Cardiovascular System Flashcards

Cardiovascular System and Related Pathologies

Introduction

• Week five overview: Discussing cardiovascular system with a focus on hypotension.
• Exam performance: Class average was 94.
  • Exam review: Available via Zoom appointment with the instructor; no video recording or verbatim notes permitted during review.
• Comprehensive fourth exam:
  • 50% new content.
  • 50% questions similar to previous exams.

Congenital Heart Disorders (CHDs)

• Etiology:
  • Maternal smoking: Linked to oxidative stress and hypoxic states during fetal development.
  • Medications:
    • Antiepileptic drugs.
    • SSRIs: Potential cause of persistent pulmonary hypertension.
  • Maternal conditions:
    • Obesity.
    • Preexisting diabetes: Uncontrolled blood sugars can lead to septal hypertrophy.
• Manifestations:
  • Vary based on the specific defect and balance (blood flow through the heart +/- lungs and body).
  • Abnormal shunting of blood flow (e.g., VSD with pulmonary hypertension causing right-to-left shunting).
  • Fetal shunts may not close immediately, leading to signs and symptoms.

Fetal Circulation

• Key differences from postnatal circulation: High lung pressure and low body pressure (opposite of postnatal).
• Oxygenated blood flow:
  • Placenta → Umbilical vein → IVC via ductus venosus.
  • Shunted from RA to LA through foramen ovale (PFO).
  • Left atria → LV → Aorta to systemic circulation.
  • Small amount goes to RA, RV, and then pulmonary artery; bypasses lungs through ductus arteriosus.
• Deoxygenated blood returns to the placenta via umbilical arteries.
• Fetus makes breathing movements for lung development and pressure regulation, not oxygenation.

Characteristics of CHDs

• Structural abnormalities occurring prenatally, involving walls, valves, or vessels.
• Incidence: Approximately 1% of newborns.
• In utero: Often silent due to placental support for oxygenation and ventilation; issues usually arise postnatally.
• Manifestation: Postnatal issues can take days to weeks (complicated system that does not change to postnatal circulation immediately).
• Diagnosis:
  • May not always be accurate prenatally due to imaging difficulties with fetal movement.
  • Some conditions, like septal hypertrophy may take an entire gestation to develop.

Cyanotic vs. Acyanotic CHDs

• Acyanotic CHDs: Do not initially change oxygenation delivered to the body.
  • Examples: Tetralogy of Fallot, VSDs, ASDs.
• Cyanotic Heart Defects:
  • Decrease oxygen delivery.
  • Classified as critical congenital heart disease (CCHD).
  • Can involve single or multiple defects, right or left heart obstruction, or mixing of blood.

Universal Newborn Screening

• Importance: 30% of infant mortality is directly associated with critical congenital heart defects.
• Method: Simultaneous O2 saturation measurements.
  • Right hand (preductal).
  • Either foot (postductal).
  • Measured between 24-48 hours of age.
• Indications for Further Evaluation:
  • Sat < 90%.
  • Sat < 95%.
  • Difference > 4% between pre and post sats.
• Interpretation of Results:
  • Difference indicates discrepancy between oxygen flow to heart/lungs vs. body (mixing lesion or difficulty with oxygenated blood distribution).
• False positives can occur with primary pulmonary diseases (like pneumonia).

Undiagnosed CCHDs

• Conditions like coarctation of the aorta or interrupted aortic arch can be missed.
• Coarctation example: Aorta narrows, and PDA closure exacerbates the problem, leading to decreased blood flow to lower extremities.
• Manifestations of Decreased Blood Flow to Lower Extremities:
  • Poor perfusion.
  • Prolonged capillary refill.
  • Discrepancy in femoral vs. brachial pulses.
  • Decreased urine output.
  • Demarcation line indicating perfusion difference.

Conditions Affecting Cardiac Output

Coronary Artery Disease (CAD)

• Risk Factors:
  • Non-modifiable: Age, family history.
  • Modifiable: Tobacco use, weight, inactivity, stress, diabetes, high lipids, hypertension.
  • Negative: High HDL cholesterol.
  • Emerging: Elevated CRP (chronic inflammation), homocysteine levels affecting vessel smoothness.
• Metabolic Syndrome: Hypertension, hyperlipidemia, and diabetes increase the risk for CAD.
• Consequences of CAD:
  • Heart failure.
  • Sudden death.
  • Myocardial ischemia.
  • Coronary vasospasms.
• Myocardial Ischemia:
  • Occurs when myocardial oxygen demand exceeds supply, often due to blockage.
  • Compensation through increased heart rate and O2 flow is impaired by blockages.
  • Atherosclerotic plaques reduce compensatory abilities, increasing risk for acute MI.
• MIs in Younger Patients:
  • Atherosclerotic plaques can rupture, move, and impede blood flow.
  • Hypercoagulable states (e.g., lupus).
  • Drug-induced vasospasms, coronary embolism, autoimmune-related issues.

Spontaneous Coronary Artery Dissection (SCAD)

• Partial dissection of the lumen of the artery.
• Management: Intense blood pressure control, potentially mesh support to arterial dissection.
• Higher risk in patients with Marfan syndrome (connective tissue disorder affecting vessel structure).

