Essay: Peripheral Vascular Disease

Summary of Disease Processes
Priority medical diagnosis: Peripheral Vascular Disease
Peripheral vascular disease includes all vascular disorders of the blood vessel system outside of the heart.
Acute and chronic vascular diseases may develop progressively from atherosclerotic plaque formation. Atherosclerosis is defined as the process of fatty substances, cholesterol, cellular waste products, calcium, and fibrin building up in the intimal and medial layers of vessel wall, resulting in plaque building up and narrowing of the lumen of the artery. The intima is the innermost layer composed of endothelial cells within a matrix of collagen and elastin fibers. The media is the thick middle layer of smooth muscle. The adventitia is the outermost layer layer composed of collagen and elastin, which is the key element in providing strength for the arterial wall. Peripheral arterial disease is a subcategory of peripheral vascular disease. It is caused primary by embolic and pathophysiological processes that alter the aorta, its visceral arterial branches, and the arteries of the lower extremities (Osborn, 2014 p1069). The presence of PAD may indicate cardiovascular disease.
Atherosclerotic plaque formation occurs in three stages. The first or early stage is the development of fatty streaks beginning from childhood. The fatty streaks are formed from foam cells, which are lipid laden macrophages. Low-density lipoprotein cholesterol is the main lipid component that makes up thes fatty streaks. The second stge is the appearance of fibrous plaque later on in life from the progression of the fatty streaks made from foam cells to a more permant fibrous plaque. These plaques often will occur at areas of bifurcation of the arterial vessels. The last stage occurs when the fibrous plaque develops into a complicated lesion with necrosis and ulceration of the plaque surface with exposure, leading to thrombogenesis through platelet aggregation and formation of a thrombus. As the lipids are collected under the inner lining of damaged artery walls, it eventually narrows or blocks the artery and obstructs blood flow. The fatty tissue breaks down the artery wall over time and causes it to diminish its elasticity. Plaque deposits can also rupture, causing debris to migrate with an artery. Most patients with PAD will present with lower extremity pain, either as classic intermittent claudication or atypical leg pain. Although the supply of blood may be adequate to meet the demands of the inactive muscle, a mismatch will occur between the supply of blood and increased demand due to activity. The mismatch is what causes the atypical lower extremity pain. Patient started with small lesion on L foot. Eventually led to necrosis of the 2nd and 3rd toe.
Autonomic neuropathy occurs when blood is shunted away from peripheral cutaneous capillary beds, which may occur in patients with PAD associated with diabetes. Motor neuropathy leads to changes in gait and thus more pressure on one leg, leading to ulceration. The loss of protective sensation and proprioception resulting in increased force with each step may lead to formation of calluses at pressure areas, which decreases elasticity and increases skin ischemia. Patient has diabetic neuropathy.
Acute occlusion of a lower extremity artery may occur with chronic PAD and development of an acute thrombosis. It is called “critical limb ischemia” when the chronic development of peripheral artery occlusive disease in the lower extremity becomes severe. It is manifested by ischemic ulcers of the foot. Ischemic ulcers often begin as minor traumatic wounds and fail to hail because the blood supply is insufficient to meet the increased demands of the healing tissue. Ulcerations caused by ischemia are typically lcated at the termination of arterial branches. They are commonly found on the tips of the toes and between the digits. They can also form at increased focal pressure, such as lateral malleolus and metatarsal heads. In addition to ulcers, patient can present a gangrenous digit or foot. Gangrene can either be dry or wet. Dry gangrene is characterized by a hard, dry texture, often with a clear demarcation between viable and black, necrotic tissue. This form of gangrene is common in patients with PAD. Wet gangrene is characterized by its moist appearance, gross swelling, and blistering. Wet gangrene is a surgical emergency. Pt presented in the ED with wet gangrene, and dry gangrene post op.
(Neschis, 2016)
Ischemia sufficient to threaten a limb occurs when arterial blood flow is insufficient to meet the metabolic demands of resting muscle or tissue. Once patient’s body is unable to maintain the metabolic needs, it goes into anaerobic metabolism, which is seen in labs as high lactic acid. Acute thrombosis of sites of stenosis in which the blood flow impairment was hemodynamically significant can occur and present with acute symptoms., such as pain, pallor, paresthesias, paralysis, pulselessness, and poikilothermia(coldness). Symptoms of parethesias and paralysis may indicate advanced ischemia that is affecting nerve pathways of the extremity. Patient had ischemic ulcer in L foot, and signs of parethesias, pulselessness, and pain.
(Baird, 2016 p590, Porth, 2011 p415)
The presence of ischemia from occlusion to a lower extremity influences the timing of revascularization, debridement, and definitive coverage/closure. Wounds will not be able to heal as well as a result of ischemia and may lead to necrotizing of the soft tissue. It may come in the form of cellulitis, myositis, and fasciitis.
