Adult Circulatory Flashcards

1
Q

Describe the different kinds of Acute Coronary Syndrome
Stable angina
Unstable angina
Non-ST elevation MI (NSTEMI)
ST elevation MI (STEMI)

A
  • Stable angina: chest pain or discomfort that is associated with physical activity
  • Unstable angina: chest pain that can occur at rest, can be a precursor to an MI
  • Non-ST elevation MI (NSTEMI): Partial occlusion of a major coronary vessel or complete occlusion of a minor coronary vessel causing reversible partial thickness heart muscle damage. EKG reveals ST depressions or T wave inversions without Q waves. Usually accompanied by elevated cardiac markers.
  • ST elevation MI (STEMI): Complete occlusion of a major coronary vessel resulting in irreversible full thickness heart muscle damage. EKG reveals ST elevationsAccompanied by elevated cardiac markers
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2
Q

Pathophysiology of Acute Coronary Syndrome

A
  • The development of any acute coronary syndrome begins with the rupture or erosion of plaque - an unstable and lipid-rich substance.
  • The rupture results results in platelet adhesions, fibrin clot formation, and activation of thrombin.
  • An acute coronary syndrome most commonly results when a thrombus progresses and occludes blood flow.
  • The effect is an imbalance in myocardial oxygen supply and demand.
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3
Q

Risk Factors of Acute Coronary Syndrome

A

Non-modifiable
- Male gender
- Postmenopausal female
- Family history
Modifiable
- Smoking
- Obesity
- High fat, high carbohydrate diet
- Sedentary lifestyle
- Hypertension
- Type II diabetes

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4
Q

Mrs. Dixon is a 62-year-old female in
the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country. VS:
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
What should you ask Mrs Dixon?

A
  • How long have you had symptoms?
  • Do you have chest pain? Location?Quality? Scale from 1-10? Duration?
  • Nausea and/or vomiting?
  • Medical/surgical history?
  • Family history?
  • Do you smoke?
  • Are you taking any medications?

Symptoms: 3-4 days
No chest pain
No vomiting, occasional nausea
History of iron-deficiency anemia, C-section X 2 & appendectomy
She does not smoke
She is not taking any medications
Father had coronary artery disease and had an MI at age 59
Women with MI: fatigue, diaphoresis, indigestion, arm or shoulder pain, nausea, and vomiting.

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5
Q

Mrs. Dixon is a 62-year-old female in
the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country. VS:
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
No chest pain
No vomiting, occasional nausea
History of iron-deficiency anemia, C-section X 2 & appendectomy
She does not smoke
She is not taking any medications
Father had coronary artery disease and had an MI at age 59
What are your priority assessments?

A
  • Mental Status: A&O x 3, a little anxious
  • Skin (look for perfusion): Cool, moist
    Decreased pulses and cold, clammy, pale skin are signs of inadequate tissue perfusion and inadequate CO. Activation of the sympathetic system with low CO will stimulate diaphoresis.
  • Respiratory: Regular and unlabored, breath sounds clear
  • Vital signs: Stable
  • Pulses: Strong and regular
  • Heart sounds: Regular S1, S2;
    no murmurs
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6
Q

Mrs. Dixon is a 62-year-old female in
the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing significantly wrong before leaving the country. VS:
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
What orders do you anticipate?

A
  • You place her on telemetry monitoring
  • Oxygen 2 L/min via NC
  • 12-lead EKG: shows ST depression on inferolateral leads (Left Coronary Artery)
  • CXR
  • ABG
  • Complete blood count (CBC)
  • Comprehensive metabolic panel (CMP)
  • Lipid panel
  • Cardiac enzymes
    *Troponin I & Troponin T
    *CK and CK-MB
    *Myoglobin
  • Lipid panel
  • Coagulation studies (in case she needs anticoagulants)
    *Prothrombin time (PT)
    *Partial thromboplastin time (PTT)
    *International normalized ratio
  • IV access (to get meds to her quickly)
    *Can also do an echo or coronary angiography
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7
Q

Mrs. Dixon is a 62-year-old female in the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing significantly wrong before leaving the country.
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
EKG reveals NSTEMI. How do you explain her symptoms?

A

Men and women have different kinds of symptoms when it comes to MI
MEN
- Burning
- Squeezing
- Crushing tightness in the substernal chest that may radiate to the left arm, neck, jaw, or shoulder blade
WOMEN
- Atypical chest pain
- Vague or a lack of chest pain
- More likely to experience a toothache or pain in the arm, shoulder jaw, neck or throat, back, breast or stomach
- Fatigue
- SOB

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8
Q

Mrs. Dixon is a 62-year-old female in the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country.
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
EKG reveals NSTEMI.
You receive several stat orders, what do you anticipate these to be?

A

“MONA”
- Morphine: control pain and relax coronary arteries, improving blood flow
- Oxygen: heart needs oxygen
- Nitroglycerin: dilates coronary arteries, increasing blood supply to the heart in an attempt to limit myocardial muscle damage and control pain. One tablet may be administered gradually every 5 minutes for a maximum of three doses as long as the patient maintains adequate BP. If pain is not controlled with three doses, IV Nitroglycerin will be started.
- Aspirin: helps prevent platelets from enlarging the existing clot or new clots from forming
- Beta-blockers (Metoprolol): decrease myocardial workload and myocardial oxygen demand, limiting extension of injury. Not to be used with a right coronary artery MI with bradycardia!
- Heparin drip: Prevent new clot formation
- Consult cardiology

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9
Q

Mrs. Dixon has a NSTEMI. Labs:
WBC: 4,000 – 10,000 uL; 5,000
Hemoglobin: 12.0 – 17.0 g/dL; 11.2 L
Hematocrit: 36.0 – 51.0%; 34.1 L
RBC: 4.2 – 5.9 cells/L; 3.80 L
Platelets: 150,000 – 350,000 uL; 245,000
Calcium: 9 – 10.5 g/dL; 9
Chloride: 98 – 106 mEq/L; 98
Magnesium: 1.5 – 2.4 mEq/L; 2.0
Phosphorus 3.0 – 4.5 mg/dL; 3.1
Potassium 3.5 – 5.0 mEq/L; 3.5
Glucose 70 – 100 mg/dL ;112 H
BUN 8 – 20 mg/dL; 20
Creatinine 0.7 – 1.3 mg/dL; 1.0
Creatine Kinase 30 – 170 U/L; 384 H
CK-MB 3–5 %; 7 % H
Cholesterol < 200 mg/dL; 268 H
Triglycerides < 150 mg/dL; 298 H
Troponin I < 0.5 ng/mL; 0.12 H
Troponin T < 10 ng/mL; 15 H
Myoglobin < 170 ng/mL; 203 H
PT 11 – 12.5 seconds; 11.5
INR 0.8 – 1.1; 0.8
aPTT 25 – 35 seconds; 32
What is significant about these labs?

A

All cardiac enzymes are elevated
- Evidence of myocardial ischemia
All values are elevated in the lipid profile
- Most cases are secondary to atherosclerosis
- Growth of cholesterol plaques slowly block blood flow in arteries
- Rupture of plaques results in thrombus formation and obstruction of coronary artery flow
H&H slightly low
- History of iron-deficiency anemia
- Not taking medications
- Possible decreased iron-binding capacity

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10
Q

Mrs. Dixon has an NSTEMI. You have started a 20 gauge IV in Mrs. Dixon’s left hand. The ER physician orders 25,000 units of heparin in 500 mL NS to infuse at 1,000 unit/hr. At what rate should the pump be set?

A

20 mL/hr

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11
Q

Mrs. Dixon is a 62-year-old female in
the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country.
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
EKG reveals an NSTEMI
Is she a candidate for fibrinolytic therapy (tPA)? Why not?

