12.1 Cardiovascular Conditions: Anatomy, Coronary Disease, Heart Failure, and Blood Pressure

12.1 Cardiovascular Conditions: Anatomy, Coronary Disease, Heart Failure, and Blood Pressure

Quick Answer: Cardiovascular and respiratory disorders represent the highest-liability emergency triage categories on the NCCAOM Biomedicine examination. Practitioners must immediately differentiate benign somatic complaints from acute crises. Acute Myocardial Infarction (AMI) presents with crushing substernal chest pressure, radiation to the left arm/jaw, diaphoresis, and dyspnea; however, women, diabetics, and the elderly frequently present atypically with isolated nausea, unexplained fatigue, or acute dyspnea without chest pain. Suspected AMI mandates immediate 911 activation, administration of chewable non-enteric aspirin 325 mg, and strictly prohibiting the patient from driving. Left-sided heart failure triggers pulmonary venous congestion manifested as orthopnea, paroxysmal nocturnal dyspnea (PND), bibasilar inspiratory crackles, and an S3 gallop, whereas right-sided heart failure causes systemic venous backup manifested as jugular venous distension (JVD) and peripheral pitting edema. Hypertensive emergencies involve blood pressure > 180/120 mmHg with acute target organ damage (e.g., encephalopathy, papilledema, aortic dissection, acute renal failure), requiring emergency department transfer. Pulmonary conditions follow in Section 12.2.

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Cardiovascular Anatomy and Electrophysiology

Safe clinical practice and accurate differential diagnosis require an exact understanding of cardiac vascular architecture, electrical conduction pathways, and mechanical cycle dynamics.

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|                        CARDIAC CONDUCTION TIMELINE                          |
+-----------------------------------------------------------------------------+
|  [SA Node] (60-100 bpm)  -->  Pacemaker: generates action potential         |
|         |                                                                   |
|         v                                                                   |
|  [Internodal Tracts]     -->  Atrial depolarization (P Wave on ECG)         |
|         |                                                                   |
|         v                                                                   |
|  [AV Node] (40-60 bpm)   -->  0.10-sec physiological delay (PR Interval)    |
|         |                                                                   |
|         v                                                                   |
|  [Bundle of His]         -->  Crosses fibrous atrioventricular skeleton     |
|         |                                                                   |
|         v                                                                   |
|  [Bundle Branches]       -->  Interventricular septum (Left & Right)        |
|         |                                                                   |
|         v                                                                   |
|  [Purkinje Network]      -->  Rapid ventricular activation (QRS Complex)    |
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Coronary Circulation and Myocardial Perfusion

The myocardium receives its oxygenated blood supply during ventricular diastole, when the aortic valve leaflets close and blood enters the coronary ostia located in the sinuses of Valsalva:

1. Left Main Coronary Artery (LMCA): Arises from the left aortic sinus and rapidly bifurcates into:
   • Left Anterior Descending (LAD) Artery: Clinically termed the "widow-maker." Travels down the anterior interventricular groove to supply the anterior two-thirds of the interventricular septum, anterior wall of the left ventricle, and the cardiac apex. Occlusion causes extensive anterior and septal wall infarctions (manifested on ECG leads V1–V4).
   • Left Circumflex (LCx) Artery: Courses along the coronary sulcus around the left cardiac border to supply the lateral and posterior walls of the left ventricle and left atrium (manifested on ECG leads I, aVL, V5, V6).
2. Right Coronary Artery (RCA): Originates from the right aortic sinus, coursing through the right atrioventricular groove. It supplies the right atrium, right ventricle, inferior wall of the left ventricle, and the sinoatrial (SA) node in 60% of individuals and the atrioventricular (AV) node in 90% of individuals. Occlusion causes inferior wall infarctions (leads II, III, aVF) and carries high risk for acute bradyarrhythmias, heart blocks, and right ventricular infarction.
3. Posterior Descending Artery (PDA): In approximately 85% of the population, the PDA arises from the RCA (designated "right-dominant circulation"); in 10% it originates from the LCx ("left-dominant"), and in 5% from both ("codominant"). The PDA perfuses the posterior third of the interventricular septum and inferior/posterior ventricular walls.

