Introduction to Cardiac Anatomy, Physiology, and EKG Analysis

Overview of Cardiac Mechanics and Anatomy

Importance of Fundamental Knowledge: Understanding the acutely, critically ill patient requires mastery of the heart's anatomy, structure, mechanics, and the meaning of cardiac output. This knowledge determines whether a heart remains strong or enters failure.
The Heart as a Machine: The heart functions as a machine that requires specific factors to operate: - Volume: Often referred to as the "gas in the tank." The heart relies on an appropriate volume to move blood through the system. Too much volume can cause overload, while too little forces the heart to work harder to meet body demands. - Force: The muscular strength needed to propel blood. - Resistance: The pressure the heart must overcome in the systemic circulation.
Structural and Flow Problems: - Structural issues include valves not opening or closing properly or muscular problems where the heart is not strong enough. - Cellular changes in the chambers can occur over time, impacting pump efficiency. - Flow problems occur when inappropriate amounts of blood move through the heart, causing systemic issues.

Blood Flow and the Cardiac Circuit

Right Side Logic: The right side of the heart is directly linked to the pulmonary circuit (lungs). - Path: Deoxygenated blood enters the Right Atrium (RA) via the Superior Vena Cava (SVC) -> Tricuspid Valve -> Right Ventricle (RV) -> Pulmonic Valve -> Pulmonary Artery -> Lungs for oxygenation. - Pulmonary Circuit: A low-pressure system. - Lungs and Right Side Connection: Chronic lung disorders (e.g., COPD, Pulmonary Hypertension) increase the workload on the right side. This can lead to RV hypertrophy or failure. Smoker’s lungs have a direct negative impact on right-sided heart work.
Left Side Logic: The left side is the high-pressure pump for systemic circulation. - Path: Oxygenated blood from the lungs -> Pulmonary Veins -> Left Atrium (LA) -> Mitral Valve -> Left Ventricle (LV) -> Aortic Valve -> Systemic Circulation. - Congestion and Backup: If the left side pump fails, congestion occurs and backs up into the lungs, eventually causing right-sided heart problems.
Atrial Kick: - Definition: The process where the atria contract, increasing blood pressure in each atrium and forcing additional blood into the ventricles. - Loss of Atrial Kick: In conditions like Atrial Fibrillation ( $Afib$ ), the loss of normal electrical conduction eliminates the atrial kick, causing the heart to speed up and eventually suffer.

Hemodynamics and Cardiac Output

Cardiac Output (CO): - Formula: $CO = \text{Stroke Volume (SV)} \times \text{Heart Rate (HR)}$ - Definition: The volume of blood pumped per minute. - Normal Range: $4\,L/min$ to $8\,L/min$ . - Compensation: If SV decreases (e.g., dehydration), the HR must increase to maintain the $4-8\,L/min$ required for organ perfusion.
Cardiac Index (CI): - Definition: A measurement of CO relative to the patient's body size. - Normal Range: $2.5\,L/min/m^2$ to $4.0\,L/min/m^2$ .
Factors Determining Cardiac Output: 1. Preload: The volume of blood that enters the heart chambers, causing a stretch at the end of diastole. Preload is essentially volume. Medications like diuretics are preload reducers. 2. Afterload: The force or resistance that opposes ventricular ejection (the systemic vascular resistance). Increased blood pressure or vasoconstriction increases afterload, causing the heart to work harder and eventually remodel (hypertrophy). Vasodilators like Nitroglycerin reduce afterload. 3. Contractility: The force or strength of the muscular contraction required to propel blood. Failing hearts lose contractility.
Systemic Vascular Resistance (SVR): The resistance the left side works against. Hypertension and vasoconstriction increase SVR, leading to structural heart changes.

Heart Valves and Ejection Fraction

Phases of Cardiac Action: - Diastole: The filling and relaxation phase. The Atrioventricular (AV) valves (Tricuspid and Mitral) are pushed open to fill the ventricles. - Systole: The pump and contraction phase. The Semilunar valves (Pulmonic and Aortic) are pushed open as ventricles propel blood into circulation.
Ejection Fraction (EF): - Definition: The percentage of blood ejected from the ventricle with each heart stroke. - Normal EF: $60\%$ to $75\%$ . - EF and Heart Failure: - $50\%$ : Mild symptoms. - $25\%$ to $40\%$ : Constant symptoms requiring a significant medication regimen. - Under $25\%$ (e.g., $20\%$ ): Usually requires hospitalization or mechanical support. - $10\%$ : Requires a machine to pump or a heart transplant.

