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Pathophysiology NRS 232 Exam 2

Terms in this set (88)

DVT
(formation of a clot) on the wall of vein is accompanied by inflammation of the vein wall and obstructed venous blood flow.
CAD VS PAD
· CAD: coronary artery disease
· PAD: peripheral artery disease
· Same cause, different symptoms
· Atherosclerosis, Moenckenberg, Arteriosclerosis
Hypertension
high blood pressure; the force of the blood against the arterial wall is too high.
Major Risk Factor for:
◦ Coronary artery disease (CAD)
◦ HF
◦ Stroke
◦ Renal failure
◦ Peripheral vascular disease
Etiology of HTN
◦ Primary Hypertension
◦ Essential hypertension: unknown etiology; most common type;
◦ CV Risk factors
◦ Outcomes: renal damage; Left Vent. Hypertrophy; MI
◦ Secondary Hypertension
◦ Known, identifiable cause
◦ Infants/peds most often have secondary hypertension
◦ Sleep apnea, drugs, CRD, Primary Aldosteronism, Cushings or steroid therapy, pheochromocytoma, thyroid or parathyroidism
◦ Emergency Hypertension (HTN crisis)
◦ That which is caused by crisis: can cause CVA, emboli, MI, HF, etc. SBP >180 and/or - DBP >120 and acute end-organ damage
Risk Factors of HTN
Non-modifiable
Inc. age
Family Hx.
Ethnicity
Modifiable
Obesity
Sedentary lifestyle
Dietary factors
Stressful lifestyle
Tobacco use
DM - insulin, glucose
Hyperlipidemia-total, HDL, LDL
Hypertriglyceridemia
Arteriosclerosis
small artery calcification
· Thickening/hardening of the vessel walls, usually r/t aging; can increase vessel resistance d/t narrowed vessels.
Describe control mechanisms and major risk factors for HTN
Diabetes
Unhealthy diet
Physical inactivity
Obesity
Excessive ETOH use
Tobacco use
Genetics / Family Hx
Age / Gender
AHA HTN guidelines
Normal: Systolic: < 120 Diastolic: < 80
Elevated: Systolic: 120-129 Diastolic: < 80
HTN Stage 1: Systolic: 130-139 Diastolic: 80-89
HTN Stage 2: Systolic: 140 or higher Diastolic: 90 or higher
Hypertensive Crisis: Systolic: Higher than 180 Diastolic: Higher than 120
Diuretics
Body dumps salt, water follows -> decreased fluid flowing through vessels

Lasix
Beta-Blockers
Block effects of the hormone - epinephrine (adrenaline)

LOL's: Metoprolol, propranolol, labetalol, carvedilol, atenolol

Used when other meds don't work.
ACE-inhibitors
Angiotensin converting enzymes; relax (dilate) vessel to decrease BP related to prevention of angiotensin production (which narrows vessels)

PRIL's: Benazepril, captopril, enalapril, lisinopril
Calcium-channel blockers
Block/prevent calcium from entering heart/arterial cells

Inhibits "squeezing" action (contraction) allowing relaxation, and decreased pressure/resistance.

Amlodipine, nicardipine, nifedipine, verapamil, diltiazem
DVT Pathology & Management
· Usually in lower leg
· Leg pain or swelling, or asymptomatic
· Serious condition r/t embolus can break off and travel to lungs causing PE
Main Causes:
· Damage to vein r/t
o Surgery
o Inflammation
o Injection
o Injury
S/Sx:
· Pain, swelling, tenderness, warm skin
· Can be asymptomatic
Risk Factors:
· Prolonged inactivity
· Hypercoagulable states
· Increased estrogen
Treatment
· Oral anticoagulants (i.e. blood thinners)
· Thrombolytics (clot busters)
· Compression stockings
· Vena Cava Filters
Describe Pulmonary Emboli manifestations, diagnostics, and treatment
PE: Small clot; DVT breaks off from leg and travels through heart into pulmonary artery.