Cardiac Conduction System and Electrocardiographic Correlates

• Sinoatrial (SA) Node: Situated at the junction of the superior vena cava and the right atrium. Functions as the primary physiological pacemaker with an intrinsic firing rate of 60–100 impulses per minute.
• Atrioventricular (AV) Node: Located in the inferior-posterior aspect of the interatrial septum. Possesses an intrinsic pacing rate of 40–60 impulses per minute. Crucially, the AV node imposes an intrinsic 0.08 to 0.12 second delay on electrical impulses, allowing the atria to contract fully and eject their volume ("atrial kick") into the ventricles before ventricular systole commences.
• Bundle of His, Bundle Branches, and Purkinje Fibers: The His-Purkinje system traverses the fibrous skeleton, dividing into the Right Bundle Branch and the broader Left Bundle Branch (which further splits into anterior and posterior fascicles). Purkinje fibers distribute impulses throughout the ventricular subendocardium at velocities up to 4 meters per second, ensuring coordinated, apex-to-base ventricular contraction. The Purkinje network possesses an intrinsic escape rate of 20–40 impulses per minute.
• Electrocardiogram (ECG) Tracing Elements:
  • P Wave: Atrial depolarization (normal duration < 0.12 seconds).
  • PR Interval: Conduction time from SA node through the AV node and His-Purkinje system to ventricular myocytes (normal duration: 0.12 to 0.20 seconds; prolongation > 0.20 seconds signifies first-degree AV block).
  • QRS Complex: Ventricular depolarization (normal duration: < 0.12 seconds; widening >= 0.12 seconds indicates bundle branch block or ventricular ectopic focus).
  • ST Segment: Plateau phase of ventricular repolarization; normally isoelectric. Elevation indicates acute transmural myocardial injury (STEMI); depression signifies subendocardial ischemia.
  • T Wave: Rapid ventricular repolarization. Peaked symmetrical T waves indicate early ischemia or hyperkalemia; inverted T waves signify ischemia or ventricular strain.

Mechanical Cardiac Cycle and Auscultation

The cardiac cycle alternates between ventricular systole (contraction and ejection) and ventricular diastole (relaxation and filling). Understanding normal and adventitious heart sounds is foundational to physical assessment:

Hemodynamic Determinants of Blood Pressure

Systemic arterial blood pressure represents the product of cardiac output and peripheral resistance:

$\text{Mean Arterial Pressure (MAP)} = \text{Cardiac Output (CO)} \times \text{Systemic Vascular Resistance (SVR)}$ $\text{Cardiac Output (CO)} = \text{Stroke Volume (SV)} \times \text{Heart Rate (HR)}$

Stroke volume is modulated by three primary parameters:

1. Preload: The myocardial sarcomere stretch at end-diastole, governed by venous return (end-diastolic volume). In accordance with the Frank-Starling mechanism, increased filling increases contractile force up to physiological limits.
2. Afterload: The mechanical resistance or impedance against which the left ventricle must pump to eject blood, determined primarily by systemic vascular tone (SVR) and aortic compliance.
3. Inotropy (Contractility): The intrinsic contractile vigor of the myocardium independent of preload and afterload, augmented by sympathetic catecholamines and cardiac glycosides, and blunted by beta-blockers, hypoxia, acidosis, and ischemia.

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Coronary Artery Disease (CAD) and Acute Coronary Syndrome (ACS)

Coronary artery disease develops through an insidious, progressive inflammatory cascade within arterial walls, culminating in acute occlusive thrombosis.