Heart Sounds and Physical Assessment

Auscultation Landmarks ("All People Enjoy Time Magazine"): - Aortic: Second Intercostal Space ( $ICS$ ), Right of the sternum. Loudest site for $S2$ . - Pulmonic: Second $ICS$ , Left of the sternum. Also reflective of $S2$ . - Erb’s Point: Third $ICS$ , Left of the sternum. A landmark with no specific valve sounds. - Tricuspid: Fifth $ICS$ , Right of the midclavicular line. Closure at the beginning of systole ( $S1$ ). - Mitral (Apex): Fifth $ICS$ , Midclavicular line. Loudest site for $S1$ .
Heart Sounds: - S1: Closure of Mitral and Tricuspid valves at the start of systole. Loudest at the apex. - S2: Closure of Aortic and Pulmonic valves at the start of diastole. Loudest at the base (Aortic area). - S3: Third heart sound. Occurs due to rapid ventricular filling or volume overload. Best heard at the apex with the patient on the left side. Normal in young adults; indicates heart failure in older adults. - S4: Fourth heart sound. Reflects slow ventricular filling and increased atrial contraction against a noncompliant ventricle. Often associated with severe hypertension. - Murmurs: Sound of turbulence crossing a diseased valve. Not an "extra" heart sound.
Assessment Techniques: To hear abnormal sounds like $S3$ or $S4$ , lean the patient forward and use the bell of the stethoscope (for low-pitched noises).

Anatomy of Heart Layers and Coronary Arteries

Heart Layers: - Epicardium: The outer, superficial layer. - Myocardium: The thickest, middle muscular layer. It is fed by coronary arteries and is responsible for the pump. - Endocardium: The innermost endothelial layer. It is closest to the valves; endocardial infections often lead to valvular problems.
Major Coronary Arteries: - Left Main Coronary Artery: Includes the Left Anterior Descending ( $LAD$ ). - Right Coronary Artery ( $RCA$ ): Supplies the right side. - Widowmaker: A clot in the $LAD$ is called a Widowmaker because it supplies a massive amount of blood to the Left Ventricle. Blockage here causes instant death or cardiogenic shock.

EKG Basics and Conduction

Cardiac Action Potential: - Polarization (Resting): No electrical activity. The inside of the cell is negatively charged. Ready to fire. - Depolarization (Contraction): Positive ions (Sodium rapidly, Calcium slowly) enter the cell, making it positively charged. Reflected as the $P$ wave and $QRS$ complex. - Repolarization (Recovery): Potassium leaves the cell, and the Sodium-Potassium pump restores the negative charge. Reflected as the $T$ wave.
Cardiac Properties: - Automaticity: Ability of cells to spontaneously initiate an impulse. - Excitability: Ability to respond to a stimulus. - Conductivity: Ability to transmit a stimulus from cell to cell.
EKG Grid Measurements (Horizontal = Time): - Small Box: $0.04\,seconds$ . - Big Box (5 small boxes): $0.20\,seconds$ . - 1 Second: 5 big boxes. - 3 Second Interval: 15 big boxes. - 6 Second Interval: 30 big boxes.
EKG Grid Measurements (Vertical = Amplitude/Voltage): - Small box: $1\,mm$ .

9-Step EKG Interpretation Process

Rate: Determine Atrial and Ventricular rates. Normal: $60-100\,bpm$ . Tachycardia: >100\,bpm. Bradycardia: <60\,bpm.
Regularity: Look at the pattern (R-to-R interval). Is it regular or irregular?
P Waves: Evaluate morphology. Should be uniform and precede every $QRS$ . Normal: $0.06-0.12\,s$ .
PR Interval: Start of $P$ to start of $Q$ . Measurement: $0.12-0.20\,s$ .
QRS Complex: Ventricular depolarization. Normal: $0.06-0.10\,s$ . Over $0.10\,s$ is considered wide.
ST Segment: From the end of $QRS$ ( $J$ point) to the start of the $T$ wave. Should be at the isoelectric line. Elevation or depression indicates ischemia or infarct.
T Wave: Ventricular repolarization. Morphology should be asymmetrical, height <5\,mm in limb leads or <10\,mm in chest leads. Peaked $T$ waves indicate hyperkalemia.
QT Interval: Time for ventricles to depolarize and repolarize. Normal: $0.34-0.44\,s$ . Prolongation increases risk for Torsades de Pointes.
U Wave: Small bump after the $T$ wave. May indicate hypokalemia.

Heart Rate Calculation Methods

6-Second Method: Count the number of $QRS$ complexes in a 6-second strip and multiply by 10. Best for irregular rhythms.
1500 Method: Count the number of small squares between two $R$ waves and divide 1500 by that number. More accurate for regular rhythms.

Sinus Rhythms and Arrhythmias

Normal Sinus Rhythm ( $NSR$ ): Rate $60-100\,bpm$ . Regular. Normal measurements.
Sinus Bradycardia: Rate <60\,bpm. - Causes: Athletes, sleep, beta-blockers, hypothermia, vagal maneuvers. - Symptomatic Bradycardia: Dizziness, hypotension, syncopy. - Treatment: Atropine ( $0.5\,mg$ IV every 3-5 min, max $3\,mg$ ), Dopamine, Epinephrine, or Transcutaneous Pacing.
Sinus Tachycardia: Rate >100\,bpm. - Causes: Fever, pain, anxiety, dehydration, caffeine, blood loss. - Treatment: Treat the underlying cause (fluids for dehydration, meds for pain).
Sinus Arrhythmia: Irregular rhythm that often cycles with breathing.
Premature Atrial Contraction ( $PAC$ ): Early beat from an ectopic focus in the atria. $P$ wave morphology differs. Usually harmless but can lead to atrial tachycardias.

