Exam 3: Ventilation And Cardiovascular Function/Dysfunction Flashcards
(128 cards)
1
Q
What are the signs of impaired ventilation?
A
*Confusion
Cyanosis (late sign)
Clubbing (sign of long-term impaired ventilation).
2
Q
What is circumoral cyanosis?
A
Bluish tinge around mouth. Late sign of not enough O2 to tissues.
3
Q
What is clubbing?
A
A compensatory mechanism of the body in finger/toes. The tissues grown larger in the hopes of drawing in more O2.
4
Q
What are early signs of chronic airflow limitation?
A
Easily fatigued (activity intolerance) Pursed lip breathing Dyspnea Chronic cough Barrel chest (COPD) Tripod position breathing Orthopnea
5
Q
Why is pursed lip breathing helpful?
A
It prolongs expiration, which keeps the alveoli open longer (increases CO2-O2 diffusion).
6
Q
Why does chronic air flow limitation lead to chronic cough?
A
Coughing helps to pop open alveoli due to the pressure in the thoracic cavity.
7
Q
Where are the respiratory control centers?
A
The medulla oblongata and the pons.
8
Q
What are the central chemoreceptors?
A
Aka “medullary chemoreceptors”
Primary initiator of Respiratory Rate
Sensitive to CO2 levels and decreased pH.
Tell the respiratory centers to INCREASE respiratory rate when CO2 increases or pH drops. (Allowing the body to blow off CO2 and return to homeostasis).
9
Q
Where are the peripheral chemoreceptors and what do they do? When are they most important to be aware of, clinically?
A
Located in the carotid body (carotid artery) and the aortic body (aortic arch).
Monitor O2 levels in arterial blood. When the O2 level drops, they signal the resp center to increase respiratory RATE and DEPTH.
In COPD patients, drop in O2 at peripheral chemoreceptors is the MAIN stimulus for breathing. Over-oxygenation can slow the breathing too much - even stop the drive to breathe.
10
Q
How do proprioceptors affect respirations? Where are they?
A
Located in muscles and joints.
Monitor activity and O2 use.
Tell respiratory to increase respiratory RATE when use increases.
11
Q
How do nociceptors affect our respiratory rate?
A
Our pain/temp/touch receptors send messages to the resp center to increase our respiratory RATE when stimulated.
12
Q
What does the Herig-Breuer reflex do? Where is it located?
A
Stretch receptors. Located in the lungs.
When they reach full compliance (maximum stretch), tell resp centers to SLOW rate and DECREASE depth.
(Via negative feedback loop).
13
Q
How does surfactant relate to lung compliance?
A
Without surfactant, our alveoli collapse a little bit and our lung tissue loses its elasticity.
After anaesthesia, you will possibly hear “crackles” (alveoli popping back open).
14
Q
Why would an increase in temperature increase respiratory rate?
A
Increase in metabolic activity and dehydration (both associated with higher temps) increase the body’s O2 demand.
The inflammatory response leads to increased lactic acid production, which decreases pH. Faster, deeper breaths blow off more CO2, increasing the body’s pH.
15
Q
What are the basics of blood oxygenation? (Which ventricle is deoxygenated blood pumped from, what is the structure of the alveoli, what is the process of oxygenation?)
A
Deoxygenated blood pumped from the R. Ventricle to the Pulmonary arteries.
Pulm. Arteries become a fine meshwork of arterioles around the alveolar sacs.
Gas exchange happens across the alveoli and the pulmonary arterioles via the process of diffusion.
Oxygenated blood returns to the heart (through the pulm vein) and gets pumped to the rest of the body via the L. Ventricle.
16
Q
What do (alveolar) type I epithelial cells do?
A
They provide structure and shape to the alveoli, allowing them to stay open.
CO2-O2 exchange happens across these cells.
17
Q
What do (alveolar) type II epithelial cells do?
A
Secrete surfactant, which allows for compliance/elasticity of the alveoli.
18
Q
What do (alveolar) resident macrophages do?
A
Allow for immediate defense against pathogens and dust
Help grow new tissue in lungs
Help grow new blood supply in lungs (angiogenesis).
CAN reproduce even when the environment is infected/inflamed.
Fun fact: phagocytize tuberculosis and encapsulate it in a granuloma.
19
Q
About how many hemoglobin molecules does one red blood cell contain? How many ferrous iron discs (Fe2+) per hemoglobin?
