Cardio day 1 Flashcards
1
Q
Describe the flow of electricity through the heart as well as the normal blood flow
A
o Electrical Flow:
o SA Node → AV Node → Bundle of His → Right and Left Bundle Branches → Purkinje Fibers.
o Blood Flow:
o Deoxygenated Blood:
o Superior/Inferior Vena Cava → Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Valve → Pulmonary Artery → Lungs.
o Oxygenated Blood:
o Lungs → Pulmonary Veins → Left Atrium → Mitral Valve → Left Ventricle → Aortic Valve → Aorta → Systemic Circulation.
2
Q
What are the 3 intrinsic factors that influence stroke volume
A
preload, afterload, contractility
3
Q
Describe preload
A
Definition: Preload is the degree of stretch of the cardiac muscle fibers at the end of diastole, just before contraction. It reflects the volume of blood filling the ventricles.
Influence on SV: According to the Frank-Starling law of the heart, an increase in preload (more blood in the ventricles) results in a stronger contraction and increased stroke volume, up to a certain point.
4
Q
Describe afterload
A
Definition: Afterload is the resistance the heart must overcome to eject blood during systole. It is influenced by systemic vascular resistance (SVR) and arterial pressure.
Influence on SV: Increased afterload (e.g., from high blood pressure) can reduce stroke volume because the heart has to work harder to eject blood. Conversely, decreased afterload can enhance stroke volume.
5
Q
Describe contractility
A
Definition: Contractility refers to the intrinsic ability of the heart muscle to contract. It is independent of preload and afterload.
Influence on SV: Increased contractility (due to factors such as sympathetic stimulation or inotropic drugs) enhances stroke volume.
Decreased contractility (due to heart failure or negative inotropic agents) reduces stroke volume.
6
Q
What are the 6 extrinsic factors that influence stroke volume
A
Heart rate, sympathetic nervous system, venous return, blood volume, aortic compliance, and medications/substances
7
Q
Describe heart rate’s influence on stroke volume
A
While heart rate itself does not directly affect stroke volume, it can influence the total cardiac output (CO). Very high heart rates can reduce the time available for ventricular filling (diastole), potentially decreasing stroke volume
8
Q
Describe Sympathetic Nervous System’s influence on stroke volume
A
Increased sympathetic activity boosts contractility and can increase stroke volume. It also has a positive chronotropic effect, which can indirectly influence stroke volume by affecting the filling time.
9
Q
Describe venous return’s influence on stroke volume
A
An increase in venous return increases preload, which can enhance stroke volume through the Frank-Starling mechanism.
10
Q
Describe Blood Volume’s influence on stroke volume
A
An increase in blood volume can lead to increased preload, thereby enhancing stroke volume. Conversely, reduced blood volume (e.g., due to dehydration or hemorrhage) can decrease stroke volume.
11
Q
Describe aortic compliance’s influence on stroke volume
A
Definition: Aortic compliance refers to the ability of the aorta to stretch and accommodate the stroke volume.
Influence on SV: Decreased aortic compliance (e.g., due to aging or arteriosclerosis) can increase afterload and reduce stroke volume.
12
Q
Describe Medications and Substances’ influence on stroke volume
A
Inotropic Agents: Medications such as digoxin or beta-agonists can increase contractility and stroke volume.
Vasodilators: Drugs that decrease systemic vascular resistance can reduce afterload and improve stroke volume.
Diuretics: By reducing blood volume, diuretics can decrease preload and potentially reduce stroke volume.
13
Q
Define Stroke volume (SV)
A
is the amount of blood ejected from the left ventricle of the heart with each heartbeat.
14
Q
Describe Cardiac output (CO)
A
the volume of blood pumped by the heart per minute and is a crucial indicator of heart function.
15
Q
Factors Influencing Cardiac Output:
A
Stroke Volume (SV):
Preload: Affects ventricular filling and stroke volume.
Afterload: Affects the resistance against which the heart pumps.
Contractility: Affects the strength of heart muscle contractions.
Heart Rate (HR):
Autonomic Nervous System Activity: Influences heart rate.
Hormones and Medications: Affect heart rate and contractility.
Exercise: Can increase heart rate and stroke volume.
Blood Volume and Venous Return:
Blood Volume: Affects preload and cardiac output.
Venous Return: Influences preload and cardiac output.
Cardiac Function and Health:
Heart Size, Function, and Intracardiac Pressures: Affect overall cardiac output.
