Vascular Disorders and Shock

• Study Guide: Vascular Disorders and Shock notes are here.

Blood Vessels

• Arteries carry oxygenated blood to organs and tissues, providing perfusion, nutrients, and healthy skin/hair.
• Veins return blood to the heart and lungs, remove waste, and collect fluid from the lymphatic system.
• At any given moment, about 30% of the blood in systemic circulation is in the arteries, 5% in the capillaries, and 65% in the veins.

Arterial Vascular Disease

• Arteriosclerosis is the hardening of arterial walls, occurring with age or post-menopausally, typically after age 60.
• Atherosclerosis, a type of arteriosclerosis, involves plaque formation in arterial walls and is associated with low HDL, high LDL & triglycerides, hypertension, genetics, diabetes, and obesity.
• Further risks include sedentary lifestyle, smoking, stress, African or Hispanic ethnicity, and older age.
• Management involves controlling blood pressure and glucose and smoking cessation.

Hypertension (HTN)

• Blood Pressure (BP) Formula: BP = (SV x HR) x PVR. HTN is an increase in either CO or PVR.
• In younger populations, HTN involves increased cardiac output (CO), whereas, in older populations, increased peripheral vascular resistance (PVR) is more prominent.
• Blood pressure classification: Normal is 120/80 mmHg; Prehypertension is 120-139/80-89 mmHg; Stage 1 HTN is 140-159/90-99 mmHg; Stage 2 HTN is >160/100 mmHg.
• Primary (Essential) HTN is not caused by another disease process, with risks including family history, smoking, obesity, diabetes, salt sensitivity, and renin elevation.
• Secondary HTN is secondary to another disease process, such as kidney disease, obesity, alcoholism, Cushing's disease, hyperthyroidism, or stimulant use.
• A hypertensive crisis is characterized by blood pressure >180/120 mmHg, potentially leading to heart failure (HF), acute kidney injury (AKI), or cerebrovascular accident (CVA).
• HTN causes include increased sodium intake, the renin-angiotensin-aldosterone system (RAAS), aldosterone, and the sympathetic nervous system.
• Management involves lifestyle modifications and antihypertensive medications like diuretics, calcium channel blockers (CCBs), ACE inhibitors, angiotensin II receptor blockers (ARBs), beta-blockers, combined alpha and beta blockers, vasodilators, and central agonists.
• Potential complications include silent killer, causing asymptomatic damage to the brain, heart, and kidneys, as well as ASCVD, HF, stroke, aneurysm, aortic dissection, and hypertensive crisis.
• Pediatric hypertension may manifest as screaming in pain, banging the head against the wall, irritability, and tenseness, with an inability to verbalize the issue.
• Children are more likely to have secondary HTN until adolescence, often related to kidney disease, CHD (coarctation of the aorta), endocrine disorders, or medications.
• Essential HTN in children is usually mildly elevated, and is treated with diet/salt restriction, exercise, and stress reduction.
• Medication becomes necessary with diuretics, beta blockers, CCBs, ACE-I, or ARBs.

Peripheral Arterial Disease (PAD)

• Peripheral Arterial Disease (PAD) causes poor perfusion and can be caused by atherosclerosis.
• PAD Symptoms include claudication (leg pain), worsening with progression, and waking the person up at night.
• Assessment findings include hairless legs, poor pulses, red when dependent, pale when elevated, and deep, necrotic ulcers on the toes.
• The 6 P's of ischemia include pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia.
• Management includes positioning, foot care, and medications (BP meds, Trental).
• Nursing care includes assessing hairless legs with poor or no pulses, red when down, and pale when elevated.
• Suspect painful, deep, necrotic ulcers on toes with pale, dry wound beds that do not heal.
• Ineffective peripheral tissue perfusion, risk for impaired skin integrity, and chronic pain are potential diagnoses.
• Plan/implementation includes positioning with legs dependent, even when sleeping, inspecting feet daily, educating on risks and claudication, and no bare feet to avoid injuries.
• Prescribed medications education (BP meds, Trental) are also important.
• Acute LIMB ISCHEMIA (Arterial occlusion) is characterized by the 6 "Ps" of ischemia.

Carotid Artery Disease

• Stenosis levels include mild (<50%), moderate (50-69%), and severe (70-99%).