Atrial Arrhythmias

Atrial Fibrillation ( $Afib$ ): Chaotic atrial activity. No discernible $P$ waves (replaced by "f" waves). Irregular $R-R$ intervals. - Risk: Clot formation in atria leading to stroke. - Treatment: Rate control (Beta-blockers, Calcium Channel Blockers), Rhythm control (Amiodarone), and Anticoagulants.
Atrial Flutter: Sawtooth appearing flutter waves. More rhythmic than $Afib$ . Treatment remains the same.
Supraventricular Tachycardia ( $SVT$ ): Rate $150-250\,bpm$ . Regular. $P$ waves often buried in $T$ waves. - Treatment: Vagal maneuvers, Adenosine (to chemically cardiovert), or Beta-blockers/Calcium Channel Blockers.

Heart Blocks (Atrioventricular Blocks)

Heart Block Poem: - If the $R$ is far from the $P$ , you have a First Degree. - Longer, longer, longer, drop, then you have a Wenckebach (Type 1). - If some $P$ s don't get through, then you have a Mobitz II. - If $P$ s and $Q$ s don't agree, then you have a Third Degree.
First Degree: Consistent $PR$ interval >0.20\,s. Usually asymptomatic.
Second Degree Type 1 (Mobitz I/Wenckebach): Progressive lengthening of $PR$ interval until a $QRS$ is dropped. Often drug-induced (Digoxin, Beta-blockers).
Second Degree Type 2 (Mobitz II): Constant $PR$ interval with randomly missing $QRS$ complexes. More serious; requires pacing.
Third Degree (Complete Heart Block): Atria and Ventricles beat independently. Severe bradycardia, hypotension. Emergency; requires a permanent pacemaker.

Junctional and Ventricular Rhythms

Junctional Rhythms: Impulse starts in the AV junction because the SA node failed. Characterized by inverted or missing $P$ waves. - Junctional Escape: Rate $40-60\,bpm$ . - Accelerated Junctional: Rate $60-100\,bpm$ . - Junctional Tachycardia: Rate >100\,bpm.
Premature Ventricular Contractions ( $PVC$ ): Early, wide, bizarre $QRS$ . No $P$ wave. - Unifocal: All look the same. - Multifocal: Look different; more dangerous. - Bigeminy: Every other beat is a $PVC$ ; Trigeminy: Every third beat.
Ventricular Tachycardia ( $V-tach$ ): Wide, bizarre $QRS$ complexes, rate >100\,bpm. Can be pulseless or have a pulse.
Torsades de Pointes: "Twisting of the points" around the isoelectric line. Associated with prolonged $QT$ interval. - Causes: Meds (Zithromax, Lasix, Haldol, Levaquin) and low Magnesium/Potassium. - Treatment: IV Magnesium ( $2\,grams$ ).
Ventricular Fibrillation ( $V-fib$ ): Chaotic quivering. Pulseless and unconscious. Treatment: Defibrillation immediately.

ACLS and Cardiac Arrest Management

Shockable Rhythms: $V-fib$ and Pulseless $V-tach$ .
Non-Shockable Rhythms: Asystole and Pulseless Electrical Activity ( $PEA$ ).
$PEA$ H's and T's (Causes): - H's: Hypovolemia, Hypoxia, Hydrogen ions (Acidosis), Hypo/Hyperkalemia, Hypoglycemia, Hypothermia. - T's: Toxins (Overdose), Tamponade (Cardiac), Tension Pneumothorax, Thrombus (Pulmonary/Coronary), Trauma.
Pharmacology of ACLS: - Epinephrine: $1\,mg$ every 3-5 minutes. - Amiodarone or Lidocaine: Used for refractory $V-fib/V-tach$ .
Defibrillation vs. Synchronized Cardioversion: - Defibrillation: Unsynchronized, random shock for pulseless rhythms. - Cardioversion: Synchronized with the $R$ wave. Used for unstable tachycardias (e.g., $Afib$ , $SVT$ ) where a pulse is present.

Pacemakers and Internal Devices

Modes: - Fixed: Fires at a set rate regardless of heart activity. - Demand: Only fires if the heart rate drops below a preset level.
Chambers: Single (one lead in RA or RV) or Dual (leads in both).
ICD (Implantable Cardioverter Defibrillator): Monitors for $V-tach/V-fib$ and delivers an internal shock.
Patient Education: - Post-procedure: No lifting arm above the shoulder (2 days to 2 weeks). - Monitor for infection (fever, positive blood cultures). - No MRIs unless device is compatible. - Carry Medical ID; inform airport security. - Avoid lingering near anti-theft devices in stores.