S17 Patho #3

Front 1

Perfusion, ventilation, respiration & diffusion as they apply to movement of gas in and out of the lungs.

Back 1

Perfusion: The movement of blood into and out of the capillary beds of the lungs to body organs and tissues.

Ventilation: Ventilation is the mechanical movement of gas or air into and out of the lungs.

Respiration: The exchange of oxygen and carbon dioxide during cellular metabolism

Diffusion:

the movement of gases between air spaces in the lungs and the bloodstream

(Huether 660)

Front 2

Most likely cause of aspiration

Back 2

Aspiration is the passage of fluid and solid particles into the lung. It tends to occur in individuals whose normal swallowing mechanism and cough reflex are impaired by central or peripheral nervous system abnormalities. Predisposing factors include an altered level of consciousness caused by substance abuse, sedation, or anesthesia; seizure disorders; cerebrovascular accident; and neuromuscular disorders that cause dysphagia. Elderly individuals also are at increased risk for aspiration.12 The right lung, particularly the right lower lobe, is more susceptible to aspiration than the left lung because the branching angle of the right main stem bronchus is straighter than the branching angle of the left main stem bronchus. (Huether 684)

Front 3

Know trachea, segmental bronchi, alveolocapillary membrane & main bronchus and their responsibility in gas exchange

Back 3

Trachea: The trachea connects the larynx to the bronchi, the conducting airways of the lungs. Conducting airway.

Segmental bronchi: The trachea branches into two main airways, or bronchi (sing., bronchus), at the carina. The right and left main bronchi enter the lungs at the hila (sing., hilum), or “roots” of the lungs, along with the pulmonary blood and lymphatic vessels. From the hila the main bronchi branch farther. Conducting airway.

alveolocapillary membrane:

The shared alveolar and capillary walls compose the alveolocapillary membrane (Figure 25-6). Gas exchange occurs across this membrane.

(Huether 663)

main bronchus: The trachea branches into two main airways, or bronchi (sing., bronchus), at the carina.

Front 4

What is the best assessment of alveolar ventilation (we talked about this in class)

Back 4

The adequacy of alveolar ventilation cannot be accurately determined by observation of ventilatory rate, pattern, or effort. If a healthcare professional needs to determine the adequacy of ventilation, an arterial blood gas analysis must be performed to measure PaCO2 (Huether 665)

Front 5

Where do Stretch receptors send afferent impulses to?

Back 5

Three types of lung receptors send impulses from the lungs to the dorsal respiratory group:

(Huether 666)

Front 6

Know how Carbon dioxide is transported in the blood

Back 6

Carbon dioxide is carried in the blood in three ways: (1) dissolved in plasma (PCO2), (2) as bicarbonate, and (3) as carbamino compounds (including binding to hemoglobin). (Huether 673)

As CO2 diffuses out of the cells into the blood, it dissolves in the plasma. (Huether 673)

Front 7

Decreased lung compliance – causes

Back 7

Chest wall compliance decreases because ribs become ossified and joints are stiffer, which results in increased work of breathing. (Huether 675)

Increased compliance indicates that the lungs or chest wall is abnormally easy to inflate and has lost some elastic recoil. A decrease indicates that the lungs or chest wall is abnormally stiff or difficult to inflate. Compliance increases with normal aging and with disorders such as emphysema; it decreases in individuals with acute respiratory distress syndrome, pneumonia, pulmonary edema, and fibrosis.

(Huether 668)

Restrictive lung diseases are characterized by decreased compliance of the lung tissue.

(Huether 684)

Some of the most common restrictive lung diseases in adults are aspiration, atelectasis, bronchiectasis, bronchiolitis, pulmonary fibrosis, inhalational disorders, pneumoconiosis, allergic alveolitis, pulmonary edema, and acute respiratory distress syndrome.

(Huether 684)

Front 8

Know Irritant receptors, stretch receptors, J-receptors, peripheral chemoreceptors, & central chemoreceptors

Back 8

Irritant receptors (C-fibers) are found in the epithelium of all conducting airways. They are sensitive to noxious aerosols (vapors), gases, and particulate matter (e.g., inhaled dusts), which cause them to initiate the cough reflex.5 When stimulated, irritant receptors also cause bronchoconstriction and increased ventilatory rate. (Huether 666)