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|                  ATHEROSCLEROTIC PLAQUE RUPTURE CASCADE                     |
+-----------------------------------------------------------------------------+
|  Endothelial Injury (Hypertension, Smoking, Hyperlipidemia, Hyperglycemia)  |
|                                    |                                        |
|                                    v                                        |
|  Subendothelial LDL Infiltration & Oxidation --> Monocyte Recruitment       |
|                                    |                                        |
|                                    v                                        |
|  Macrophage Phagocytosis of Ox-LDL --> Foam Cells & Fatty Streak Formation  |
|                                    |                                        |
|                                    v                                        |
|  Smooth Muscle Proliferation & Collagen Deposition --> Stable Fibrous Cap   |
|                                    |                                        |
|                                    v                                        |
|  Macrophage Metalloproteinase Secretion --> Cap Thinning & Vulnerability    |
|                                    |                                        |
|                                    v                                        |
|  Plaque Rupture / Fissuring --> Subendothelial Tissue Factor Exposure       |
|                                    |                                        |
|                                    v                                        |
|  Platelet Adhesion & Aggregation + Coagulation Cascade Activation           |
|                                    |                                        |
|                                    v                                        |
|  [Intraluminal Thrombus] --> Partial (UA/NSTEMI) or Complete (STEMI) Block  |
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The Clinical Spectrum of Myocardial Ischemia

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Clinical Presentation of Acute MI & Emergency Clinic Protocols

Recognizing an acute myocardial infarction in an outpatient acupuncture setting is an essential life-safety competency evaluated on the NCCAOM board examinations.

Classical Clinical Presentation

• Quality: Intense crushing, squeezing, aching, burning, or suffocating pressure behind the breastbone. Patients frequently place a clenched fist over the sternum (Levine's sign).
• Radiation: Pain classically radiates to the left shoulder, down the ulnar aspect of the left arm into the 4th and 5th digits, into the neck, the lower jaw/mandible, teeth, epigastrium, or interscapular region.
• Associated Autonomic Symptoms: Profuse cold diaphoresis (clammy skin), severe dyspnea, nausea, vomiting, dizziness, lightheadedness, pallor, and a profound psychological sense of impending doom (angor animi).
• Timing: Discomfort persists for > 20–30 minutes and is not alleviated by rest, position change, or sublingual nitroglycerin.

High-Yield Atypical Presentations: The High-Risk Triad

A substantial percentage of fatal myocardial infarctions present without classic crushing substernal chest pain. The NCCAOM examination heavily tests atypical presentations occurring in three vulnerable patient cohorts:

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|                     ATYPICAL PRESENTATIONS OF ACUTE MI                      |
+-----------------------------------------------------------------------------+
|  Vulnerable Populations:                                                    |
|  1. Diabetic Patients     --> Autonomic Neuropathy blunts visceral pain      |
|  2. Female Patients       --> Microvascular dysfunction & hormonal factors  |
|  3. Elderly Patients      --> Altered pain processing, cognitive changes     |
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|  Atypical Symptom Profile (Absence of Classic Substernal Pain):             |
|  * Sudden, unexplained shortness of breath (isolated dyspnea)               |
|  * Profound, overwhelming, unexplained exhaustion / sudden acute fatigue    |
|  * Indigestion, heartburn, epigastric burning, or postprandial fullness     |
|  * Isolated nausea, vomiting, or cold sweating                              |
|  * Unexplained acute confusion, delirium, syncope, or near-syncope          |
|  * Isolated jaw pain, neck ache, or isolated scapular discomfort            |
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Mandatory In-Clinic Emergency Action Protocol

If a patient exhibits symptoms suspicious for Acute Coronary Syndrome or Acute MI during an acupuncture visit, the practitioner must execute the following protocol immediately:

1. Call 911 Immediately: Activate Emergency Medical Services (EMS). Clearly state: "I have a patient experiencing signs of an acute myocardial infarction. The patient is at [Clinic Address]."
2. Administer Chewable Non-Enteric Aspirin (325 mg): Provide one adult 325 mg tablet (or four 81 mg baby aspirins). Instruct the patient to chew and swallow the tablets immediately. Chewing facilitates rapid buccal and sublingual mucosal absorption, achieving platelet cyclooxygenase-1 (COX-1) inhibition and suppressing thromboxane A2 synthesis within 15 minutes. Contraindications: Documented true severe anaphylactic allergy to aspirin, or active, visible massive gastrointestinal hemorrhage.
3. Patient Positioning and Needle Management: Cease all acupuncture treatment immediately. Swiftly and calmly remove all retained acupuncture needles. Position the patient in a comfortable semi-Fowler's position (head and torso elevated 30 to 45 degrees) to reduce venous return, lower cardiac workload, and ease dyspnea. Loosen tight neckwear and belts.
4. Oxygen and Sublingual Nitroglycerin Considerations:
   • Oxygen: If clinic supplemental oxygen is available, administer via nasal cannula at 2–4 L/min only if SpO2 measures < 90% or the patient is in overt respiratory distress (routine hyperoxia in non-hypoxemic MI causes coronary vasoconstriction and is contraindicated).
   • Nitroglycerin: If the patient possesses their own previously prescribed sublingual nitroglycerin, they may take one dose (0.4 mg sublingually every 5 minutes, up to 3 doses), provided their systolic blood pressure is >= 90 mmHg and heart rate is 50–100 bpm. Absolute Contraindication: Do NOT allow nitroglycerin if the patient has taken a phosphodiesterase-5 (PDE-5) inhibitor for erectile dysfunction or pulmonary hypertension within the prior 24 hours (sildenafil / Viagra, vardenafil / Levitra) or prior 48 hours (tadalafil / Cialis); concurrent administration produces catastrophic, refractory, fatal hypotension.
5. Monitor Vital Signs and Prepare AED: Obtain serial blood pressure, pulse, and oxygen saturation readings. Have the clinic Automated External Defibrillator (AED) at the patient's side. If the patient loses consciousness and becomes pulseless, immediately initiate high-quality cardiopulmonary resuscitation (CPR at 100–120 compressions/min) and attach the AED pads.
6. Strict Driving Prohibition: NEVER allow the patient to drive themselves to the emergency room, and NEVER allow a spouse or friend to transport them by personal vehicle. Patients suffering an evolving AMI are at extreme risk of developing lethal ventricular arrhythmias (ventricular fibrillation / ventricular tachycardia) within the first hour of symptom onset. EMS vehicles are mobile intensive care units equipped with 12-lead ECG tele-transmission, intravenous access, defibrillators, antiarrhythmic agents, and the ability to pre-activate the hospital cardiac catheterization laboratory before arrival.

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Heart Failure (Congestive Heart Failure - CHF)

Heart failure is a complex clinical syndrome resulting from structural or functional impairment of ventricular filling (diastolic dysfunction) or blood ejection (systolic dysfunction).

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|                      PATHOPHYSIOLOGY OF HEART FAILURE                       |
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|                                                                             |
|   [LEFT-SIDED HEART FAILURE]                 [RIGHT-SIDED HEART FAILURE]    |
|        (LV Dysfunction)                           (RV Dysfunction)          |
|               |                                          |                  |
|               v                                          v                  |
|    Elevated LV Diastolic Pressure             Elevated RV Diastolic Pressure |
|               |                                          |                  |
|               v                                          v                  |
|     LA Pressure Elevation                      RA Pressure Elevation        |
|               |                                          |                  |
|               v                                          v                  |
|    Pulmonary Vein Congestion                 Systemic Vein Congestion       |
|               |                                          |                  |
|               v                                          v                  |
|    Pulmonary Capillary Transudation          Vascular Fluid Transudation    |
|               |                                          |                  |
|               v                                          v                  |
|    * Pulmonary Edema                          * Jugular Venous Distension   |
|    * Orthopnea & PND                          * Hepatojugular Reflux        |
|    * Bibasilar Crackles (Rales)               * Dependent Pitting Edema     |
|    * S3 Gallop & Tachypnea                    * Congestive Hepatomegaly     |
|                                                                             |
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Left-Sided Heart Failure (Pulmonary Congestion & Low Output)