Necrotizing cellulitis include anaerobic infection and Meleny’s syngergistic gangrene. Anaerobic cellulitis can be divided into clostridial anaerobic cellulitis and non-clostridial anaerobic cellulitis. Clostridial anaerobic cellulitis is usually caused by C. perfringens. These organisms may be introduced into the subcutaneous tissue via trauma, surgical contamination, or spread of infection from the bowel to the perineum, abdominal wall, or lower extremities. The presence of foreign debris and necrotic tissue in a wound provides an appropriate environment for the proliferation of clostridial cells. Nonclostridial anaerobic cellulitis is caused by various non-spore-forming anaerobic bacteria(Bacterioides specis, peptostreptococci, and others) either alone of mixed with facultative organisms such as coliform bacilli, streptococci, staphylococci. Meleney’s synergistic gangrene is a rare infection that occurs in post-operative patient. It’s characteristic is a slowly expanding ulceration that is confined to the superficial fascia and results from a synergistic interaction between S. aureus and microaerophillic streptococci.
Necrotizing myositis, also known as spontaneous gangrenous myositis is relatively rare. It is a necrotizing infection of skeletal muscle caused by group A Streptococcus or other beta-hemolytic streptococci. It may be preceded with skin abrasions or blunt trauma. The infection will progress over several hours and involve muscle groups and soft tissue. If the patient develops streptococcal toxic shock syndrome, then they have an onset of hypotension. These patients will not have evidence of gas formation in tissue on physical or radiographic examination.
Necrotizing fasciitis in an infection of the deeper tissues that results in progressive destruction of the muscle fascia and overlying subcutaneous fat. Infection is usually spread along the muscle fascia due to it’s relatively poor blood supply. The process progresses rapidly over several days, from erythematous area to change in skin color from red-purple to patches of blue-gray. Within three-five days onset, skin breakdown with bullae will occur and frank cutaneous gangrene can be seen. By this time, the involved area is no longer tender but has become anesthetic secondary to thrombosis of small blood vessels and destruction of superficial nerves in the subcutaneous tissue. There are two types of necrotizing fasciitis.
Type I of necrotizing fasciitis is a mixed infection caused by aerobic and anaerobic bacteria. Risk factors include diabetes, PVD, immune compromised, and recent surgery. Type II necrotizing fasciitis is generally monomicrobial. It is caused by group A Streptococcus or other beta-hemolytic streptococci that is either alone or in combination with other pathogens, most commonly S. aureus. Patient’s culture came back with growth of Staphlococcus aureus.
(Stevens, 2016)
The Society for Vascular Surgery Lower Extremity Threatened Limb Classification System, WIfI, is a system for classifying the severity of limb threat that is intended to reflect clinical considerations that impact management and amputation risk. WIfI is an acronym for wound, ischemia, and foot infection. Each category has a different grade.
For wound, a grade 0 is rest pain; no wound; no ulcer; no gangrene. Grade 1 is a small shallow ulcer(s) on distal leg or foot, any exposed bone is only limited to distal phalanx(ie. Minor tissue loss, limb salvageable with possible simple digital amputation or skin coverage). Grade 2 involves a deeper ulcer on distal leg or foot with exposed bone, joint, or tendon, or shallow heel ulcer without involvement of the calcaneus( ie. Major tissue loss: salvageable with >3 digital amputations or standard transmetatarsal amputation plus skin coverage). Grade 3 is an extensive deep ulcer of the forefoot and/or midfoot, or full thickness heel ulcer with or without involvement of the calcaneus(ie. Extensive tissue loss: salvageable only with complex foot reconstruction or nontraditional TMA). Patient is a grade 2 for wound because he had a deep ulcer.
Ischemia also has grades 0-3. Grade 0 is ABI (ankle-brachial index) > 0.8, with ankle systolic pressure >100mmHg, toe pressure(TP) >60. Grade 1 is ABI 0.6-0.79, ankle systolic pressure 70-100mmHg, TP 40-59. Grade 2 is ABI 0.4-0.59, ankle systolic pressure 50-70mmHg, TP 30-39. Grade 3 is ABI <0.39, ankle systolic pressure <50mmHg, TP <30.
The third category is foot infection. Grade 0 is no symptoms or signs of infection. Grade 1- infection is present and at least 2 of the following are present: local swelling, erythema >0.5 to <cm around ulcer, local tenderness or pain, local warmth, or purulent discharge. Other causes of an inflammatory response of the skin have been excluded(gout/fracture). Grade 2 is a local infection is present as defined for Grade 1, but extends > 2cm around ulcer, or involves structure deeper than the skin and subcutaneous tissues(eg. Abscess, osteomyelitis, septic arthritis, fasciitis). No clinical signs of systemic inflammatory response. Grade 3 is a local infection that is present as defined for Grade 2, but clinical signs of systemic inflammatory response are present as manifested by 2 or more of the following: temperature >38°C or <36°C; heart rate >90 beats per minute, respiratory rate >20 breaths per minute or PaCO2 <32 mmHg; white blood cell count >12,000 or <4000 (cu/mm) or >10 percent immature band forms present. Patient is grade 2 for foot infection, in which he had a local infection on his foot that was 2cm by 2cm, and involves structure deeper than the skin and subcutaneous tissues.
