Much of the basic information about the chambers, valves, and great vessels is covered in the cardiac exam page, and is worth reviewing. Also covered in that page are the events occurring diastole and systole.
Cardiologist think of the anatomy of the heart in a variety of ways. The way that medical students need to be familiar with is "territories," which refers to those areas of the heart supplied by a particular coronary artery. The aorta gives rise to the LCA (left coronary artery) and the RCA (right coronary artery) immediately after the aortic valve.
During systole, the heart muscle itself becomes stiff, and much of the blood leaving the left ventricle bypasses the takeoffs of the coronary arteries. This results in poor perfusion of the heart during systole. The majority of coronary artery filling occurs during diastole, when the peripheral arteries apply pressure back on the aortic valve, and therefore into the openings of the coronary arteries. If diastole is compromised, by being shortened as a result of a tachyarrythmia for example, the heart becomes poorly perfused and the patient is said to be experiencing diastolic dysfunction.
The RCA gives off marginal arteries, which supply the inferior wall of the heart. In most patients (~80%), the RCA becomes the PDA (posterior descending artery), which runs between the ventricles on the posterior aspect of the heart, and which supplies the posterior wall of the heart. Patients whose PDA comes from the RCA are said to be "right dominant."
The LCA splits almost immediately into the LAD (left anterior descending artery) and the CFX (circumflex artery). The LAD runs between the ventricles on the anterior aspect of the heart, and is responsible for supplying blood to the anterior wall of the heart. The CFX runs between the L atrium and ventricle, and is responsible for the blood supply to the lateral wall of the heart. In some patients (~20%), the CFX becomes the PDA. These patients are referred to as being "left dominant."
The SA node is supplied by the first branch of the RCA. The AV node is supplied by a branch of the PDA.
When a patient has an infarct in a certain area of the heart, you're expected to know which artery is likely to be involved.
|Artery||Area||Structures||EKG Leads Involved|
|CFX||Lateral & anterolateral||Left Ventricle||I, aVL, V1, V4-V6|
|LAD||Anterior & anteroapical||Left Ventricle||V1-V4|
|Left Main||Lateral & anterior||Left Ventricle||All V leads, and may also involve inferior leads in left-dominant patients|
|PDA||Posterior||Left & Right Ventricles*||V6 (also R>S in V1)|
|RCA||Inferior||Left & Right Ventricles*|
Proximal RCA can also injure atria and cause a-fib
|II, III, aVF|
|* Be certain to perform an EKG with right-sided leads if you suspect inferior or posterior damage|
There are 3 major areas of a normal heart that can play the role of pacemaker.
The first is the SA node, which lives at the top of the right atrium. It receives input from various parts of the body, most notably the vagus nerve, the aortic arch, and from various circulating agents in the body such as epinephrine. Left to its own devices, it beats at approximately 60 bpm. It sends out impulses via three internodal tracts (on the way to the AV node), and excites the atria. The contraction of the atria is responsible for the P wave (the SA node itself doesn't create enough voltage to register on an EKG).
Next is the AV node, which lives in between the right atrium and right ventricle. Usually it is triggered by input from the SA node, but in the event of loss of communication, it can generate its own rhythm at ~40 bpm. It sends out impulses through the common AV bundle, which is then divided into a right and left bundle branch. These travel down their respective sides of the interventricular wall towards the apex of the heart along purkinje fibers - once they reach the apex, they bend back up along the ventricular walls and terminate in cardiac muscle.
Electrical impulses travel most quickly and efficiently along these conduction tracts, but they also travel through the cardiac muscle itself. Once an area of cardiac muscle is stimulated, it contracts, and the stimulus spreads to adjoining tissue in a ripple pattern. If things work correctly, the atria are stimulated by the SA node, there is a delay at the AV node, and then the impulse is sent to the apex of the heart to contract the ventricles from the bottom up, forcing blood up into the great arteries. Ventricular contraction produces the QRS complex on the EKG. If conduction is primarily through muscle (instead of along tracts), the contraction is much slower - causing a wider QRS - and less efficient.
In conduction abnormalities, sometimes the nodes fire either infrequently or not at all. In these situations, cardiac muscle itself can generate an impulse, usually at ~20 bpm.
