which causes irreversible damage. The primary patient complaint is chest pain, also called angina.
Angina is classified into two categories, stable and unstable angina.
Stable angina is chest pain or discomfort that is associated with physical activity.
Unstable angina refers to chest pain that can occur at rest. Of the two types of angina, unstable angina is the most concerning.
Percutaneous transluminal coronary angioplasty is the procedure most commonly performed to relieve symptoms caused by atherosclerotic changes in the coronary vessels.
ATHEROSCLEROSIS/ARTERIOSCLEROSIS
Terms often incorrectly used interchangeably.
Both are types of vascular disease, but not the same.
Arteriosclerosis: hardened arteries.
Atherosclerosis: plaque build-up in arteries.
Patient with atherosclerosis have arteriosclerosis.
Patients often have both conditions.
Arteriosclerosis:
Thickening or hardening of arterial wall associated with aging.
Causes stiffness and a loss of elasticity.
Includes 3 possible pathologic processes:
Medial calcific sclerosis, which occurs when calcium is deposited in the arterial wall.
Arteriolar sclerosis.
Low-density lipoproteins (LDL) build up in arterial wall.
Epidemiology:
Emerging epidemic of atherosclerotic disease in developing countries may start in childhood.
Tobacco smoke greatly worsens atherosclerosis.
Pathophysiology:
LDL particles build up in the arterial wall.
Clinical Manifestations:
May be no symptoms until critical narrowing of the artery results in an emergency.
May result in sudden cardiac death.
Atherosclerotic disease in carotids may result in stroke (sudden weakness, dizziness, loss of coordination, difficulty talking, facial droop, sudden vision problems, and sudden and severe headache).
Depending on the artery involved, plaque formation and/or rupture can lead to myocardial infarction, unstable angina, sudden cardiac death, or stroke.
Management:
Identifying and controlling lifestyle risk factors-modifiable risk factors.
Medications used to lower lipid levels.
Surgical intervention is reserved for irreversible manifestations such as chest pain or gangrene.
Intractable chest pain and coronary artery disease require coronary bypass surgery.
Gangrene (if blood supply is totally cut off peripherally to the affected body part) may require amputation.
Peripheral Vascular Disease (PVD)
Disorders that change the natural flow of blood through the arteries and veins of the peripheral circulation causing decreased perfusion to body tissue.
Diagnosis implies arterial disease, not venous.
It is possible that a Patient will have both arterial and venous complications.
PERIPHERAL ARTERIAL DISEASE
Epidemiology:
Majority are 65 years or older.
African Americans are affected more often than any other group.
Pathophysiology:
Progressive and chronic condition.
Obstruction of blood flow through the large peripheral arteries causes arterial occlusion.
Stages of PAD.
The most common risk factor for PAD is Atherosclerosis. Therefore, the risk factors for atherosclerosis apply to PAD as well.
They include key modifiable risk factors such as smoking, hypertension, diabetes, dyslipidemia, sedentary lifestyle, obesity, and ineffective stress management.
This obstruction can be caused by a combination of atherosclerosis, inflammation, stenosis, embolus, and thrombus.
Peripheral arterial disease deprives the lower extremities of oxygen and nutrients.
The result of this inadequate tissue perfusion can be ischemia and necrosis, or cell death.
Stages of PAD:
Stage 1: Asymptomatic. No claudication is present. Bruit or aneurysm may be present. Pedal pulses are decreased or absent.
Stage 2: Claudication. Muscle pain, cramping, or during occurs with exercise and is relieved with rest. Symptoms are reproducible with exercise.
Stage 3: Rest Pain. Pain while resting commonly awakens the patient at night. Pain is described as numbness, burning, toothache-type pain. Pain is relieved by placing the extremity in a dependent position.
Stage 4: Necrosis/Gangrene. Ulcers and blackened tissue occur on the toes, forefoot and heel. Distinctive gangrenous odor is present.
Clinical Manifestations:
May be asymptomatic
Identified by a reduced ankle BP
Manifest symptoms of intermittent claudication or severe chronic leg ischemia
Management:
Provide relief of symptoms, prevent progression of arterial disease and cardiovascular complications
Improve quality of life and provide education
Pharmacology agents
Intermittent claudication is a diagnosis given for muscle pain—ache, cramp, numbness, or sense of fatigue, classically in the calf muscle, that occurs during exercise and is relieved by a short period of rest.