• Primary Etiologies: Ischemic heart disease (CAD / prior MI), long-standing systemic hypertension, dilated cardiomyopathy, aortic valve stenosis, and mitral regurgitation.
• Pathophysiology: Impaired left ventricular ejection or relaxation elevates left ventricular end-diastolic pressure (LVEDP). Pressure transmits backward into the left atrium and pulmonary veins, driving pulmonary capillary hydrostatic pressure above plasma oncotic pressure (typically > 20–25 mmHg). Fluid transudates into the pulmonary interstitial space and alveoli, impairing gas exchange.
• Clinical Manifestations:
  • Dyspnea on Exertion (DOE): The earliest and most sensitive symptom of left ventricular decompensation.
  • Orthopnea: Shortness of breath occurring when recumbent, caused by the redistribution of pooled venous blood from the lower extremities and splanchnic bed into the central pulmonary circulation. Quantified clinically by the number of pillows required to sleep comfortably (e.g., "three-pillow orthopnea").
  • Paroxysmal Nocturnal Dyspnea (PND): Sudden awakening 1 to 2 hours after falling asleep with severe air hunger, diaphoresis, and coughing, forcing the patient to sit upright or seek an open window.
  • Physical Findings: Bibasilar, fine, inspiratory crackles (rales) that do not clear with coughing; dullness to percussion at lung bases (pleural effusion); lateral and downward displacement of the apical Point of Maximal Impulse (PMI); an audible S3 ventricular gallop; tachypnea; and in acute flash pulmonary edema, expectoration of pink, frothy sputum.

Right-Sided Heart Failure (Systemic Venous Congestion)

• Primary Etiologies: The single most common cause of right heart failure is left-sided heart failure (elevated pulmonary pressures create backward afterload against the thin-walled right ventricle). Isolated right heart failure arises from chronic pulmonary disease (cor pulmonale secondary to severe COPD, pulmonary fibrosis, or recurrent pulmonary emboli), pulmonary arterial hypertension, and tricuspid valve disease.
• Pathophysiology: Right ventricular contractile failure leads to elevated right atrial pressure and retrograde venous stasis throughout the superior and inferior vena cava networks.
• Clinical Manifestations:
  • Jugular Venous Distension (JVD): Elevation of the internal jugular venous pulsation > 3–4 cm vertically above the sternal angle of Louis with the patient reclined at a 45-degree angle. Reflects directly elevated central venous pressure.
  • Positive Hepatojugular Reflux: Sustained, firm manual pressure applied over the right upper quadrant for 10–15 seconds produces a persistent elevation of >= 3 cm in the jugular venous column.
  • Dependent Peripheral Pitting Edema: Symmetrical pitting edema in the lowest gravitational tissues—pretibial areas, ankles, and dorsum of the feet in ambulatory patients; presacral and posterior thigh edema in bedridden patients.
  • Congestive Hepatomegaly and Ascites: Passive vascular congestion stretches the liver capsule, causing dull right upper quadrant tenderness, palpable smooth hepatomegaly, splenomegaly, and peritoneal transudate accumulation (ascites).
  • Gastrointestinal Congestion: Venous congestion of the stomach and bowel walls produces early satiety, anorexia, nausea, and abdominal bloating.

New York Heart Association (NYHA) Functional Classification

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Severe Hypertension vs. Hypertensive Emergency

Hypertension affects over one-third of adult clinical populations. Acupuncturists frequently perform baseline vital sign screenings and must know how to distinguish severe asymptomatic blood pressure elevation from a life-threatening crisis.