If there is a block between the SA node and the AV node, the atria still respond to the SA node rhythmically, creating regular P waves. However, the AV node doesn't receive regular signals, and fires at its own pace, occasionally being stimulated by the atria contracting. This "disconnect" is referred to as A-V (atrial - ventricular) dissociation.
The electrical impulses are generated and transmitted by electrochemical means. There are a number of important electrolytes that need to be in balance for the system to function properly. Most important are magnesium, potassium, and sodium.
There are three findings that must be interpreted on an EKG to determine whether an arrhytmia is present, and if so, what its type is. These are atrial activity (P wave), venrticular activity (QRS complex), and the relationship between atrial and ventricular activity.
|Sinus Tachycardia: Normal waveforms, normal conduction, regular, but rapid - >100 bpm by definition. Caused by exercise, pain, stress, hyperthyroid, hypovolemia, shock, PE, drug toxicity. Treat by treating underlying condition.|
|Sinus Bradycardia: Normal waveforms, normal conduction, regular, but slow - <60 bpm by definition. Seen in healthy athletes. Caused by sick sinus, MI, vasovagal, drug toxicity. Treat with atropine, beta agonist (isoproterenol), pacing, or by reversing drug toxicity.|
|Premature Atrial Contraction (PAC): Normal AV groups with additional early P waves - which may or may not be conducted to the ventricles. Usually caused by an additional focus in the atria that fires independently and "re-triggers" the SA node. Immediate causes include catecholamines and drug toxicity. Treat if symptomatic with beta blockers, quinidine, procainamide.|
|Multifocal Atrial Tachycardia (MAT): Irregular atrial rate (P-P interval), irregular ventricular rate (R-R interval), and inconsistent morphology of P waves - three or more variations in shape. >100 bpm by definition - usually between 100 and 180. Seen in patients with COPD, respiratory failure, or cardiac damage. Treat by treating underlying condition to degree possible - medications have limited effectiveness.|
|Atrial Fibrillation: No P waves due to fibrillating (quaking) atria, which generate from 400-700 impulses per minute. Generally 140-180 of these are conducted through the AV node. Caused by CHF, cardiac disease (S/P MI / rheumatic), or idiopathic. Treat with electric cardioversion &/or procainamide if new onset. If >72 hours, clot may have formed, and warfarin therapy should be initiated x 3-4 weeks prior to cardioversion. If cannot be converted, must remain on anticoagulation.|
|Atrial Flutter: "Sawtooth" flutter waves at ~300 bpm, commonly with 2:1 block (ventricular rate of ~150). Vagal maneuvers (valsalva, carotid massage) can increase block and heighten appearance of sawtooth morphology. Caused by CHF, cardiac disease (S/P MI, rheumatic), or idiopathic. Treat with electric cardioversion, verapamil, dig, adenosine.|
|Premature Ventricular Contraction (PVC): Normal waveforms, normal conduction with additional QRS complexes that are not accompanied by P waves. These extra QRS complexes appear "ventricular," or wide. Caused by hypokalemia, cardiac muscle damage or ischemia, or drug toxicity. Treat if symptomatic with lidocaine.|
|Idioventricular Rhythm: Ventricular pacing due to lack of supraventricular triggering, usually at ~35 bpm. No P waves, ventricular (wide) waveform. Treat with observation.|
|Ventricular Tachycardia: Ventricular waveforms at >100 bpm, a result of re-entrant impulses in the ventricular conduction system. Usually preceded by PVC's. Treat with cardioversion, procainamide.|
|Torsade de Pointes: V Tach with a sinusoidal, or "bowtie" appearance over time. Caused by long Q-T, hypokalemia, 3rd degree heart block, hypomagnesemia, liquid protein diet, drug toxicity. Treat with cardioversion, mag sulfate, isoproterenol.|
|Ventricular Fibrillation: Chaotic wide waveforms - the disorganized nature of the electrical activity precludes effective contraction of the ventricles, which is obviously deadly. Caused by DKA, hyperkalemia, hypothermia, hypovolemia, OD, or direct cardiac damage such as in MI. Treat with cardioversion, epinephrine, lidocaine.|
|1st Degree A-V Block: Normal EKG but consistent, longer than normal P-R interval (>0.20 seconds). Caused by increased vagal tone, AV blocking drugs, primary heart disease. Treat Not necessary unless caused by dig toxicity - then reduce dig.|
|2nd Degree A-V Block, Wenkebach (Mobitz I): Progressively larger P-R interval until a P wave not conducted. Caused by increased vagal tone, AV blocking drugs, primary heart disease. Treat if symptomatic with atropine, pacing, isoproterenol.|
|2nd Degree A-V Block, Mobitz II: Consistent pattern of non-conducted P waves (2:1, 3:1, etc.). Caused by damage to conduction system, i.e. MI, surgery. Treat with pacing.|
|3rd degree A-V Block: No relation between P waves and QRS complexes - no P waves conducted. aka "Complete Heart Block." Caused by damage to conduction system. Treat with pacing.|
Can have many causes, only one of which is MI. Consider aortic dissection, cholecystitis/cholelithiasis, esophagitis, foreign body aspiration, fractured rib, GI pain, hiatal hernia, intercostal muscle pain, neoplasm(s), pancreatitis, pericarditis, pleuritis, pneumo/hemothorax, PE, zoster.