Signs:
Moderate:
◦ Fluid and blood fill the alveoli in area,
◦ Reflective vasoconstriction
◦ Increase in blood vessel pressure
Large:
◦ 60% or more of lung tissue
◦ Leads to right-sided heart failure, acute cor pulmonale
◦ Decrease cardiac output on left side
◦ Shock, sudden death
Symptoms:
· Chest pain
· Cough
· Dyspnea
· Sudden onset of tachypnea and dyspnea
· Later hemoptysis and fever
· General sympathetic reaction: anxiety, restlessness, pallor
· Massive PE: low BP, rapid weak pulse, loss of consciousness
· Fat emboli: petechial rash on trunk
Risk Factors: Cardiac disease, surgery, cancer, clotting disorders, smoking, obesity, pregnancy, estrogen supplements
Diagnosis: CXR, V/Q lung scan, heical CT scan, D-Dimer, ABG's, pulmonary angiogram if other dx tests (above) are not conclusive d/t expensive and invasive
Treatment: Anticoagulation therapy (heparin, warfarin), Thrombolytics, embolectomy, vena cava filters.
Atherosclerosis
large arteries hardened and narrows; a buildup/deposits of fatty material/yellowish plaques containing cholesterol in arterial walls.
· Thickening/hardening within inner arterial lining
o Intima -smooth tissue - endothelium
· Causes blood flow obstruction
· Plaques may rupture leading to acute arterial occlusion via clot
· Often no Sxs until plaque ruptures leading to blocked blood flow.
-Mainly affects large and medium arteries
· CAD (coronary)
· CVA (cerebral, carotid)
· Femoral Arteries
Risk Factors
Modifiable:
· Resiliency/Stress mitigation
· Diet/exercise/obesity
· HTN
· High cholesterol/TRGS
· Smoking
· Glucose intolerance
· Stress
Non-Modifiable:
· Age/Gender/Ethinicity/Hereditary
Treatment - closely related to high blood pressure treatment
· Healthy diet and exercise
· Medications
o Statins, other cholesterol drugs
o Aspirin
o BP medications
· Procedures to open blocked arteries
Symptoms (vary greatly)
· Chest pain or angina
· Pain in leg, arm, anywhere that has a blocked artery
· Cramping in buttocks while walking
· Fatigue
· Confusion, which occurs if the blockage affects circulation to brain
Arterial PVD
Narrowed arteries: blocked, spasm r/t fatty deposits & Ca+ build up in arterial walls

Cold, decrease hair growth, glossy appearance
Pallor when elevated; rubor when dependent
Sharp pain with activity, improved at rest
Ulcer development: heels, malleolous, distal phalanges

Risk Factors: Age, diabetes, smoking
Raynaud's syndrome
relatively rare condition of the smaller arteries. Note: evidenced by brief vasospasms and narrowing of blood vessels (vasoconstriction)

• Smaller arteries supplying blood to skin become narrowed
• Narrowing r/t vasospasm
• Vasospasm r/t cold temps or stress
• Mostly affects arteries of hands and feet, distal extremities, earlobes and nose
• Most common in females (e.g., puberty to menopause)
• Emotional stress and cold triggered
Acute Arterial Occlusion
Cause: acute thrombus /embolism, trauma, external compression
· Necrosis/Gangrenous
· Six P's:
Pallor
Paresthesia
Paralysis
Pain
Polar (cold)
Pulseless
Describe Thromboangiitis Obliterans
AKA Buerger Disease; caused by small blood vessels that are inflamed and swollen
· Vessels narrow or are blocked by thrombosis
· Mostly affect hands and feet
· Affect arteries more than veins
Risk Factors: Tobacco use (smoking/chewing)
Etiology: men; 20-40; higher in Israel, Asia, India
Patho: Inflammatory disease of small to medium peripheral arteries & veins; causes obstruction to arterial blood flow
Cause: unknown (note: due to the rarity, research is limited)
S/S: numbness/tingling, pale, reddish, or blue tinted skin, intermittent pain, inflammation distal extremity ischemia; pain at rest; ulcerations
TX: antibiotics; amputation; good wound care; stop smoking; prostaglandins, hyperbaric oxygen TX
Chronic Venous Insufficiency (Stasis Ulcerations)
Venous stasis, usually in lower extremities; chronic venous insufficiency
Etiology: aging; poor CV output; poor venous return
Clinical manifestations
o Reddish-brown color (distal to proximal)
o Pain in dependent position
o Edema & inflammation
Management:
· BR
· Elevate lower extremities
· Safety
· Hygiene
· Dressings
· Stop smoking
Thrombosis
Formation of a clot in the blood vessel
· Arterial clots can form in chambers of heart
· More commonly in venous system - legs or pelvis (DVT)
Contributing Factors:
· Pregnancy
· Age
· Post surgery
· Smoking
· Long travel time
· Obesity
· Drugs(BCP or erythropoietin)
· Thrombophilia
What are manifestations of DVTs?
· Redness
· Swelling
· Increase warmth
· Skin changes
· Pain
· Positive Homan's sign (not that predictive in dx of DVT)
· Can be asymptomatic
What are management strategies for pulmonary emboli?
Anticoagulation Therapy: Unfractionated Heparin, Low-molecular weight heparin, and oral anticoagulation (e.g., warfarin) at time of diagnosis

Thrombolysis: tx if hemodynamic compromise

Embolectomy: massive PE, can have fibrinolysis tx.