Aortic Diseases

• Aneurysms can occur at any point on any artery with AAA and TAA being the most common.
• Risk factors are the same as for PAD & include genetics, Marfans, Syphilis, bicuspid aortic valve and Kawasaki disease.
• Diagnosed by CT with contrast & blood pressure should be controlled to avoid rupture.
• Aortic Dissection presents as a sudden tear in the intima, causing a false lumen.

Other Arterial Health Problems

• Buerger's disease causes night leg pain from claudication and is related to smoking.
• Raynaud's phenomenon induces painful vasospasms in extremities.
• Subclavian Steal causes arm pain from obstruction of subclavian flow.
• Thoracic Outlet Syndrome happens when there is positional compression of the subclavian artery.

Peripheral Venous Disease (PVD)

• PVD is caused by Accumulation of Fluid and Waste.
• Superficial Thrombophlebitis has localized warmth and tenderness as symptoms.

Venous Thromboembolism (VTE)

• VTE is a clot due to endothelial injury, venous stasis, or hypercoagulability (Virchow's Triad), with swelling present distal to the clot.
• You want to assess for risk factors and prevention measures.
• Tests included D-Dimer, PT, aPTT, INR, H/H, ultrasound, and CTA to assess for PE. -Venous Insufficiency has stasis dermatitis, stasis ulcers, and edema.
• Varicose Veins occur due to chronic venous insufficiency from backpressure.

Shock

• Shock has inadequate oxygen delivery, leading to life-threatening cellular hypoxia.
• Blood Pressure Regulation: BP = CO x PVR, CO = HR x SV, and MAP = (2/3 Diastole) + (1/3 Systole).

Types of Shock

• Hypovolemic shock is with low preload, SV, CO, & MAP, due to blood or fluid loss.
• Cardiogenic shock is with low SV, CO, & MAP, due to heart pump failure.
• Distributive shock is with low preload, SV, CO, & MAP, due to leaky capillaries or vasodilation.
• Obstructive shock is with low SV, CO, & MAP, due to blocked blood flow.

Stages of Shock

• The initial stage presents with cellular hypoxia.
• The compensatory stage has the body attempting to maintain perfusion involving baroreceptors and RAAS activation.
• The progressive stage causes decompensation and metabolic acidosis worsens.

Stages of Shock (Detailed)

• The initial stage of shock involves hypoperfusion with subtle or no clinical manifestations.
• In the non-progressive stage, vasoconstriction, RAAS/ADH, increased PVR, and glycogenolysis occur, leading to restlessness, confusion, tachycardia, weak pulses, tachypnea, respiratory alkalosis, oliguria, hypoactive bowel sounds, hyperglycemia, and pale, cool, clammy skin.
• Progressi is marked by increased shunting and failure of the Na/K pump, resulting in lethargy, coma, hypotension, dysrhythmias, anuria, absent bowel sounds, severe metabolic and respiratory acidosis, and cool extremities.
• Refractory presents with systemic anaerobic metabolism, hypoxia, coma, hypotension, severe acidosis, organ failure, and tissue ischemia.
• Compensatory phase involves neural (baroreceptors, Epi, NorEpi, Alpha1, Beta1, Beta2), endocrine (kidneys, RAAS, aldosterone, ADH) and the chemical (chemoreceptors, tachypnea) responses.
• Physiologic responses during non-progressive shock: Baroreceptors sense a drop in BP, releasing Epi and Norepi & Alpha1, Beta1, and Beta2 receptors cause vasoconstriction, increased heart rate and force, dilation of the bronchi, and increased blood flow to the heart and brain.
• The renin-angiotensin-aldosterone system is activated with decreased renal perfusion, which stimulates the release of renin, and vasoconstriction and sympathetic stimulation also occur, causing the release of ADH and aldosterone (Na, H20).
• Antidiuretic Hormone (ADH) is released with the posterior pituitary sensing hypovolemia and kidneys resorbing sodium and water.

Physiologic Responses During Progressive (Decompensated) Shock

• Altered capillary permeability causes fluid and proteins to leak into interstitial space.
• Respiratory insufficiency causes pulmonary edema and impaired gas exchange.
• Cardiac depression causes a decreased Preload, SV, CO, BP/MAP.
• Tissue Hypoperfusion causes organ ischemia (kidneys, intestines, skin).
• Neurological Response causes decreased cerebral flow and AMS.