Of these, the ones that need to be ruled out emergently include aortic dissection, pericarditis (effusion can lead to tamponade), pneumo/hemothorax, PE (pulmonary embolus), and MI.
Hx: Quality of pain is often described as "tearing," although this is not a reliable indicator. Patients often present with no pain or pain of a different character. Patients may note numbness or coolness in extremities, particularly left upper extremity, as branches of aorta become occluded.
Dx: On exam, there is often a new murmur of aortic regurgitation, as the valve becomes distended from the stretched aorta. Look for asymmetric pulses or changes in cognition (including unconsciousness) as aortic branches become occluded. CXR may show a "shadow" outside of an aortic calcification - this represents the false lumen.
Tx: Treat with surgery, although varies with specific subclassification.
Hx: Pain typically increases with inspiration and may be relieved by leaning forward, and is often described as similar to angina (in chest, may radiate to arms, neck, back).
Dx: On exam, there may be a pericardial friction rub. Tamponade suggested by distant heart sounds, tachycardia, low blood pressure, small pulse pressure (difference between systolic and diastolic pressures), distended neck veins, and paradoxical pulse (decrease in systolic pressure during inspiration of >10 mm). Typically accompanied by diffusely elevated ST segments with no reciprocal depression and no Q waves. Effusion is confirmed with echo (ultrasound of heart).
Tx: Treat with antibiotics, and cardiocentesis if symptomatic.
Hx: Difficulty breathing, sensation of drowning, diffuse chest pain.
Dx: On exam, there is often a weakened pulse, distant heart sounds, lung sounds may be diminished or absent over area of buildup. CXR will show trachea shifted from midline away from side of buildup. If pneumothorax, will be area of increased penetration (black) with no lung markings - typically on the periphery of the lung fields, and the lung border may be visible as a separate line from the ribcage. In hemothorax, chest will contain fluid (opaque on x-ray). Can be confirmed with ultrasound or CT scan, although placement of chest tube is usually initial step in management of this potentially life-threatening condition, and its aspirate can confirm the diagnosis.
Tx: Treat with chest tube if symptomatic.
Hx: Dyspnea, fever, diaphoresis, apprehension, hemoptysis.
Dx: On exam, there may be evidence of DVT (LE edema, calves painful to palpation). Often accompanied by tachycardia, murmur of tricuspid insufficiency, S3. EKG may show classic finding of SIQIIITIII pattern &/or inverted T-waves in V1-V4, although neither is reliable. ABG can also be negative, but may show decreased pH, decreased pO2, and decreased pCO2. A-a gradient (see ABG page) is better marker - tends to increase in PE. V-Q scan is typically performed, although it lacks specificity in the absence of a "low probability" or "high probability" report combined with clinical suspicion that agrees with report [PIOPED is a famous study that discusses the diagnostic utility of the V-Q scan]. The "gold standard" of diagnosis is the pulmonary angiogram.
Tx: Treat with thrombolytic if acute onset. Heparin for prophylaxis.
Hx: Quality of pain varies, but often sharp or "crushing" pain in substernal area radiating to arm(s), neck, jaw, shoulders, back. Often accompanied by diaphoresis, nausea/vomiting, dyspnea, apprehension. See risk factors, below.