Other Etiologies for MIs in Young Patients:

• Cocaine use.
• Drug overdose.
• Hypoxic events (e.g., choking).
• Recreational nitrous oxide use.

Evaluating Chest Pain

• Troponin Levels:
  • Normal: Consider non-cardiac causes.
  • Elevated: Concern for acute MI.
• Evaluation Steps:
  • Traditional CV risk factors.
  • Drug use history (urine drug screen).
  • Coronary assessment even if drug screen is negative.
  • Consider drug-induced AMI even if the drug screen is positive.

Potential Findings During Evaluation:

• Focal stenosis or isolated thrombus.
• Non-obstructive CAD.
• Occlusion that resolves with nitro or calcium channel blockers suggest vasospasm.
• Focal dissection (SCAD).
• Avascular necrosis.

Biomarkers for Myocardial Infarction

• CK-MB:
  • Detects myocardial necrosis after six hours.
  • Useful even if we see specificity of skeletal muscle damage.
  • Quick, cost-effective, early detection.
• Myoglobin:
  • Sensitive and can detect MI within two hours.
  • Also detects reperfusion.
  • Low specificity for skeletal muscle injury, so may need further validation.
  • Must be drawn within 1-2 hour window.
• Troponins:
  • Greater sensitivity and specificity than CK-MB.
  • Can detect recent MI up to two weeks prior.
  • Important to trend with the timeline of the symptoms presenting.
  • New high sensitivity troponin tests trending.

Conditions Affecting Tissue Perfusion

Peripheral Vascular Disease (PVD)

• Upper and Lower Extremities Impacted:
  • Likely peripheral arterial disease; investigate arterial occlusive disorders.
• One Arm Impacted:
  • Atherosclerosis.
  • Arterial thrombus.
• Risk Factors:
  • Similar to atherosclerosis - age, diabetes, dyslipidemia, smoking, hypertension.
• Symptoms:
  • Develop with stenosis or blockage.
  • Pain: Persistent with activity, relieved by rest (intermittent claudication); worsened with elevation.

Manifestations of PVD

• Erectile dysfunction occurs with vascular disease involving the aortoiliac artery.
• The "Six P's" (Emergency):
  • Pallor.
  • Pulselessness.
  • Paresthesia.
  • Paralysis.
  • Poikilothermia (cold).
  • Pain.

PVD Testing and Management

• Diagnosis: Ultrasound, blood pressures in upper and lower extremities, CTA, MRA.
• Labs: Lipid panel, homocysteine, CRP.
• Treatment: Depends on progression and physical exam findings.
  • Raynaud's: Warm extremity, beta blockers.
  • Severe tissue loss concern: Aggressive clot diagnosis to address any stenosis.

Arterial vs. Venous Thrombus

Different presentation depending on the clot location

• Pulse:
  • Pulse present in venous.
  • Pulse weaker or absent distal to the clot located in an arterial position.
• Skin Color:
  • Congestion, red/purple in venous thrombus.
  • Cyanotic, pale with arterial thrombus.
• Skin Temperature:
  • Warm with venous thrombus.
  • Cool in arterial thrombus.
• Edema:
  • Present in venous thrombus.
  • Minimal/absent with arterial.

Deep Vein Thrombosis (DVT)

• Veins Most Affected: Popliteal, femoral, common femoral, iliac veins.
• Risk Factors:
  • Decreased blood flow, increased venous pressure, mechanical injury, inflammation.
  • Non-smooth vessel lining promotes clot formation.
  • Increased blood viscosity will also yield the same effects.
  • Anatomic differences in the venous anatomy promotes catch blood products more easily.
  • Dehydration will make blood thicker.

Increased Risk of Coagulation:

• Genetic Factors: Abnormal protein C/S, antithrombin III deficiency, factor V Leiden.
• Acquired Risks: Cancer, sepsis, MI, heart failure, vasculitis, lupus.

Virchow's Triad

• Describes pathophysiology for DVT development:
  • Damage to vessel wall.
  • Blood flow turbulence.
  • Hypercoagulability.
• Significance of Vessel Wall Damage: Can be minimal, e.g., trauma, PICC line attempts, surgery, PICC line attempts, surgery.
• Implications Between Thrombosis and Fibrinolysis: Dynamic counteraction

Conditions Resulting in Changes in Cardiac Output and Perfusion

• Blood Pressure =$\$ Cardiovascular Resistance$\$ * Systemic Vascular Resistance.
• Cardiac Output: Blood pumped per minute (function of resistance and heart rate).
• Stroke Volume: Amount of blood leaving the heart with each contraction.
• Blood Pressure Regulation:
  • Controlled through multiple mechanisms involving adrenal gland hormones, kidneys, and more.
  • Adrenal Gland Hormones epinephrine & ADH: Vasopressin, increased water reabsorption.
  • RAAS: Decreased blood flow to the kidneys release renin resulting in vasoconstriction.
  • ANP or nitretic hormones: Sodium, chloride, and water losses.