Stretch receptors are located in the smooth muscles of airways and are sensitive to increases in the size or volume of the lungs. They decrease ventilatory rate and volume when stimulated, an occurrence sometimes referred to as the Hering-Breuer expiratory reflex. This reflex is active in newborns and assists with ventilation. In adults, this reflex is active only at high tidal volumes (such as with exercise) and may protect against excess lung inflation. Stretch receptors called rapidly adapting receptors (RARs) have been found to be an important mediator of cough

(Huether 666)

J-receptors (juxtapulmonary capillary receptors) are located near the capillaries in the alveolar septa. They are sensitive to increased pulmonary capillary pressure, which stimulates them to initiate rapid, shallow breathing, hypotension, and bradycardia (Huether 666)

The peripheral chemoreceptors are somewhat sensitive to changes in PaCO2 and pH but are sensitive primarily to oxygen levels in arterial blood (PaO2).7 As PaO2 and pH decrease, peripheral chemoreceptors, particularly in the carotid bodies, send signals to the respiratory center to increase ventilation. (Huether 666)

The central chemoreceptors are sensitive to very small changes in the pH of CSF (equivalent to a 1 to 2 mm Hg change in PCO2) and can maintain a normal PaCO2 under many different conditions, including strenuous exercise.6 If inadequate ventilation, or hypoventilation, is long term (e.g., in chronic obstructive pulmonary disease), these receptors become insensitive to small changes in PaCO2 (“reset”) and regulate ventilation poorly (Huether 666)

Front 9

Diseases of lung: mycobacterium tuberculosis, pulmonary edema, emphysema, pneumothorax, types (restrictive, obstructive, acute, communicable), asthma (effect of inflammatory cytokines), pulmonary hypertension, pulmonary fibrosis, atelectasis, bronchiectasis, aspiration, bronchiolitis, flail chest, pleural effusion, exudative effusion

Back 9

* Exudative effusion: high concentrations of white blood cells and plasma proteins

Front 10

Bacteria in the secretions of bronchitis

Back 10

Bronchitis causes increase hyper secretions of mucous in the lungs.

Front 11

Effects of obesity, kyphoscoliosis, and neuromuscular disease on chest wall

Back 11

Chest wall compliance is diminished by obesity and kyphoscoliosis, which compress the lungs, and by neuromuscular diseases that impair chest wall muscle function.

(Huether 704)

Impairment of respiratory muscle function caused by neuromuscular disease also can restrict the chest wall and impair pulmonary function. Muscle weakness can result in hypoventilation, inability to remove secretions, and hypoxemia.

(Huether 682)

Front 12

Know effect of inflammatory cytokines in relationship to norepinephrine, acetylcholine, epinephrine & immunoglobulin and the effect on asthma

Back 12

acetylcholine: which cause bronchial smooth muscle contraction and mucus secretion

(Huether 689)

IgE: Causes mast cell degranulation with the release of inflammatory mediators including histamine, bradykinins, leukotrienes and prostaglandins, platelet activating factor, and interleukins (see Figures 5-8 and 7-9 for additional details).35 These mediators cause vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and mucus secretion from mucosal goblet cells with narrowing of the airways and obstruction to airflow

(Huether 689)

Epinephrin/norepinephrin: Bronchodilation

Front 13

Know cyanosis in relation to Hemoglobulin

Back 13

Cyanosis is a bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin (which is bluish) in the blood. It generally develops when 5 g of hemoglobin is desaturated, regardless of hemoglobin concentration.

(Huether 680)

Front 14

Hyperventilation, hypocapnia, hypercapnia

Back 14

Hyperventilation is alveolar ventilation exceeding metabolic demands. Lungs remove CO2 faster than it is produced by cellular metabolism, resulting in decreased PaCO2

Hypocapnia is decreased PaCO2 (PaCO2 is less than 36 mm Hg). Results in a respiratory alkalosis.

Hypercapnia is increased CO2 concentration in the arterial blood (increased PaCO2). Is caused by hypoventilation of the alveoli.

Front 15

Know the difference between: Restrictive Cardiomyopathy, Hypertrophic Cardiomyopathy, & Dilated cardiomyopathy

Back 15

Restrictive cardiomyopathy is characterized by restrictive filling and increased diastolic pressure of either or both ventricles with normal or near-normal systolic function and wall thickness. (Huether 612)