A
Approximately 300 hemoglobin molecules per RBC.
4 Ferrous Irons per hemoglobin.
20
Q
Why is it important to know what a patient’s Fe2+ levels are? How does this relate to Nitroglycerin?
A
O2 binds with Fe2+
Nitroglycerin, however, oxidizes Fe2+ to Fe3+, which doesn’t bind to O2 as readily.
Result: worse oxygenation.
If pt is on Nitroglycerin OR sulfonamides (do the same thing) and they are not oxygenating well, look at their Fe2+ levels.
21
Q
How does carbon monoxide affect O2 binding? How will CO poisoning present?
A
Carbon monoxide has a much higher affinity for Fe2+ than O2 does. It prevents O2 from binding to the hgb molecule.
Presents as:
Confusion
Nausea/vomiting
Unconsciousness, then death.
22
Q
What are the pleura and how do they work?
A
Double-layered sac around the lungs.
Separated by serous fluid, which allows for glide and adherence.
23
Q
What are the 4 roles of the pulmonary artery?
A
Bring blood from heart to lungs for gas exchange.
Remove blood clots.
Act as a blood reservoir (500mLs) for the heart.
Make A.C.E in its endothelial cells (for Angio I to Angio II conversion).
24
Q
What are the bronchial arteries? What do they do?
A
Bring oxygenated blood to the lung tissue.
Humidify incoming air
CAN undergo angiogenesis to help keep lung tissue alive during a pulmonary embolism.
25
What are the three things that lung compliance depends on?
Elasticity of lung tissue
Alveolar surface tension
Compliance of the thoracic/chest cage
26
What is Distensibility (related to lungs)?
Ease of inflation.
27
What is stiffness (related to lungs)? What makes lung tissue stiff or not stiff?
Resistance to stretch.
Elastin allows for stretch.
Collagen is not stretchy at all.
Collagen replaces elastin in remodeling due to chronic inflammation - lung disease and pulmonary fibrosis. Permanent loss of elasticity.
Increased fluid in the lungs (like in pulmonary edema) leads to a reversible decrease in elasticity.
28
What does elastic recoil refer to? What common disease results in loss of recoil?
The ability of stretched parts to return to original state/size.
Emphysema results in lungs that are easier to inflate but difficult to deflate due to a loss of elastic recoil.
29
How does surface tension relate to alveolar function?
Surface tension develops between the liquid film and the air of the alveoli. Increased surface tension = increase in inflation difficulty.
30
How does surfactant help with breathing?
Lowers surface tension, making inflation easier.
Keeps alveoli dry inside.
31
What common advice would you give to both post-op patients and immobile patients regarding their breathing?
Breathe Deeply. Increased air volume in lungs spreads the surfactant around.
Shallow breathing from immobility will prevent the spread of surfactant throughout lungs.
Already decreased surfactant (from anaesthesia) will spread more effectively (and sooner) if pt breathes deeply.
32
What factors increase Hemoglobin’s affinity for O2?
- Presence of each O2 molecule on the hgb further increases hgb’s desire to bind.
- alkalinity (increased pH)
- hypocapnia (decreased CO2)
- decreased body temp
(Makes sense because O2 wants to bind to the molecule in conditions where it won’t take it away from cells that need O2).
33
What factors decrease hemoglobin’s affinity for O2?
Acidosis (or decreased pH in tissues)
Hypercapnia (or increased CO2 concentration)
Increased temp/fever
(These make sense because tissues in these conditions need O2 to be released to them quickly).
34
What independent nursing interventions can use use for a patient in respiratory distress?
```
Turning/repositioning (to move around fluid)
Coughing (to increase intrathoracic pressure and open alveoli)
Deep breathing (to increase volume)
```
35
What interventions would a patient with potential hypoxia/acidosis receive? (Both nursing and from a provider)
O2 supplementation
Improve blood flow (movement?)
Bicarb (acid buffer)
Calcium or sodium blockers (not sure of reasoning yet)
36
Do nursing interventions typically promote a right shift or a left shift in the oxyhemoglobin assoc/dissoc curve?
Right shift (helps oxygenate cells)
37
How do oxygen and hemoglobin behave in a right shift?
O2 is more likely to dissociate from hemoglobin
| Promotes tissue oxygenation
38
What independent nursing interventions would help a patient who has a left shift?
