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Cardiac Emergencies

2.5 Contact Hours including 2.5 Advanced Pharmacology Hours
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This peer reviewed course is applicable for the following professions:
Advanced Practice Registered Nurse (APRN), Athletic Trainer (AT/AL), Certified Nurse Practitioner, Certified Registered Nurse Practitioner, Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Nursing Student, Physical Therapist (PT), Physical Therapist Assistant (PTA), Registered Nurse (RN), Registered Nurse Practitioner
This course will be updated or discontinued on or before Friday, December 19, 2025

Nationally Accredited

CEUFast, Inc. is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. ANCC Provider number #P0274.

CEUFast, Inc. (BOC AP#: P10067) is approved by the Board of Certification, Inc. to provide education to Athletic Trainers (ATs).

FPTA Approval: CE24-951523. Accreditation of this course does not necessarily imply the FPTA supports the views of the presenter or the sponsors.

≥ 92% of participants will know the current recommendations and guidelines for managing cardiac emergencies.


After completing this continuing education course, the participant will be able to meet the following objectives:

  1. Formulate the patterns of cardiac disease, epidemiology, and factors directly influencing mortality rates.
  2. Generalize the latest research findings in the diagnosis of cardiac emergencies.
  3. Integrate the stages of disease progression with associating presenting symptoms.
  4. Explain the latest findings and guidelines on care and monitoring for cardiac emergencies.
  5. Summarize alternative therapy options to improve disease prognosis.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

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Cardiac Emergencies
To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Jassin Jouria (MD)


In modern medicine, cardiac emergencies primarily fall under the large classifications of cardiovascular diseases (CVDs) - a collection of disease states characterized by physiological and cellular impairment to the heart and blood vessel structures. Considering the biological complexities of the cardiovascular system (CVS), a wide array of disease states can arise, hampering its primary function of blood circulation, oxygen distribution, and the production of chemical entities for self-regulation.

For ease of study and classification, clinical inquiries examining the pathophysiology of these disease states have largely been published under four main headings. These include coronary artery disease (CAD) - a condition characterized by decreased myocardial perfusion with symptomatic manifestations of angina and myocardial infarction with or without heart failure; cerebrovascular disease - conditions largely classified to include transient ischemic attack (TIA) and stroke; peripheral artery disease (PAD) - conditions considered primarily to be arterial diseases that may result in claudication in the limb; and aortic atherosclerosis - disease states including thoracic and abdominal aneurysms.

Generally, disease conditions of the cardiovascular system, including the heart, are closely related to the CAD class. CAD class conditions account for about one-third of CVD cases diagnosed globally. In recent years, epidemiological surveys have reported an upsurge in the number of CAD and CVD-related conditions diagnosed globally. Trend statistics showed a significant upsurge in developing and third-world countries. An increased industrialization drive of the global economy with a resultant shift from the conventional model of work to remote and sedentary models has been proposed as a leading risk factor. A change in the global consumerism model favoring longer commute minutes, decreased leisure time and exercise, and longer work hours may also have contributed to this increase.

High intake of high-calorie diet, processed sugars, and saturated fat have been associated with the development of different metabolic disease states linked to CVDs (Curry et al., 2018). For a broader perspective on CVS-related conditions, Podolec et al. (2019) further classified rare cardiovascular maladies presenting with urgencies and requiring immediate expert care into a few groups. These include:

  • Rare afflictions of the system (class I) and pulmonary circulation (class II)
  • Rare cardiomyopathies (class III)
  • Rare congenital cardiovascular disorders (class IV)
  • Rare cardiac arrhythmias (class V)
  • Cardiac tumors and cardiovascular conditions related to cancer (class VI)
  • Cardiovascular sickness in pregnancy (class VII)
  • Other types of rare cardiovascular illness (class VIII)

For clarity, this course will describe clinical emergencies of the cardiac systems cutting across the different groups of this classification.