Hypertrophic cardiomyopathy refers to two major categories of thickening of the myocardium: (1) hypertrophic obstructive cardiomyopathy (asymmetric septal hypertrophic cardiomyopathy or subaortic stenosis) and (2) hypertensive or valvular hypertrophic cardiomyopathy. Hypertrophic obstructive cardiomyopathy is the most commonly inherited cardiac disorder. It is characterized by thickening of the septal wall (Figure 23-27), which may cause outflow obstruction to the left ventricle outflow tract. Obstruction of left ventricular outflow can occur when heart rate is increased and intravascular volume is decreased. This type of hypertrophic cardiomyopathy is a significant risk factor for serious ventricular dysrhythmias and sudden death, and has been implicated in more than 33% of sudden deaths in young athletes.8,103 Hypertensive or valvular hypertrophic cardiomyopathy occurs because of increased resistance to ventricular ejection, which is commonly seen in individuals with hypertension or valvular stenosis (usually aortic). (Huether 612)

Dilated cardiomyopathy is usually the result of ischemic heart disease, valvular disease, diabetes, renal failure, alcohol or drug toxicity, peripartum complications, genetic disorder, or infection. It is characterized by impaired systolic function leading to increases in

intracardiac volume, ventricular dilation, and systolic heart failure (Figure 23-26)

(Huether 612)

Front 16

Define shock & factors that impair oxygen use in all types of shock:

Back 16

An abnormal condition of inadequate blood flow to the body's tissues, with life-threatening cellular dysfunction. The condition is usually associated with inadequate cardiac output, hypotension, oliguria, changes in peripheral blood flow resistance and distribution, and tissue damage. Causal factors include hemorrhage, vomiting, diarrhea, inadequate fluid intake, or excessive fluid loss, resulting in hypovolemia.

(Huether 1097)

Front 17

Function of papillary muscles, catecholamine, vagal stimulation vagus nerve

Back 17

The papillary muscles are extensions of the myocardium that pull the cusps together and downward at the onset of ventricular contraction, thus preventing their backward expulsion into the atria.

(Huether 554)

catecholamine: Any one of a group of sympathomimetic compounds.

(Mosby 307)

Sympathetic nervous activity enhances myocardial performance. Stimulation of the SA node by the sympathetic nervous system rapidly increases heart rate. Furthermore, neurally released norepinephrine or circulating catecholamines interact with β-adrenergic receptors on the cardiac cell membranes. The overall effect is an increased influx of Ca++, which increases the contractile strength of the heart and increases the speed of electrical impulses through the heart muscle and the nodes. Finally, increased sympathetic discharge dilates the coronary vessels.4

(Huether 560)

vagal stimulation vagus nerve:

The parasympathetic nervous system affects the heart through the vagus nerve, which releases acetylcholine. Acetylcholine causes decreased heart rate and slows conduction through the AV node. Acetylcholine also causes coronary vasodilation

(Huether 560)

Front 18

Know Sarcolemma sclerotic plaques, Intercalated disks, Trabeculae carneae, Bachmann bundles

Back 18

Sarcolemma sclerotic plaques: Sarcolemma sclerotic plaques, Intercalated disks, Trabeculae carneae, Bachmann bundles

Intercalated disks: Electrical impulses are transmitted rapidly from cardiac fiber to cardiac fiber because the network of fibers is connected at intercalated disks, which are thickened portions of the sarcolemma. The intercalated disks contain two junctions: desmosomes, which attach one cell to another; and gap junctions, which allow the electrical impulse to spread from cell to cell (see Chapter 1). Together, these junctions provide a low-resistance pathway for impulse propagation.

(Huether 560)

Trabeculae carneae:

any one of the irregular bands and bundles of muscle projecting from the inner surfaces near the apex of the ventricles of the heart.

(Mosby 1794)

Bachmann bundle, conducts the impulse from the SA node to the left atrium.

(Huether 557)

Front 19

Describe Frank-Starling law –

Back 19

The Frank-Starling law of the heart describes the length-tension relationship of VEDV (preload) to myocardial contractility (as measured by stroke volume). Muscle fibers have an optimal resting length from which to generate the maximum amount of contractile strength. Within a physiologic range of muscle stretching, increased preload increases stroke volume (and therefore cardiac output and stroke work) (Figure 22-16, curve B). Excessive ventricular filling and preload (increased VEDV) stretches the heart muscle beyond optimal length and stroke volume begins to fall. Factors that increase contractility cause the heart to operate on a higher length-tension curve (Figure 22-16, curve A). Factors that decrease contractility (Figure 22-16, curve C) cause the heart to operate at a lower length-tension curve. Figure 22-17 illustrates the relationship between VEDV and stroke volume, cardiac output, and stroke work.