Based on these considerations, the patient with PAD can be placed into one of four amputation risk categories (very low, low, moderate, high). Patient had to amputate his 2nd and 3rd L toes.
(Mills, 2014)
Femoropopliteal bypass is indicated when arteriography reveals that the superficial femoral artery or proximal popliteal artery is occluded and that the patient popliteal artery has luminal continuity with any of its three terminal branches. With a popliteal occlusion, a bypass to an isolated segment of popliteal artery is usually effective if the segment is greater than 7 cm in length. If the isolated popliteal segment is less than 7 cm or there is severe gangrene of the foot, a sequential bypass to the popliteal and then to a more distal vessel should be considered. Patient had a fem-pop bypass on 2/18 because his angiography showed occluded left superficial femoral artery distal reconstitution of the popliteal artery through collateral vessels consistent w/ chronic occlusion. Two vessel runoff in the calf.
(Neschis, 2016)
Sepsis is a syndrome of physiologic, pathologic, and biochemical abnormalities caused by a dysregulated inflammatory response to infection. It may lead to multiple organ dysfunction syndrome and death. The patient is susceptible to sepsis because he has a L foot wound that is infected with MRSA.
Traditionally, the SIRS criterion was first used to identify sepsis, however, it was unanimously considered to be unhelpful. Infection and bacteremia may be early forms of infection that can progress to sepsis. However, there is no formal definition of ‘early sepsis’.
The SIRS(systemic inflammatory response syndrome) criteria included 2 or more of the following: temperature >38C or <36C, heart rate >90bpm, respiratory rate >20/min, PaCO2<32mmHg, WBC count >12000/mm3 or <4000/mm3 or >10% immature bands. The SIRS criteria does not necessarily dictate a dysregulated , life threatening response. It is also present in many hospitalized patients. Instead, organ dysfunction can be identified as an acute change in total SOFA score > 2 points consequent to infection. The baseline SOFA score is assumed to be 0 in patients that has no pre-existing organ dysfunction. A SOFA score > 2 reflects an overall mortality risk with suspected infection. qSOFA(quick SODA) incorporates altered mentation, systolic BP of 100mHg or less, and respiratory rate >22/min, provides a simple bedside criteria to identify adult patients with suspected infection whose condition are likely to worsen. Additional screening includes a multivariable logistic regression identified that any 2 of 3 clinical variables – GCS 13 or less, systolic BP 100mmHg or less, and respiratory rate 22/min or greater.
Second on the sepsis continuum, the patient needs to present 2 of the SIRS criteria and a positive culture of sputum, blood, or urine that reflects growth of bacteria.
Severe sepsis is classified when there is sepsis and hypo-perfusion with organ dysfunction that is unresponsive to fluid resuscitation. It has more recently been viewed as endothelial dysfunction resulting from overwhelming inflammatory mediation, in conjunction with profound, unopposed coagulation. The capillary vasculature sustains a significant injury due to the cascade of events that ends in capillary occlusion. The greater the occlusion, the greater risk for organ failure because cellular level circulation requires a functional capillary network for delivery of oxygen and nutrients and removal of cellular metabolic waste products.
When infection or injury prompts an initially widespread inflammatory response (SIRS), the normally smooth surface of the microvascular endothelium is roughened and damaged by the response. In addition, the release of inflammatory mediations promotes vasodilation with an increase in capillary permeability. This causes little holes in the endothelium that the systemic mediators try to facilitate the healing of. The four main factors associated with severe sepsis is hyperinflammation, hypercoagulation, microvascular obstruction, and endothelial responses that leads to accelerated formation of microclots on the non-smooth surface of the endothelium. This consumes plates and inhibits clot lysis. This progresses to uncontrolled alterations in the vascular tone with vasodilation. In severe sepsis, the balance between vasodilators(nitric oxide) and vasoconstrictors(endothelin) cannot be maintained. Consequently, the maldistribution of blood flow in addition to loss of vascular tone at the macro and microvascular levels results in ischemia and hyperemia in the cells. Myocardial depressant factor is also released and may contribute to the loss of the compensatory CO that is required to keep blood moving through the vascular beds.