Vena Cava Filters: if unable to do anticoagulation tx, hx of massive PE and suspected recurrence
What are the general processes of atherosclerosis? (DILPIP)
Damage to the endothelial surface
Inflammatory response with increased wall permeability
LDL breach layer, Leukocytes drawn
Platelet aggregate: release platelet growth factor
Increase growth of smooth muscle, proliferate (thrombus CAD)
PLAQUE: smooth muscle cells, lipoproteins, inflammatory debris
Repeated
What are patient education strategies for Raynaud's syndrome?
1. Avoid the cold, stressors, and smoking.
2. S/Sx are not serious.
3. Wear insulated clothing.
4. Use warm water soaks to warm extremities.
5. Teach biofeedback and relaxation techniques

Other: Biofeedback & relaxation techniques
Calcium channel blockers (Nifedipine)
Topical NTG ointment to fingers & dorsumof hand
Prostaglandin therapy
How are varicose veins different than stasis ulcerations?
Varicose Veins: affect superficial veins
Stasis Ulcerations: affect deep veins
Varicose Veins
• Damaged valves allow back flow; Dilated, torturous veins, usually in legs
• Veins become enlarged, dilated, twisted, overfilled with blood
• Generally benign, more cosmetic
• Affects more superficial veins
• More common in females
• Patho: valve problems in veins; can't move blood from extremities
• Causes: obesity; congenital; venous obstruction; standing
• S/S: mild to severe pain; legs cramps; swelling, appear raised, bluish-purple, red
• TX: surgery; cosmetics; antiembolic stockings; elevate legs often; prevention
Systolic blood pressure
(the first number) - indicates how much pressure your blood is exerting against your artery walls when the heart beats.

(Korotkoff sound begins) pressure exerted by blood when ejected from the left ventricle
Diastolic blood pressure
(the second number) - indicates how much pressure your blood is exerting against your artery walls while the heart is resting between beats.

pressure that occurs when the ventricles are relaxed (korotkoff sound disappears)
What are the 5 hypertension categories? [AHA 2021 Guidelines]
1) Normal: Less than 120/80 mm Hg
2) Elevated 120-129 systolic and less than 80 mm Hg diastolic. People with elevated blood pressure are likely to develop high blood pressure unless steps are taken to control the condition.
3) Hypertension Stage 1 -139 systolic or 80- 89 mm Hg diastolic; doctors are likely to prescribe lifestyle changes and may consider adding blood pressure medication based on your risk of atherosclerotic cardiovascular disease.
4) Hypertension Stage 2 140/90 mm Hg or higher; doctors are likely to prescribe a combination of blood pressure medications and lifestyle changes.
5) Hypertensive Crisis over 180/120 mm Hg, requires immediate medical attention
Heart rate vs. BP
Heart rate and blood pressure do not necessarily increase at the same rate. A rising heart rate does not cause your blood pressure to increase at the same rate. Even though your heart is beating more times a minute, healthy blood vessels dilate (get larger) to allow more blood to flow through more easily. When you exercise, your heart speeds up so more blood can reach your muscles. It may be possible for your heart rate to double safely, while your blood pressure may respond by only increasing a modest amount.
RAAS
balanced by naturistic peptides (ANH & BNP.)

1) Drop in BP or blood volume is sensed by the kidneys which secrete renin →

2) targets the liver to secrete Angiotensinogen → Renin converts angiotensinogen to angiotensin I