Nursing Prioritization Of Care in Shock

• Secure the airway.
• Assist with breathing with oxygen.
• Focus on circulation with intravenous access and fluids.
• Determine the cause.
• Watch MAP carefully and watch the vital signs. Pay attention to urine output as UOP is a great indicator of vital organ perfusion.
• Note skin perfusion because CSMT, Cap Refill, and Pulses are a good indicator of how the patient is doing.
• Note mental status as that is a good indicator of cerebral perfusion.
• Conduct invasive monitoring (art line, PA/CVP cath) & treat the underlying cause.

Medical Interventions

• VOMIT (Vitals, Oxygen, Monitors, IV Access, Treat Underlying Cause)
• Hypovolemic shock treatments include replacing fluid (plasma or blood), addressing dehydration/hemorrhage, and identifying and correcting the problem.
• Vasopressors can be used once volume is replaced. Monitor H&H, UOP, and I&O.
• Cardiogenic shock treatments includes addressing Left Ventricular Pump Failure from MI, Cardiomyopathy, and Cardiac Arrest
• Volume can be given GENTLY and Monitor carefully for FVO
• Inotropes to increase the effectiveness of contractions, being careful as depending on BP, drugs that decrease afterload may help as well.
• Obstructive shock treatments include addressing what is causing the decreased Cardiac output to be decreased due to a NON-CARDIAC problem
• Treat pericardiac and/or cardiac problems as needed.
• Distributive Neurogenic shock Treatments include reversing the Loss of Sympathetic Tone and 3rd spacing caused in CNS/cord injuries.
• Treat the underlying problem using cautious fluid administration, vasopressor drips to increase PVR, and atropine/TCP if bradycardic.
• Distributive Anaphylactic shock treatments include reversing the Life-Threatening Systemic Hypersensitivity to an allergen.
• Causes widespread histamine and heparin release, third spacing (urticaria, angioedema, stridor, hypotension), and remove the offending agent if possible Epinephrine, Oxygen, IV fluids, Antihistamines, Steroids should be administered.

Sepsis and SIRS

• Sepsis stems from a widespread infection leading to an inflammatory response (SIRS).
• Complications include Multiple Organ Dysfunction Syndrome (MODS).
• Drug Therapy includes administering antibiotics, IV fluids, Vasopressors, and Corticosteroids
• Sepsis remains the 10th leading cause of death in the US.
• Infectious organisms that enter the body can cause sepsis, for example, lung infections or ventilated patients.
• Susceptible patients include People with increased susceptibility (age- over 85, immunocompromised, poor nutrition, malignancy)
• Complications of sepsis include DIC and MODS.
• MODS is when Sequential failure of organ systems from hypoxia and acidosis occurs, with an extremely high mortality rate.
• Treatment in sepsis involves the following: decreased PVR = ↓ preload = ↓ stroke volume = ↓ cardiac output = ↓ blood pressure = ↓ organ perfusion & it is important to treat the fever.
• The clinical manifestations of sepsis include patients will present with irritability, restlessness, confusion and are initially flushed, febrile, tachycardic, with decreased urine output.
• As the patient worsens, those patients will become pale with clammy skin and weak pulses.

Medical and Nursing Management of sepsis & shock

• Prevention and treatment of sepsis includes pulmonary, urinary, and skin care.
• Treatment includes obtain cultures and review sensitivity to ensure correct antibiotic is prescribed, and antibiotics as soon as possible are critical to stopping the progression of shock
• Ongoing assessment is needed where vital Signs, MONITOR URINE OUTPUT, watch labs, and signs of bleeding need to be reviewed.
• Pertinent labs include WBC, H&H, Lactic acid, Cultures, D-dimer, ABGs.
• Oxygen, IV fluids as needed with antibiotics and vasopressors should be prescribed.

General Management of Shock

• Assessment needs to watch for early signs (tachycardia, tachypnea, pallor, thirst, and decreased urine output).
• Specific Treatment needs to take Ventilatory Support (Airway, breathing, oxygenation), Cardiovascular Support (IV fluids, vasopressors), Monitor (Vital signs, urine output, CBC, ABGs), and fixing the underlying cause (Stop bleeding, treat infections, and correct hypovolemia).
• Pediatric Shock warning signs include Restlessness, tachypnea, tachycardia, and pallor.
• Treat by administering Fluid Boluses of 20 mL/kg NS & give Vasopressors if that does not work.
• Fix underlying imbalances.