```
Warm the patient
Encourage movement (increases CO2 and decreases pH by increasing cellular metabolic activity)
```
39
What is anemia? What two components are referred to in the “title” of different types of anemias?
Decreased oxygen-carrying capacity of the blood.
```
RBC size (macrocytic vs microcytic vs normocytic)
Hemoglobin/iron content (hypochromic vs normochromic)
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40
What are the characteristics of macrocytic-normochromic anemia? What is an example?
Large RBCs with normal hemoglobin/iron content.
The quantity of the RBCs is decreased because of their large size - they tend to die within 50-60 days (instead of 120) because pushing through the capillary bed damages them.
Caused by a B12 or folate deficiency (required by the bone marrow to properly form RBCs).
Example: Pernicious anemia
41
What happens in pernicious anemia? How is it treated?
Parietal cell injury in the stomach (due to autoimmune disorder or a gastric ulcer) prevents the production of INTRINSIC FACTOR.
Intrinsic factor is supposed to attach to B12, forming a complex that allows it to be absorbed by microvilli during digestion. Then it travels to the bone marrow to be used for red blood cell formation.
In pernicious anemia, B12 gets excreted in the stool. Results in a deficiency and abnormal RBCs. Can be treated by B12 injections.
42
What is microcytic-hypochromic anemia? What does it result from? How is it diagnosed?
Small RBCs and low iron.
RBCs are pulled out of the bone marrow when they are too young.
Insufficient dietary intake of iron can cause this.
Low iron results in RBCs leaving the bone marrow with too little iron to carry O2 in the blood.
Lab values of less than 12 g/dL, but symptoms probably won’t appear until 7-8 g/dL.
Can also test CBC and serum iron levels.
43
What kind of iron do you want to make for good hemoglobin production?
Ferrous iron (Fe2+)
(Ferric iron, Fe3+, will not produce hemoglobin well).
44
What are normal hemoglobin and hematocrit levels?
Normal hemoglobin: 12-18 g/dL
Normal hematocrit: 35-50%
45
What are the symptoms of all anemias?
Fatigue
Weakness
Shortness of breath
Paleness (especially in conjunctiva)
46
What are the three types of atelectasis and what is the common characteristic they all share?
Compression
Absorption
Surfactant
All are characterized by collapsed alveoli.
47
What are the symptoms of atelectasis?
```
Cough
Dyspnea
Decreased SpO2
Tachypnea
Tachycardia
Decreased breath sounds
Accessory muscle usage
Change in level of consciousness
Cyanosis
```
48
What causes compression atelectasis? How do you treat it and/or prevent it?
Alveoli shrink due to disuse from pressure on the pleural space (high BMI puts pressure on the lungs; immobility = inability to take full, deep breaths).
Both treatment AND prevention: Incentive spirometer (inhalation) - breathing in and holding the ball at a particular space exercises the alveoli, opens the airway and improves oxygenation.
49
What is absorption atelectasis? How do you prevent it? How would you notice it?
Caused by high flow O2 for too long (10 L/m for 1-2 days). The ratio of nitrogen to oxygen in room air is what keeps the alveoli open. (N=78%).
Prevent with incentive spirometer.
Pt would present with a drop in O2 and crackles.
50
What is surfactant impairment?
Collapsed alveoli and pulmonary edema because of reduced surfactant and inability to keep the alveoli.
Be aware of this for post-op patients.
Some will also be on high-flow O2 and already at risk for absorption atelectasis.
51
What is pneumonia? What are its causes, what symptoms will present and what are nursing interventions?
Inflammation in the lower respiratory regions.
Bacterial, viral, ventilator-associated nosocomial/HAI
Colored Sputum differentiates this from other resp problems.
Plus, Fever, productive cough, dyspnea, crackles on INHALATION, pleural pain.
Independent Nursing interventions: Move, turn, cough, breathe deeply.
Dependent: Incentive spirometer, antibiotics.
52
What is Pulmonary edema? What causes it? What are the symptoms? What medications can help it?
Excess (non-mucous) fluid in lungs that mostly accumulates outside the alveoli. Looks frothy and whitish or clear.
Primary cause is Left Ventricular heart failure.
The thickened intraventricular radius leads to decreased stroke volume, which increases preload.
Excess preload backs up to lungs.
The back pressure is higher than the ability of albumin/oncotic pressure to keep the lungs dry.