3) targets the lungs to release ACE → converts Angiotensin I → Angiotensin II

4) Angiotensin II Causes:
1) Vasoconstriction → Increase in BP
2) Adrenal cortex releases aldosterone → sodium and water retention → increase in blood volume → Increase in BP
Homeostasis of Body Fluids
ADH and Aldosterone
What are nursing considerations for hypertension management?
Check BP
Check HR
Check urine output
Check reduction of dependent edema
Check Na+, K+, Cl-, BUN and Creatinine.
Monitor for side effects
Monitor for compliance
Pt education
HTN Drug Therapy
Diuretics - decrease preload
Beta-blockers - dec. HR and contractility
ACE inhibitors - RAAS pathway
Angiotensin II receptor blocker- RAAS pathway
Aldosterone Receptor Blocker - RAAS pathway
Ca++Channel Blocker - heart and vessel contraction
Alpha1 blockers - Dec. HR and vessel contractility
· Vasodilators
Aldosterone
Aldosterone is released from the adrenal gland in response to Angiotensin II, and targets the kidneys where it signals for the reabsorption of sodium (Na+); smaller volume of urine - "Saltwater Hormone" (Salt retaining)
ADH
Antidiuretic Hormone is released from the Posterior Pituitary gland in response to volume receptors sensing the decrease in plasma volume, and targets the nephron tubules of the kidneys, where it signals for reabsorption of H2O; makes a smaller volume of more concentrated urine - "Tap-water Hormone"
Blood Composition
Fluid component transporting blood cells throughout body
Whole Blood (Plasma & Formed elements)
7 - 8% of body weight
♀ average of 9 pints
♂ average of 12 pints
55% Plasma
Glucose
Hormones
Proteins
Mineral salts
Fats
Vitamins
45% Formed Elements
Erythrocytes
Leukocytes
Thrombocytes
Erythropoiesis
Production of red blood cells is controlled by erythropoietin, a hormone produced primarily by the kidneys. Red blood cells start as immature cells in the bone marrow and after approximately seven days of maturation are released into the bloodstream.
Erythropoiesis steps (PBPORM)
Proerythroblast
Basophilic erythroblast
Polychromatophilic erythroblast
Orthochromic erythroblast
Reticulocyte
Mature RBC
Hemoglobin Synthesis
• Begins in the mitochondrion
• Two main components:
1) Globin production
2) Heme synthesis
• Iron is essential to build the heme
Hgb Structure and Function
• Hemoglobin carries oxygen and transports carbon dioxide
• Each hemoglobin molecule binds with four oxygen molecules
• Oxyhemoglobin - a hemoglobin molecule bound to 4 oxygen molecules
• Utilizes iron in the ferrous state
• Lungs - C02 is released while 02 diffuses into blood
• Tissue - C02 is bound for transport to lungs while 02 is released
• Oxygen saturation, denoted as Sa02, is the percentage or fraction of oxyhemoglobin relative to total hemoglobin in blood.
• Normal Sa02 is 95-100%. (Sp02 = Sa02)
• Venous oxygen saturation (SvO2) is a measure of the oxygen content of the blood returning to the right side of the heart after perfusing the entire body. When the oxygen supply is insufficient to meet the metabolic demands of the tissues, an abnormal SvO2 ensues and reflects an inadequacy in the systemic oxygenation.
• Normal SvO2 is 60 - 80%.
• Pulmonary Capillaries
• Have a loose and reversible bond due to a high partial pressure, allowing 02 and C02 exchange.
• PaO2 80 - 100mm Hg
• PvO2 is 35 - 45mm Hg.
Evaluate the Oxygen-Hemoglobin Dissociation Curve
The dissociation curve show how hemoglobin saturation with 02, (S02) is related to the partial pressure of 02 in the blood, (P02).
Factors recognized to influence the Oxygen Dissociation Curve (ODC) include local prevailing C02 partial pressure (PC02), pH, and temperature.
Hyperventilation - leads to alkalosis, and hypocapnia
Exercise causes an increase in acidity, temperature and metabolic intermediates and a decrease in oxygen in your muscle tissues. This causes an increased dissociation of oxygen (right shift) from your blood flowing through your muscles, supplying them with much needed oxygen.
Describe Carbon Dioxide transport
transported via blood by 3 methods:
Dissolved gas in solution (5%)
Buffered with water (75%) - Carbonic Acid
Bound to proteins (~ 20%) - Particularly hemoglobin (Hb)
75% transported in RBCs
25% transported in Plasma
Largest majority transports as part of bicarb system
• Bicarb system uses blood and C02 to maintain pH while C02 is transported to lungs to be exhaled
• Diffuses easily into pulmonary capillaries
Describe Oxygen transport
1) Oxygen combines with heme from RBC → oxyhemoglobin
2) Oxyhemoglobin is carried to tissue and released
Tissue cellular metabolism occurs via carbonic acid formation
3) Carbonic acid → Hydrogen and bicarb dissociation
Hydrogen and bicarb are eliminated via lungs and kidneys
Anemia manifestations
· SOB
· Dizziness
· Fatigue
· Pain
· Increased HR - dystythmias
· Headache
· Pale yellow skin
· Cold hands/feet
· Peds- growth problems
What are laboratory tests used to diagnose anemia?
Complete Blood Count (CBC), Comprehensive Metabolic Panel (CMP), Hemoglobin & Hematocrit (H&H), Reticulocyte Count (percentage of immature RBCs), Coagulation factors, Peripheral smear
Describe Anemias with decreased RBC production
1) Vitamin Deficiency Anemia
B12 and/or Folate not available for RBC production
Larger than normal RBCs
↓ RBCs
↓ WBCs
↓ Platelets
2) Iron Deficiency Anemia
Iron unavailable for hemoglobin synthesis
Smaller than normal RBCs
↓ RBCs
↓ WBCs
↓ Platelets
3) Aplastic Anemia
Stem cell disorder in bone marrow
↓ RBCs
↓ WBCs
↓ Platelets
4) Anemia R/T chronic renal failure
Impaired erythropoietin production
Renal system destroys RBCs
Describe Anemias related to RBC inherited disorders
SICKLE CELL DISORDER
• RBC "sickles" with 02 levels
• Sickled RBCs occlude small arteries
• Hemolysis in spleen
• Excruciating pain
GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY (G6PD)
• Genetic enzyme deficiency
• Found in 11% of African American males
• Increased in areas w/malaria
• Damaged RBCs
THALASSEMIA
• Irregular hemoglobin formation
• Destruction of erythroblasts in marrow
• RBCs, very tiny
• Enough an be made to be asymptomatic
• Usually affects people of Mediterranean, African, Middle Eastern and Southeast Asian descent
• Can be mild to life threatening
• Severe form: Cooley's Anemia
SPHEROCYTOSIS
• Genetic condition
• Defective RBCs
• RBC is spherical, missing concave sides
Describe the three types of polycythemia
A condition in which there is an excessive number of RBCs.
· Thickens blood
· Slows blood flow
· Can lead to clots