The ankle-brachial index (ABI) uses a Doppler probe to compare the BP obtained at the ankle with the pressure obtained at the brachial artery. Normally, BP readings in the ankle are higher than those in the upper extremities.
Plethysmography is another noninvasive test used to evaluate arterial flow in the lower extremities.
Pulse volume recordings are plethysmographical tracings that detect changes in the volume of blood flowing through a limb. Pressure cuffs are placed on the thigh, calf, ankle, or foot.
A graded exercise treadmill test may give valuable information about the degree of peripheral arterial narrowing in patients who experience intermittent claudication.
Radiographical imaging assessment consists of arteriography of the lower extremities. This is done to quantify the narrowing of the occluded vessels.
Make sure to educate patients not to cross legs and avoid wearing restrictive clothing. Further, educate on how to properly inspect their feet daily.
Critical limb ischemia
Acute limb ischemia
Complications:
Percutaneous transluminal angioplasty
Laser-assisted angioplasty
Rotational atherectomy
Critical limb ischemia (CLI) is the sustained, severe decrease of arterial blood flow to the affected extremity, which leads to chronic ischemia, rest pain, ulceration, gangrene, and ultimately limb loss if left untreated.
Acute limb ischemia (ALI) is the sudden decrease in blood flow to an extremity that threatens tissue viability.
Percutaneous transluminal angioplasty is a nonsurgical, minimally invasive method of improving arterial blood flow.
Laser-assisted angioplasty is another minimally invasive intervention that can be done for patients with PAD. During this procedure, a laser probe is advanced through a cannula that is inserted into or above an occluded artery.
Rotational atherectomy is another technique used to improve blood flow to the ischemic limbs of people with PAD. Rotational atherectomy is more commonly used for very hard, calcified stenotic lesions that are not amenable to balloon angioplasty.
Surgical or revascularization procedures are indicated when patients have severe pain at rest or claudication that interferes with the ability to perform activities of daily living (ADLs) or threatens loss of a limb.
Acute Peripheral Arterial Occlusion
The onset of acute arterial occlusion is sudden and dramatic.
An embolus (piece of a clot that travels and lodges in a new area) is the most common cause of peripheral occlusions, although a local thrombus may be the cause.
More common in lower extremities.
Emboli originating from the heart are the most common cause of acute arterial occlusions.
Most patients with an embolic occlusion have had an acute myocardial infarction (MI) and/or atrial fibrillation within the previous weeks.
Severe pain below the level of the occlusion that occurs even at rest.
The affected extremity is cool or cold, pulseless, and mottled. Small areas on the toes may be blackened or gangrenous due to lack of perfusion.
Those with acute arterial insufficiency often present with the “six Ps” of ischemia:
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Poikilothermy (coolness)
Anticoagulant therapy with unfractionated heparin (UFH) is usually the first intervention to prevent further clot formation. The patient may undergo angiography.
A surgical thrombectomy or embolectomy with local anesthesia may be performed to remove the occlusion.
The HCP makes a small incision, which is followed by an arteriotomy (a surgical opening into an artery).
A catheter is inserted into the artery to retrieve the embolus. It may be necessary to close the artery with a synthetic or autologous (patient’s own blood vessel) patch graft.
After an arterial thrombectomy, observe the affected extremity for improvement in color, temperature, and pulse every hour for the first 24 hours or according to the postoperative surgical protocol.
Monitor patients for manifestations of new thrombi or emboli, especially pulmonary emboli (PE). Chest pain, dyspnea, and acute confusion (older adults) typically occur in patients with PE. Notify the health care provider or Rapid Response Team immediately if these symptoms occur.
Buerger’s Disease
Claudication in feet and lower extremities worse at night.
Causes ischemia and fibrosis of vessels in extremities with increased sensitivity to cold.
Ulcerations and gangrene on digits.
Unknown cause but is associated with smoking.
Interventions:
Medications
Chronic pain management
Management of ulceration
Lifestyle Modifications:
Smoking cessation
Avoid cold
Managing stress
Avoid Caffeine
Medications:
Vasodilating drugs such as Nifedipine (Procardia). Make sure to educate patient on use of Vasodilation medication side effects (Facial flushing, hypotension, headaches).
While taking Nifedipine teach patient to avoid grapefruit and grapefruit juice to prevent severe side effects including possibly death.