```
Symptoms:
Dyspnea
Increased work of breathing (WOB)
Inspiratory crackles
Pink/clear/white frothy sputum
Tripod position
Confusion
Cyanosis
```
Treatment goal: decrease preload and afterload.
- A.C.E. Inhibitors
- ARBs
- Diuretics
53
What are A.C.E. Inhibitors? In what conditions would you use them?
They prevent the conversion of Angio I to Angio II by preventing ACE production in the lungs.
- inhibits preload by decreasing water retention
- inhibits afterload by decreasing vasoconstriction
54
What are ARBs? How do they work?
Angiotensin Receptor Blockers. Prevent Angio II from attaching to post pituitary and endothelial cells.
Inhibit preload by decreasing water retention
Inhibit afterload by decreasing vasoconstriction
55
What is a pulmonary embolism? What causes it? What are its symptoms? What are some treatments?
Obstruction of the pulmonary vessel
#1 cause is DVT (deep vein thrombosis), but can also be caused by hypercoagulation.
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Symptoms:
JVD on both sides
Hemoptisis (coughing up blood)
Chest pain at one spot in the lung
Anxiety, Headache
Tachypnea
Hypotension
Obstructive shock then death.
```
Treatments: thrombectomy, anticoagulants, fibinolytics.
56
What are risk factors for deep vein thrombosis? What are preventions?
Risk factors:
- Anything that inhibits venous return or impairs circulation
- Immobility
- hypercoagulation/elevated hematocrit (polycythemia)
- excess glucose in blood (thickens it)
- floppy venous valves (you’d see excessive varicose veins)
Prevention:
-ROM exercises to increase venous return (immobile or post-op)
-Hydration, blood thinners, transfusions (hypercythemia/hypercoagulation)
-
57
What is a pneumothorax? What are the 3 different types? What causes it? How does it present?
Air or gas in the pleural space
Suction on the lung occurs and it collapses in on itself.
```
Spontaneous (usually in tall, white adolescents in a rapid growth phase).
Traumatic
Tension (air comes in but doesn’t go out. Pressure on heart & trachea. Hypotension, decreased preload and tracheal shift.)
```
Symptoms:
Pain
Dyspnea
Decreased breath sounds.
(Tension pneumothorax ONLY will have tracheal shift and decreased BP).
58
Acute Respiratory Failure - primary cause, effects and symptoms? Treatments?
Alveolar flooding occurs as a result of severe pulmonary edema
#1 cause: Sepsis
Degranulation of mast cells in EVERY vascular space, including the arterioles around the alveoli.
Albumin accumulates inside the alveoli and causes protein-rich edema, pulling fluid inside the vascular space.
This fluid prevents gas exchange d/t the fluid between the alveolus and the vascular space.
```
Symptoms:
Excessive dyspnea
Excessive hypoxemia
Hypotension with decreased cardiac output
Acidosis
```
Treatments: Antibiotics, mechanical ventilator
59
What is COPD? What are the two primary manifestations? What are the symptoms?
Airflow limitations, usually on expiration, that get progressively worse.
Emphysema
Chronic bronchitis
(These can occur simultaneously)
Symptoms:
- hypercapnia (CO2 is trapped)
- difficulty exhaling
- chronic acidosis
- bronchial edema (chronic bronchitis)
- hypersecretion of mucus (chronic bronchitis)
- alveolar inflammation with loss of elasticity (emphysema)
60
What happens in emphysema?
The alveoli lose their elasticity, becoming flaccid and weak.
Air easily enters, but they have trouble with recoil and can’t release CO2.
There is also a loss of surface area for gas exchange.
61
What happens in chronic bronchitis?
Chronic macrophage activity causes remodeling of the inside of the bronchial tube.
Thickening and Bronchial constriction result.
This traps CO2 and causes excess mucus production.
62
What is asthma? What causes it? What are the symptoms and long term effects?
Chronic, recurring episodes of bronchospasm, d/t a hypersensitivity reaction of the bronchial mucosa, usually an allergic response.
Allergic inflammatory response (acute) results in:
- increase in capillary permeability
- edema in the lung tissue
- excess mucus/mucus plugs
Chronic episodes lead to:
- fibrosis and airway modeling
- narrowing of bronchi (permanent)
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Presents with:
Wheezing
Mucous production
Inflammation
Dyspnea
```
(Tx: nebulizers)
63
A patient presents with fatigue, weakness, dyspnea and paleness of the conjunctiva. What do you suspect? What would you test for?