Hypertension

Generally considered a disease to the arteries..

• Types: Primary/essential, prehypertension, familial, secondary, orthostatic/postural, complicated, isolated systolic, and malignant hypertension.
• Pregnancy-Induced Hypertension (PIH): Now termed gestational hypertension; can progress to preeclampsia and eclampsia.
• Impact: Impacts cardiac output and perfusion.

Conditions Affecting Myocardial Function

• Effective Myocarditis.
• Cardiomyopathies:
  • Hypertrophic: Walls are hypertrophied, decreasing chamber space reduces cardiac output due to decreased chamber volume.
  • Dilated can cause some hypertrophy, but also thinning of the walls which makes it so the chambers themselves are generally don't squeeze as well
  • Restrictive: Walls not as great at pumping.
• COVID related cardiomyopathy.
  • Can affect cardiac function and cardiac output in the long run.

Consequences of Abnormal Heart Structure

• Poor perfusion.
• Poor tolerance to exercise/activity.
• Change in pulses, capillary refill, mentation.
• Potential ischemia including coronary from reduced cardiac output.

Tamponade

• Acute event where pericardial sac fills with fluid.
• Compromises heart's ability to beat, decreasing cardiac output/stroke volume.
• Signs/Symptoms: Muffled heart sounds, failure, cardiogenic shock, tachycardia, hypotension, respiratory distress.
• Treatment: Remove fluid from the pericardial sac, increase preload with volume while the team figures out how to treat the problem.

Shock

Characterized by not enough tissue perfusion

• Due to decreased O2 delivery, increased O2 demand, or abnormal O2 use.

• Classification:

  • Compensated shock: Initial response with tachycardia.
  • Decompensated shock: Blood pressure drops, perfusion compromised.

• Categories:

  • Distributive (anaphylaxis).
  • Cardiogenic (related to heart function).
  • Hypovolemic (related to fluid volume).
  • Neurogenic
  • Septic
    Distributive, Cardiogenic, Neurogenic and Septic:

• Fluid is already in the body, it has shifted into the wrong places.

Hypovolemic:

Fluid in the body has shifted out and needs an IV bolus.

Cardiogenic Shock

Resulting from left ventricle cannot maintain adequate cardiac output.

• Compensatory mechanisms (increase heart and respiratory rate), although this will eventually lead to multisystem organ dysfunction and failure because of decreased contractility.
• Most Common Cause: acute Myocardial Infarction specifically of the Anterior Wall

Congestive Heart Failure (CHF)

Where the heart cannot pump enough blood to meet the body's metabolic needs.

• There will be decreased preload, decreased cardiac output and decreased afterload.
• Also signs and symptoms include decresed myocardial contractility and stroke volume.
• This can also lead to structural issues, congenital causes, post-surgery causes and MI based causes.
• CHF gets worse with pulmonary hypertension.

Right vs Left Sided:

There is a little bit of overlap with both and for purposes of school we can agree that

• Left Sided: will have pulmonary congestion, SOB, dyspnea and exercise intolerance, fatigue. X-ray will show pulmonary congestion.

• Right-Sided: the main sign there is an issue with congestion which is why hepatomegaly, ascites, edema and weight gain will occur. Dyspnea, exercise, intolerance, weakness, and fatigue occur as the effect of the actual heart not being able to pump correctly.

  JVD (Distended Neck Veins), flushed face, headache will signal a further issue is going on.

Hypotension Management

• Manage underlying cause (e.g., antibiotics for sepsis, treat low fluid states).
• Methods: Modify vascular resistance with pressors; increase cardiac output with fluid.
• Inotropes and Vasopressors:
  • Vasopressors: Cause vasoconstriction, increase resistance, improve MAP.
  • Inotropes: Increase contractility, improve cardiac output.

Pressors:

If the tank isn't filled, don't give these.

• Phenylephrine, Norepi, Epi, Vasopressin, Dopamine is a dose-dependent catecholamine.
• Inotropes: Dovuta and Milrinone- more niche, if there's concern with low afterload due to pulmonary hypertension.

Sepsis Management

• The way to go is norepinephrine: This works quicker and shows that it increases blood pressure in research and evidence based tactics- closes Vessels= increases blood pressure.
• Fluid: Should always be at the forefront- but needs to correlate with whatever shock management you are trying to achieve.
• Never JC = IVJC is the end of the road.

Neurogenic Shock.

• With these the main goal is to have a systolic that is greater than 90 or MAP >85 for first 7 days
• This will help adequately perfuse the brain which includes Epi or Phelyephine
• Be careful administering Phenylehrine because of the potential reflex of bradycardia.*

Cardiogenic:

Treat for dysrhythmias *NEVER DO DOPA WITH SEPSIS *.
Neuropathic and Dysrhythmias should be a very important component. And should recommend using this to help augment what is going well.

• Recommend Using Either ( Vasopressors and or inotropes depending on The Patient.
• Levophedrin Has A Very Small Portion of Inotropy*

With most shock and especially hypotension management remember, understanding what the meg is and why you are administering it is most important