16
Q
What is the difference between systole and diastole
A
systole is the contraction of a ventricle
diastole is the relaxation of the ventricle
17
Q
How do you calculate cardiac output
A
CO = SV*HR
80 mL/beat*70 beats/min = 5600 mL /min=5.6L/min
18
Q
What do positive chronotrope medications do?
A
Positive chronotropes speed things up (epi, atropine)
19
Q
What do negative chronotrope medications do?
A
negative chronotropes slow them down (beta blocker)
20
Q
What affects afterload
A
Afterload: Resistance ventricles must overcome to pump the blood influenced by (how tight the arteries are) :
Hypertension
Atherosclerosis
Vasoconstriction
21
Q
What is a resting CO
A
resting is 5-6 L /min
22
Q
Name an example of the heart compensating for an increased SV, by decreasing HR
A
Cardiovascular conditioning
23
Q
Name an example of the heart compensating for compensate decreased SV by increasing the HR
A
Hypovolemia
24
Q
How much urine should be produced an hour if the kidneys are being well perfused
A
need 30ml/hour
25
what does a chemistry panel tell us about heart function/health
Calcium: Abnormal calcium levels can affect heart rhythm and contractility. High calcium (hypercalcemia) can lead to arrhythmias, while low calcium (hypocalcemia) can also impact heart function and lead to muscle cramps or spasms.
Potassium (K+): Potassium is essential for proper heart rhythm, muscle function, and nerve transmission. High potassium (hyperkalemia) can cause dangerous cardiac arrhythmias, while low potassium (hypokalemia) can also affect heart rhythm and muscle function.
Magnesium: Magnesium is essential for the normal functioning of cardiac ion channels, including those that regulate sodium, potassium, and calcium influx and efflux in heart cells. Adequate magnesium levels help maintain a regular heart rhythm and prevent arrhythmias (irregular heartbeats). Magnesium deficiency is associated with increased vascular resistance and higher blood pressure.
26
What is BNP
Definition: B-type natriuretic peptide (BNP) is a hormone produced by the heart's ventricles in response to increased pressure and stretching of the heart muscle.
Production: BNP is released when the heart is under stress, such as in heart failure, and helps regulate blood pressure and fluid balance by promoting vasodilation (widening of blood vessels) and increasing sodium excretion through the kidneys.
27
Name the most commonly known cardiac enzyme and what it indicates
Troponin
Proteins involved in muscle contraction. They are highly specific to cardiac muscle. Troponin levels rise within a few hours after myocardial injury and can remain elevated for several days. They are the most sensitive and specific markers for myocardial infarction (MI or heart attack).
28
Describe the importance of total cholesterol lab findings
High Total Cholesterol: Elevated total cholesterol levels can be a marker of increased risk for cardiovascular diseases, including atherosclerosis (hardening of the arteries), coronary artery disease, and heart attacks.
LDL Cholesterol: High levels of LDL cholesterol are particularly concerning as they contribute to the formation of atherosclerotic plaques in the arteries, which can lead to reduced blood flow and increased risk of heart disease.
HDL Cholesterol: Low levels of HDL cholesterol are associated with a higher risk of cardiovascular disease, as HDL helps remove LDL cholesterol from the bloodstream.
29
Describe the importance of triglyceride lab findings
High triglycerides usually mean you aren't metabolizing energy stores from food correctly. High tri can contribute to the formation of atherosclerotic plaques and are often seen in conditions such as metabolic syndrome, diabetes, and obesity.
30
What is the purpose of an echocardiogram
look at heart structure and measure output and check valve function
31
Why would you perform a cardiac stress test
looking for abnormal change in rhythm during exercise
32
What is a Percutaneous Transluminal Coronary Angioplasty (PTCA)
go in with a balloon and widen the narrowed artery
33
What is a Directional Coronary Atherectomy (DCA):
screws plaque out of the artery
34
What do you need to ensure as a nurse prior to your patient's cardiac cath
ensure that the patient does not have allergy to iodine/shellfish before procedure
35
Describe the post-cardiac cath procedure protocol
Vital signs every 15 minutes x 4
every 30 minutes x 2
then every hour x4
then every 4 hours
PERFORM NEURO CHECKS EVERY TIME
36
Describe the post-cardiac cath procedure protocol WHEN THE FEMORAL ARTERY WAS ACCESSED
Patient has to lay flat for prescribed time (usually 6 hours)
37
How do you assess a patient's pulse and sensation is intact after a cardiac cath procedure
check a pulse site that is DISTAL to the catheter insertion site
38
Where does the borrowed vein attach on the heart during a CABG procedure
Attach borrowed vascular at aorta and place the other end BELOW WHERE BLOACKAGE IS so the tissue gets direct perfusion
39
Describe the best-case post-op CABG outcome
Extubated as soon as possible (as soon as 4 to 8 hours after surgery)
Pt meets VS parameters set by the surgeon
After stable and extubated, patient is encouraged to walk and move as much as possible
discharge by post-op day 2-3
40
How do you monitor for adequate perfusion
Level of consciousness, blood pressure, UrineOP, cap refill etc.