Anemia
Test for B12 levels and maybe B9 levels (pernicious)
Test for Hgb & Hematocrit & serum iron (micrycytic hypochromic)
64
A patient presents with cough, complains of shortness of breath, increased heart and respiratory rate. SpO2 is decreased, patient is irritable and you hear decreased breath sounds with some crackles. What do you suspect? What do you do?
Atelectasis.
Incentive spirometer
Encourage cough (open alveoli)
Encourage deep breathing (move around surfactant).
65
A patient presents with fever, pain, dyspnea and a productive cough. They tell you their sputum is yellowish-green. You hear crackles on inspiration. What do you suspect? What do you do?
Pneumonia
```
Antibiotics
Incentive spirometer
Mobility
Turning (move fluid)
Cough (open alveoli)
Deep Breathing (increase volume)
```
66
A patient presents with difficulty breathing, crackles on inspiration, frothy clear sputum. The patient seems irritable and is sitting in the tripod position. What do you suspect? What do you do?
Pulmonary edema
Best treatments are all dependent:
ACE inhibitors
ARBs
Diuretics
(Decrease preload and afterload)
67
A patient presents with JVD, chest pain, a headache, and complains of coughing up blood. You take the blood pressure and it is low, as is the heart rate. What do you suspect? What do you do?
Pulmonary embolism.
Get to doctor asap! - thrombectomy, anticoagulants, fibrolytics needed to break up or remove the clot.
68
A patient complains of sudden and intense pain in the chest and difficulty breathing. You have a hard time hearing sounds on one side. What do you suspect?
Pneumothorax.
69
A patient who has had an indwelling urinary catheter suddenly presents with extreme respiratory distress, confusion and combativeness, and low blood pressure. What do you suspect?
Acute respiratory failure d/t sepsis
Treatment: antiobiotics, mechanical ventilator
70
A patient complains of difficulty when breathing out and she has a chronic cough. Her sputum is normal colored. What do you suspect?
COPD - probably chronic bronchitis.
Would check SpO2 and CO2 levels - would anticipate hypercapnia.
71
A patient arrives in the ED with severe respiratory distress and wheezing. What do you suspect?
Asthma
72
What are the long-term risks of asthma?
Chronic inflammatory response leads to airway remodeling and narrowing of the bronchi.
73
How does oncotic pressure relate to pulmonary edema and acute respiratory failure?
Pulmonary edema: back pressure (from backflow) from the L ventricle to the pulmonary vascular system overrides the oncotic pressure of the albumin in the vascular space that usually keeps the lungs dry.
Respiratory failure: septic/histamine response allows albumin into the alveolar space and fluid follows.
74
A patient who has just come out of surgery has difficulty breathing, and when you listen to her lungs you hear crackles. What do you suspect? What do you do?
Surfactant impairment atelectasis
And, possibly absorption atelectasis as well, if she’s on high-flow O2.
Use an incentive spirometer
Encourage her to turn, cough, and breathe deeply.
75
What are normal lab values for Potassium?
3.5-5.0
76
What are normal lab values for Sodium?
135-145
77
What are normal lab values for serum calcium?
8.6-10.2
78
What is the body’s normal pH range?
7.35 to 7.45
79
During the action potential, what happens with the influx of Calcium?
Calcium channels open at the peak of the AP. Calcium enters, causes a plateau to occur. In myocytes (cardiac and skeletal), the cell then stores the calcium in the sarcoplasmic reticulum.
80
What happens to excitable cells with hyperkalemia values of 5.3-6.0? What’s the first thing that will happen to the EKG?
```
RMP is closer to threshold
Faster depolarization (d/t closeness to threshold)
Faster repolarization (d/t excess K+ rushing in)
```
EKG will show a peaked T-wave (after the QRS complex).
81
What happens to excitable cells with hyperkalemia K+ values at 6.0-7.0? What will you see in the EKG?
RMP is almost level with threshold.
EKG SLOWS down (sodium-gated channels open, cells lose)
Total cardiac block and stop can occur
EKG: Wide, low p-wave, Wide QRS complex, long T-wave.
82
How will excitable cells respond to low Ca++ levels in the blood? Why?