Case Study

Bermada's Early Life

Bermada lived all his life in Massachusetts, playing big in the real estate business. Originally born in Morocco, he immigrated with his parents to the United States at the tender age of two. Bermada had his fair share of struggles as an African immigrant. In his early thirties, he worked mostly on construction sites, skipping college to augment the income of a family of seven, a dying father, and an unemployed mum. At 37, Bermada lost his dad to a sudden heart attack while he slept. Now 45, Bermada had made it big in the real estate scene, working all hours to amass an empire.

On a fateful afternoon, Bermada reported to the emergency department of a hospital with complaints suggestive of postprandial chest pain lasting for more than 24 hours. He had initially paid less attention to the pain while self-medicating on successive doses of over-the-counter ibuprofen to relieve the pain. Since it persisted with increased severity, Bermada presented to the hospital.

At the Clinic

Bermada is a known smoker, has hypertension, and has a family history of myocardial infarction. He explained how the chest pain had started without any prior symptoms. On physical examination, he had a heart rate of 103 beats per minute (bpm) and a blood pressure of 127/110 millimeters of mercury (mmHg). Lung examinations revealed no alterations and heart assessment revealed a systolic murmur in the mitral area. An initial electrocardiogram (ECG) was ordered.

The ECG showed a heart rate of 110 bpm, sinus rhythm, first-degree atrioventricular (AV) block, low-voltage QRS complexes in the frontal plane, and extensive arterial wall infarction.

Initial Management

Oral aspirin and 5 milligrams (mg) intravenous (IV) metoprolol were initiated. However, Bermada's response was minimal as cardiovascular arrest in pulseless electrical activity developed, though reversed after five minutes. Bermada subsequently developed peripheral hypoperfusion and hypotension. On the attending physician's advice, Bermada was promptly transferred to a cardiology specialist clinic. On admission at the cardiology clinic, Bermada had received continuous IV norepinephrine, IV morphine, and heparin. Blood pressure was down to 65/40 mmHg. A second ECG was ordered.

The ECG disclosed a heart rate of 121 bpm, junctional escape rhythm with sinus arrest, low QRS complex in the frontal plane, ST elevation at V1 to V5, an inactive area in the inferior wall, and an extensive ongoing anterior acute myocardial infarction. Coronary angiography disclosed anterior interventricular branch occlusion with images suggestive of intracoronary thrombus and a lesion in the circumflex artery and the right coronary artery.

Angioplasty was promptly performed with a stent implant in the anterior interventricular artery. A combination of antithrombotic therapy, oxygen, and IV glycoprotein IIb/IIIa inhibitors (GP IIb/IIIa) was promptly started. Forty-eight hours later, Bermada showed clinical signs suggestive of improved reperfusion with a blood pressure of 127/85 mmHg and a heartbeat of 89 bpm. Direct feedback suggests chest pain had significantly resolved, although his analgesic regimen was continued for another day. A week later, Bermada was scheduled for long-term antithrombotic therapy.

Case Aspects

Bermada's case highlights a 45-year-old with a family history of cardiovascular emergencies and a strong risk factor for acute coronary syndrome. He presented on account of radiating chest pain, a strong initial clinical sign of a progressing cardiac emergency. A clinical presentation of prolonged chest pain, as in this case, raises the possibility of an impairment in the cardiovascular system. In this case, performing an ECG offered valuable diagnostic and prognostic insight. An ST-segment elevation in the anterior wall strongly backed the initial suspicion of acute coronary syndrome. Bermada's case highlights how prompt diagnostic and management approaches to cardiac emergencies rapidly improve prognosis and reduce the risk of mortality.