41
Medications that lower heart rate include:
Beta-blockers (e.g., atenolol, metoprolol)
Calcium channel blockers (e.g., verapamil, diltiazem)
Digoxin
Antiarrhythmics (e.g., amiodarone, sotalol)
Centrally acting agents (e.g., clonidine)
42
Describe the cardiac diet
Low saturated fat (lean meat)
high complex carbohydrate diet (oatmeal)
High fiber diet (reduces fat in blood)
Possible fluid or sodium restriction
Diabetes control (hypergly effects outcomes)
No alcohol (causes cardiomegaly) or Smoking
43
Describe the symptoms of coronary artery disease
Angina Pectoris: Chest pain or discomfort, often described as a squeezing or pressure sensation, that occurs when the heart muscle does not get enough oxygen-rich blood. It may radiate to the left arm, neck, jaw, or back.
Shortness of Breath: Especially during physical activity or stress.
Fatigue: Unusual tiredness, particularly during physical exertion.
Palpitations: Irregular or rapid heartbeats
Nausea or Indigestion: Often mistaken for gastrointestinal issues.
Sweating: Excessive sweating or cold sweat, particularly with chest pain.
Asymptomatic CAD:
Silent Ischemia: Some individuals may not experience noticeable symptoms but may still have underlying CAD, especially in individuals with diabetes.
44
Describe lab findings of coronary artery disease
Lipid Profile:
Total Cholesterol: Elevated levels increase CAD risk.
Low-Density Lipoprotein (LDL) Cholesterol: High levels are associated with increased risk of atherosclerosis.
High-Density Lipoprotein (HDL) Cholesterol: Low levels are a risk factor for CAD.
Triglycerides: Elevated levels can also contribute to cardiovascular risk.
2.2 Cardiac Biomarkers:
Troponin: Elevated levels may indicate myocardial injury, such as in acute coronary syndrome.
BNP: Elevated levels can suggest heart failure, which may be associated with CAD.
Other Tests:
Fasting Blood Glucose or HbA1c: Elevated levels may indicate diabetes, a risk factor for CAD.
High-Sensitivity C-Reactive Protein (hs-CRP): Elevated levels may indicate inflammation associated with CAD.
45
Describe the diagnostic tests used to dx coronary artery disease
Electrocardiogram (ECG):
Purpose: Detects abnormal heart rhythms and ischemic changes in the heart muscle.
Findings: May show ST-segment elevation or depression, T-wave inversions, or Q-waves indicative of ischemia or myocardial infarction.
Stress Testing:
Exercise Stress Test: Evaluates the heart’s response to physical exertion and identifies exercise-induced ischemia.
Pharmacologic Stress Test: Used when exercise is not possible; involves medications like dobutamine to simulate exercise effects.
Imaging Studies:
Chest X-Ray: Helps assess heart size, shape, and any fluid accumulation.
Echocardiogram: Uses ultrasound to evaluate heart function, structure, and blood flow.
Coronary Angiography (Coronary Catheterization): Provides detailed images of coronary arteries to identify blockages or narrowing.
Computed Tomography (CT) Angiography: Non-invasive imaging to visualize coronary arteries and assess for coronary artery disease.
3.4 Coronary Artery Calcium (CAC) Score: Measures the amount of calcium in coronary arteries, providing an estimate of atherosclerotic plaque burden.
46
Describe the different treatments for coronary artery disease
Medications:
Antiplatelet Agents:
Aspirin: Reduces the risk of blood clots and heart attacks.
Clopidogrel: Often used in combination with aspirin in certain cases.
Statins:
Examples: Atorvastatin, Simvastatin.
Purpose: Lower LDL cholesterol levels and stabilize atherosclerotic plaques.
Beta-Blockers:
Examples: Metoprolol, Carvedilol.
Purpose: Reduce heart rate and myocardial oxygen demand.
ACE Inhibitors:
Examples: Enalapril, Lisinopril.
Purpose: Lower blood pressure and reduce cardiac workload.
Calcium Channel Blockers:
Examples: Amlodipine, Diltiazem.
Purpose: Dilate coronary arteries and reduce angina.
Nitrates:
Examples: Nitroglycerin.