A
  • Symptoms must be present for less than 12 hours
  • Best outcomes occur in those treated in 1-2 hours
  • Fibrinolysis is not effective for treatment of a MI without ST segment elevation (NSTEMI)
  • Mrs. Dixon has an NSTEMI and has had symptoms for 3-4 days
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12
Q

Mrs. Dixon is a 62-year-old female in the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country.
BP: 140/82
PULSE: 84
RR: 16
O2 SAT: 97% RA
TEMP: 98.2 F
EKG reveals an NSTEMI.
The cardiologist arrives within 30 minutes and has elected to take the pt to the cardiac cath lab for percutaneous coronary intervention. Why is the timing significant?
What happens in the percutaneous coronary intervention?

A
  • Door-to-balloon time is a key performance quality metric in the treatment of MI.
  • The American Heart Association’s guidelines recommends that the artery be reopened within 90 minutes for best outcomes.
  • Remember: door to balloon – 90 minutes!
  • Balloon angioplasty is performed using a thin tube called a catheter, with a small deflated balloon at its tip. The catheter is inserted into a large artery in the leg or via the radial artery in the forearm, and then carefully guided to the blocked portion of the artery. The balloon is then inflated to push the accumulated plaque against the walls of the artery, restoring normal blood flow to the heart muscles.
  • Pt must lay down 2-6 hours afterward
  • Coronary artery stenting, a small wire mesh, is often used to prevent the blocked artery from re-narrowing after a balloon angioplasty.
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13
Q

Mrs. Dixon is a 62-year-old female in
the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country. EKG reveals an NSTEMI.
The cardiologist arrives within 30 minutes and has elected to take the pt to the cardiac cath lab for percutaneous coronary intervention. It is successful and she is discharged home.
What medications do you anticipate at discharge?

A

Aspirin 81 mg or 325 mg daily
- Inhibits clotting mechanisms within the clotting cascade or prevents platelet aggregation; used for unstable angina, acute myocardial infarction, and coronary interventions.
Plavix 75 mg daily
- Inhibits clotting mechanisms within the clotting cascade or prevents platelet aggregation; used for unstable angina, acute myocardial infarction, and coronary interventions.
Lisinopril 10 mg daily (ACEI)
- Prevents the conversion of AI to AII, resulting in lower levels of AII, which causes an increase in plasma renin activity and a reduction of aldosterone secretion; also inhibits the remodeling process after myocardial injury.
Metoprolol 25 mg daily
- Results in decreased SNS response such as decreased heart rate, blood pressure, and cardiac contractility;
Atorvastatin 80 mg daily
- To lower lipid levels
NTG SL 0.4 mg PRN
- Directly relaxes smooth muscle, causing vasodilation of the systemic vasculature bed; decreases myocardial oxygen demands; secondary effect is vasodilation of responsive coronary arteries
Stool softeners (Docusate sodium)
- We don’t want her to be straining
Iron sulfate?
- For her anemia, need to increase binding sites for O2

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14
Q

Mrs. Dixon is a 62-year-old female in the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing significantly wrong before leaving the country. EKG reveals an NSTEMI.
The cardiologist arrives within 30 minutes and has elected to take the pt to the cardiac cath lab for percutaneous coronary intervention. It is successful and she is discharged home.
What are priority discharge instructions/teaching for Mrs. Dixon?

A
  • Regular follow-up with cardiologist or PCP
  • Purpose, dose, and side effects of medications
  • Cardiac rehabilitation including progressive exercise
  • Immediately report signs and symptoms of MI such as chest pain and chest discomfort or increased shortness of breath.
  • Diet low in cholesterol and sodium, high in fiber (breaks down fat)
  • Healthy weight
  • Smoking cessation if pt smokes
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15
Q

Mrs. Dixon is a 62-year-old female in the emergency department for “achiness” in the elbows that is atypical and worsening over the last 3 - 4 days. She says that the feeling awakens her in the middle of the night. Mrs. Dixon complains of increased fatigue, shortness of breath, and stress at work. She and her husband have a cruise planned in a couple of days and wants to confirm that there is nothing
significantly wrong before leaving the country. EKG reveals an NSTEMI.
The cardiologist arrives within 30 minutes and has elected to take the pt to the cardiac cath lab for percutaneous coronary intervention. What would an alternative treatment be if PCI was not possible or she had extensive multivessel disease?

A

Coronary artery bypass grafting (CABG)
* Surgical revascularization intervention that bypasses blockages in the coronary arteries causing the myocardial muscle damage.
* Indications for CABG include unsuccessful PCI or not a candidate for PCI, failure of medical management, or critical left main or three vessel disease.
* During CABG, a healthy artery or vein, typically the internal thoracic (mammary) artery or saphenous vein, is grafted to the blocked coronary artery. One end is attached to the aorta, with the other end attached to the blocked coronary distal to the occlusion, thereby bypassing the blocked portion of the artery allowing blood flow to the cardiac tissue.

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16
Q

Valvular Heart Disease
3 Types: Pathophysiology

A
  • Stenosis: stiffening and thickening of the valve leaflets, caused by calcium deposits or scarring, narrow the opening, and obstruct flow
  • Regurgitation: blood flows or leaks backward – ventricle to atria, aorta to the left ventricle, pulmonic circulation to the right ventricle – because of incomplete closing of the valve
  • Prolapse: valve leaflets bulge backward and do not close, causing regurgitation
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17
Q

Risk Factors of Valvular Heart Disease

A
  1. Infectious diseases
    - Infective endocarditis (IE)
    - Rheumatic fever (from untreated
    streptococcal infections)
  2. Coronary artery disease
  3. Myocardial infarction
  4. Heart failure
  5. Congenital defects
  6. Cardiomyopathy
  7. Degenerative changes (older age)
  8. Pregnancy: Due to increased workload on the heart
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18
Q

Valvular Heart Disease
Clinical Manifestations

A
  • One of the first clinical signs is the auscultation of a murmur.
  • A murmur can be the result of a high rate of blood flow through a valve, forward blood flow through a narrowed valve (stenosis), or backward blood flow through an incompetent valve (regurgitation).
  • They can be classified as systolic, diastolic, or continuous based on where in the cardiac cycle it is best heard.
  • Others:
    SOB, dyspnea, orthopnea
    Crackles
    Angina
    Syncope, dizziness
    Dysrhythmias (Atrial fibrillation most common)
    Palpitations
    Fatigue
    Weight gain
    Edema
    Cool, pale extremities with weak pulses
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19
Q

Valvular Heart Disease
Systolic Murmurs
- When are they heard?

A
  • Systolic murmurs can be heard during S1 or lub when
    the ventricles are contracting.
  • During this time, the aortic and pulmonic valves should
    be open, and the mitral and tricuspid valves should be
    closed.
  • Therefore, a systolic murmur can be heard with aortic or pulmonic stenosis or mitral or tricuspid
    regurgitation.
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20
Q

Valvular Heart Disease
Diastolic Murmurs
- When are they heard?

A
  • Diastolic murmurs can be heard during S2 or dub when
    the ventricles are relaxing, and the heart is filling.
  • The mitral and tricuspid valves should be open to allow
    for ventricular filling, and the aortic and pulmonic valves should be closed.
  • Therefore, a diastolic murmur can be heard with aortic or pulmonic valve regurgitation or mitral or tricuspid stenosis.
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21
Q

Mr. Spitale is a 54-year-old male who presents to your
clinic with complaints of intermittent episodes of
dyspnea, chest pain, palpitations, and dizziness for 6 months. He says that he used to exercise regularly but cannot tolerate increased physical activity. He is concerned and does not know what to do. He is alert and oriented currently and is asymptomatic. Vital signs:
BP: 176/87
HR: 82 (irregular)
RR: 20
O2 sat: 98% RA
Temp: 98.6 F
What should you ask Mr. Spitale?