(Huether 563-564)

Front 20

Know what causes mitral regurgitation, mitral stenosis, pulmonary edema & jugular vein distention

Back 20

Mitral regurgitation permits backflow of blood from the left ventricle into the left atrium during ventricular systole, producing a holosystolic (throughout systole) murmur heard best at the apex, which radiates into the back and axilla.

(Huether 615)

Mitral regurgitation has many possible causes, including mitral valve prolapse, rheumatic heart disease, infective endocarditis, MI, connective tissue diseases (Marfan syndrome), and dilated cardiomyopathy.

(Huether 615)

Mitral stenosis impairs the flow of blood from the left atrium to the left ventricle. Mitral stenosis is more common in women and occurs in 40% of individuals with a history of rheumatic heart disease.8 Autoimmunity in response to group A β-hemolytic streptococcal M protein antigens leads to inflammation and scarring of the valvular leaflets. Scarring causes the leaflets to become fibrous and fused, and the chordae tendineae cordis become shortened

(Huether 614)

pulmonary edema:

the accumulation of extravascular fluid in lung tissues and alveoli, caused most commonly by congestive heart failure.

(Mosby 1490)

jugular vein distention: Excessive blood in vein due to causes that interfere with the filling of the right atrium or ventricle. Causes may include: right-sided heart failure, restrictive pericarditis, narrowing/blockage of the superior vena cava, hypervolemia, narrowing (stenosis) of right AV valve.

Front 21

Know the outcomes of the sympathetic, parasympathetic, somatic & Spinal nervous systems

Back 21

Sympathetic

- enhances myocardial performance.

- Stimulation of the SA node

- rapidly increases heart rate

- stimulates the release of norepinephrine or circulating catecholamines interact with β-adrenergic receptors on the cardiac cell membranes.

- causes influx of Ca++

- increases the contractile strength of the heart and increases the speed of electrical impulses through the heart muscle and the nodes.

- dilates the coronary vessels.

Parasympathetic:

- Affects heart through vagus nerve, which releases acetylcholine

- Acetylcholine causes decreased heart rate and slows conduction through AV node

- Acetylcholine also causes coronary vasodilation

Somatic:

Front 22

Know autonomic regulation, somatic regulation, autoregulation & metabolic regulation

Back 22

Autonomic Regulation

Although the coronary vessels themselves contain sympathetic (α- and β-adrenergic) and parasympathetic neural receptors. Despite this blood flow is regulated locally through metabolic autoregulation (overrides neurogenic influence).

Autoregulation (automatic self-regulation) enables individual vessels to regulate blood flow by altering their own arteriolar resistances. Autoregulation in the coronary circulation maintains constant blood flow at perfusion pressures (mean arterial pressure) between 60 and 180 mm Hg, provided that other influencing factors are held constant. Thus autoregulation ensures constant coronary blood flow despite shifts in the perfusion pressure within the stated range.

(Huether 578-579)

The metabolic hypothesis of autoregulation proposes that autoregulation of coronary vessels originates in the myocardium. The stimulus is an increase in the metabolic needs of the myocardium (e.g., because of strenuous exercise). With an increased myocardial oxygen requirement, myocardial cells release substances that promote vasodilation.

(Huether 579)

Front 23

Myogenic regulation of blood vessel diameter and subsequent blood flow through a vessel is an example of _____ of blood vessels.

Back 23

Autoregulation

Front 24

Know how substances pass from capillaries and interstitial fluid

Back 24

High hydrostatic pressures in the capillaries cause vascular fluid to exude into the interstitial space. pg 590, 569

* diffusion through the endotheal cell membrane.

Front 25

Action of Brain Natriuretic Peptide, Atrial Natriuretic Peptide & C-type Natriuretic Peptide Cause of atherosclerosis and role of LDL’s

Back 25

Atrial natriuretic peptide (ANP) is a hormone secreted from cells in the right atrium when right atrial blood pressure increases. ANP increases urine sodium loss, leading to the formation of a large volume of dilute urine that decreases blood volume and blood pressure.

(Huether 576)

Brain natriuretic peptide (BNP) is secreted from cardiac cells and also increases sodium loss from the kidney. It is used both as a marker and as a treatment for acute heart failure.

(Huether 576)

C-type natriuretic peptide (CNP) is found throughout the vascular endothelium and in cardiac, renal, skeletal, and reproductive tissues. It has been found to promote vasodilation, increase cardiac contractility, and inhibit smooth muscle proliferation and vascular remodeling.

(Huether 576)

Atherosclerosis is a form of arteriosclerosis characterized by thickening and hardening of the vessel wall. It is caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a plaque.