Purpose: Relieve angina by dilating coronary arteries and reducing myocardial oxygen demand.
Interventional Procedures:
Angioplasty and Stent Placement (Percutaneous Coronary Intervention):
Purpose: Open narrowed coronary arteries and place a stent to keep the artery open.
Coronary Artery Bypass Grafting (CABG):
Purpose: Bypass blocked coronary arteries using grafts to improve blood flow to the heart muscle.
47
Describe the pathophys of angina pectoris
Atherosclerosis: The most common cause, involving the buildup of fatty plaques in the coronary arteries, which narrows and hardens the arteries, reducing blood flow to the heart muscle.
Coronary Artery Spasm: Temporary tightening or constriction of the coronary arteries that reduces blood flow, which can occur in conditions such as Prinzmetal’s angina.
Other Causes: Can include coronary artery dissection, severe anemia, or a high heart rate.
Mechanism:
Increased Myocardial Oxygen Demand: During physical exertion or stress, the heart’s demand for oxygen increases.
Reduced Myocardial Oxygen Supply: If the coronary arteries are narrowed or obstructed, they cannot supply enough oxygen-rich blood to meet the increased demand, leading to ischemia.
Ischemia: Insufficient oxygen to the heart muscle causes pain or discomfort, often described as angina.
48
Describe the clinical Manifestations of Angina Pectoris
Symptoms:
Chest Pain or Discomfort: Often described as a squeezing, pressure, heaviness, or burning sensation. It typically occurs in the center or left side of the chest and may radiate to the left arm, neck, jaw, or back.
Shortness of Breath: Often accompanies chest pain, especially during physical activity.
Nausea or Indigestion: Sometimes mistaken for gastrointestinal issues.
Fatigue: Unusual tiredness, particularly during exertion.
Sweating: Cold sweat, particularly with chest pain.
Palpitations: Irregular or rapid heartbeats.
Types of Angina:
Stable Angina: Predictable and occurs with physical exertion or emotional stress. Relieved by rest or nitroglycerin.
Unstable Angina: Occurs unpredictably and may happen at rest. It is more severe and prolonged and indicates a higher risk of myocardial infarction.
Prinzmetal’s Angina (Variant Angina): Caused by coronary artery spasm, often occurring at rest and may be relieved by medications that treat spasm
49
Describe the lab findings of angina pectoris
3.1 Cardiac Biomarkers:
Troponin: May be normal in stable angina but elevated in unstable angina or myocardial infarction.
Creatine Kinase-MB (CK-MB): Typically normal in stable angina but may be elevated during myocardial injury.
BNP or NT-proBNP: Elevated in heart failure, which may accompany severe or chronic angina.
3.2 Lipid Profile:
Total Cholesterol: Elevated levels can indicate increased cardiovascular risk.
LDL Cholesterol: High levels are associated with atherosclerosis.
HDL Cholesterol: Low levels are a risk factor for cardiovascular disease.
Triglycerides: Elevated levels can contribute to cardiovascular risk.
3.3 Other Tests:
Fasting Blood Glucose or HbA1c: Elevated levels indicate diabetes, a risk factor for angina.
50
Describe diagnostic tests for angina pectoris
Electrocardiogram (ECG):
Purpose: Detects ischemic changes during episodes of angina. It may show ST-segment depression or T-wave inversions.
Findings: May be normal between episodes or show transient ischemic changes during pain.
4.2 Stress Testing:
Exercise Stress Test: Assesses the heart’s response to physical exertion and identifies exercise-induced ischemia.
Pharmacologic Stress Test: Used when exercise is not possible, using medications like dobutamine to simulate the effects of exercise.
4.3 Imaging Studies:
Echocardiogram: Evaluates heart function and structure and can detect ischemia or damage to heart muscle.
Coronary Angiography: Provides detailed images of coronary arteries to identify and evaluate blockages or narrowing.
Cardiac CT Angiography: Non-invasive imaging to visualize coronary arteries and assess for coronary artery disease.
4.4 Coronary Artery Calcium (CAC) Score:
Purpose: Measures the amount of calcium in coronary arteries, indicating the extent of atherosclerotic plaque.
51
Describe tx of angina pectoris
5.2 Medications:
Nitrates:
Examples: Nitroglycerin, Isosorbide dinitrate.
Purpose: Relieve angina by dilating coronary arteries and reducing myocardial oxygen demand.
Beta-Blockers:
Examples: Metoprolol, Atenolol.
Purpose: Reduce heart rate and myocardial oxygen demand.
Calcium Channel Blockers:
Examples: Amlodipine, Diltiazem.