Global Stats on Epidemiology, Disease Burden, and Patient Demographics

1990s to 2010 (Decades of Clinical Observation)

Since 2010, the number of published studies on the epidemiology of CVDs - including cardiac emergencies - has increased significantly. A meta-review of these studies provides a succinct view of the global disease burden of these conditions. In the Global Burden of Disease study of 2010, researchers considered tobacco (including secondhand smoke), heavy use of alcohol, high blood pressure, and a diet low in protein as the leading risk factors for cardiovascular-related diseases. Lim (2013) reported a quantified risk assessment for these factors, with high blood pressure responsible for 7.0% of global disability-adjusted life years (DALYs), tobacco smoking and secondhand smoke responsible for 6.3%, alcohol use 5.5%, and diets low in fruits 4.2%.

The authors also noted a significant change in risk value assessment if estimated values in 2010 were considered retrospective. For instance, in 1990, high blood pressure only ranked fourth on the list of higher DALYs, with smoking, household pollution, and being underweight during childhood completing the top 3 spots. Between 1990 and 2000, epidemiologists studying the observable changes in global CVS-related risk factors attributed these changes to steady epidemiological transitions in different dimensions of human existence across the globe. Aggregating published reviews during this period of 'epidemiological transitions' also revealed important observations. It is worth noting that while these transitions occurred globally, there were significant regional disparities in the recorded estimations of risk factors of CVS-related diseases.

In Africa and developing countries of Asia, household air pollution, poor diet structuring, an epidemic of iron deficiency, and being overweight contributed largely as top risk factors for diseases, particularly CVS-related diseases. However, in North and South America, Europe, and Asia-Pacific, high blood pressure, indiscriminate alcohol use, tobacco smoking and secondhand smoke, and elevated BMI contributed more significantly to the burden of CVS-related diseases (Murray et al., 2012). As expected, studies evaluating the epidemiological transition to increased CVS-related diseases in the early 2000s also completed reviews and published submissions on the mortality rates and actual mortality numbers with direct links to the subject matter. Studies published by Lozano et al. (2012) reported an estimated 52.8 million deaths collectively in 2010.

Comparative analysis of actual mortality numbers suggests that as of 1990, stroke (11.1%) and ischemic heart disease (13.3%) were the two leading causes of mortality in the global population. However, the proportion of deaths related to these conditions had increased from one-fifth in 1990 to one-quarter in 2010. Likewise, the proportion of global years of life lost (YLL) linked with ischemic heart disease and stroke had increased by 28% and 17%, respectively, over the two decades of observation. These conditions were reportedly positioned as the first and third causes of YLL over this period. As a side note, mortality attributed to atrial fibrillation or flutter also increased significantly, emphasizing the role of cardiac emergencies in the global mortality outlook since the 1990s.

2015 and Beyond

In an early attempt to understand the impact of cardiac emergencies on the global mortality outlook, Mensah et al. (2019) published a study describing how CVS-related diseases contributed largely to the rising cost of medical care globally. In a review of the burden of CVD in Sub-Saharan Africa, Mensah et al. (2015) noted how age-standardized mortality rates of CVS-related diseases have declined by 27.3%. Still, the number of deaths increased by an estimated 42% from 1990 to 2015. In the same period, diseases caused by medical emergencies reportedly led to over 17 million deaths globally, which by statistical extension translated to 330 million YLL and about 35.6 million years lived with a disability (YLD) by 2017. Based on this trajectory, about 23 million deaths are expected to be caused by CVS-related emergencies by 2030 globally.

A World Health Organization (WHO) review highlighted how over three-quarters of CVS-related deaths have occurred in low- and middle-income countries in recent years. A larger outlook on evaluating the statistical importance of cardiovascular emergencies was published by Roth et al. (2020). Estimated prevalence values highlight how diagnosed cases of CVS-related emergencies almost doubled from 271 million cases in 1990 to 523 million cases in 2019. By 2019, the number of deaths related to these emergencies had also increased steadily to 18.6 million from 12.1 million in 1990. In this period, the global trends of DALYs, YLLs, and YLDs also changed considerably. YLDs doubled from 17.7 million in 1990 to an estimated 34 million in 2019.