Similar to hyperkalemia
Faster/more APs
Faster depolarization and repolarization
Reason: Ca++ no longer lining channels enough to prevent Na+ from entering.
83
What nerve innervates the SA node?
Cranial Nerve 10
| Vagus nerve
84
What is the SA node?
Heart’s primary pacemaker - sets and maintains the rate.
60-100bpm.
85
What part of the EKG corresponds with the SA node? What else does this signify?
P-wave
| Signifies atrial depolarization
86
How do you know if you’re looking at a sinus rhythm?
If there is a p-wave
| P-wave = SA node starting the beat & atrial depolarization
87
What does the AV node do?
Signals the bundle of His after receiving signal from the SA node, causing the Purjinke fibers to stimulate ventricular contraction.
88
What do the QRS complex and T-wave correspond to?
QRS complex: ventricular depolarization
(Atrial repolarization hidden in here)
T-wave: ventricular repolarization
89
What happens if the SA node stops working? What will you see on the EKG?
The AV node will work as a backup, with a BPM of 45-50.
EKG will show NO p-wave
Instead, there will be a PVC - preventricular contraction.
90
What roles do Actin, Myosin and Troponin play in muscle contractions?
Actin & Myosin slide together to shorten/contract muscle
Troponin facilitates by binding with calcium and cross-bridging between myosin and actin.
91
What do we need to know about Troponin (especially Troponin-1)?
Troponin 1 is a protein from the phospholipid bilayer of myocytes.
Found in greater quantities in heart muscle.
Cell death (like in MIs) releases Troponin 1 into bloodstream.
Bloodstream levels of Troponin 1 tell you how bad an MI is/was.
Shows up at 3 hours, 1st peak at 5 hours, 2nd peak at 10 hours.
92
What are the stroke volumes of a normal person vs someone with left ventricular hypertrophy?
Normal: 60-80 mL/stroke
L. Ventricular hypertrophy: 25-40mL/stroke.
93
What is the primary cause of left ventricular hypertrophy?
Chronic increased afterload from atherosclerosis (plaque in arteries).
94
What symptoms are associated with L. Ventricular heart failure?
Excess fluid (due to RAAS activation from low bp/volume).
- peripheral dependent edema (ankles, legs, sacrum)
- pleural effusion (AROUND lungs)
- pulmonary edema (IN lungs)
Vasoconstriction of peripheral arteries
Oliguria
95
What is the RAAS supposed to compensate for? What does it do to heart conditions?
RAAS is supposed to compensate for shock/low blood volume.
It worsens heart conditions by increasing blood volume and vascular resistance.
96
Why do we give heart patients ARBs and ACE inhibitors?
To prevent/slow down the effects of the RAAS.
(ARB - angiotensin receptor blockers - so Angio II doesn’t act on post-pit and kidneys)
(ACE inhibitors - so Angio II is never made from Angio I)
97
What do we know about Parasympathetic control of the heart?
PNS control is “cholinergic” (uses acetylcholine as the primary NT).
Slows heart rate, AV node conduction, and causes coronary vasodilation.
Uses Vagal nerve/CN X to receive/conduct signals.
Vagal nerve stimulation (carotid/aortic baroreceptors) creates bradycardia. (Valsalva maneuver, carotid massage, trendelenberg).
98
Why is carotid massage or the valsalva maneuver dangerous for those with ventricular heart failure?
This pt already has decreased cardiac output.
Overstimulation of vagal nerve will override nodes, inhibit ventricular contractions and further decrease cardiac output.
99
What is the hormone cascade for SNS control of the heart?
SNS stimulation: Thalamus -> hypothalamus: “release ACTH” (adrenocorticotropic hormone).
ACTH -> adrenal glands: “release epinephrine & norepinephrine” (catecholamines)
100
What does Epinephrine do to the heart? Airways?
Attaches to Beta receptors in heart
-increases rate (chronotropic activity)
-increases strength of contractions (inotropic activity)
(This happens b/c it increases calcium influx during APs, which shortens the refractory period between beats).
-Vasodilates coronary blood vessels.
Vasodilates upper airways
101
Why doesn’t norepinephrine vasoconstrict heart vessels?
There are very few alpha receptors in the heart.
102
What does norepinephrine do?
Attaches to alpha receptors
Causes vasoconstriction of renal, intestinal and peripheral arteries
-activates the RAAS and improves vascular volume.