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|                      HYPERTENSIVE CRISES DIFFERENTIATION                    |
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|                        Severe BP Elevation                                  |
|             (Systolic > 180 mmHg and/or Diastolic > 120 mmHg)               |
|                                     |                                       |
|                    Assess for Acute Target Organ Damage                     |
|                                     |                                       |
|                  +------------------+------------------+                    |
|                  |                                     |                    |
|                  v                                     v                    |
|       [Target Organ Damage PRESENT]         [Target Organ Damage ABSENT]    |
|                  |                                     |                    |
|                  v                                     v                    |
|       HYPERTENSIVE EMERGENCY                 SEVERE HYPERTENSION            |
|                  |                                     |                    |
|  * Encephalopathy / Acute Stroke       * Severe headache, anxiety, epistaxis|
|  * Papilledema / Retinal Hemorrhage    * Outpatient oral medication titration|
|  * Acute Pulmonary Edema / Acute MI    * Gradual reduction over 24-48 hours |
|  * Aortic Dissection / Acute AKI       * Do NOT rapidly drop BP with IV meds|
|                  |                                     |                    |
|                  v                                     v                    |
|  [IMMEDIATE 911 / ICU ADMISSION]       [SAME-DAY / 24-HR MEDICAL REFERRAL]  |
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Severe Hypertension Without Target Organ Damage (Formerly "Hypertensive Urgency")

The 2025 AHA/ACC high blood pressure guideline replaced the older term "hypertensive urgency" with severe hypertension: a blood pressure above 180/120 mmHg without signs of acute target organ damage. The criteria and management principles below are unchanged; only the label is new. Older texts and some exam items still use the old term.

• Diagnostic Criteria: Systolic blood pressure > 180 mmHg and/or diastolic blood pressure > 120 mmHg, in the absence of acute target organ damage.
• Clinical Presentation: Patients are often entirely asymptomatic, or present with nonspecific complaints such as mild occipital tension headaches, generalized anxiety, lightheadedness, or minor epistaxis.
• Management Strategy: Severe hypertension without organ damage does not warrant emergency 911 dispatch or sudden intravenous antihypertensive therapy. In fact, precipitously dropping the blood pressure can induce cerebral hypoperfusion, watershed ischemic stroke, or acute myocardial ischemia. Management requires contacting the patient's primary care physician for initiation or dosage titration of oral agents (e.g., clonidine, captopril, or labetalol) with outpatient follow-up within 24 to 48 hours.

Hypertensive Emergency

• Diagnostic Criteria: Blood pressure > 180/120 mmHg with objective evidence of acute, ongoing, life-threatening target organ damage.
• Target Organ Manifestations:
  1. Central Nervous System: Hypertensive encephalopathy (manifesting as severe bursting headache, altered mental status, confusion, projectile vomiting, seizures, or coma), acute ischemic stroke, or intracerebral/subarachnoid hemorrhage.
  2. Ophthalmologic (Malignant Hypertension): Funduscopic examination demonstrates bilateral papilledema (blurring of optic disc margins), flame-shaped retinal hemorrhages, cotton-wool exudates, and acute visual blurring or blindness.
  3. Cardiovascular & Great Vessels:
     • Acute Aortic Dissection: Characterized by sudden onset of excruciating, "ripping," "tearing," or "knife-like" chest pain radiating directly through to the interscapular region of the back, accompanied by marked blood pressure asymmetry between the left and right arms (> 20 mmHg discrepancy) or pulse deficits.
     • Acute Left Ventricular Failure & Pulmonary Edema: Acute dyspnea, orthopnea, frothy sputum, and rales.
     • Acute Coronary Syndrome: Myocardial infarction or unstable angina provoked by extreme myocardial wall stress and afterload.
  4. Renal System: Acute kidney injury (AKI) characterized by rapid deterioration of renal function, marked oliguria, microscopic or gross hematuria, and proteinuria.
• Management Protocol: Activate 911 immediately for transport to an emergency department and intensive care unit (ICU). Patients require continuous arterial line monitoring and carefully titratable intravenous antihypertensives (e.g., labetalol, nicardipine, clevidipine, or nitroprusside). The clinical target is typically to reduce MAP by no more than 20–25% within the first hour to prevent cerebral ischemia (except in acute aortic dissection, where rapid reduction of systolic BP to < 120 mmHg within 20 minutes is mandatory).

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Other Cardiovascular Conditions on the 2026 Outline

The 2026 BIOM appendix also lists the conditions below. Know how each presents and what it means for referral and treatment.