Septic shock is a subset of sepsis(4th on the continuum), in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. It is a type of vasodilatory or distributive shock that is severe sepsis with cardiovascular dysfunction(primary loss of vascular tone). Patients with septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate level >2mmol/L(18mg/dL) despite adequate volume resuscitation.
MODS(Multiple organ dysfunction syndrome) refers to a progressive organ dysfunction in an acutely ill patient, in which homeostasis cannot be maintained without interventions. It is at the severe end of the sepsis spectrum because it involves both infectious(sepsis, septic shock) and noninfectious conditions(SIRS). MODS can be broken further into primary or secondary. Primary MODS is when organ dysfunction occurs early and can be attributable to itself. Secondary MODS is organ failure that is not in direct response to itself, but is a consequence of the host’s response.
(Baird, 2016 p1009; Neviere, 2017)
Risk factors
• Family or personal hx of tobacco abuse, hyperlipidemia, hypertension, diabetes, obesity, stress, sedentary living, cardiovascular disease, renal insufficiency, clotting disorders, foot ulcers, or noncomplicance with medical management Pt has history of smoking, hyperlipidemia, hypertension, diabetes, obesity, cardiovascular disease, renal insufficiency, and foot ulcer!
• Age <50 years, w/ diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, HTN, or hyperhomocysteeinemia)
• Age 50-69 years with hx of smoking or diabetes
• Age >70 Pt is 78 y/o
• Leg symptoms w/ exertion(suggestive of claudication) or ischemic rest pain Pt states LLE claudication
• Abnormal lower extremity pulse examination Absent pedal pulses
• Known atherosclerotic coronary, carotid, or renal artery disease
• Male, Black ethnicity Pt is male and African American
(Baird, 2016 p592)
Clinical manifestations
• Intermittent claudication (cramping with exertion, relieved at rest) Pt reports bilateral LE claudication, worse in left leg.
• Nocturnal rest pain
• Fatigue/numbness in an extremity Pt came in to ED for generalized weakness
• Pain – Patient reports LLE pain constant and hurting
• Pallor
• Pulselessness Pt has absent pedal pulses
• Poikilothermia (coldness)
• Paralysis
• Poor hair growth
• Parethesia(abnormal physical sensation-prickling, tingling, numbness)
• Poor healing of sores or ulcers Pt has nonhealing wound on L foot, led to amputation of 2nd and 3rd toe
• Bruits – indicate disturbance in flow (plaque formation)
• Edema – Pt has bilateral LE w/ 2+ pitting edema from knee down
(Baird, 2016 p595, Osborn, 2014 p1069)
Common lab & diagnostic tests
• CBC ( to check for anemia r/t surgical blood loss or post op bleeding, platelet level for evaluating for increased clotting/bleeding propensity, increased WBCs indicating possible infection – High WBC(19.7,14.8, 12.9)-infection, Low RBC(3.22)infection, Low Hgb (32.9/25.9) anemia, renal disease – Low Hct (32.9, 25.9) – anemia, renal disease, acute blood loss
• BMP (fluid shift or volume changes w/ increased use of IV fluids, kidney disorders) – Elevated BUN(92/92/94) renal disease r/t HF , High Cr (3.71,3.3,3.96) – HTN,high K (6.5) lactic acidosis
• Coagulation studies(evaluate increased clotting/bleeding propensity)- Elevated PT (22.8, 20.5) & PTT(41.6)
• HgbA1C
• Liver enzymes, CPK (evaluating for reperfusion injuries) Elevated ALT, AST, Alk Phos, Osmo Calc, CPK r/t liver disease, CHF, acute MI
• Lactic acid (compensation for metabolic acidosis) (high ; 4.7 on admission – lactic acidosis r/t CHF & COPD)
• Ankle-brachial index ( detects PAD of LE by assessing pressure of foot and brachial)
• Doppler waveforms( Assess for LE stenosis)
• Duplex US (sound waves to identify areas of stenosis in arterial vessels and defines severity) Occluded left superficial femoral artery distal reconstitution of the popliteal artery through collateral vessels consistent w/ chronic occlusion. Two vessel runoff in the calf.
• Treadmill exercise arterial studies (decreased ABI following exercise indicates arterial insufficiency)
• Angiography(Visualizes anatomy, areas of stenosis and/or occlusion) Long segment occlusion of the distal superficial femoral/popliteal artery. Severe narrowing of the popliteal artery above the knee two – vessel run off through the posterior tibial and peroneal artery to the foot. Marked stenosis in the proximal portion of the posterior tibial artery.
• CT Scan (Visualizes anatomy, areas of stenosis and/or occlusion)
• MRI and MRA (Visualizes anatomy, areas of stenosis and/or occlusion)
(Baird, 2016 p596-597, Osborn, 2014 p1071)
Treatment
Patients with PVD should receive lifelong antiplatelet therapy with aspirin. Aspirin has antithrombotic effects and inhibits platelet aggregration. Other medications in this class include Ticlid, Plavix, and Pletal. Ticlid and Plavix are theinopyridine derivatives that inhibit adenosine diphosphate(ADP) –induced platelet aggregration.
