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176 Week 7 notes Day 1
176 Week 7 notes Day 1
Perfusion
Perfusion is the circulation of blood throughout the body.
Key rule: Air goes in and out, blood goes round and round.
Factors Affecting Perfusion
Perfusion issues can be:
Temporary: e.g., acute myocardial infarction (MI) causing a drop in blood pressure.
Long term: e.g., chronic hypertension.
Permanent: e.g., heart failure.
Cardiac Anatomy
Blood flow:
Superior vena cava to right atrium.
Right atrium squeezes to right ventricle.
Right ventricle squeezes through pulmonary arteries to lungs (to pick up oxygen, drop off CO2).
Pulmonary veins back to left atrium.
Left atrium squeezes to left ventricle.
Left ventricle squeezes to the body through the aorta.
Heart has four chambers and four valves.
Heart muscle gets blood during diastole (coronary arteries fill).
Central perfusion involves the heart and lungs.
Cardiac Output
Cardiac output (CO) is the amount of blood the heart pumps in one minute.
Cardiac Output = Heart Rate * Stroke Volume
Heart rate (HR): number of beats per minute.
Stroke volume (SV): amount of blood ejected with each beat.
Changes in heart rate affect cardiac output.
Factors Affecting Heart Rate
Cardiac arrhythmias.
Blood volume: Insufficient blood volume reduces cardiac output.
Heart's ability to squeeze (contractility): Issues arise in heart failure.
Heart attacks: Damage from heart attacks affects the heart's ability to pump.
Medications: Can improve heart function.
Heart disease.
Preload vs. Afterload
Preload: Volume or stretch in the ventricles as they fill with blood.
Afterload: Pressure required to open the aortic valve.
Cardiac output is determined by stroke volume and heart rate: CO = SV * HR
Stroke volume is impacted by preload, afterload, and contractility.
Preload Explained
Preload is the stretch on the ventricles during diastole as they fill with blood, think of it like filling a balloon.
Measured by central venous pressure (CVP).
Factors decreasing preload:
Decreased blood volume (e.g., hemorrhage).
Factors increasing preload:
Heart failure.
Renal failure.
Afterload Explained
Afterload is the resistance the ventricle must overcome to open the aortic valve during systole.
Measured by systemic vascular resistance (SVR).
Factors decreasing afterload:
Low blood pressure.
Factors increasing afterload:
Hypertension.
Vasoconstriction.
Treatment Strategies
Low preload: Administer blood products or fluids to increase volume and stretch.
High preload: Administer diuretics or ACE inhibitors to decrease volume and stretch.
High afterload: Administer vasodilators to reduce resistance.
Low afterload: Administer vasoconstrictors to increase resistance.
Cardiac Medications
Diuretics (e.g., Lasix, spironolactone): Reduce preload by decreasing fluid volume.
ACE inhibitors, ARBs, and nitrates: Reduce afterload by vasodilation.
Inotropes (e.g., milrinone, dopamine, dobutamine, digoxin): Improve contractility, making the heart squeeze better.
Chronotropes:
Beta blockers (olol):
Rate control.
Calcium channel blockers (pines):
Rate control.
Digoxin: Slows heart rate; watch for toxicity (visual disturbances, bradycardia, GI upset).
Rate control.
Antiarrhythmics (e.g., amiodarone): Control rhythm.
Signs of Low Cardiac Output
Decreased level of consciousness.
Chest pain.
Wet, crackly lung sounds.
Cold, clammy skin.
Decreased urine output.
Weak peripheral pulses.
Dangerous Arrhythmias with No Cardiac Output
Pulseless ventricular tachycardia.
Ventricular fibrillation.
Asystole.
Risk Factors for Perfusion Issues
Age: Connective tissues and heart muscle stiffen with age.
Social and economic factors: Low income, low education, healthcare disparities.
Noncompliance with treatment.
Stress.
Poor eating habits (high sodium, fat, cholesterol).
Age-Related Changes
Connective tissue becomes denser and less stretchy.
SA node has fewer cells.
Fewer bundle of His and Purkinje fibers.
Blood vessels develop atherosclerosis and stiffen.
Increased risk of arrhythmias.
Heart valves thicken and stiffen, leading to stenosis or regurgitation (murmurs).