Dx: On exam, there may be signs of heart muscle damage - increased JVP, presence of S3 &/or S4, edema, lung crackles, poor perfusion, etc. Pallor is common. EKG is commonly performed on admission, with emphasis on looking for ST segment elevations (early) or depressions (late) &/or Q waves (typically seen in infarction as opposed to ischemia). Q waves classically suggest a transmural (entire thickness of cardiac muscle) infarction. Cardiac enzymes (CK-MB and Troponin I) should be drawn on admission. CK-MB becomes elevated ~6 hrs after cardiac injury, >5 ng/ml suggests MI. Troponin I is more specific for cardiac muscle, and is typically used to diagnose cardiac muscle damage (including ischemia, non-Q-wave MI). Also becomes elevated 4-6 hrs after injury, but remains elevated for days (vs. hours for CK-MB).
Tx: Initial treatment for any patient with suspected MI should include MONA - Morphine, O2, Nitrates, Aspirin.
Proven lifesaving interventions: ASA, beta-blocker, thrombolytics (<6 hours, preferably <3) or angioplasty
Commonly used, but not proven: O2, nitrates, morphine (useful for C/P refractory to O2, nitrates, beta-blocker), heparin
For unstable angina (C/P with no EKG changes): the 2b3a inhibitors
Think P Q R R R S T for those factors which lead you to believe chest pain is cardiac in origin:
|ACE (Angiotensin-Converting Enzyme) Inhibitors||Antihypertensives, recommended for patients after anterior MI to help improve LV function and aid in remodeling. Captopril, Enelapril, etc.|
|Adenosine||Used in PSVT (paradoxical supraventricular tachycardia), and to temporarily slow arrythmias in order to better visualize rhythms.|
|Amrinone||Used for refractory CHF|
|Atropine||Vagolytic. Used for sinus bradycardia. Also used in PEA (pulseless electrical activity) and asystole|
|Beta-blockers||Antihypertensive, slows conduction from SA to AV node. Used to convert arrhytmias to sinus, to slow tachycardias. Recommended as prophylaxis for any patient who has had a previous MI. Atenolol, Esmolol, Lebetolol, Metoprolol, Propranolol, etc.|
|Bretylium||Last-ditch drug for V-tach, V-fib|
|Calcium-Channel Blockers||Antihypertensive, reduce contractility. Used to slow ventricular response in a-fib or a-flutter. Diltiazem, Verapamil|
|Digoxin||Slows ventricular response. Used in a-fib or a-flutter|
|Dobutamine||Used in CHF if Pt not in shock. Increases contractility ("inotropic") and increases BP ("pressor")|
|Dopamine||Used in CHF. Raises BP ("pressor") of patients who are in shock. Increases contractility ("inotropic")|
|Epinephrine||aka adrenaline. Used in V-tach, V-fib, PEA (pulseless electrical activity), asystole. Also useful in bradycardia or anaphylaxis|
|Furosemide||aka Lasix. Loop diuretic, used to reduce fluid load, also reduces K+|
|Heparin||Anticoagulant, works by blocking antithrombin III, part of "intrinsic" pathway. Monitored by PTT. Used as prophylaxis in patients with a-fib, significant carotid stenosis, or Hx of DVT/PE|
|Isoproterenol||Last-ditch for Torsades|
|Lidocaine||Antiarrhythmic. Used in V-tach, V-fib|
|Mag Sulfate||Used in Torsades, refractory V-fib|
|Morphine||Used to decrease agitation (and therefore heart rate) as well as pain during MI|
|Nitrates||Increase coronary artery perfusion, reduce afterload. Used sublingually for angina. Nitroglycerin, Nitroprusside, Nitro Paste|
|Norepinephrine||aka noradrenaline. Used for cardiogenic shock, emergent hypotension (SBP <70).|
|Oxygen||Used pretty much all the time with most cardiac conditions. A primary effect of reduced cardiac function is reduced ability to transport O2, so additional O2 can be supplied to maximize available capacity.|
|Procainamide||Refractory or recurrent V-tach or V-fib. Also used for rapid a-fib with WPW (Wolff-Parkinson-White, a syndrome of ventricular pre-excitation, associated with "delta waves" on EKG)|
|tPA (Tissue Plasminogen Activator)||Thrombolytic, used to "bust clots" and reperfuse damaged areas in MI, PE, CVA. Used if therapy can be initiated <3 hrs after onset of Sx. Similar uses for streptokinase, retaplase|