Endovascular repair is the treatment of vascular disease from endoluminal(inside the blood vessel) and includes angioplasty, stenting, and radiation therapy. Percutaneous transluminal angioplasty (PTA) is indicated for patients who are limited by their pain or treatment of some arterial occlusive disease and is an invasive procedure. Other adjunctive interventional techniques to treat the iliac, femoral, popliteal, and tibial arteries include the use of lasers, cutting balloons, atherectomy devices, and thermal devices.
Surgical management can be performed for debilitating peripheral vascular disease. This include arterial bypass to surgically revascularize. Surgery can be done when a patient has disabling claudication and/or limb-threatening ischemia due to blocked arteries in the lower extremities. Other bypasses include aortoiliac bypass, aortobifemoral bypass, iliac endarterectomy, or iliofemoral bypass, axillofemoral bypass, and femoropopliteal bypass. Amputation may be required for uncontrolled infection, uncontrolled pain, extensive tissue loss, and in cases where revascularization cannot be accomplished.
Hyperbaric oxygen therapy is also used an as adjuvant therapy in wound care. It involves intermittent treatment of the entire body with 100% oxygen at 20 times greater than normal atmospheric pressures. It reduces amount of hypoxic leukocyte dysfunction occurring within an area of hypoxia and infection. It provides oxygenation to otherwise ischemia areas and arterial blockage by stimulating growth of new blood vessels.
(Osborn, 2014 p.1070, 1912)
Patient is on 81mg of aspirin and Plavix for antithrombotic effects. Patient had a femoropopliteal bypass done on 2/18 in an attempt to revascularize to his L foot. However, the doctors recommended amputation of the 2nd and 3rd toe because of extensive tissue loss and revascularization cannot be accomplished. The patient is also receiving hyperbaric oxygen therapy for wound healing in addition to controlling his blood glucose levels.
DM type II
Type 2 Diabetes is a heterogeneous group of disorders characterized by decreased liver, muscle, and adipose tissue sensitivity to insulin and a defect in insulin secretion from the pancreatic beta cells. Type 2 Diabetes results from decreased insulin production by the pancreas and increased insulin resistance, which is characterized by an inability to use insulin effectively.
In the first stage, genetic factors probably influence both insulin sensitivity and insulin secretion. There is an initial period of hyperinsulinemia in which the pancreatic beta cells are able to overcome insulin resistance. In the second stage, insulin resistance continues to increase, and this compensatory hyperinsulinemia becomes insufficient to maintain normal glucose homeostasis. Under conditions of insulin resistance, visceral adipose tissue is very sensitive to the effects of catecholamines, and insulin resistance is associated with enhanced lipolysis. This leads to increased fatty acid production and mobilization, exacerbating resistance in liver and muscle tissue. In addition, impairments in insulin-mediated glucose transport into skeletal muscle, the major target for glucose disposal, becomes impaired. Also in this stage, physiologic stress states that increase the production of hormones such as catecholamine, cortisol, growth hormone, and glucagon will cause hyperglycemia.
In the third stage, there is further increase in insulin resistance. The restraining effects of insulin on hepatic glucose production become impaired, and plasma glucose levels increase. Fasting and postprandial hyperglycemia result from increased insulin resistance, unrestrained hepatic glucose production and glucose toxicity.
Wound healing is slowed when the patient is diabetic. Macrovascular and microvascular changes are due to elevated blood sugar levels that can cause fatty deposits to stick to the endothelial lining of vessels and cause narrowing and then blockage of circulation. Narrowed blood vessels lead to decreased blood flow and oxygen to a wound. An elevated blood sugar level also decreases the function of RBCs that carry nutrients to the tissue. This lowers the efficiency of the white blood cells that fight infection. Without sufficient nutrients and oxygen, the wound would heal slowly.
Diabetic neuropathy is when the nerves in the body are affected and the patient develops a loss of sensation because their blood glucose levels are uncontrolled. The elevated blood glucose over time affects the myelin sheath surrounding the nervers and degrades the sheath, exposing the nerves. Sometimes, patients do not feel the blister, infection, or wound problem, which may lead to increased severity and complications. Pt has uncontrolled Type 2 DM which interferes with his non-healing wound.