1) Polycythemia Vera (primary)
§ Malignancy of bone marrow stem cells, blood cancer
§ ↑RBCs, leukocytosis, thrombocytosis
§ Rare
2) Secondary Polycythemia
↑ stimulation of RBC production
High altitude, lung disease
3) Relative Polycythemia
Dehydration, endocrine disorders
Related to decreased plasma volume
↑ hematocrit with normal to high RBC numbers and low normal to decreased plasma volume
Increased risk for thromboembolic events
What are the nutritional requirements for erythropoiesis?
Folate, Vitamin B12, and Iron
What does a "shift to the left" mean as related to the oxygen-hemoglobin dissociation curve?
• Increased 02 affinity/retention
• Prevents 02 unloading in peripheral tissue → low tissue 02 concentration
Causes of left shift:
· Binding with one CO molecule (carbon monoxide)
· ^ pH
· Low temp
· Hyperventilation r/t decreased CO2
What is absolute anemia?
Actual decrease in # of RBCs
What is characteristic of thalassemia?
· Irregular hemoglobin formation
· Destruction of erythroblasts in marrow
· RBCs, very tiny
· can be asymptomatic
· Mediterranean, Middle Eastern, Southeast Asian decent
· Severe form: Cooley's Anemia
What is hemolytic anemia?
RBCs destroyed faster than they can be replaced
Can develop Quickly or slowly
Can be mild or serious
Describe ventilation processes and the mechanics of breathing
AIRWAY RESISTANCE
Relationship between pressure & flow.
Resistance increases as airway passages narrow.
· Mucous
· Smooth muscle constriction
· Foreign body

LUNG COMPLIANCE
Ability to inflate & chest wall expandability.
Neonates/Pediatrics
increased lung compliance up to 3.5 yo r/t chest wall flexibility
Elderly
decreased compliance/t loss of elastic fibers in lungs, rib rigidity
OPPOSING FORCES
Elasticity vs. Expandability
§ Expandability measured with pulmonary function test (PFT)
Describe neurological control of ventilation
Receptors receive stimuli from within body and send that information to the respiratory center.
NEURAL CONTROL CENTERS
• Medulla oblongata
o muscle stimulation
• Pons
o respiratory rate, blocks ramp signal
PERIPHERAL CHEMORECEPTORS
• Aortic arch and carotid bodies
o Respond to arterial Pa02
o Respond to C02
CENTRAL CHEMORECEPTORS
• Monitor/Respond to systemic PaC02 changes in immediate environment (brain)
• CSF pH changes
PROPRIOCEPTORS
• Muscles & tendons
o Increase respiration with exercise
LUNG
STRETCH RECEPTORS
• Alveolar
• Bronchi
• Bronchioles
BARORECEPTORS (PRESSURE)
• Aortic arch and carotid arteries
o Increased BP
o Decreased respiration
Perfusion
Distribution of blood flow can be uneven.
Affected by
Body position
Exercise
Pressure of capillaries vs. alveoli.
hypoventilation and hyperventilation
HYPOVENTILATION- Delivery of air to alveoli is insufficient
(in delivery of 02 and removal of C02)
EXAMPLES:
• Medications
• Sleep apnea
• Chest wall damage