A

Do you have any medical history?
- “Small” heart attack 5 years ago. Never followed up with cardiology.
- I “might” have high blood pressure, but I don’t take anything for it.
Do you smoke, drink alcohol or use illicit drugs?
- Smoked a pack per day for 15 years but quit 5 years ago.
- Drinks 2 beers each night. Never used drugs.
Do you take any medications?
- None
Family medical history?
- Unknown. Adopted as a child.
Social history?
- Married for 25 years with 2 grown children.
- Works as a foreman for a construction company.
- Denies outside stressors.

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22
Q

Mr. Spitale is a 54-year-old male who presents to your
clinic with complaints of intermittent episodes of
dyspnea, chest pain, palpitations, and dizziness for 6 months. He says that he used to exercise regularly but cannot tolerate increased physical activity. He is concerned and does not know what to do. He is alert and oriented currently and is asymptomatic. Vital signs:
BP: 176/87
HR: 82 (irregular)
RR: 20
O2 sat: 98% RA
Temp: 98.6 F
What are your priority physical assessments?

A

Vital Signs
- BP 176/87, HR 82 and irregular
Pain assessment
- None currently
- Could have chest pain, palpitations
Breath sounds
- Clear bilaterally
- Crackles are indicative of pulmonary congestion
Heart sounds (and rhythm)
- Systolic murmur, 2nd ICS right sternal border (aortic stenosis)
Peripheral vascular assessment
- Warm, dry and intact. No edema.
- Strong pulses.
- Poor color, cool extremities, weak peripheral pulses, delayed capillary refill, and edema can indicate inadequate cardiac output
Activity tolerance
- Dyspnea, fatigue and dizziness

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23
Q

Mr. Spitale is a 54-year-old male who presents to your
clinic with complaints of intermittent episodes of
dyspnea, chest pain, palpitations, and dizziness for 6 months. He says that he used to exercise regularly but cannot tolerate increased physical activity. He is concerned and does not know what to do. He is alert and oriented currently and is asymptomatic. Vital signs:
BP: 176/87
HR: 82 (irregular)
RR: 20
O2 sat: 98% RA
Temp: 98.6 F
Priority labs/diagnostics?

A
  • EKG
  • CXR - may indicate cardiomegaly and pulmonary edema
  • CBC
  • CMP
  • Cardiac enzymes
  • Echocardiogram with TEE can identify valve abnormalities
  • Hearth cath is definitive for stenosis
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24
Q

Mr. Spitale is a 54-year-old male who presents to your
clinic with complaints of intermittent episodes of
dyspnea, chest pain, palpitations, and dizziness for 6 months. He says that he used to exercise regularly but cannot tolerate increased physical activity. He is concerned and does not know what to do. He is alert and oriented currently and is asymptomatic. Vital signs:
BP: 176/87
HR: 82 (irregular)
RR: 20
O2 sat: 98% RA
Temp: 98.6 F
Labs are normal, CXR is clear. What further testing can be done?

A

Transesophageal Echocardiography
(TEE)
- Patient lies on bed on left side
- Doctor places TEE probe into mouth and down esophagus
- Sound waves create a picture of the heart
- Identifies valve abnormalities and Ejection Fraction

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25
Q

Mr. Spitale has completed a TEE and the study reveals aortic stenosis and will be referred to cardiology for potential valve replacement.
What are the most common valvular diseases?

A
  • The most common valvular diseases are aortic stenosis and mitral regurgitation.
  • The least commonly affected valves are the tricuspid and pulmonic valves because of the low-pressure system in the right heart.
  • Valvular disease can affect one or more valves at the same time.
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26
Q

Mr. Spitale has completed a TEE and the study reveals aortic stenosis and will be referred to cardiology for potential valve replacement.
What medications do you anticipate for him?

A

Beta-blockers (Metoprolol, atenolol, esmolol)
- Reduce heart rate and blood pressure
ACE inhibitors (Lisinopril)
- If side effects (annoying cough, angioedema), go to ARBS
- Decrease BP
Angiotensin II receptor blockers (Losartan, valsartan)
- Decrease BP
Anticoagulant (Warfarin)
- Patients who undergo valve replacement with a mechanical prosthetic valve will need to be anticoagulated for life to prevent thrombotic events such as stroke
NTG
- Vasodilator

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27
Q

Mr. Spitale has completed a TEE and the study reveals aortic stenosis and will be referred to cardiology for potential valve replacement. What education/teaching do we need to provide for Mr. Spitale?

A
  1. Medication teaching
  2. Restrict sodium and caffeine (so Afib does not become worse)
  3. Monitor for signs and symptoms of heart failure (dyspnea, pedal edema, orthopnea, and fatigue)
  4. Daily weight monitoring
  5. If on warfarin, anticoagulant precautions:
    - Use electric razor for shaving
    - Limit alcohol consumption
    - Fall precautions
    - Regular PT/INR checks
    - Limit green leafy vegetables (High in vitamin K)
  6. Regular follow-up with cardiologist, PCP
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28
Q

Carotid Artery Disease
Pathophysiology
Severity

A
  • Like atherosclerotic changes in other arteries, carotid artery disease is characterized by vessel wall thickening, plaque formation, and a progressive narrowing of the carotid artery.
  • Plaque disruption and thrombus formation contribute to progressive narrowing of the lumen of the artery, which can cause adverse clinical events.
  • Stenosis is most significant at the carotid bifurcation. This area is known as the carotid bulb, where the common carotid artery branches into the internal and external carotid arteries. The carotid bifurcation is an area of low-flow velocity and low-shear stress.
  • When blood circulates through the carotid bifurcation, there is separation of flow into the low-resistance internal carotid and the high-resistance external carotid artery.
  • With increasing degrees of stenosis in the internal carotid artery, flow becomes more turbulent, increasing the risk of atheroembolization.
  • The severity of stenosis is commonly divided into three categories according to the luminal diameter reduction: Mild (<50%), Moderate (50% - 69%) & Severe (70% - 99%
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29
Q

Carotid Artery Disease
Risk Factors

A

Modifiable
* Smoking
* Hypertension
* Diabetes
* Dyslipidemia
* Sedentary lifestyle
* Obesity
* Ineffective stress management
* People with coronary artery disease have a greater risk of developing carotid artery disease
Nonmodifiable
* Age
* Gender: Male
* Ethnicity
* Family history

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30
Q

Mr. Hamilton is a 75-year-old man with a history of hypertension for 10 years treated with Amlodipine 10 mg and Lisinopril 20 mg daily. Mr. Hamilton considers his hypertension controlled. He also has a 5-year history of hyperlipidemia and takes
Atorvastatin 10 mg daily. His PCP has recommended a carotid duplex ultrasound of his carotid arteries as part of a systematic screening because of his vascular risk factors. Vital signs:
BP: 152/101
HR: 92
RR: 20
O2 sat: 97% RA
Temp: 97.4
What key physical assessment might make you suspicious that Mr. Hamilton has carotid artery disease?
What other cues might indicate that Mr. Hamilton will need this study?

A

Auscultation of the carotid arteries. Asymptomatic carotid artery stenosis may be identified by the presence of carotid bruits, sounds created by blood flow through a stenosed vessel on auscultation. This can be done by placing the bell of the stethoscope over the side of the neck anterior to the sternocleidomastoid muscle.
Other cues:
- Hypertensive (152/101)
- Advanced age (75)
- Male
- History of hyperlipidemia (Takes Atorvastatin 10 mg daily)

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31
Q

Mr. Hamilton is a 75-year-old man with a history of hypertension for 10 years treated with Amlodipine 10 mg and Lisinopril 20 mg daily. Mr. Hamilton considers his hypertension controlled. He also has a 5-year history of hyperlipidemia and takes
Atorvastatin 10 mg daily. His PCP has recommended a carotid duplex ultrasound of his carotid arteries as part of a systematic screening because of his vascular risk factors. Vital signs:
BP: 152/101
HR: 92
RR: 20
O2 sat: 97% RA
Temp: 97.4
Mr. Hamilton is not currently symptomatic. If he was symptomatic, what clinical manifestations might we observe?