Regional disparities in mortality rates also seem to appear noticeably. In 2019, age-standardized mortality rates for CVS-related diseases and emergencies were highest in Uzbekistan, the Solomon Islands, and Tajikistan. The rates in Peru, France, and Japan showed a 6-fold decline in 2019, leading epidemiologists to infer that age-standardized rates for prevalence and YLDs may be important drivers in the global outlook of CVS-related emergencies. On the gender scene, it appears total CVS-related DALYs are higher in men than women before age 80 to 84. Beyond age 84, this pattern appears to be reversed. Differences in DALYs, when considered based on gender, are more prominent in the 30 - 60-year-old population.

Pathophysiology, Clinical Staging, and Diagnostic Care of Selected Cardiac Emergencies

Congenital Heart Disease

Congenital heart anomalies describe heart defects present at birth, including defects that occur singly or in groups. In these abnormalities, the cardiac chambers, valves, or vessels present structural malformations that resultantly impair the normal flow of blood from and to the heart. In individuals with these malformations, complications such as cardiac arrhythmia, valve insufficiency, and heart failure are commonly reported (Institute Of Medicine, 2010). In 2019 alone, an estimated 3.12 million cases of congenital heart anomalies were reported, representing an estimated 2,300 cases per 100,000 live births. In the same year, a total of 13.3 million people reportedly lived with different forms of congenital heart anomalies, with about 217,000 deaths linked to these conditions. When considered across a spectrum, congenital heart disease is broadly classified into six groups (Chowdhury, 2007);

Left-to-right shunts:

  • Atrial level: atrial septal defect (ASD), total anomalous pulmonary venous connections (TAPVC)
  • Ventricular level: ventral septal defect (VSD)
  • Great artery level: patent ductus arteriosus (PDA), aortopulmonary (AP) window
  • Truncus arteriosus
  • Coronary level: anomalous left coronary artery (ALCAPA), coronary fistula

Right-to-left shunts:

  • Tetralogy of Fallot (TOF) physiology
  • Transposition of the great arteries (TGA) physiology

Left-sided obstructive lesions:

  • Obstructed veins
  • Mitral stenosis
  • Aortic stenosis
  • Coarctation
  • Interrupted aortic arch
  • Hypoplastic left heart syndrome

Right-sided obstructive lesions:

  • Pulmonary stenosis/atresia
  • Tricuspid stenosis
  • Hypoplastic right heart

Single ventricle


  • Ventricular rings
  • Venous anomalies
  • AV fistula

In line with the scope of this course, only classifications that are considered prevalent or commonly reported will be extensively discussed.

Left-to-Right Shunts

Regarding recent reports on the epidemiology of congenital heart diseases, left to right shunts are considered the most diagnosed impairment. This group of anomalies is characterized by the return of oxygenated blood back to the lungs for re-oxygenation, creating a physiological redundancy in the circulatory system. There is an increased venous return from the lungs through the pulmonary veins to the left atrium and ventricle. As a result, a volume overload is created on the left ventricle and decreases systemic cardiac output. The resulting physiological alterations associated with the shunt are determined by the magnitude of the anomaly and the post-infancy changes in pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR).

In the fetal stage of development, shunt defects have minimal or no physiological effect since a high PVR limits blood flow to the lungs. Oxygen administration, low arterial carbon dioxide tension, nitric oxide, and other interventions or maneuvers that decrease the PVR automatically increase the left-to-right shunt at the cost of decreasing systemic output. Continued shunting damages the pulmonary vasculature, ultimately causing pulmonary hypertension and hyperplasia of the vessel walls. A reversal or discontinuation of shunting has been reported to normalize PVR.