(Osborn, 2014 p1896; Porth, 2011)
CAD
CAD is a chronic process that affects the arteries perfusing the heart, brain, and kidneys. CAD includes arteriosclerosis(thickening, reduced elasticity, and calcification of the arterial wall), atheroschlerosis(type of arteriosclerosis that causes reduced myocardial blood flow), and arteritis(inflammation of the arterial wall, usually due to infection or auto-immune response). Atherosclerosis causes reduced blood flow to the myocardium because of buildup of plaque like cholesterol, lipids, and cellular debris infiltrating the intimal lining of the arterial wall. The myocardium normally extracts 75% of available oxygen from the coronary arteries. If the oxygen requirement is not met, then the myocardial blood flow needs to be increased. However, the arteries in CAD are not able to dilate because of the plaque buildup and calcification. As a result the heart needs to increase force of contraction in order to increase blood flow, and thus increasing cardiac output. “The result of all the unmet oxygen needs is the shift to anaerobic metabolism and myocardial tissue hypoxia, which results in angina.” CAD and HTN contribute to HF because the heart needs to increase the force and contractility to maintain tissue perfusion.
(Osborn, 2014 p920)
CHF
CHF includes cardiovascular response to inadequate perfusion and series of neurohormonal response in addition to structural abnormality. The systemic response to compensate for inadequacy is to increase cardiac output. Cardiac output is determined by heart rate and stroke volume. Additionally, stroke volume is influenced by three factors; contractility, preload (the volume of blood in the left ventricle at the end of a diastole), and afterload (pressure of resistance the ventricles must overcome to eject blood during systole).
Preload is assessed by measuring the right atrial pressure and is affected by any restriction. The example that Figueroa & Peters (2006) provides is an increase in positive pleural pressure (seen in COPD or asthma) will reduce ventricular filling. The compensatory mechanism that responds to the decrease preload by decreasing stretch is called the Frank-Starling law. The optimal filling pressure is between 10-12mmHg. The force of ventricular contraction will decrease when the pressure exceeds 12mmHg and the myocardial fibers are overstretched. A prolonged decrease force of contraction will lead to heart failure.
Contractility is the force generated by contracting myocardium and is expressed as the ejection fraction. The contraction of the myocardium depends on the ability of the ventricular muscle fibers. Structure of the heart such as valvular abnormalities can affect contractility. According to Figueroa & Peters (2006),” A heart with normal systolic function will maintain an ejection fraction over 50-55%.” As mentioned before, overstretching the myocardial fibers will lead to heart failure.
Afterload is the pressure or resistance the ventricles need to overcome to eject blood during systole and is assessed by the mean arterial pressure. According to Figueroa & Peters (2006), afterload represents three factors that are impaired in CHF patients; vascular resistance, wall tension, and intrathoracic pressure. (Osborn, 2014 p901-903)
When cardiac output action is compromised, the sympathetic nervous system and renin-angiotensin-aldosterone system is activated. The activation of the sympathetic nervous system releases norepinephrine, which causes vasoconstriction in an attempt to increase ventricular preload. Myocardial contractility and heart rate increases to increase cardiac output. Circulating levels will increase fluid retention by increasing sodium absorption of the kidney. The increased intravascular volume will improve blood pressure and cardiac output. An additional function of norepinephrine allows renal vasoconstriction that maintains the glomerular filtration at a stable rate despite decreased renal perfusion. However, these mechanisms cannot be maintained extensively because it causes cardiac wall stress by constantly increasing pressure. Effects of long term maintenance include,” ..hypertrophy of the heart(cardiomegaly), chamber dilation, increased myocardial oxygen consuming, worsening myocardial ischemia, and pulmonary and systemic congestion (Osborn, 2014 p1029).”
The renin-angiotensin-aldosterone system activates in response to decreased renal perfusion. A series of hormones is released in this system to increase preload, cardiac output, and blood pressure. Renin is released from the kidneys to convert angiotensin I to angiotensin II. Angiotensin II is a strong vasoconstrictor that increases afterload and stimulates the secretion of aldosterone. Aldosterone is a hormone that causes sodium and fluid retention of the kidneys to increase intravascular volume. Like the activation of the sympathetic nervous system, this system has long term effects that will lead to heart failure. These long-term effects include,” increased cardiac workload, pulmonary and systemic congestion, and chamber dilation. Abnormal cell growth manifested by myocardial hypertrophy and adverse remodeling is also triggered by angiotensin II(Osborn, 2014 p1029).” Patient’s chest radiography showed cardiomegaly as a result of abnormal cell growth due to increased workload of the heart.
In addition to decreased renal perfusion, decrease in cardiac output can affect other organs as well. Decrease cardiac output leads to ischemia because the oxygen demand from the organs is still there, however there is inadequate blood pumped by the heart to meet these demands. As a result, less oxygen is carried by red blood cells is getting to the organs.