A

Stroke symptoms
- Symptoms resembling a CVA or TIA (altered cerebral perfusion)
- Weakness (sometimes on one side)
- Dizziness
- Loss of coordination
- Difficulty talking
- Facial droop
- Vision problems
- Headache

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32
Q

Mr. Hamilton is a 75-year-old man with a history of hypertension for 10 years treated with Amlodipine 10 mg and Lisinopril 20 mg daily. Mr. Hamilton considers his hypertension controlled. He also has a 5-year history of hyperlipidemia and takes
Atorvastatin 10 mg daily. His PCP has recommended a carotid duplex ultrasound of his carotid arteries as part of a systematic screening because of his vascular risk factors. Vital signs:
BP: 152/101
HR: 92
RR: 20
O2 sat: 97% RA
Temp: 97.4
Mr. Hamilton undergoes a carotid duplex ultrasound of his carotid arteries. His ultrasound showed an atherosclerotic stenosis at the site of the left carotid bifurcation. Data was consistent with a severe carotid stenosis estimated about 70%.
What additional tests do you anticipate?

A
  • Lipid profile
  • CBC
  • Comprehensive metabolic profile
  • CTA, MRA, MRI, Carotid angiography (invasive)
  • all but MRI use contrast dye -> BUN/Cr
  • CTA: Utilizes IV contrast dye to highlight the carotid arteries
  • MRA: Utilizing IV contrast dye, the MRA uses magnetic fields and radio waves to show blockages inside the arteries.
  • Carotid Angiography: Involves inserting a catheter into an artery. Contrast dye is injected through the catheter that allows visualization of the carotid arteries via radiographical imaging.
  • EKG
  • Cardiac echocardiogram
  • Heart catheterization
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33
Q

Mr. Hamilton is a 75-year-old man with a history of hypertension for 10 years treated with Amlodipine 10 mg and Lisinopril 20 mg daily. Mr. Hamilton considers his hypertension controlled. He also has a 5-year history of hyperlipidemia and takes
Atorvastatin 10 mg daily. His PCP has recommended a carotid duplex ultrasound of his carotid arteries as part of a systematic screening because of his vascular risk factors. Vital signs:
BP: 152/101
HR: 92
RR: 20
O2 sat: 97% RA
Temp: 97.4
Mr. Hamilton undergoes a carotid duplex ultrasound of his carotid arteries. His ultrasound showed an atherosclerotic stenosis at the site of the left carotid bifurcation. Data was consistent with a severe carotid stenosis estimated about 70%.
What treatment do you anticipate for Mr. Hamilton?

A
  1. Antiplatelet therapy
    - Aspirin
    - Clopidogrel (Plavix)
  2. Increase antihypertensive
    therapy
  3. Increase Statin therapy
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34
Q

Mr. Hamilton is a 75-year-old man with a history of hypertension for 10 years treated with Amlodipine 10 mg and Lisinopril 20 mg daily. Mr. Hamilton considers his hypertension controlled. He also has a 5-year history of hyperlipidemia and takes
Atorvastatin 10 mg daily. His PCP has recommended a carotid duplex ultrasound of his carotid arteries as part of a systematic screening because of his vascular risk factors. Vital signs:
BP: 152/101
HR: 92
RR: 20
O2 sat: 97% RA
Temp: 97.4
Mr. Hamilton undergoes a carotid duplex ultrasound of his carotid arteries. His ultrasound showed an atherosclerotic stenosis at the site of the left carotid bifurcation. Data was consistent with a severe carotid stenosis estimated about 70%.
What priority teaching/discharge instructions do you anticipate for Mr. Hamilton?

A
  • Teach patient how to recognize signs and symptoms of stroke
  • Medication teaching
  • Lifestyle changes
    *Exercise
    *Smoking cessation
  • Limit alcohol consumption
  • DASH diet (Dietary Approaches to Stop Hypertension)
35
Q

Surgical Interventions for Carotid Artery Disease

A

Carotid Artery Stenting with EPD
- During carotid angioplasty, a balloon catheter is then guided to the area of the blockage or narrowing.
- Once in place, the balloon is inflated, the fatty plaque is compressed against the arterial wall to increase the lumen of the vessel and improve blood flow.
- During the angioplasty procedure, a carotid stent (a small, metal mesh tube) is placed inside the carotid artery at the site of the blockage to provide support to keep the artery open.
- Prior to stent insertion, an emboli protection device (EPD) is deployed to capture distal emboli to prevent clots from traveling to the brain.
- Following EPD deployment, the stent is placed.
Carotid Endarterectomy (CEA)
- Surgery to remove plaque causing occlusion in the carotid arteries
- The plaque and arterial intima, along with portions of the media of the artery, are removed
- A patch of autogenous vein or prosthetic material is then put in place
- Wide fluctuations in the patient’s BP are common and excessive hypertension or hypotension may produce stroke. Perioperatively, the patient should have an arterial catheter in place to monitor BP so that cerebral perfusion can be maximized.

36
Q

Heart Failure Pathophysiology

A
  • Heart failure is inadequate pumping / filling up the heart, insufficient blood to meet the oxygen needs of tissues, impaired cardiac output from changes in preload, afterload, contractility, and heart rate.
  • Classified based on ejection fraction (EF), which is the percentage of blood that is ejected from the
    ventricle with each contraction. Normal values range from 55% to 70% of the total volume.
  • Patients with low EF are diagnosed with heart failure with reduced ejection fraction (HFrEF), formerly called systolic heart failure. These patients have a weakened contraction, with an EF of 45% or less.
37
Q

Left Sided Heart Failure s/s

A
  • Dysfunction of the left ventricle
  • Weakened contraction results in poor peripheral perfusion
  • Backflow of blood that causes fluid accumulation in the lungs
  • Symptoms include
  • Dyspnea
  • Orthopnea
  • Fatigue
  • Weight gain
  • Poor color
  • Elevated PCWP
  • Tachypnea
  • Blood-tinged sputum
  • S3 or S4 gallop upon auscultation
38
Q

Right Sided Heart Failure s/s

A
  • Inability of the right side of the heart to effectively pump blood to the pulmonary vasculature
  • Results in a backflow of blood into the right atrium and venous circulation
  • Symptoms include
  • JVD
  • Generalized edema
  • Hepatomegaly
  • Ascites
  • Loss of appetite
  • Nausea/Vomiting
  • Increased abdominal girth
39
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Vital signs:
BP: 178/112
HR: 116
RR: BiPAP delivered rate at 16 breaths per minute, FiO2 at 100%
O2 sat: Unable to read
Tympanic temp: 97.1
What are your priority physical assessments?

A
  1. Shortness of breath
  2. Crackles, rales bilaterally
    - Crackles indicate pulmonary congestion.
  3. Skin pale, cool and diaphoretic (inadequate cardiac output)
  4. Tachycardia (compensation)
    - Tachycardia can be present as the heart attempts to compensate for decreased cardiac output
  5. Hypertensive
    - Hypertension is present because of the increased afterload.
  6. Fatigue
  7. O2 saturation?
  8. Heart sounds
    - Listen for S3 or S4
40
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Vital signs:
BP: 178/112
HR: 116
RR: BiPAP delivered rate at 16 breaths per minute, FiO2 at 100%
O2 sat: Unable to read
Tympanic temp: 97.1
What are your primary labs/diagnostics?

A
  1. Stat portable CXR!
    - Assess for heart size or cardiomegaly
    - Pulmonary congestion
  2. EKG
    - May show hypertrophy or other structural disease
    - Assess for cardiac dysrhythmias
  3. Comprehensive metabolic panel
    - Include renal/liver function
  4. CBC
  5. Cardiac enzymes
  6. ABGs
  7. BNP & NT-pro BNP

(Also, MUGA, coronary angiography)

41
Q

BNP & NT-pro BNP
What do the values mean?