Atrial Septal Defect

In atrial septal defects, left-to-right shunting occurs at the atrial level, resulting in the dilatation of the right ventricle and right atrium. Pulmonary venous return to the left atrium is also noticeably increased. These alterations cause a volume overload to the left atrium. Considering evidence from recent research, right ventricle volume overload is consistent with the alterations in ASD. Irreversibility of the PVR progressively occurs with time as symptomatic presentation of volume overload occurs.

graphic of atrial septal defect

Atrial Septal Defect

Ventricular Septal Defect

Embryologically, abnormalities of the ventricular septum arise from a membranous portion of the septum or the muscular portions. In a few cases, they may occur near the aortic or AV valves. Physiological manifestations of VSD reportedly depend on the relative resistance of the pulmonary and systemic circulation and the magnitude of the VSD. In combination, these factors largely dictate the direction of blood flow. In the fetal development stage, pulmonary and systemic circulations have equivalent resistance, increasing the chances of little shunting through the VSD. Post-birth observations have shown how the pulmonary resistance declines significantly, causing an imbalance between the right ventricular pressure (lower) and the left ventricular pressure (higher), consequently establishing a left-right shunt.

graphic showing ventricular septal defect

Ventricular Septal Defect

Shunting is prominent during systole as blood from the left ventricle is ejected to the pulmonary circulation, causing a volume overload to the left atrium in the left ventricle. Since blood movement during systole physiologically takes it directly into the pulmonary circulation, there is no volume overload to the right ventricle. In a large VSD, both the right and left ventricles are at systemic pressure. However, blood movement still shunts left to right as a result of lower PVR distally.

Right-to-Left Shunts

Physiologically, right-to-left shunts are characterized by the return of deoxygenated blood from the tissues back to the body without re-oxygenation.

Tetralogy of Fallot

In this anomaly, there is a characteristic displacement of the outflow tract (infundibular) portion of the interventricular septum. The displacement principally results in four different physiological defects:

  • Subvalvular pulmonic stenosis due to the displaced septum
  • Right ventricular hypertrophy due to pulmonic stenosis
  • VSD due to malalignment of the interventricular septum
  • Overriding aorta that receives blood from both ventricles

graphic of tetralogy of follot

Tetralogy of Fallot

As a result of right ventricular blood outflow tract obstruction, a right-to-left shunt occurs across the large non-restricted VSD. A commonly reported symptomatic manifestation of this abnormality is cyanosis in patients due to a lack of pulmonary blood flow. Since blood flow is impaired, the left ventricle is smaller than the right ventricle as the pulmonary venous return decreases. Spasm of the infundibular muscle prompts total blood flow from the right ventricle into the shunt across the VSD to the systemic circulation. The occurrence - commonly described as a 'tet spell' - is physiologically reversed by increasing the SVR to subsequently increase the preload of the right heart. The right-to-left shunt declines, and blood flow across the pulmonary valve improves.

Left Heart Obstructive Lesion

Coarctation of the Aorta

Constriction of the aortic lumen in regions usually close to the ductus is described as the coarctation of the aorta. In many cases, the primary cause of obstruction is unknown. However, many research reviews have faulted low blood flow through the left heart and aorta during fetal development since low blood supply has a primary link with growth impairments of the cardiovascular system. Decreased lumen caused by coarctation increases afterload in the left ventricle.

graphic showing coarctation of the aorta

Coarctation of the Aorta

Although vessels branching off the aorta before the site of coarctation receive normal blood flow, those after the coarctation may be underperfused. As a result of this, the carotid artery and upper extremities are essentially the only region properly perfused. Differential cyanosis is a common symptom reported in this case.

Diagnosis of Congenital Heart Abnormalities

With the advent of technological innovations in medicine, many experts have proposed different diagnostic standards for congenital heart disease across the spectrum of patients' demography. Across the board, the consistent theme in these proposals is a multi-system diagnosis method recommending the use of physical examination, magnetic resonance imaging (MRI), echocardiography, cardiac catheterization, cardiac computed tomography (CT), and open-heart surgery. An accurate diagnosis may be difficult, especially in the adult population. However, a multidisciplinary approach involving special expertise and training may increase the chances of accurate diagnosis (Institute of Medicine, 2010).