Purpose: Dilate coronary arteries and reduce angina.
Antiplatelet Agents:
Examples: Aspirin, Clopidogrel.
Purpose: Reduce blood clot formation and decrease cardiovascular risk.
Statins:
Examples: Atorvastatin, Simvastatin.
Purpose: Lower LDL cholesterol and stabilize atherosclerotic plaques.
5.3 Interventional Procedures:
Angioplasty and Stent Placement (Percutaneous Coronary Intervention):
Purpose: Open narrowed coronary arteries and place a stent to keep the artery open.
Coronary Artery Bypass Grafting (CABG):
Purpose: Bypass blocked coronary arteries using grafts to improve blood flow to the heart muscle.
52
1. Pathophysiology of Myocardial Infarction
1.1 Cause:
Atherosclerosis: The most common cause, involving the buildup of atherosclerotic plaques (fats, cholesterol, and other substances) in the coronary arteries, which can rupture and form a blood clot.
Coronary Artery Thrombosis: A blood clot that forms on top of a ruptured plaque, obstructing blood flow to the heart muscle.
Coronary Artery Spasm: Rarely, severe spasm of a coronary artery can cause temporary obstruction leading to MI.
1.2 Mechanism:
Reduced Blood Flow: When a coronary artery is blocked, blood flow to a part of the heart muscle is reduced or completely cut off.
Ischemia and Infarction: The affected heart muscle undergoes ischemia (lack of oxygen) and then infarction (tissue death) if the blood supply is not restored promptly.
Cellular Damage: Deprivation of oxygen leads to cellular damage, release of intracellular enzymes, and eventually necrosis of the myocardial tissue.
53
2. Manifestations of Myocardial Infarction
2.1 Symptoms:
Chest Pain or Discomfort: Typically described as a pressure, squeezing, fullness, or pain in the center or left side of the chest. It may radiate to the left arm, neck, jaw, back, or stomach.
Shortness of Breath: Often accompanies chest pain and may occur independently of chest pain.
Nausea and Vomiting: Can be present, especially in inferior MIs.
Diaphoresis: Cold, clammy sweat.
Fatigue: Unusual tiredness, which may be present even without chest pain.
Palpitations: Irregular or rapid heartbeats.
2.2 Silent Myocardial Infarction:
Some patients, particularly diabetics or the elderly, may have an MI without the classic symptoms.
54
3. Laboratory Findings of myocardial infarction
3.1 Cardiac Biomarkers:
Troponin I and T: Highly specific and sensitive for myocardial injury. Levels rise within 3-12 hours of infarction and can remain elevated for days.
Creatine Kinase-MB (CK-MB): Rises within 4-6 hours of infarction and peaks around 24 hours. It is less specific than troponin but still used to assess myocardial injury.
Myoglobin: An early marker of myocardial injury, but not as specific as troponin.
3.2 Additional Labs:
BNP or NT-proBNP: Elevated levels may indicate heart failure, which can be associated with MI.
Lipid Profile: Assess for dyslipidemia, a risk factor for MI.
Complete Blood Count (CBC): May show signs of anemia or inflammation.
55
Diagnostic Tests for myocardial infarction
Diagnostic Tests
4.1 Electrocardiogram (ECG):
Purpose: Detects electrical changes in the heart related to ischemia or infarction.
Findings:
ST-Segment Elevation Myocardial Infarction (STEMI): Characterized by ST-segment elevation in specific leads.
Non-ST-Segment Elevation Myocardial Infarction (NSTEMI): May show ST-segment depression or T-wave inversions.
Q-Waves: May develop over time and indicate past myocardial infarction.
4.2 Stress Testing:
Purpose: Used after initial management to assess the extent of ischemia and the heart’s response to stress.
4.3 Imaging Studies:
Echocardiogram: Evaluates heart function, identifies areas of myocardial damage, and assesses for complications like left ventricular dysfunction or pericardial effusion.
Coronary Angiography (Coronary Catheterization): Provides detailed images of coronary arteries to identify and evaluate blockages.
Cardiac MRI: Can assess myocardial tissue damage and viability.
4.4 Chest X-Ray:
Purpose: Helps rule out other causes of chest pain, such as pulmonary issues, and assesses heart size and shape.
56
Tx for myocardial infarction
5.1 Initial Management:
Aspirin: Administered to inhibit platelet aggregation and reduce clot formation.
Oxygen Therapy: Given if oxygen saturation is low or if there is significant respiratory distress.
Analgesics: Morphine may be used for pain relief and to reduce anxiety.