HYPERVENTILATION- Increased amount of air entering
alveoli (leads to hypocapnia=decrease of C02 in blood)
EXAMPLES:
• Pain
• Fever
• Anxiety
hypoxemia and hypoxia
HYPOXIA- Deficient tissue oxygenation
Examples:
• Restlessness
• Headache
• Confusion
• Anxiety
• Tachycardia (abnormally fast HR)
• Tachypnea (abnormal rapid breathing)
• SOB (shortness of breath)
HYPOXEMIA- Deficient blood oxygen
Example:
• Pa02 < 80
• SP02 < 95%
Respiratory Distress VS Respiratory Failure
Respiratory Distress- Inability to regulate gas exchange
Examples:
• Too little 02
• Too much C02
Signs/symptoms:
• Severe shortness of breath, labored breathing,
unusually rapid HR, Low BP, confusion, extreme
fatigue, color changes, grunting, nose flaring,
retractions and sweating
NEEDS to be on supplemental 02
Respiratory failure- severe inability to regulate gas exchange.
Examples:
• Altered oxygenation
• Altered ventilation
• Metabolic requirements (can be fatal if left untreated)
Signs/symptoms:
• Same as distress but more severe
• Hypertension and tachycardia
• Happens quickly/sometimes w/out warning
MIGHT need intubation
What are the structures of the upper airway?
Nasopharynx
Oropharynx
Laryngopharynx
(Mouth, Nose, Throat)
What are the three dimensions of the dead space?
The volume of air inhaled but does not participate in gas exchange.
Remnants in conduction airways
Alveoli perfused poorly or not at all
Consideration - not all the air in each breath is available for gas exchange
What are several causes of airway resistance?
Relationship between pressure & flow.
Resistance increases as airway passages narrow.
Causes:
Mucous
Smooth muscle constriction
Foreign body
What is the process of "shunting"?
Normally about 3% of blood pumped by right ventricle does NOT perfuse alveolar capillaries
The higher amount of shunted blood, the greater hypoxia
What are several causes for hypoventilation?
Medication, sleep apnea, chest wall damage
What are clinical manifestations of acute respiratory failure?
Severe SOB, labored breathing, tachypnea, hypotension, confusion, extreme fatigue, color changes, grunting/nose flaring, retractions, sweating, tachycardia. Can come on quickly!
What is the pathology of pulmonary hypertension?
A type of hypertension that affects arteries in the lungs and right side of heart
SIGNS/SYMPTOMS
• Short of breath
• Dizziness
• Chest pain
Medications and 02 therapy can lessen symptoms and improve quality of life
UNDERLYING CAUSES
• Coronary artery disease
• High blood pressure
• Liver disease (cirrhosis)
• Lung blood clots
• Chronic lung disease (ie., emphysema)
What are clinical manifestations of pulmonary malignancies?
LUNG CANCER
Men - 1/3 of all cancer deaths
Women - 1/4 of all cancer deaths
Etiology - smoking (85% of cases)
Patho - altered cell / altered cell function
Sign / Symptoms - weight loss, anemia, dyspnea, cough, chest pain, hemoptysis, increased sputum
Management - chemo, radiation, laser therapy, surgery
Review the basics of acid-base imbalances
Acid = A molecule that can contribute
an H Ion (weak acid does not let go of
hydrogen easily; strong acid "gives up"
hydrogen)
BASE = A molecule that can accept or
remove an H Ion

PH = Concentration of H Ions
Result as byproduct of metabolism
(EX: Lactic Acid; Ketoacids)
Describe pH regulators
Buffer Systems (act like sponges to absorb H+)
◦ HCO3 system* (extracellular)
◦ PO4 system (intracellular & urine)
◦ Hb buffers (RBCs)
◦ Protein buffers (intracellular & blood)
Lungs: ↑Carbonic Acid stimulate respiratory center to ↑RR (2nd line of defense)
Kidneys:
*HCO3- (normally conserved)
*Excrete H+ from non H2CO3 acids (non-volatile; metabolic acids = lactic acid)
◦ Less efficient in infants & older adults
◦ Cannot excrete carbonic acid but can excrete other acids to compensate
Buffer Systems
Bicarbonate Buffers Carbonic Acid & HC03