103
What role does the stress response play in heart attacks?
Stress response releases epinephrine,
Heart cells surrounding damage are already working harder
The inflammatory response that ensues is going to damage even more cells.
Add epinephrine and norepinephrine and you’re making the heart work harder and faster and increasing your afterload and volume.
Anyone in an active MI, calm the best you can.
104
What are arrhythmia and dysrhythmias? Where do they originate? What kind are the most dangerous?
Disorders of cardiac rhythm.
Can be from the SA or AV nodes - supraventricular, or
Ventricular (most dangerous)
105
What are causes of dysrhythmias and arrhythmias?
Anything making membranes hyperexcitable
-electrolyte imbalance (Na, K, Ca)
Ischemia to heart cells
Acidosis
ANS dysfunction
-PNS activation supersedes SNS activation - Neurogenic shock
106
Why would Chron’s disease or dehydration lead to dysrythmias?
Inability to absorb ions (Chron’s) or ion imbalance in bloodstream (severe dehydration) = electrolyte disturbance = AP problems at heart.
107
What is the primary reason for neurogenic shock? What is the result, systemically?
Closed head injury
PNS becomes more activated than SNS
-Damage to Thalamus = no ACTH from hypothalamus = no epinephrine/norepinephrine release
Result: Decreased heart rate, decreased cardiac output. Hypoperfusion with vasodilation.
108
What is heart block? What can cause it?
Signal between the SA and AV nodes is blocked. Will show up as missing impulses on the EKG.
Causes:
- ischemia to that part of the heart (R atrium)
- Acidosis at or below 7.0 pH
- Severe hyperkalemia
Potentially fatal.
109
What is an Ectopic Pacemakes? What causes it?
Instead of the SA node setting the beat, a hyperexcitable group of cells below the AV node (in the ventricles) initiates the beat.
Shows up as a PVC/premature ventricular complex
Causes:
Acidosis
Electrolyte imbalance
110
What is fibrillation? What causes it? What can happen to the patient? How can you mitigate these risks?
Uncoordinated, random signals in the heart - ends up as quivering. Can be atrial or ventricular.
Causes:
Ischemia or decreased blood flow leading to necrosis (especially around the SA node). (Can make the SA node hyperexcitable and prevent QRS signaling).
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Effects:
Hypercoagulatory state (like ice cream maker) = embolism risk
Pulmonary edema (blood regurgitated back into the pulmonary space)
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Give patient anticoagulants
Hydrate patient
111
Which valves are associated with S1?
Tricuspid and Mitral
112
Which valves are associated with S2?
Pulmonic and Aortic valves
113
What is valve regurgitation? What can cause it? What can it do to the patient?
Valve prolapse causes leakage/regurgitation of blood into the space it just came from.
Caused by:
Overwork (excessive afterload over time)
A congenital birth defect
Patient effects:
- Decreased cardiac output (due to increased preload)
- Stetched myocardium (leads to cardiac remodeling) due to increased preload.
114
What is valve stenosis? What causes it? What happens to the patient?
Thickened, stiff, fibrotic and/or non-compliant valves. Tend to be on the L side of the heart (like Aortic valve stenosis).
Causes:
- aging
- calcium deposits
- chronic macrophage activity
- hyperparathyroidism (results in excess serum calcium)
Effects on patient:
Hypertrophy of the L. Ventricle, which means decreased cardiac output.
115
What is ventricular failure? What is one symptom that presents?
Heart can’t push out the blood it needs to in order to supply the body.
Excess pressure on the pulmonic and aortic valves result in an S3 sound.
116
What is arteriosclerosis and what causes it? What are its effects?
Stiff, non compliant arteries due to calcium deposits in vessel walls.
Causes:
-Decreased NO production due to damage to endothelial cells
AGES or ROS damage - diabetes increases risk
Calcium deposits in vessel walls -hyperparathyroidism increases risk
Age -atrophy/declining function
Effects:
HTN
Tissue Damage (from a Map over 110 - damages endothelial cells further, further decreases NO production)
117
Differentiate between stage I and stage II hypertension
Stage 1: Systolic 120-139, Diastolic 80-89.
Stage 2: Systolic 140+, Diastolic 90+.
118
What are some causes of hypertension?