Nitrates: To reduce myocardial oxygen demand and improve blood flow.
Anticoagulants: Medications like heparin or low molecular weight heparin to prevent further clot formation.
5.2 Reperfusion Therapy:
Thrombolytics: Medications like tissue plasminogen activator (tPA) are used to dissolve the blood clot and restore blood flow. Best administered within the first few hours of symptom onset.
Percutaneous Coronary Intervention (PCI): Angioplasty with stent placement to open the blocked coronary artery. Often preferred over thrombolytics in many cases.
5.3 Medications:
Antiplatelet Agents:
Clopidogrel or ticagrelor to prevent further clot formation.
Beta-Blockers:
Examples: Metoprolol, Carvedilol to reduce heart rate and myocardial oxygen demand.
ACE Inhibitors:
Examples: Enalapril, Lisinopril to reduce blood pressure and prevent heart failure.
Statins:
Examples: Atorvastatin, Simvastatin to lower cholesterol and stabilize atherosclerotic plaques.
Anticoagulants:
Examples: Warfarin, rivaroxaban for longer-term prevention of clot formation.
5.4 Post-Acute Management:
Cardiac Rehabilitation: A structured program of exercise, education, and counseling to improve cardiovascular health and recovery.
Lifestyle Modifications: Diet, exercise, smoking cessation, and weight management.
Long-Term Follow-Up: Regular monitoring and management of cardiovascular risk factors.
57
Pathophysiology of Heart Failure
Coronary Artery Disease (CAD): Often leads to myocardial infarction and subsequent heart failure.
Hypertension: Increases the workload on the heart, leading to hypertrophy and eventually heart failure.
Valvular Heart Disease: Conditions like aortic stenosis or mitral regurgitation can impair heart function.
Cardiomyopathies: Diseases of the heart muscle, such as dilated or hypertrophic cardiomyopathy.
Chronic Lung Disease: Can lead to right-sided heart failure due to increased pressure in the pulmonary circulation (cor pulmonale).
Arrhythmias: Abnormal heart rhythms can impair the heart's pumping efficiency.
Other Conditions: Include congenital heart defects, diabetes, and thyroid disorders.
1.2 Mechanisms:
Systolic Dysfunction: Reduced ability of the heart to contract and eject blood, often due to weakened heart muscle.
Diastolic Dysfunction: Impaired filling of the heart with blood due to stiff or hypertrophied heart muscle.
Compensatory Mechanisms: The body attempts to compensate for reduced cardiac output through mechanisms like increased heart rate, fluid retention, and hypertrophy of the heart muscle. While initially adaptive, these mechanisms can eventually worsen heart failure.
58
clinical Manifestations of Heart Failure
2.1 Symptoms:
Dyspnea: Shortness of breath, especially on exertion or when lying flat (orthopnea).
Fatigue: Unusual tiredness due to reduced cardiac output.
Edema: Swelling of the legs, ankles, or abdomen due to fluid retention.
Cough: Often dry or productive with frothy sputum, indicating pulmonary congestion.
Decreased Exercise Tolerance: Difficulty performing physical activities.
Paroxysmal Nocturnal Dyspnea: Sudden shortness of breath during sleep, waking the patient up.
Ascites: Fluid accumulation in the abdominal cavity, common in right-sided heart failure.
2.2 Signs:
Rales (Crackles): Heard on auscultation due to fluid in the lungs.
Jugular Venous Distention (JVD): Elevated jugular veins due to increased central venous pressure.
Hepatomegaly: Enlarged liver due to congestion.
Pitting Edema: Swelling in the extremities that leaves an indentation when pressed.
59
Laboratory Findings of heart failure
3.1 Biomarkers:
B-type Natriuretic Peptide (BNP) or NT-proBNP: Elevated levels indicate heart failure and can help differentiate it from other causes of dyspnea.
Troponin: May be elevated in acute heart failure or myocardial injury.
Renal Function Tests: Elevated creatinine or blood urea nitrogen (BUN) may indicate renal impairment associated with heart failure.
3.2 Other Labs:
Electrolytes: Imbalances, such as low potassium or sodium levels, can occur with heart failure and its treatment.
Lipid Profile: Evaluates cardiovascular risk factors.
60
Diagnostic tests for heart failure
4.1 Electrocardiogram (ECG):
Purpose: Identifies underlying arrhythmias, ischemic changes, or signs of left ventricular hypertrophy.
Findings: May show signs of prior myocardial infarction or atrial fibrillation.
4.2 Echocardiogram:
Purpose: Assesses heart function, structure, and evaluates ejection fraction (EF), which helps classify heart failure as systolic or diastolic.