Management of Congenital Heart Disease

Surgical interventions for managing congenital heart anomalies have been popular since the mid-1990s. However, advances in this care have not been widely accepted until recently. These include the development of catheter heart placement and staged palliation for hypoplastic left heart syndrome. Drug regimens developed recently also provide care options for physiological complications, including pulmonary hypertension, arrhythmia, and heart failure.

Advances in Catheter Methods

Clinical studies and observations on the effectiveness of these methods are commonly described in managing pulmonary valve stenosis and ASDs. In ASD repair, a specialized catheter is digitally guided to the patient's heart from a large vessel in the groin. In the septum, the catheter is deployed, releasing an umbrella-shaped device maneuvered expertly to plug the hole between the atria. It is secured in place as the catheter is withdrawn from the heart. Post-treatment surveys have estimated a 6-month duration for the normal tissue to grow in place and on the closure device. In the absence of clinical complications, the closure device is not replaced as the child ages.

In pulmonary stenosis, the catheter is threaded through a large vessel to the pulmonary valve. With the help of a tiny balloon feature on the catheter, the valves are pushed apart while the balloon is quickly inflated. Once through the valves, the balloon is deflated as the catheter is withdrawn—the maneuver repairs narrow valves in the heart. Based on recent image guidance technology developed for these procedures, the prognosis of congenital anomalies has significantly improved in the global population. Surgeons can now expertly use coronary angiography, echocardiography, and transesophageal echocardiogram to guide specialized catheters through large and small vessels of the heart.

An open heart surgery option is considered in clinical presentations requiring extensive or multiple repairs that are not possible with the use of catheters. Depending on the severity of the congenital anomaly, one or more open heart surgeries may be required. Cases exclusively requiring open heart surgery may present with closed holes in the heart, widened arteries or openings to the valves, poorly developed heart valves, and complexities in the blood vessels near the heart. A heart transplant may be required if multiple defects in the same patient are too complex to repair.

Heart Failure

Unlike other cardiac emergencies discussed in this course, heart failure is a complex clinical syndrome with associating etiologies rather than being a specific disease condition itself. With regards to conventional definitions, heart failure describes conditions resulting in;

  1. a functional defect impairing the physiological ability of the heart to pump or fill with blood
  2. a structural abnormality resulting in a significantly inadequate cardiac output
  3. an adequate cardiac output secondary to compensatory neuronal activation and increased left ventricular pressure

In all, these observations severely impair the functional capacity of the patients and dramatically increase the risk of mortality. In a recent epidemiological study completed by the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee, an estimated 6.2 million people in the United States reported symptoms consistent with heart failure between 2013 and 2016 (Virani et al., 2020). The Global Health Data Exchange registry put the 2022 worldwide prevalence of chronic heart failure at 63.34 million cases, translating to 9.91 million YLDs and an estimated $346 billion in care expenses.

Comparative analysis across age groups suggests that prevalence is noticeably dependent on age groups as it increases steeply with advancing age. Concerning race, the African-American community expressed a 25% higher prevalence of heart failure compared to Caucasians. The American Heart Association (AHA) also considers heart failure as the primary cause of CVS-related mortalities in the United States, with a higher prevalence and incidence rate among African Americans, Native Americans, Hispanic Americans, and migrants from developing countries (Benjamin et al., 2017).