Peripheral vessels stiffen, impairing vasoconstriction and vasodilation.
Impaired Central Perfusion
Leads to hypoxia due to poor blood flow and oxygenation.
Can result in tissue death if unmanaged.
Diagnostic Tests
Lab Tests
Cardiac enzymes:
Troponin (gold standard): Elevates with heart muscle damage; monitored in series.
Creatinine kinase: Released with muscle damage.
Myoglobin: Positive indicates heart attack.
Serum lipids: High cholesterol contributes to plaque formation.
Complete blood count (CBC):
Checks red blood cell count.
Hemoglobin levels.
Blood coagulability:
Platelets.
PT/INR.
PTT.
D-dimer: Positive indicates a clot is present.
Bone marrow biopsy: Assesses red blood cell production (if H&H is abnormal).
Electrocardiogram (ECG/EKG)
Assesses electrical activity of the heart.
Stress Tests
Treadmill/stationary bike with heart monitoring.
Pharmacological stress test: Uses drugs to simulate exercise.
Radiograph Studies
Chest X-ray: Assesses heart size.
Ultrasound
2D echocardiogram: Assesses chamber size, wall thickness, valve function, and blood flow (Doppler studies).
Arteriogram and Mammograms
Imaging of vessels with dye.
Cardiac Interventions
Pacemaker Placement
Used when the SA or AV node is not functioning correctly.
Typically placed in the upper left chest.
Can be temporary or permanent.
Diet Therapy
Low sodium, low fat, low cholesterol.
Monitor potassium levels (3.5-5 mEq/L).
Immediate Actions for Chest Pain
Prioritize over almost everything except lack of breathing.
Administer oxygen to maximize hemoglobin saturation.
CPR: Essential skill.
Temporary Pacemakers
Transvenous: Inserted through the subclavian vein.
External: Applied through the skin (painful, requires sedation).
Pacemaker Purpose
Restore regular heart rhythm.
Improve cardiac output.
Basic Cardiac Rhythms
Five Steps for EKG Interpretation
Rate: Count R peaks, multiply by 10 (normal: 60-100 bpm).
Rhythm: Check if R peaks are evenly spaced (regular).
P Wave: Present with every QRS complex.
PR Interval: Should be five mini boxes or less (0.10-0.20 seconds).
QRS: Present, upright, and not wide (three little boxes or 0.12 seconds).
Normal Sinus Rhythm
Has PQRST for every beat.
Regular.
Rate between 60-100 bpm.
Sinus Bradycardia
Regular, has all parts (PQRST).
Rate below 60 bpm.
Symptoms: Asymptomatic or low confusion.
Causes: Drug-induced (digoxin, beta blockers).
Treatment: Atropine, pacemaker.
Sinus Tachycardia
Has all parts (PQRST).
Regular.
Rate: 100-150 bpm.
Symptoms: Similar to bradycardia.
Causes: Dehydration, stress, fever, caffeine toxicity.
Treatment: Address the primary cause, minimize caffeine, manage anxiety, beta blockers.
Dysrhythmias
Atrial: Originates in the SA node or atria.
Junctional: Originates at the AV node.
Ventricular: Originates below the AV node.
Atrial Fibrillation (A-Fib)
Irregular rhythm (only irregular rhythm in this class).
No visible P waves.
Increased risk of clot formation due to quivering atria.
Complications: Clots can travel to the lungs, brain, or other areas.
Treatment:
Control rate (new onset: 100-150 bpm).
Anticoagulate to prevent clots.
Cardioversion (synchronized).
Ventricular Tachycardia (V-Tach)
Check for a pulse.
Wide, bizarre QRS complexes.
Fast rate (up to 250 bpm).
Treatment:
No pulse: CPR, defibrillation.
Pulse and unstable: Cardioversion.
Pulse and stable: Amiodarone and cardioversion.
Ventricular Fibrillation (V-Fib)
Ventricles quiver (no contraction).
No cardiac output.
Disorganized electrical activity.
Treatment: CPR, defibrillation.
Asystole
No electrical or mechanical activity.
No pulse or respiration.
Treatment: CPR, epinephrine, atropine, transcutaneous pacing (not guaranteed to work).
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