Phosphate buffers Phosphate; HCL; NA Hydroxide

Protein Buffers: Made of Amino Acids (located in cells)
Identify acid-base control mechanisms
Respiratory control
◦ Lungs control level of CO2
◦ Begin to compensate in 2-3 hours
Kidneys: (Metabolic)
◦ Eliminate H+ & conserve HCO3-
◦ Eliminate ammonium (NH4)
◦ Ion exchanges
Na + & Cl-
Cl- & HCO3-
Acid Base Imbalance Normal Ranges
pH: 7.35-7.45
CO2: 35-45
HCO3: 22-26
O2: 96-100%
Respiratory Acidosis
Low pH, High CO2

Primary Factor: hypoventilation
Causes:
Impaired ventilation
o Depression of the central nervous system
o Drug overdose
o Head Injury
Diseases of the airways or lungs
o Bronchial asthma
o Emphysema
o Chronic bronchitis
o Respiratory distress in the newborn
o Pneumonia
o Pulmonary edema
Disorders of chest wall or respiratory muscles
o Chest injuries
o Kyphoscoliosis
o Extreme obesity
o Treatment with curare-type drugs
o Upper airway obstruction
o Aspiration of foreign body
o Obstructive sleep apnea
o Laryngospasm
· Increased carbon dioxide inhalation
o Breathing air that is high in carbon dioxide content
Manifestations
ph less than 7.35
pCo2 greater than 45 mmHg
Depression of Neural function
Headache
Weakness
Confusion and disorientation
Behavioral changes
Depression
Paranoia
Hallucinations
Tremors
Paralysis
Stupor and coma
· Skin
Warm and flushed
· Compensatory mechanisms
Increased loss of hydrogen in the urine
Treatment
Correct Cause
Improve ventilation as this is caused by hypoventilation
Perhaps mechanical ventilation will be necessary
Examples:
*Pulmonary disease
*Drugs
*Obesity
*Mechanical asphyxia
*Sleep
Sleep Apnea causes respiratory acidosis via hypoventilation
Metabolic Acidosis
low pH, low HCO3

Primary factor: addition of large amounts of fixed acids to body fluids or ↑ loss of HCO3-
Causes:
· Increased anion gap
· Decreased pH seen in metabolic acidosis
· Kidney failure or dysfunction
· Loss of intestinal secretions
· Diarrhea
· Intestinal suction
· Intestinal or biliary fistula
· Increased renal losses
· Renal tubular acidosis
· Treatment with acetazolamide
· Increased chloride levels
· Abnormal chloride reabsorption by the kidney
· Sodium chloride infusions
· Treatment with ammonium chloride
· Parenteral hyperalimentation
Manifestations:
· ph below 7.35
· Bicarbonate below 24 mEq/liter (24 mmol/liter)
· Altered gastrointestinal function
· Anorexia
· Nausea
· Vomiting
· Abdominal pain
Depression of Neural Fx
· Weakness
· Lethargy
· General malaise
· Confusion
· Stupor
· Coma
· Depression of vital functions
Cardiovascular manifestations
· Cardiac arrhythmias
· Heart unresponsive to
· catecholamines
· Decreased heart rate
· Decreased cardiac output
· Skin: Warm and flushed
Management
· Correct Cause
o Reverse DKA (Hyperglycemia)
o Correct GI Disturbance
· NOTE: Supplemental bicarb is
o controversial, particularly in
o lactic acidosis
EXAMPLES OF EXCESS PRODUCTION: Lactic acidosis (circulatory failure) Ketoacidosis (diabetes, starvation) Acid ingestion (salicylates) Severe infection Alcoholic ketoacidosis
Respiratory Alkalosis
high pH, low CO2

Primary Factor: hyperventilation
Causes:
· Increased ventilation (hyperventilation)
· Anxiety and psychogenic hyperventilation
· Lung disease that reflexively stimulates ventilation
· Hypoxemia
· Local lung lesions
Stimulation of respiratory center
Elevated blood ammonia
Salicylate toxicity
Encephalitis
Anxiety
Mechanical ventilation
Manifestations: pH above 7.45; Bicarbonate below 24 mEq/l) as an attempt to compensate by the renal system (Metabolic)
Increased excitability of the nervous system
Numbness and tingling of finger and toes
Dizziness, panic and lightheadedness
Tetany
Positive Chvostek's and Trousseau's signs (Due to
· Hypocalcemia
Convulsions
· Cardiovascular manifestations: Cardiac dysrhythmias