Clinical Classification, Symptom Profile, and Diagnosis of Heart Failure

Since studies on the clinical importance of heart failure began in the early 1980s, experts have proposed multiple clinical classifications based on factors such as disease severity, pathophysiology, clinical presentation complications, and disease progression. The New York Heart Association's functional classification system is based on symptom severity. The American College of Cardiology (ACC) classification on disease progression stages from A to D (Heidenreich et al., 2022). These classifications include:

  • Stage A - Patients at risk of developing heart failure
  • Stage B - Patients with a structural defect but asymptomatic
  • Stage C - Patients with heart failure and symptomatic
  • Stage D - Patients with advanced heart failure

Although these clinical classifications provide a simple categorization of patients, they are not exactly considered for practical purposes. Heart failure is widely discussed based on left ventricular ejection fraction (LVEF) for functional and practical purposes. The LVEF below 40% is termed 'heart failure with reduced ejection fraction' or HFrEF. If the LVEF is greater than 40%, it is termed 'heart failure with mildly reduced ejection fraction.' On the other hand, patients with an LVEF greater than 50% are considered to have 'heart failure with preserved ejection fraction.' These criteria are the results of discrete LVEF considered as cut-off points used as selection criteria in clinical trials and studies evaluating the clinical efficacy of drug candidates and surgical procedures in managing heart failure (Yancy et al., 2017).

In itself, heart failure is not considered a diagnosis but a syndrome with multiple clinical presentations. Presenting symptoms relate to significant reductions in cardiac output and elevated filling pressures. In many cases, symptoms presented by patients are non-specific, and reduced ejection fraction is only identified on acute admission to the hospital. Clinically presenting with reduced ejection fraction is often considered the ultimate stage in a long process involving chronic pressure overload of the left ventricle accompanied by subacute decompensation on a background of chronic cardiovascular impairments.

Physical examination of patients presenting with heart failure requires a comprehensive assessment. Generally, the most commonly reported symptoms include shortness of breath related to positional changes (orthopnea) or exertion. Other commonly reported symptoms include fatigue, anorexia, palpitation, recurrent cough, and chest pain. The general appearance of patients with chronic heart failure may also include anxiety, diaphoresis, and malnutrition. In acute decompensated heart failure, wheezing may be noticed. In advanced stages of pulmonary congestion, frothy and blood-stained sputum may also be present.

A jugular venous extension has also been reported in a few patients, including cases of paradoxical increase in jugular venous distention with respiration (Kussmal sign). On examination of cardiac signs, S3 gallop, pulsus alternans, and accentuation of P2 may be noticed. Mitral and tricuspid regurgitation have been reported to be present in cases of decompensated dilated cardiomyopathy. If there are enough physical signs to suspect heart failure, serum B-type natriuretic peptide (BNP) or N-terminal component (NT-proBNP) should be measured as definitive diagnostic examinations. Although highly sensitive, these markers are poorly specific for heart failure (Haydock & Flett, 2022).

The National Institute for Health and Care Excellence (NICE) published a detailed illustration of the steps for chronic heart failure diagnosis in 2020 (Haydock & Flett, 2022).

graph showing guideline for the diagnosis of suspected heart failure

NICE Guideline for the Diagnosis of Suspected Heart Failure. Adapted from the National Institute for Health and Care Excellence (2018)

Pathophysiology and Management of Heart Failure

The overactivation of the neuronal axis, particularly the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), is implicated in the development of HFrEF. In the early stages of heart failure, this adaptive feature is required to maintain the overall contractile processes of the heart and becomes maladaptive. These include the Frank-Starling mechanism, changes in myocyte regeneration, myocardial hypertrophy, and myocardial hypercontractility (Kemp & Conte, 2012). The myocardium attempts to compensate in the face of increased wall stress by initiating eccentric remodeling, further worsening the loading condition and wall stress. A resultant decrease in cardiac output activates the RAAS, ultimately leading to salt and water retention and increased vasoconstriction (Kimeu et al., 2023).

Generally, the goal of therapy for chronic heart failure is the improvement of symptom profile and an overall decrease in mortality score. These goals have been observed to decrease the frequency of hospitalization and significantly improve the quality of life. Patients with a diagnostic classification of HFrEF should be placed on a disease management plan. Loop diuretics are considered first-line treatment agents in the management of heart failure. In cases of renal comorbidities, high doses or IV administration of diuretics may be considered. In cases of symptom improvement by other therapies, the dose of administered diuretic may need to be reduced.

