for blood flow and microbubbles for capillary blood flow contrast. transthoracic echocardiogram (tte): echocardiogram of the heart through the thorax external to the body. much easier to perform than tee because it is non-invasive and takes less time, but has several disadvantages (namely clarity of images). transesophageal echocardiogram (tee): echocardiogram of the heart through the esophagus. tee can require sedation or general anesthesia and the patient must be npo. cardiovascular magnetic resonance imaging (cmr): magnetic resonance imaging (mri) of the heart that utilizes the ecg for gating and to look at specific mechanical functions of the heart. cardiac stress test – testing of the cardiovascular system through controlled exercise or drugs. auscultation – listening to sounds (e.g., heart sounds) with a stethoscope. electrocardiography (ecg or ekg): measurement of the electrical activity of the heart, typically with 4 or 10 electrodes on the skin. holter monitor – portable ecg device for continuous monitoring. electrophysiology study – studying the electrical activity of the heart through the use of catheters placed in the heart via veins or arteries. sphygmomanometer – blood pressure cuff used to measure arterial blood pressure. cardiac marker – testing for biomarkers in the blood that may indicate various conditions. coronary catheterization – catheterization of the coronary arteries. fractional flow reserve (ffrmyo): testing the blood flow through a stenosis of a coronary artery to determine the perfusion of the heart. intravascular ultrasound (ivus): ultrasonography of a coronary artery. optical coherence tomography (oct): testing through the use of optical scattering for coronary artery disease. drugs main article: list of cardiac pharmaceutical agents there are several classes of pharmaceutical drugs used in cardiology to manage various diseases and a lot of drugs have cardiovascular side effects. drugs for the cardiovascular system drugs that manipulate the cardiovascular system do so through several ways. the first is ion channels, which are often manipulated to manage arrhythmias. the second is receptors of various types. the third is manipulation of enzymes. ion channels ion channels are responsible for cell membrane voltage, depolarization, and repolarization. these actions lead to conduction of signals down nerves and contraction of cardiomyocytes. perhaps the most prominent manipulation of ion channels is through antiarrhythmic agents. these agents are commonly classified by the type of ion they manipulate and named the vaughan williams classification: class i — sodium channel blockers class ia — fast sodium channels (quinidine, ajmaline, procainamide, disopyramide) class ib — sodium channels (lidocaine, phenytoin, mexiletine, tocainide) class ic — decrease conductivity (encainide, flecainide, propafenone, moricizine) class ii — beta blockers (carvedilol, propranolol, esmolol, timolol, metoprolol, atenolol, bisoprolol) class iii — potassium channel blockers (amiodarone, sotalol, ibutilide, dofetilide, dronedarone) class iv — calcium channel blockers (verapamil, diltiazem) class v — other (adenosine, digoxin, magnesium sulfate) specifically, types i, iii, & iv manipulate ion channels while the others are not. receptors the adrenergic receptor is a set of receptors that are commonly manipulated. four properties of the heart — chronotropy, dromotropy, inotropy, & lusitropy — are manipulated by adrenergic receptors. for example, the β1 receptor increases all four of these properties: chronotropy at the sa node, dromotropy through the av node, inotropy of the cardiomyocytes through increased calcium, and lusitropy through phosphorylation of phospholamban. catecholamines are a set of drugs and hormones that manipulate the adrenergic receptors. the natural catecholamines are norepinephrine, epinephrine, and dopamine. there are numerous other drugs (e.g., dobutamine, ephedrine, isoproterenol) that manipulate the adrenergic receptors and have variable specificity for the receptors and are, thus, used for various reasons. angiotensin ii receptor antagonists (arbs) block the angiotensin ii receptors that are linked to hypertension and heart failure, mainly through vasodilation & heart remodeling inhibition. enzymes ace inhibitors works upstream from angiotensin ii receptor antagonists and have similar effects on management of hypertension and heart failure. sodium nitroprusside and nitroglycerin function by causing vasodilation through nitric oxide, which manipulates cgmp levels through guanylate cyclase. cox inhibitors (namely aspirin), warfarin, direct xa inhibitors, direct thrombin inhibitors, heparin, low-molecular weight heparins, antibodies (e.g., abciximab), and a few others are used for anticoagulation therapy. this is important in those predisposed to blood clots (e.g., factor v leiden) but also for thrombus formation when an atherosclerotic plaque rupture that would, otherwise, lead to myocardial infarction. drugs with cardiovascular side effects numerous drug classes have well-known cardiovascular side effects. anesthetics – as a general rule, all agents used in anesthesia have depressant effects on the cardiovascular system with notable exception of ketamine. chemotherapy – doxorubicin is one agent known to have heart toxicity (leads to dilated cardiomyopathy). diuretics – the primary effect of diuretics is removal of intravascular volume, which then has secondary benefits to the cardiovascular system in diseases like heart failure. lithium – teratogenic effect of causing ebstein's anomaly in mothers taking lithium. opioids – decreases blood pressure. selective serotonin reuptake inhibitors (ssri) – toxicity causes arrhythmias including sinus tachycardia, junctional rhythms, and trigeminy. ssri's also have interactions with anti-coagulation therapy and increases the risk of bleeding while on them. serotonin–norepinephrine reuptake inhibitors (snri) – due to manipulation of norepinephrine, snri's can cause hypertension and so hypertension should be reduced before starting an snri. tricyclic antidepressants (tcas) – tcas behave like type ia antiarrhythmics and could terminate ventricular fibrillation and decrease contractility. they can also cause tachycardia and hypotension. cardiology organizations american college of cardiology american heart association heart rhythm society indian heart association national heart foundation of australia cardiology publications acta cardiologica american journal of cardiology annals of cardiac anaesthesia cardiology cardiology in review circulation circulation research clinical and experimental hypertension clinical cardiology ep – europace european heart journal experimental & clinical cardiology heart heart rhythm international journal of cardiology journal of the american college of cardiology pacing and clinical electrophysiology persons influential in cardiology robert atkins (1930–2003) – known for the atkins diet eugene braunwald (born 1929) – editor of braunwald's heart disease and 1000+ publications wallace brigden (1916-2008) – identified cardiomyopathy willem einthoven (1860–1927) – a physiologist who built the first practical ecg and won the 1924 nobel prize in physiology or medicine ("for the discovery of the mechanism of the electrocardiogram") werner forssmann (1904–1979) – who infamously performed the first human catheterization on himself that led to him being let go from berliner charité hospital, quitting cardiology as a speciality, and then winning the 1956 nobel prize in physiology or medicine ("for their discoveries concerning heart catheterization and pathological changes in the circulatory system") andreas gruentzig (1939–1985) – first developed balloon angioplasty max holzmann (1899-1994) – co-founder of the swiss society of cardiology, president from 1952 to 1955 samuel a. levine (1891–1966) – recognized the sign known as levine's sign as well as the current grading of the intensity of heart murmurs, known as the levine scale bernard lown (born 1921) known for being the original developer of the defibrillator henry marriott (1917–2007) – ecg interpretation and marriott's practical electrocardiography jacqueline noonan (born 1928) – discoverer of noonan syndrome that is the top syndromic cause of congenital heart disease john parkinson (1885–1976) – known for wolff–parkinson–white syndrome helen b. taussig (1898–1986) – founder of pediatric cardiology and extensively worked on blue baby syndrome paul dudley white (1886–1973) – known for wolff–parkinson–white syndrome louis wolff (1898–1972) – known for wolff–parkinson–white syndrome stewart wolf (1914–2005) – known for his research into the roseto effect