A

Biomarkers elevated due to overstretching of the ventricles
BNP
* < 100 pg/mL – HF unlikely
* > 400 pg/mL – HF likely
* 100 – 400 pg/mL use clinical judgment
NT-pro BNP
* > 300 ng/mL – HF likely

42
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
pH: 7.10 L
PO2: 169 H
PCO2: 35
HCO3: 22 – 26 mEq/L 11 L
Base Excess -2 to +2 - 10.5 L
Lactate 0.5 – 1 mmol/L 4.9 H
How does lactic acidosis occur?

A
  • Reduction of blood flow and oxygen throughout the body.
  • If cells are deprived of oxygen, instead of using aerobic metabolism (with oxygen) to function, the
    cells use the anaerobic (without oxygen) pathway to produce energy.
  • Lactic acid is formed as a by-product of anaerobic metabolism.
  • Ultimately will lead to cell death and organ failure.
43
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Why is an EKG clinically significant? CKR?

A
  • Dysrhythmias are a common adverse effect of heart failure.
  • Atrial fibrillation is THE most common.
    His EKG shows Afib
    CXR shows enlargement of heart
44
Q

Cardiomyopathy patho
Types: Ischemic vs. Nonischemic

A

Ischemic
* Secondary to MI: Greatly reduced ejection fraction
Nonischemic
* Dilated cardiomyopathy
- Most common, 3rd leading cause of HF. Starts with the dilation of the muscle in the left ventricle which causes the inside of the chamber to enlarge. The dilated chambers result in poor systolic function, impaired contractility, thus decreasing CO.
* Hypertrophic cardiomyopathy
- The heart muscle, typically the left ventricle, thickens, enlarges, and becomes stiff. Contraction is not typically weakened, but filling is impaired creating a diastolic or filling dysfunction.
* Restrictive
- Characterized by stiff ventricular muscle resulting diastolic function and impaired filling. Normal heart muscle is replaced by fibrosis and scarring.

45
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Vital signs:
BP: 178/112
HR: 116
RR: BiPAP delivered rate at 16 breaths per minute, FiO2 at 100%
O2 sat: Unable to read
Tympanic temp: 97.1
In Lactic acidosis
EKG shows Afib, CXR shows heart enlargement
What orders do you anticipate for Mr. Ruiz?

A

Rapid Sequence Intubation
Induction agents
* Ketamine (1.5 mg/kg IV)
* Etomidate (0.3-0.4 mg/kg IV)
* Fentanyl (2-10 mcg/kg)
* Midazolam (0.3mg/kg)
* Propofol (1-2.5 mg/kg)
Neuromuscular blockers
* Succinylcholine (1.5mg/kg)
* Vecuronium (0.15 mg/kg)
Beta- blocker
* Metoprolol, sotalol
Diuretics
* Lasix or spironolactone
* Reduces volume, thus cardiac preload
Nitrates
* NTG (transdermal or IV)
* Decreases venous return, thus cardiac preload, and afterload
* Increases myocardial oxygen supply
Heparin drip
* Atrial fibrillation on the monitor
* Reduces clot formation
Morphine may also be considered

46
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Vital signs:
BP: 178/112
HR: 116
RR: BiPAP delivered rate at 16 breaths per minute, FiO2 at 100%
O2 sat: Unable to read
Tympanic temp: 97.1
In Lactic acidosis
EKG shows Afib, CXR shows heart enlargement

He goes into Vtach. What do you do?
He then goes into Vfib. What do you do?

A
  1. Check for a pulse
  2. If no pulse -> CPR
    Place Biphasic defibrillator pads
    Shock 120-200 Joules!
    Same thing again for Vfib
    First thing after shocking and seeing a new rhythm: Check for pulse
    If Pulseless Electrical Activity -> give CPR
47
Q

Mr. Ruiz is an obese 61-year-old man who presents to the ED via ambulance with acute shortness of breath. He was placed on bilevel positive airway pressure (BiPAP) ventilation on arrival. He is unable to speak to you due to the BiPAP machine and acute shortness of breath and is not accompanied by a family member. He is pale, diaphoretic and skin is cool to touch. Crackles and rales bilaterally upon auscultation. 18 gauge IV in his left forearm.
Vital signs:
BP: 178/112
HR: 116
RR: BiPAP delivered rate at 16 breaths per minute, FiO2 at 100%
O2 sat: Unable to read
Tympanic temp: 97.1
In Lactic acidosis
EKG shows Afib, CXR shows heart enlargement
He goes into Vtach. Shock. He goes into Vfib. Shock.
Normal rhythm comes back.
BP: 82/48 (MAP 59)
HR: 32 - Sinus Bradycardia
What orders do you anticipate for
Mr. Ruiz?
What happened?

A
  • Atropine 0.5 mg IV
  • Sinus Bradycardia
  • Increases HR
  • Dopamine 2-20 mcg/kg/min OR Norepinephrine (Levophed) 8-12 mcg/min OR Epinephrine 2-10 mcg/min
  • Dopamine 3-10: increases contractility and HR. Greater than 10: vasoconstriction and increased BP
  • Norep and Epi: Vasoconstriction and increases BP

Cardiogenic shock happened

48
Q

Cardiogenic Shock Patho

A
  • Condition of diminished cardiac output that severely impairs tissue perfusion
  • Ventricular dysfunction initiates a series of compensatory mechanisms that attempt to increase cardiac output and, in turn, maintain vital organ function
  • As cardiac output falls, baroreceptors in the aorta and carotid arteries initiate responses in the sympathetic nervous system. These responses, in turn, increase HR, left ventricular filling pressure, and afterload to enhance venous return to the heart
  • These compensatory responses initially stabilize the patient but later cause the patient to deteriorate as the oxygen demands of the already compromised heart increase
49
Q

Mr. Ruiz just experienced cardiogenic shock due to heart failure. He has a central venous catheter in place, an arterial line in his right upper extremity, and is on a mechanical ventilator. He is on Levophed at 10 mcg/min, NS at 50 ccc/hr, and a Propofol drip to titrate for sedation. He has diuresed 860
cc urine. His vital signs are as follows:
BP: 116/68 (MAP 84)
HR: 76 (irregular)
RR: Mechanical vent settings
O2 sat: 97%
Mr. Ruiz is taken to the cardiac cath lab where he was discovered to have a 90% occlusion of the left coronary artery (left main) with biventricular failure. His ejection fraction is 30%. After revascularization, he has an intra-aortic balloon pump inserted. What is the benefit?

A
  • To increase myocardial oxygen supply and demand
  • The balloon at the tip of the catheter (just below the aortic arch) inflates at the start of diastole and deflates just before systole
  • When the balloon inflates, blood is displaced toward the coronary arteries and into the systemic circulation
  • Improves coronary and systemic perfusion
  • Deflating the balloon decreases afterload, thus decreasing the workload of the left ventricle
50
Q

AICD: what is it, who is it for?

A
  • Recommended for patients with with reduced ejection fraction (<30%), who are at high risk for lethal dysrhythmias
  • Monitors for lethal ventricular dysrhythmias and delivers a shock if needed
51
Q

Mr. Ruiz just experienced cardiogenic shock due to heart failure. HE has a central venous catheter in place, an arterial line in his right upper extremity, and is on a mechanical ventilator. He is on Levophed at 10 mcg/min, NS at 50 ccc/hr, and a Propofol drip to titrate for sedation. He has diuresed 860 cc urine. His vital signs are as follows:
BP: 116/68 (MAP 84)
HR: 76 (irregular)
RR: Mechanical vent settings
O2 sat: 97%
Mr. Ruiz is taken to the cardiac cath lab where he was discovered to have a 90% occlusion of the left coronary artery (left main) with biventricular failure. His ejection fraction is 30%. After revascularization, he has an intra-aortic balloon pump inserted.
After a two-week hospitalization, Mr. Ruiz makes a full recovery.
What medications do you anticipate
upon discharge?