Systolic dysfunction, also known as left ventricular systolic dysfunction(LVSD), results in volume overload and decreased contractility. It is diagnosed when the left ventricular ejection fraction (LVEF) is less than 40%. Normal LVEF is 55%-70%. Patient’s ejection fraction is 25-30% with cardiomyopathy. LVEF is the proportion of blood ejected during each ventricular contraction compared to the total ventricular filling volume. Cardiac remodeling occurs when prolonged activation of the sympathetic nervous system and renin-angiotensin-aldosterone leads to damaged and maladaptation of the myocardium. Myocytes will “revert to a fetal-type expression and ultimately changes the myocyte geometry from elliptical to spherical (Osborn, 2014 p1027).” The change in shape at the cellular level will manifest to changes in the size, shape, and function of the heart. There are three types of heart failure depending on the anatomy of the ventricles; right, left, or biventricular heart failure.
Right-sided heart failure is characterized as impairment to the pumping ability of the right side of the heart. The cause of right-sided defectiveness is left-sided dysfunction, isolated right ventricular myocardial infarction, and a process where blood cannot flow into the pulmonary vasculature in the lungs. The backup of blood leads to congestion and elevated pressure in the systemic veins and capillaries. Manifestation of right-sided heart failure includes elevated neck veins, abdominal ascites, edema, poor appetite, nausea and vomiting, and lower extremity swelling of the ankles and calves. Pt reports poor appetite, N/V, and has +2 pitting edema in LLE.
Left-sided heart failure is characterized as impairment to the pumping ability of the left side of the heart. Blood that is backed up in the pulmonary circulation increases pressure in the pulmonary veins and capillaries. Signs and symptoms that will occur as a result include poor concentration/mentation, pulmonary congestion, cough, paroxysmal nocturnal dyspnea, orthopnea, crackles, and activity intolerance.
Biventricular heart failure occurs when both ventricle function of the heart is impaired. The manifestations is a combination of right-sided and left-sided heart failure.
Diastolic dysfunction of the heart is also referred to as heart failure with preserved LVEF. According to Figueroa & Peters (2006), the diastolic function is determined a passive process, elasticity of the left ventricle and an active process, the process of myocardial relaxation. The left ventricular filling generates a suction effect when relaxing the myocardium. Ventricular filling is impaired due to ”..restrictive, obstructive, non-obstructive, hypertrophic, and infiltrative cardiomyopathies(Osborn, 2014 p1028).” It is diagnosed when patients have a normal LVEF but manifest the symptoms of heart failure.
(Osborn, 2014 p1028-1030)
MI
Myocardial infarction results from necrosis of myocardial tissue caused by relative or absolute lack of blood supply to the myocardium. Apoptosis results in a permanent loss of myocardial muscle function. Most acute MI are caused by atherosclerosis, which results in plaque formation within the coronary arteries. Plaque deposition that results in endolelial changes causes narrowing of the lumen of the coronoary artery. If an unstable plaque ruptures, the immune system responsds with localized infection; platelets aggregate at the site of injured plaque and a thrombus forms. If the lesion is large enough to fill the vessel lumen, then it will result in a occlusion of blood flow. Occlusion can also be caused by coronary artery vasospasm.
Non-ST segment elevation myocardial infarction(NSTEMI) shares a common pathophysiology and clinical presentation as unstable angina because both usually occur as a result of transient subtotal occlusion of a coronary artery with reduced coronary blood flow resulting from plaque disruption. It can occur when perfusion pressure is low, and in sudden hypotension, or when there is increased myocardial workload, as in aortic stenosis caused by tremendous resistance to ejection created by narrowed aortic valve. Patient’s PVD, CHF, and CKD contribute to this.
ST segment elevation myocardial infarction (STEMI) refers to myocardial injury associated with ST segment elevation on the ECG. The presence of this elevation indicates myocardial tissue is undergoing severe anoxia and cellular damage. This is most likely due to complete coronary artery blockage from thrombotic occlusion over an underlying plaque lesion. Apoptosis occurs if blood flow is not reestablished within 20 minutes because the blockage is sustained.
(Osborn, 2014 p948; Baird, 2016 p479)
HTN
Hypertension is a consistent average blood pressure than is higher than the accepted normal value. Long term elevation of blood pressure can be caused by hemodynamic, neural, humoral, and renal mechanisms(Osborn, 2014 p1060). Increase in blood pressure leads to increase in cardiac output and peripheral vascular resistance. This is caused by the SNS releasing vasoconstrictor substances. Another organ that influences blood pressure is the kidney. The kidney increases excretion of Na and water when the blood pressure rises. Heart failure and CAD can cause secondary hypertension because of the prolonged activation of SNS and RAAS. The need for increase in cardiac output over a long period of time causes HTN.
The wall of a stressed vessel causes the release of humoral vasoconstrictors, which increases the systemic vascular resistance. As a result, “the increased pressure causes a cycle of endothelial damage, local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and release of more vasoconstrictors(Baird,2016 p578).” The cycle of vascular injury leads causes tissue ischemia and autoregulatory dysfunction. This affects perfusion to other organs, such as decreased circulation to the kidneys causes hypoperfusion, leading to CKD.