Findings: Can reveal left ventricular hypertrophy, valvular heart disease, and other structural abnormalities.
4.3 Chest X-Ray:
Purpose: Evaluates heart size, pulmonary congestion, and fluid accumulation.
Findings: May show cardiomegaly, pulmonary edema, or pleural effusion.
4.4 Cardiac MRI:
Purpose: Provides detailed images of heart structure and function and helps assess myocardial tissue characteristics.
Findings: Useful for evaluating cardiomyopathies and assessing myocardial fibrosis or inflammation.
4.5 Stress Testing:
Purpose: Assesses the heart’s response to stress and evaluates exercise tolerance.
61
Describe the anatomy of the vasculature that contributes to CAD
tunica intima most innermost lining.
Tunica media contracts.
Tunica externa faces outside environment.
When intima is damaged it causes healing reaction that plaque can opportunistically attach to, causing plaque buildup at injury site
62
If you see elevated CRP (c-reactive protein) you should suspect which cardio disease process
coronary artery disease
62
What medication should you give to a pt with CAD that needs to decrease risk of complete occlusion
Niacin (decreased LDL cholesterol )
Aspirin, warfarin (Antiplatelet/anticoagulant therapy)
63
T/F: You need a low sodium, low fat, high fiber diet to treat pts with CAD
False: No need for strict sodium restriction unless further compromise noted
Focus on low fat, high fiber diet
64
How do you treat ER pts with shoulder, neck, substernal, or back pain?
These types of pain you treat for angina until ruled out in ER
65
What type of angina causes chest pain from SPASMING (media narrows randomly) not plaques/occlusion necessarily.
Variant Angina, also known as (Prinzmetal’s)
Related to stimulant use. Happening during sleep or randomly.
CAN RESULT IN ELEVATED ST SEGMENT.
66
What's the difference between stable and unstable angina
Stable: pain can be predicted based on level of activity. Plaque isn't getting bigger because it's capped, but still is occluding enough to cause some pain.
Unstable: pain is unpredictable and can wake someone up at night. Characterized by becoming worse over time (more painful, lasts longer) EMERGENCY UNTIL PROVEN NOT AN MI
67
Pt presents to the ER with torso pain that seems to be getting worse. He has HYPOTENSION, weak and thready pulse, and tachycardia. What do you suspect
Angina
68
If CK-MB is up but troponin is low, it means they are...
actively having a new cardiac event.
69
Why would you draw a myoglobin or CK-MB for a pt experiencing unstable angina
Myoglobin is the first to spike during muscle/heart damage, closely followed by CK-MB.
70
A patient's cardiac labs come back normal despite the patient's complaints of sustained chest and shoulder pain. Should you send them home?
No, because they could be about to have a cardiac event.
71
what does st elevation vs st depression mean
ST elevation (ST-elevated MI (STEMI)
When the ST segment is abnormally high above the baseline, this indicates transmural myocardial ischemia. This can be caused by a rupture, erosion, or dissection of a coronary artery that supplies blood to the heart.
OR
ST depression: non-ST-elevated MI (NSTEMI)
When the ST segment is abnormally low below the baseline, this indicates less severe myocardial ischemia. This can be caused by a number of conditions, including hypokalemia, myocardial ischemia, and a left bundle branch block
72
T/F: The gold standard diagnostic test to rule out MI with a patien currently experiecing chest pain is a Stress Test and Calcium scan
False
stress tests are contraindicated for chest pain and calcium scans should not be performed during a crisis.
73
What are the first interventions for a pt with unstable angina
Aspirin
Oxygen
IV
Diagnose as STEMI or NSTEMI
74
What supplement should cardiac pts take
omega-3
low fat, high fiber, high complex carb diet. NO REFINED SUGAR OR ALCOHOL
75
Hoe many times can you admin nitro to an angina pt
3 times
76
What's the biggest thing you want to look out for in a pt with a suspected MI
CHANGES in medication efficacy, pain, breathing, BP/HR.
REPORT IMMEADIATLEY.
77
Whats the difference between type 1 and type 2 myocardial infarction
Type 1 MI
Caused by a rupture or erosion of coronary plaque, which leads to thrombosis and vessel occlusion.
Type 2 MI
Caused by an imbalance between the supply and demand of oxygen to the heart muscle, which is often due to an extracardiac stressor like hypotension, tachycardia, or hypertension.