A
  1. Beta-blockers (Metoprolol)
    - Decrease the sympathetic nervous system response to decreased CO and decrease the workload of the heart, thus reducing myocardial oxygen consumption
  2. ACE inhibitors (Lisinopril)
    - Reduce afterload or systemic vascular resistance (SVR), making it easier for the heart to eject blood
  3. ARBs (Losartan, Valsartan)
    - Reduces afterload
  4. Digoxin (Lanoxin)
    - Positive inotropic agent, slows HR and enhances contractility of the heart
  5. ARNIs (Sacubitril/valsartan)
    - By blocking neprilysin, natriuretic peptides remain active in increasing urine output and dilating blood vessels
    - Reduces preload and afterload
  6. Diuretics (Lasix, Spironolactone)
    - Spironolactone: Aldosterone agonist; Reduces preload
    - Lasix: Loop diuretic, Reduces preload
  7. NTG
    - Decreases venous return and decreases cardiac preload and afterload
  8. Inodilators (Milrinone)
    - Positive inotrope and vasodilator
    - Increases contractility and reduces afterload
  9. Vasodilators (Hydralazine, isosorbide dinitrate)
    - Reduce afterload
52
Q

Mr. Ruiz just experienced cardiogenic shock due to heart failure.
Mr. Ruiz is taken to the cardiac cath lab where he was discovered to have a 90% occlusion of the left coronary artery (left main) with biventricular failure. His ejection fraction is 30%. After revascularization, he has an intra-aortic balloon pump inserted.
After a two-week hospitalization, Mr. Ruiz makes a full recovery.
What is the priority teaching/discharge issues?

A

*Medication management.
- Understanding and adhering to the medication treatment plan are essential for effective medication treatment AND prevention of rehospitalization.
*Provide education about safe use of oxygen.
- Home use including portable devices, compressors, proper storage indications for use and assessing oxygen saturation.
*Rest and pace activities.
- Maintain activity as tolerated.
- Alternate rest and activity periods.
*Educate on fall prevention and accessing emergency assistance.
*Signs and symptoms of worsening heart failure checklist. Remember “FACES.”
- Fatigue,
- Limitation of activity
- Cough and congestion
- Edema
- Shortness of breath
*Daily weights on the same scale every day, preferably in the morning after voiding.
- Report to provider weight gain of >2.5 lbs in one day or 5 lbs in one week.
*Reinforce collaborative plan to include smoking cessation, limiting alcohol consumption, mild exercise, low sodium diet, moderate caffeine, and reduced saturated fats.
*Teach patient to reduce high-sodium sources of food.
- Processed meats, canned foods, baked goods, and snacks
- Teach about non-sodium flavor enhancers.
*Cardiac rehabilitation.
- Reduces mortality, improves functional status, reduces hospitalization, and improves quality of life.
*Eat a potassium rich food each day including a banana, orange juice in absence of potassium supplement.

53
Q

Shock Patho

A
  • Shock is a life-threatening syndrome that occurs when the circulatory system is unable to supply adequate amounts of oxygen to the tissues to meet basic metabolic requirements.
  • This creates a state of tissue hypoxia, which is an imbalance of cellular oxygen supply and demand.
  • Shock can result from ineffective cardiac function, inadequate blood volume, or inadequate vascular
    tone.
  • Without immediate treatment to reverse this imbalance, organ system failure and death may
    result
54
Q

Describe the 4 types of shock
Hypovolemic
Cardiogenic
Distributive
Obstructive

A

Hypovolemic
- Rapid fluid loss resulting in inadequate circulating volume.
- Most commonly, secondary to blood loss from penetrating trauma, blunt trauma, or severe GI bleeds
Cardiogenic
- Inadequate pumping of the heart results in decreased cardiac output (CO) and poor perfusion at the tissue level.
Distributive
- The result of diseased states such as sepsis, anaphylaxis, or neurogenic shock.
- Causes poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling. Venous pooling causes a decreased venous return to the right heart.
Obstructive
- Caused by a mechanical barrier to ventricular filling or emptying (increased afterload), causing decreased CO.

55
Q

Mr. Jones is a 79-year-old man presenting to the Emergency Department reporting an acute onset of ”ripping” lower abdominal pain radiating to his back. The pain started earlier the same day, had become progressively worse, and was not relieved by changes in position. He denies hematuria, dysuria, constipation, diarrhea, or any recent trauma. He is diaphoretic and complains of nausea and feeling faint.
Vital signs:
BP: 104/66
HR: 110
RR: 16
O2 sat: 98%
Temp: 98.6
What are we going to ask Mr. Jones?

A

Onset of pain?
Description of pain?
Severity of pain? (Scale from 1-10)
Does the pain radiate? If so, where?
Medical history?
Family history?
Peripheral sensation?
Do you smoke?
Nausea and/or vomiting?
Recent trauma?

Pain began earlier in the day and became progressively worse
Now acute
Pain is a “8” on a 1-10 scale
Abdomen radiating to his back, “ripping”
History of hypertension, HLD, atherosclerosis, coronary artery disease
Father had a history of the same
Peripheral sensation intact but diaphoretic
Smoked one pack per day for 25 years but quit 10 years ago
Nausea, no vomiting
Denies trauma

56
Q

Mr. Jones is a 79-year-old man presenting to the Emergency Department reporting an acute onset of ”ripping” lower abdominal pain radiating to his back. The pain started earlier the same day, had become progressively worse, and was not relieved by changes in position. He denies hematuria, dysuria, constipation, diarrhea, or any recent trauma. He is diaphoretic and complains of nausea and feeling faint.
Vital signs:
BP: 104/66
HR: 110
RR: 16
O2 sat: 98%
Temp: 98.6
Pain is a “8” on a 1-10 scale
Priority Physical Assessments?

A
  • Vital signs (Currently WNL)
  • Look for blood loss, BP differing in extremities
  • Hypotension and tachycardia may indicate hypovolemia secondary to blood loss
  • Blood pressure may vary between extremities if dissection is occurring because of the lessening of blood flow distal to the dissection
  • Pain ( “8” on a 1-10 scale)
  • Pain is an indicator of a change such as dissection or rupture
  • Peripheral pulses, skin color and temperature (WNL)
  • Peripheral sensation and motor response (WNL)
  • Pressure on arteries supplying spinal cord -> paralysis
  • Gentle abdominal auscultation and palpation (No bruit, no mass)
  • Pulsatile abdominal masses may indicate a AAA
  • A bruit is caused by turbulent flow through the aneurysm
57
Q

Aortic Dissection

A
  • Thought to be caused by a sudden tear in the aortic intima creating a false lumen in the artery opening the way for blood to enter the aortic wall.
  • Degeneration of the aortic media may be the primary cause for this condition, with hypertension being an important contributing factor.
  • Classic signs and symptoms of aortic dissection are sudden onset of severe and persistent pain described as “tearing” or “ripping” in the anterior chest or back and extending to the shoulders, epigastric area, or abdomen.
  • Diaphoresis, nausea, vomiting, faintness, and tachycardia are also common.
  • Blood pressure is often markedly different from one extremity to another and often decreases because of loss of blood.
58
Q

Mr. Jones is a 79-year-old man presenting to the Emergency Department reporting an acute onset of ”ripping” lower abdominal pain radiating to his back. The pain started earlier the same day, had become progressively worse, and was not relieved by changes in position. He denies hematuria, dysuria, constipation, diarrhea, or any recent trauma. He is diaphoretic and complains of nausea and feeling faint.
Vital signs:
BP: 104/66
HR: 110
RR: 16
O2 sat: 98%
Temp: 98.6
Pain is a “8” on a 1-10 scale
Priority Diagnostics?