Treatment: Correct Cause
Increase PO2
Rebreathing expired air

EXAMPLES:
Overventilation on a ventilator
Response to acidosis
Bacteremia
Thyrotoxicosis
Fever
Hepatic failure
Response to hypoxia
"Panic attack"
Metabolic Alkalosis
high pH, high HCO3

Primary Factor: retention of base or removal of acid from body fluids
Causes:
· Increase in gain of bicarbonate
· Ingestion of sodium bicarbonate or alkaline salts
· Milk-alkali syndrome
Bicarbonate Retention
o Loss of chloride (hydrogen with bicarbonate retention
o Vomiting
o Gastric suctioning
o Diuretic therapy
o Potassium deficit with hydrogen ion excretion
Excessive levels of adrenal cortical hormones
Decreased potassium intake
Increased potassium losses
Contraction alkalosis (loss of body fluids)
Manifestations:
· pH greater than 7.45
· Bicarbonate greater than 26 mEq/liter (26 mmol/liter)
· Increased excitability of the nervous system (develops late because bicarbonate crosses blood-brain barrier slowly)
· Confusion
· Hyperactive reflexes
· Muscle hypertonicity
· Tetany
· Convulsions
Treatment:
· Correct Cause
· Give Potassium Chloride to replace it
· Fluid replacement
EXAMPLES:
Excessive gastric drainage
Vomiting
K+ depletion (diuretic therapy)
Excessive NaHCO3 administration
What is the difference between strong acids and weak acids?
Strong Acids
◦ Break apart (dissociate) completely in water & can not recombine
◦ Example: HCL + H2O → H+ + Cl-
Weak Acids
◦ Partially break apart in water
◦ Can also recombine
◦ Example: H2CO3 →H+ + HCO3
What systems of the body control acid-base components?
-Lungs: Control level of CO2. Increased carbonic acid stimulates respiratory center to increase respiratory rate and exhale CO2 (inverse is also true); begin to compensate in 2-3 hours
Kidneys: Eliminate H+ and conserve bicarb (HCO3-), can excrete hydrogen ions from acids other than carbonic acid to compensate (non-volatile; metabolic acids = lactic acid). Eliminate ammonium (NH4). Ion exchanges in the kidneys: Na+ & Cl-; Cl- & HCO3
What are causes of respiratory acidosis?
Factors that cause hypoventilation can induce respiratory acidosis. Primarily: pulmonary disease, drugs, obesity, mechanical asphyxia, sleep.
What are management strategies for respiratory alkalosis?
Brown paper bag to increase CO2 retention; give potassium chloride to replace; fluid replacement
How does the renal system compensate for respiratory acidosis?
Kidneys increase secretion of H+ into urine while retaining HCO3
How do the lungs compensate for metabolic acidosis conditions?
Through Kussmaul breathing (deep, fast, and labored breathing). It is a form of hyperventilation.
What are causes of metabolic acidosis?
Excess production of metabolic acids (increased anion gap): Lactic acidosis (circulatory failure), ketoacidosis (diabetes, starvation), acid ingestion (salicylates), severe infection, fasting and starvation, ketogenic diet, and alcoholic ketoacidosis.-Kidney failure or dysfunction-Loss of intestinal secretions: diarrhea, intestinal suction, intestinal or biliary fistula-Increased renal losses: renal tubular acidosis, treatment with acetazolamide
What are management strategies for metabolic alkalosis?
Correct cause (bicarb retention due to excessive levels of adrenal cortical hormones, decreased potassium intake, increased potassium losses, and contraction alkalosis (aka loss of body fluids)).-Give potassium chloride to replace potassium levels-Fluid replacement
How does hypoventilation cause an acid-base imbalance?
When a patient is hypoventilating, CO2 (which is acidic) is released more slowly than usual, causing a build-up in the blood and changing the pH of the blood to be more acidic
Pulmonary Circulation
begins at R side of heart → Lungs →Blood picks up O2 and drops off CO2 → delivers to left side of heart
deoxygenated blood travels:
1) R ventricle pumps
2) Semilunar valve
3) pulmonary trunk
4) Splits into R and L pulmonary arteries
5) Pulmonary arterioles
6) Pulmonary capillaries → pick up O2, drop off CO2 (Blood is now oxygenated)
7) Pulmonary venules
8) Pulmonary vein
9) left atrium
10) Mitral (Bicuspid) valve
11) left ventricle
Veins Vs Arteries
Veins: carry blood towards the heart
Arteries: carry blood away from heart
Left Ventricle vs Right Ventricle
LEFT VENTRICLE: Oxygenated Blood; systemic circulation
RIGHT VENTRICLE: Deoxygenated blood; pulmonary circulation
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