AGES -> endothelial cell damage = decreased NO = decreased compliance
Chronic Angio II release
Adrenal gland tumors -> increased Aldosterone release (Na+ retention)
Arteriosclerosis
Atherosclerosis
119
What is Atherosclerosis? What causes it? What are its effects?
LDLs enter the intima/intimal layer of the blood vessels
Too many LDLs in the intima will make the mast cells release histamine and chemotactic factors.
-monocytes arrive, eat LDLs, become macrophages, become “fat-filled foam cells”.
Then, they sit in the intimal layer and GROW
- release cytokines
- promote angiogenesis and collagen formation
These create resistance and increase afterload
Effects:
-L. Ventricular hypertrophy, which can lead to L. Heart failure.
120
What are the four proteins that we might track in lab values to evaluate cardiac muscle damage?
Troponin I (most specific to heart muscle)
Troponin T (mildly specific)
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Myoglobin (less specific)
Creatinine kinase (less specific)
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As inflammatory process and tissue death progresses, these values (especially Troponin I) will continue to rise.
121
What is a myocardial infarction? What causes it? What are the symptoms?
Oxygen delivery to the myocardium is not sufficient to meet metabolic demands.
Can be caused by:
- thickening
- clot
- ischemia (decreased blood flow)
- hypoxemia (decreased o2)
- infarction (trickle of blood or total occlusion)
Symptoms:
- Acidosis
- Pain (especially radiating to arm - dermatome pattern)
- Electrolyte imbalance (hypoxic cell injury will lead to increase in potassium, which will cause more injury)
122
What happens during an MI on a cellular level? What are our primary goals? How can we achieve them?
8-10 seconds of insufficient O2 to cells will create a hypoxic cascade.
Results:
Anaerobic metabolism in cells
Glycolysis
High blood glucose levels. (Liver releases glycogen during hypoxic cell injury and/or stress response).
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Primary Goal:
Decrease preload/volume
-prevent pulmonary edema
-decrease workload for heart
Decrease afterload
-decrease workload for heart
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Treatment:
- Give insulin (to deal with glucose in bloodstream)
- Diuretics (to decrease volume/preload)
- NPO
- ACE Inhibitors & ARBs (decrease volume/preload and vasconstriction/afterload)
- Decrease environmental stimuli (decrease afterload)
- Give nitroglycerin (vasodilation - mimics NO - decreases afterload)
- Loosen tight clothing (socks, compression stockings, etc) (decrease afterload).
123
What happens after an MI, both on a cellular and a systemic level? What are our goals?
The still-functional tissue has to work harder to perfuse the rest of the body - undergoes hypertrophy.
Ventricular muscle contractility is weaker, which means stroke volume is decreased.
Body activates the RAAS because of decreased fluid volume
Body activates epinephrine/norepinephrine because of stress response.
Post-MI goals are to decrease cardiac workload by decreasing preload and afterload.
124
What is a normal ejection fraction? What is the ejection fraction of someone with heart failure? What does this result in?
EF Normal: 60-75%
EF Heart failure: less than 40%
Means that 60% is still left in ventricles, which means excess preload.
This will likely result in pulmonary edema.
125
What happens with chronically overstretched cardiac muscle cells?
They don’t snap back well, are weaker.
This causes increased ventricular wall tension, which increases oxygen demand.
Negative inotropes (medication) will decrease the contractility of the heart.
126
What are the symptoms/effects of Right-Sided Heart failure?
Backup on the venous side
- edema/congestion of peripheral tissues
- If severe, ascites (edema in peritoneal space)
- edema/congestion in GI tract
- weight loss
- anorexia (loss of appetite)
- GI distress
- Liver congestion
- easy bruising and bleeding (decrease in clotting factors)
- buildup of toxins in bloodstream (creatinine and ammonia)
- Oliguria
127
What are the symptoms/effects of Left-sided heart failure?
Backup/regurgitation into the lungs
Pulmonary edema/congestion
-Orthopnea
-white or pink frothy sputum
Impaired gas exchange (d/t fluid in the lungs)
-signs of hypoxia
Decreased Cardiac Output
-hypotension
-activity intolerance (fatigue readily)
-poor tissue perfusion (decrease in pedal pulse strength).
128
What is a classic sign of MIs in EKG readings? Why?
S-T elevation
Excess calcium enters the cell (with sodium), prolonging the AP and keeping K+ on the outside)
Tells you that the delivery of O2 & Glucose is decreased to heart cells.