A

CBC
- H/H is low
Chemistry
- Glucose is high
Lipid Profile
- High
Coagulation studies
Cardiac enzymes
EKG
- Rule out MI because complications of aneurysm involve chest pain
CT abdomen with IV contrast
- Considered gold standard for assessing size and location of abdominal or thoracic aneurysm
Abdominal ultrasound / TEE
- Preferred screening modalities
- Noninvasive

59
Q

Mr. Jones is a 79-year-old man presenting to the Emergency Department reporting an acute onset of ”ripping” lower abdominal pain radiating to his back. The pain started earlier the same day, had become progressively worse, and was not relieved by changes in position. He denies hematuria, dysuria, constipation, diarrhea, or any recent trauma. He is diaphoretic and complains of nausea and feeling faint.
Vital signs:
BP: 104/66
HR: 110
RR: 16
O2 sat: 98%
Temp: 98.6
Pain is a “8” on a 1-10 scale
Abdominal ultrasound demonstrates a 10- cm AAA with a large retroperitoneal hematoma consistent with dissection.
What orders do you anticipate?

A

Emergent vascular surgery consult
Blood typing and crossmatching
Two large bore IVs
Oxygen
IVFs ( Normal saline, lactated ringers)

60
Q

Mr Jones: Abdominal ultrasound demonstrates a 10- cm AAA with a large retroperitoneal hematoma consistent with dissection.
Mr. Jones becomes unconscious. His skin is cool and clammy.
Vital signs:
BP: 68/40
HR: 160
RR: 6
O2 sat: 72%
What’s happening?

A

Hypovolemic Shock
- Rapid fluid loss resulting in inadequate circulating volume.
- Possibly due to ruptured AAA.
- Blood loss from the vascular system reduces the volume of venous blood returning to the heart.
- In the event of acute hemorrhaging (internal bleeding), the venous blood, the blood volume and consequently cardiac output are reduced, and progresses inevitably to inadequate tissue perfusion and cardiocirculatory arrest and death.

61
Q

Mr Jones: Abdominal ultrasound demonstrates a 10- cm AAA with a large retroperitoneal hematoma consistent with dissection.
Mr. Jones becomes unconscious. His skin is cool and clammy.
Vital signs:
BP: 68/40
HR: 160
RR: 6
O2 sat: 72%
Hypovolemic Shock
What are our priority interventions?

A
  • Prepare for mechanical ventilation
  • Cardiac monitoring including pulse oximetry
  • ABGs
  • Rapid fluid resuscitation and blood transfusion
  • Hemodynamic monitoring
  • Foley catheter
  • Repeat CBC / chemistry
  • Lactate level
62
Q

Mr Jones: Abdominal ultrasound demonstrates a 10- cm AAA with a large retroperitoneal hematoma consistent with dissection.
Mr. Jones becomes unconscious. His skin is cool and clammy.
Vital signs:
BP: 68/40
HR: 160
RR: 6
O2 sat: 72%
Hypovolemic Shock
Priority Medications?

A
  1. Dobutamine
    - Stimulates B1 receptors, increasing contractility and HR
  2. Dopamine
    - Dose of 1-3 mcg/kg/min stimulates dopaminergic receptors on arteries in the heart, kidneys, brain, abdomen, resulting in vasodilation; this will produce an increase in urine output
    - Dose of 3-10 mcg/kg/min stimulates B1, increasing contractility and HR
    - Dose of greater than 10 mcg/kg/min stimulates B1, resulting in vasoconstriction and increased BP
  3. Epinephrine, Norepinephrine, Phenylephrine
    - Stimulates alpha 1 receptors resulting in vasoconstriction and increasing blood pressure
  4. Vasopressin
    - Arterial vasoconstriction through smooth muscle contraction, increasing blood pressure
63
Q

Describe placement of an arterial line
What does it measure?

A
  • Transducer secured at the phlebostatic axis; midpoint at the right atrium, at the fourth intercostal space in the midaxillary line with the patient in the supine position.
  • If the transducer is placed too low, the reading will be falsely high.
  • If too high, the reading will be falsely low.
  • Maintain mean arterial pressure (MAP) between 70—100 mm Hg (At least 60!)
64
Q

How to calculate MAP
What is Mr. Jones’?
BP: 68/40

A

(2 X diastolic) + systolic / 3
Mr. Jones is at 49

65
Q

Advantages of Central Venous Catheter

A

Lines goes through Superior Vena Cava
1. CVP and ScvO2 monitoring
2. Monitor preload and right heart filling pressures
3. Volume resuscitation
4. Frequent blood draws
5. Long-term IV antibiotics
6. Parenteral nutrition
7. Transvenous pacemaker insertion

66
Q

What values would we expect to see in hypovolemic shock?
CO
CVP
PCWP
ScvO2
SvO2
SVR
MAP
BP and HR

A
  1. Decreased CO (< 4 – 8 L/min)
  2. Decreased CVP (< 2 -6 mm Hg)
  3. Decreased PCWP/PAOP ( < 4– 12 mmHg)
  4. Decreased central venous oxygen saturation / ScvO2 ( < 70%)
  5. Decreased mixed venous oxygen saturation / SvO2 ( < 60%)
  6. Increased systemic vascular resistance ( > 800 – 1200)
  7. Decreased MAP ( < 60 mm Hg)
  8. Hypotension and tachycardia
67
Q

Mr Jones: Abdominal ultrasound demonstrates a 10- cm AAA with a large retroperitoneal hematoma consistent with dissection.
Mr. Jones becomes unconscious. His skin is cool and clammy.
Vital signs:
BP: 68/40
HR: 160
RR: 6
O2 sat: 72%
Hypovolemic Shock
What are our priority nursing interventions?

A

Monitor vital signs
- Hypotension and tachycardia may be present because of decreased CO
Monitor hemodynamic readings
- Decreased CO, CVP, PCWP, Scvo2, MAP,
- Increased SVR
Monitor neurological status
- Decreased level of consciousness occurs because of decreased cardiac output
Monitor urine output
- Decreased urine output occurs because of decreased cardiac output and stimulation of compensatory mechanisms that increase reabsorption of sodium and water
Skin color and temperature
- Cold and clammy skin may be a sign of decreasing peripheral perfusion and progressing shock
Monitor ABGs
- Early shock pH is elevated reflecting respiratory alkalosis due to tachypnea
- Late stages reflect metabolic acidosis due to anaerobic metabolism
Venous oxygen saturation (ScvO2)
- Decreased
Monitor H&H
- Assess for decreased Hgb & Hematocrit
Monitor metabolic profile
- Renal failure – increased BUN & creatinine
- Liver failure – increased liver function studies
Monitor lactic acid level / base excess
- Increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level
Administer IVF, medications

68
Q

What is base excess?

A
  • Reflects the level of HCO3- and
    other bases such as protein and hemoglobin
  • Normal range is -2 to +2
  • A base excess less than -2
    indicates an acid excess (metabolic acidosis)
  • A base excess greater than +2
    indicates an acid deficit (metabolic
    alkalosis)
69
Q

Mrs. Simmons remains in the ICU. It has been determined that she is in severe ARDS and is in septic shock. She remains on a mechanical ventilator in A/C mode, FiO2 of 70%, Vt of 400, f of 16, PEEP of 10. She has an arterial line in place to monitor MAP. She has a foley in place. Vital signs:
BP: 80/50 (MAP 60)
HR: 110
RR: 16
O2 sat: 90%
Temp: 96.3
Labs:
- High WBC
- Low H/H, RBC, platelets
- Low potassium
- High glucose
- High BUN/Cr
- High Liver enzymes
- High PT, INR, aPTT
- High lactic acid
- High d-dimer
What is your interpretation?