78
What symptoms are specific to an MI
CRACKLES
JVD
FEELING OF IMPENDING DOOM
79
What lab is specific to CARDIAC MUSCLE DEATH within the past few hours
troponin
80
What lab do you need to check when a pt is dx with an MI
PT/INR: bleeding risk
81
ST _______ often occurs with myocardial ischemia
ST __________ often occurs with complete occlusion
depression
elevation
82
To Dx a STEMI or NSTEMI on an ECG there must be ST elevation/depression for __ consecutive leads
3
83
What are the first two goals of treatment for MI
First: ECG w/ in 90 min
Second: Reperfusion therapy (Cath lab) w/ in 90 min
84
T/F: The patient should avoid eating foods high in fat and sodium during an MI, but needs to keep their energy up with carbohydrates and lean protein.
False
MI pts must be NPO during an acute event
Low-sodium, low-saturated fat, low-cholesterol diet after the acute period
85
Name 3 clinical manifestations of Cardiogenic shock d/t severe STEMI
Hypotension, diaphoresis, tachycardia
86
T/F: You can tell someone is in cardiogenic shock because they display signs of Heart Failure and Pulmonary Edema
False
Sx of HF and pulm edema usually manifests weeks after AMI
86
How do you treat cardiogenic shock?
Administer vasopressors, oxygen, etc. until heart can recover from insult
87
What are the differences in Sx for early and late stage HF
Early stage (left side only HF): Fatigue, edema, pulmonary congestion, kidney issues
Late stage (left and right side HF): JVD, hepatomegaly, pink frothy sputum
88
define ejection fraction
percentage of how much blood the left ventricle pumps out with each contraction
89
How do you calculate ejection fraction
Ejection Fraction = (Stroke Volume/End Diastolic Volume)x100
90
What is a normal ejection fraction
55%-65%
91
What is Hefref
Heart Failure with Reduced Ejection Fraction
Also known as systolic heart failure
The left ventricle is weakened and the EF (BELOW 55-65%) is decreased as a result
This decrease in EF is what causes hypoperfusion
92
What is Hefpef
Heart Failure with Preserved Ejection Fraction
Also known as diastolic heart failure
The left ventricle is stiff (usualy congenital) and/or physiologically smaller
This means that while the EF is at 55-65% or higher, the total amount being pumped out of the LV is not enough to meet metabolic demands
Still results in hypoperfusion and the same s/s of heart failure
93
Simply put, Hefref is best summarized as
a pump problem
94
Simply put, Hefpef is best summarized as
a DECREASED SIZE OF CHAMBER PROBLEM
95
what is cardiomyopathy
the heart muscle to become enlarged, thickened, or stiff, and in rare cases, scar tissue can replace the muscle
96
Difference between left and right sided HF manifestations
Left-Sided HF Manifestations: dyspnea, orthopnea, crackles, non-productive cough, wheezes, pink and frothy sputum, weight gain
Right-Sided HF Manifestations
ascites, JVD, edema, weight gain, fatigue
97
Is it possible to have right sided HF without left sided HF
yes, R sided (w/ out being caused by L) can be caused by cor pulmonale.
98
The labs on someone with HF might look like
diluted blood/electrolytes from fluid retention r/t kidneys reaction to decreased CO
severe anemia from kidney injury
metabolic acidosis
liver function test may be whacky from r sided HF
99
How do you measure exact blood pressure in the right side of the heart
Central venous pressure (CVP)
100
What do you need to look at before giving furosemide (a diuretic)
don't give if K, or BP is low
101
When should you not give nitro
ONLY GIVE IF THEY HAVE A CONFIRMED BLOCKAGE.
If BP is low don't give
102
Why would you give morphine to a pt with HF
decreases afterload
103
What do you give if you want to improve the contractility/strength of the heart
positive inotropes: dopamine, dobutamine, milrinone
104
Why would you give milrinone
Milrinone improves the contractility/strength of the heart but doesn’t really increase HR
105
Whats a chronotrope and why would you use it for a HF pt
Increases HR and can help with contractility.
Ex: epinephrine) dopamine/dobutamine
106
T/F: You can give inotropes/chromotropes for CHF
No, Give these temporarily until the patient is out of crisis and can diuresis Etc. on their own.
107
What HF intervention is considered the last thing to do as it's considered an end of life decision
Ventricular Assist Device (VAD)
108
When would you want to restrict your patient's sodium intake
Heart Failure
109
What are unit "norms" for HF patients on cardiac floors
Monitor I&O
Daily weights
Maintain dietary restrictions (low sodium, fluid restrictions, low fat, high fiber/carb)
Check electrolyte levels, ABGs to ensure therapy is working
Administer oxygen
Elevate Head Of Bed
Elevate feed if edema is present