(Osborn, 2014 p1060)
CKD Stage 3
Chronic kidney disease is the progressive loss of kidney function and symptoms do not appear until renal capacity has decreased to 10-15% of normal function. Diagnosis of presence of kidney damage and level of renal function is through the measurement of glomerular filtration rate(GFR). Chronic kidney disease can be defined on the basis of two independent criteria: (1)kidney damage(structural or functional seen on laboratory, pathology, or imaging studies) for more than 3 months with our without a decreased GFR and/or (2) GFR less than 60mL/min//1.73m2 for more than 3 months with or without kidney damage. Chronic Kidney Disease also has 5 stages that is classified according to level of renal function. Stage 1 is kidney damage with normal or increased GFR, GFR >90 mL/min/1.73m2. Stage 2 is kidney damage with mild decrease in GFR, GFR is 60-89 mL/min/1.73m2. Stage 3 is moderate decrease in GFR, GFR is 30-59 mL/min/1.73m2.Stage 4 is severe decrease in GFR, GFR is 15-29 mL/min/1.73m2. Stage 5 is kidney failure, GFR <15 mL/min/1.73m2 or dialysis.
Patient’s history of diabetes and HTN contributes to CKD. Hyperglycemia,hyperperfusion, and increased glomerular pressure damages the nephrons. Vascular changes in hypertension causes a decrease in circulation to the kidneys, gradually damaging the nephrons, causing nephrosclerosis. EPIC states patient is in stage 3 of CKD but his GFR is 16/18/15, which puts him in Stage4/5.
(Osborn, 2014 p1227-1228)
COPD
Chronic obstructive pulmonary disease encompasses two types of obstructive airway disease: emphysema (enlargement of air spaces and destruction of lung tissue) and chronic obstructive bronchitis( increased mucus production, obstruction of small airways, and a chronic productive cough). Chronic bronchitis is caused by inflammation and fibrosis of the bronchial wall causing mismatching of ventilation and perfusion. Hypertrophy of the sub-mucosal glands and hyper-secretion of mucus are symptoms of COPD. There is loss of elastic lung fibers(which normally provides traction and hold the airways open, impairs the expiratory flow rate, increases air trapping, and predisposes to airway collapse). With loss of lung elasticity and hyperinflation of the lungs, the airways often collapse during expiration because pressure in surrounding lung tissues exceeds airway pressure. Destruction of alveolar tissue decreases the surface area for gas exchange. Patients with predominant emphysema are referred to as (pink puffers), a reference to the lack of cyanosis. Chronic bronchitis involves the use of accessory muscles and pursed-lip(“puffer”) breathing. Air becomes trapped in the alveoli and lungs, producing an increase in the antero-posterior dimensions of the chest; “barrel chest” is typical in patients with emphysema.
Manifestations of COPD are associated with episodes of moderate-severe respiratory impairment due to obstruction of airflow, which is greater on expiration than inspiration, resulting in increased work of breathing but decreased effectiveness. Pt’s chest X-ray showed cardiomegaly with mild vascular congestion and retrocardiac atelectasis.
In patients that have moderately severe COPD, their drive to breathe becomes oxygen because their body retains too much carbon dioxide. This will increase the risk of patients developing hypercapnia and requiring supplemental oxygen therapy. An increase in arterial carbon dioxide leads to an increase depth and rate of respiration. Over time, COPD patients will have high arterial levels of carbon dioxide and low levels of oxygen. The central chemoreceptors become less sensitive to these changes, consequently the stimulus to breathe is now managed by the peripheral chemoreceptors located in the carotid bodies and the aortic arch. These receptors are stimulated by low arterial levels of oxygen, and leads to hypercapnia. Thus, if supplemental oxygen is required, small changes to the rate of administration can have significant effects in those who have a hypoxic drive to breathe.
(Porth, 2011)
GERD
Gastroesophageal reflux is the backward flow of stomach contents into the esophagus without associated vomiting. It is caused by relaxation of the lower esophageal sphincter. Normal LES pressure is 10-30 mmHg and is under muscular, hormonal and neural control. In patients with GERD, the pressure is less than 10 mmHg. The decreased pressure is what allows the reflux stomach contents. Mucosal damage and erosion can result form this disease because the esophageal mucosa does not have the same protective lining mechanism as the stomach. This disease becomes chronic when the esophagus is exposed to gastric contents for a prolonged period, and an inflammatory process is initiated. The normal squamous epithelial cells are replaced with columnar epithelium, which is more resistant to damage by acidic stomach contents and supports healing of the erosions. This new epithelium is called Barrett’s epithelium.. However, this epithelium is premalignant tissue and increases the risk for esophageal cancer.
(Osborn, 2014 p1119)