Raynaud’s Disease
Painful vasospasms of arteries and arterioles in extremities
Causes red-white-blue skin color changes when exposed to cold
Unknown causes
Occurs more in women
Smoking cessation
Avoid cold
Managing stress
Avoid Caffeine
DEEP VEIN THROMBOSIS
Epidemiology:
Blood clot in a large vein, usually in the leg or pelvis
Less common in the pediatric population
Pathophysiology:
Develops in the deep veins of the calf muscles
Less frequently in the proximal deep veins of the lower extremity or upper arm
Sometimes a DVT detaches from the site of formation and becomes mobile in the bloodstream. If the circulating clot moves through the heart to the lungs, it can block an artery supplying blood to the lungs.
This condition is called pulmonary embolism.
350,000-900,000 Americans suffer from DVT and PE each year.
Disease process that includes both DVT and PE is called Venous Thromboembolism (VTE).
Approximately 100,000 die from VTE annually.
10%-30% of those that survive first VTE event, have a second within 5 years.
According to Virchow’s triad, venous thrombosis occurs via three mechanisms: decreased flow rate of the blood, damage to the blood vessel wall, and an increased tendency of the blood to clot. The precise cause of these events remains unknown; however, predisposing risk factors have been identified.
Normal Blood flowwith small tear in lumen of vein.
Blood clot (Thrombus)forms at site of venousdamage.
Blood flow occluded by a thrombus, causswelling and pain.
Asymptomatic
Calf or groin tenderness, Pain
Sudden onset edema
Hardened area on affected extremity
Erythema
Increased warmth
Never assess Homan’s sign
Patient may be asymptomatic
Diagnostics include a combination of a pretest risk assessment, D-dimer testing, and compression ultrasonography
TEDs, SCDs, Anticoagulation Therapy
Surgical management is rarely utilized
The D-dimer test is a global marker of coagulation activation and measuring fibrin degradation products produced from fibrinolysis (clot breakdown).
Ultrasonography has become widely accepted as a primary diagnostic procedure in routine clinical practice for the work-up of clinically suspected DVT.
Computed tomography venography and MRI venography may serve as an alternative or complementary imaging tool to ultrasound.
Contrast venography has been used traditionally as the golden standard for diagnosing DVT. Treatment can be withheld safely when a technically adequate contrast venogram shows no evidence of DVT. However, venography has many disadvantages.
Medication therapy typically consists of anticoagulation with Heparin or low molecular weight heparin (LMWH) such as Lovenox followed by long-term oral anticoagulation with warfarin.
Patients can be placed on Heparin drip initial to better manage DVT. Make sure coagulation labs are performed per protocol.
Normally on a Heparin drip the PTT goal is between 60-90 seconds for therapeutic effect.
Thrombectomy is the most common surgical procedure for removing a clot.
Venous Insufficiency
Occurs as a result of prolonged venous hypertension that stretches veins and damages the valves.
Standing/sitting for long periods of time in one position.
Obesity
Thrombus formation
Thrombophlebitis
Non-surgical unless complicated with venous stasis ulcer.
Compression stockings
Elevate legs for at least 20 minutes 4-5 times a day
Dietary and lifestyle changes
Varicose Veins
Distended, protruding veins that appear darkened and twisting.
Can occur at any age, but normally see in adults over 30 yo
Prolonged standing or heavy physical activity
Vein wall weakens and dilates, venous pressure increases.
Valves in vein, become defective causing venous reflux.
Defective valves enhance vessel dilation and veins become twisted and distended.
Telangiectasias (spider veins)
3 E’s (Elastic compression hose, exercise and elevation)
Surgical ligation and/or removal of veins
Sclerotherapy
Endovenous ablation
Amputation
The removal of part of the body.
Can be surgical or Traumatic (non-surgical)
Complications of Amputation:
Hemorrhage leading to hypovolemic shock
Infection
Phantom limb pain
Neuroma
Flexion Contractures
Bleeding (post-op)
Site of amputation determined by circulation and requirements for prosthesis
Levels of amputation:
Toes
Mid-foot
Syme – ankle disarticulation
Below the knee (BKA)
Above the knee (AKA)
Pain control with opioids
Long-term phantom pain-Gabapentin for nerve pain
PT/OT
Promote mobility
Prosthesis (have patient with lower extremity amputations push limb into bed to help prepare for future prosthetic.)
Antibiotics (post-op)
Psychological and emotional health