A

Multiple Organ Distress Syndrome (MODS)
- Can be defined as the development of potentially reversible physiologic derangement involving two or more organ systems not involved in the disorder that resulted in ICU admission and arising in the wake of a potentially
life-threatening physiologic insult.
- The initial organ affected is generally the lungs, with the development of ARDS. Sequential failure is followed by the renal system, the hepatic system and then the GI system

70
Q

Mrs. Simmons remains in the ICU. It has been determined that she is in severe ARDS and is in septic shock. She remains on a mechanical ventilator in A/C mode, FiO2 of 70%, Vt of 400, f of 16, PEEP of 10. She has an arterial line in place to monitor MAP. She has a foley in place. Vital signs:
BP: 80/50 (MAP 60)
HR: 110
RR: 16
O2 sat: 90%
Temp: 96.3
MODS
Treatment?

A
  1. Treat underlying cause! (IV antibiotics)
  2. Maximize oxygenation – mechanical ventilation
  3. IVF to maintain intravascular volume
  4. Blood products as necessary to maintain adequate hemoglobin levels
    Three or more systems are associated with an 80% - 90% mortality rate
71
Q

Disseminated Intravascular Coagulopathy (DIC) Patho

A
  • Occurs because of enhanced coagulation that
    results from the release of procoagulant factors as
    a part of the inflammatory response associated
    with sepsis.
  • Diagnosis is made based on clinical picture of
    cyanosis and ischemia in combination with
    laboratory results.
  • Excessive bleeding from wounds and puncture
    sites may be present because of consumption of
    clotting factors in DIC.
72
Q

Disseminated Intravascular Coagulopathy (DIC) Treatment

A
  1. Treat underlying cause!
  2. Maximize oxygenation – mechanical ventilation
  3. Volume replacement
    - Crystalloids (NS)
    - Blood replacement
    - Plasma
    - Fresh frozen plasma
    - Replacement of clotting factors
73
Q

Pulmonary Artery
(Swan-Ganz)
Catheter
Distal Port
What is it used for?

A
  • May be used to draw SvO2 samples (60 – 80%)
  • This value reflects the oxygen saturation of blood returned to the heart from both the superior and inferior vena cava therefore reflecting total body venous oxygen saturation.
  • PA and PAWP (PAOP) pressures
  • Pulmonary artery pressures reflect the BP in the pulmonary artery. It is generated by the right ventricle ejecting blood into the pulmonary circulation.
  • PA Systolic 15-30 mm Hg
  • PA Diastolic 4– 12 mm Hg
  • MPAP = (PA Systolic pressure +2 PA Diastolic pressure) / 3
  • Normal MPAP is 20 mm HG
  • Considered elevated at > 25 mm Hg with rest or > 30
    mm Hg with exertion
  • PAWP (PAOP) 4-12 mm Hg
  • The PAOP reflects left heart preload or left ventricular end diastolic pressure. This pressure is obtained when the balloon is inflated and floats into a wedge position in the pulmonary artery which occludes that branch of the pulmonary artery obscuring data from the right heart.
74
Q

Pulmonary Artery
(Swan-Ganz)
Catheter
Proximal Port
What is it used for?

A
  • Located approximately 30 cm from the tip of the catheter in the right atrium
  • Used to monitor right atrial pressure or CVP
  • Reflects right heart preload and right ventricular end diastolic volume
  • Normal CVP 2– 6 mm Hg
  • Injection for CO injectate
  • Infusion of fluids and drugs
75
Q

Pulmonary Artery
(Swan-Ganz)
Catheter
Thermistor Port
What is it used for?

A
  • Sits at the tip of the PA catheter
  • Measures the temperature of ambient blood continuously
  • To obtain a thermodilution CO, cool NS is injected through the through the proximal port.
  • The time it takes for the cold injectate to pass
    the sensor is measured in liters of blood pumped per minute.
  • Normal CO is 4 – 8 L/min
76
Q

Central Venous Pressure (CVP)
2 – 6 mm Hg
When is it abnormally high or low and what is the treatment?

A

Central venous pressure is a reflection of right heart preload or right ventricular end-diastolic volume.
* Abnormal low: Hypovolemia or peripheral vasodilation
* Treatment: Fluid bolus, vasopressors
* Abnormal high: Right heart failure, tension pneumothorax, pulmonary hypertension, or pericardial tamponade
* Treatment: Inotropic or vasodilator therapy

77
Q

Pulmonary Artery (PA) Pressure
PAS 15– 30 mm Hg
PAD 4– 12 mm Hg
MPAP 20 mm Hg
When is it abnormally high and what is the treatment?

A

Reflects BP in pulmonary artery. It is generated by the right ventricle ejecting blood into the pulmonary circulation
* Abnormal high: Pulmonary hypertension, right heart failure
* Treatment: Inotropic and vasodilator therapy, diuretics

78
Q

Pulmonary Capillary Wedge Pressure (PCWP)
4 – 12 mm Hg
When is it abnormally high and what is the treatment?

A

The PAOP reflects left heart preload or left ventricular end diastolic pressure. This pressure is obtained when the balloon is inflated and floats into a wedge position in the pulmonary artery which occludes that branch of the pulmonary artery obscuring data from the right heart.
* Abnormal high: Pulmonary hypertension, cardiogenic shock, hypoxia and ARDS
* Treatment: Inotropic and vasodilator therapy, diuretics

79
Q

Cardiac Output / Cardiac Index
CO : 4– 8 L/min
CI : 2.5 – 4 L/min
When is it abnormally high or low and what is the treatment?

A

CO = volume of blood pumped out the heart each minute
CI = CO that is calculated based on the pt’s body surface area
* Abnormal low: Myocardial infarction, all forms of shock except for early septic shock
* Treatment: Fluid bolus, inotropic therapy, treatment of cause (MI)
* Abnormal high: Septic shock (early), hypervolemia, hyperthermia
* Treatment: Only if concerns present

80
Q

Systemic Vascular Resistance (SVR)
800 – 1200
When is it abnormally high or low and what is the treatment?

A

Left heart afterload is reflected in the systemic vascular resistance (SVR) and is representative of the force that the left heart must pump against to deliver the SV into the periphery.
* Abnormal low: Causes of vasodilation such as distributive shock (anaphylaxis, sepsis)
* Treatment: Fluid bolus, vasopressors, treat underlying cause
* Abnormal high: Causes of vasoconstriction such as hypovolemia, hypotension, cardiogenic shock
* Treatment: Vasodilators

81
Q

Pulmonary Vascular Resistance (PVR)
Less than 250
When is it abnormally high and what is the treatment?

A

Right heart afterload is reflected in the pulmonary vascular resistance (PVR).
Abnormal high: Pulmonary hypertension
Treatment: Vasodilators

82
Q

Mixed Venous Oxygen Saturation (SvO2)
60% - 70%
When is it abnormally low and what is the treatment?

A

This value reflects the oxygen saturation of blood returned to the heart from both the superior and inferior vena cava therefore reflecting total body venous oxygen saturation.
* Abnormal low: Increased oxygen needs of tissues, low cardiac output, low hemoglobin, low oxygenation
* Treatment: Increase cardiac output, increase oxygenation, increase hemoglobin

83
Q

Bundle of Care for sepsis

A

The Surviving Sepsis campaign developed a bundle of care to help standardize the very complex treatment needed by patients in severe sepsis. They may vary hospital to hospital, but the basic elements should be adhered to in order to optimize treatment. The bundle includes activities that must be completed in one hour.
1. Measure lactate levels. Reassess if initial lactate is >2 mmol/L
2. Obtain blood cultures (prior to administering antibiotics)
3. Administer broad-spectrum antibiotics
4. Administer 30 mL/kg of crystalloid if patient is hypotensive or lactate level at least 4 mmol/L
5. Administer vasopressors if blood pressure is unresponsive during or after fluid resuscitation; maintain mean arterial pressure (MAP) at 65 mmHg or above