Front 26

Know role of norepinephrine, renin-angiotensin-aldosterone, & angiotensin II on myocardium

Back 26

* Renin secreted by kidneys (also found in adrenal cortex, brain, arterial smooth muscle in vascular endothelium, etc) in response to drop in renal perfusion as well as beta-adrenergic stimulation, low plasma potassium concentrations, etc.
* Once in circulation, renin casues conversion of angiotensin I into angiotensin 2
* angiotensin 2 causes increased blood pressure.

Front 27

Describe the difference between a healthy and unhealthy vessel wall

Back 27

Healthy blood vessels are smooth and elastic; An unhealthy vessel wall is characterized by thickening and hardening of the vessel wall, caused by the accumulation of lipid-laden macrophages within the wall (plaque). (Pg 594)

Front 28

Describe Thromboangiitis Obliterans

Back 28

Thromboangiitis obliterans (Buerger disease) is an inflammatory disease of the peripheral arteries. It is strongly associated with smoking, and there is some evidence for a link with severe periodontal disease.39 Thromboangiitis obliterans is characterized by the formation of thrombi filled with inflammatory and immune cells and accompanying vasospasm. Over time, these thrombi become organized and fibrotic and result in permanent occlusion and obliteration of portions of small- and medium-sized arteries in the feet and sometimes in the hands (Huether 593)

Front 29

Difference between inflammation, ischemia, infarction, & necrosis

Back 29

Inflammation – first response to injury: increased size of blood vessels, which causes slower blood velocity and increases blood flow to the injured site, increased vascular permeability (pg. 121)

· Ischemia – a local state in which the cells are temporarily deprived of blood supply; they remain alive but cannot function normally (pg. 597)

· Infarction – persistent ischemia or the complete occlusion of a coronary artery causes the acute coronary syndromes including infarction, or irreversible myocardial damage; infarction constitutes the often-fatal event known as a heart attack (pg. 598)

· Necrosis – cellular death; the sum of cellular changes after local cell death and the process of cellular self-digestion (pg. 85)

Front 30

Greatest risk factor of CAD

Back 30

atherosclerosis

Front 31

Meaning of lab values for HDL, LDL, BNP, ESR, CRP, Troponin, CK, LDH in relationship to CAD

Back 31

HDL= High density lipo-protein. Good cholesterol, does not cause coronary artery disease

LDL= low density lipoprotein, causes macrophages to line the arteries with cholesterol. Would cause CAD

BNP= Brain natriuretic peptide.

In hypertension, increased ANP and BNP levels are linked to an increased risk for ventricular hypertrophy, atherosclerosis, and heart failure.

(Huether 589)

ESR:

The erythrocyte sedimentation rate is a measurement of the rate at which red blood cells sediment in a tube over a prescribed time span (usually an hour). Although increased erythrocyte sedimentation is a nonspecific reaction, it is considered a good indicator of an acute inflammatory response.

(Huether 133)

C-reactive protein (CRP) is a protein mostly synthesized in the liver and is used as an indirect measure of atherosclerotic plaque–related inflammation. An elevated serum level of hs-CRP is correlated with an increased risk for coronary events, but is a nonspecific measure of inflammation and may indicate the presence of other inflammatory conditions.

(Huether 599)

a protein in the striated cell ultrastructure that modulates the interaction between actin and myosin molecules.

(Mosby 1819)

The more damage to the heart = more troponin in the blood.

a blood test used to detect damage to the heart muscle, skeletal muscles, and brain. Serum CK levels are elevated whenever such damage occurs. CK is the main cardiac enzyme studied in patients with heart disease.

(Mosby 456)

lactate dehydrogenase (LDH),

an enzyme that is found in the cytoplasm of almost all body tissues, where its main function is to catalyze the oxidation of l-lactate to pyruvate.

(Mosby 1004)

a LDH blood test used to detect levels of LD, which is widely distributed throughout the body. Disease or injury to body tissues such as the heart, liver, red blood cells, kidneys, skeletal muscles, brain, and lungs will result in higher-than-normal blood levels.

(Mosby 1004)

Front 32

REVIEW ABG : Normal values and their meaning in regards to respiratory & metabolic and alkalosis & acidosis.

Back 32

•Respiratory Acidosis = pCO2 above 45

•Respiratory Alkalosis = pCO2 below 35

•Metabolic Acidosis = HCO3 below 24

•Metabolic Alkalosis = HCO3 above 28