Pillars of Heart Failure Management

The 2022 AHA/ACC/ Heart Failure Society of America (HFSA) Guideline for the Management of Heart Failure provided a patient-focused recommendation for healthcare professionals in the management of heart failure. These recommendations, now commonly segmented under different headings for simplicity, have been described by different review journals as the 'Pillars of Heart Failure Management.' These pillars address clinical recommendations effective in the management of heart failure in patients with a degree of renal impairment or other forms of comorbidities.

Pillar 1: Angiotensin-converting enzyme inhibitors/angiotensin receptor blockers/angiotensin receptor neprilysin inhibitor

As a result of a significant reduction in cardiac output, the renal architecture becomes poorly perfused, ultimately triggering the release of renin from the juxtaglomerular apparatus. Renin release prompts the increased conversion of angiotensin II to angiotensin I, resulting in the further reabsorption of sodium and water, rising aldosterone and antidiuretic hormone levels, and arteriolar vasoconstriction. In this case, angiotensin-converting enzyme inhibitors (ACEIs) are recommended as first-line therapy since they significantly reduced the mortality score and improved symptom profile in multiple clinical studies. Angiotensin II receptor blockers (ARBs) are considered second-line agents, considering there are less robust mortality data from clinical studies (Sun et al., 2023).

In modern practice, however, the combination of sacubitril/valsartan should be considered first before resorting to ARBs alone. An experimental combination of ARBs+angiotensin receptor neprilysin inhibitors (ARNIs) with sacubitril/valsartan has reportedly demonstrated more therapeutic efficiency compared to ACEIs in patients with HFrEF. Sacubitril seems to inhibit neprilysin - an entity responsible for the breakdown of natriuretic peptides. A combination therapy of ACEIs and ARNIs, though popularly discussed in clinical reviews, has been contraindicated due to the increased risk of angioedema. Presently, it is common practice to establish an ACEI/ARB combination and consider other pillars of therapy before switching to ARNIs in patients who do not respond.

Pillar 2: Mineralocorticoid receptor antagonism

Mineralocorticoid receptor antagonists (MRAs) directly block the physiological effects of aldosterone - an action that effectively negates the dynamics of salt and water retention and the profibrotic action on the myocardium. Spironolactone, a broad-spectrum MRA, is widely considered in heart failure cases with comorbidities of hypertension and hypertensive crisis. Eplerenone, a specific aldosterone blocker, is better tolerated, particularly in males with lower blood pressure. It has been demonstrated to reduce mortality scores in patients with heart failure after myocardial infarction. Considering clinical evidence evaluating the effects of aldosterone blockers, the combination of spironolactone and eplerenone reportedly reduces the mortality index in HFrEF by an estimated 30% when added to an ACEI (Zannad et al., 2011).

Pillar 3: Antagonism of the sympathetic system with selected beta blockers

In HFrEF, sympathetic processes are usually overactive. As with the other adaptive mechanisms in the early stages of heart failure, the increased peripheral vasoconstriction and elevated heart rate in attempting to maintain cardiac output and improve the perfusion rates of vital organs eventually become maladaptive; this worsens the myocardial ischemia, and the resulting high levels of catecholamines may increase myocyte automaticity and the risk of ventricular arrhythmia. A selected range of beta blockers has been shown to reduce the relative mortality score of HFrEF by 35% compared with placebo groups (The Cardiac Insufficiency Bisoprolol Study II [CIBIS-II] Investigators and Committees, 1999). Clinicians must be careful in initiating beta-blockers in heart failure as they may worsen acute heart failure. A stepwise clinical assessment is recommended to ensure patients with HFrEF are not decompensated by beta-blocker initiation.

Pillar 4: Sodium-glucose cotransporter-2 inhibitors

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are popular therapeutic agents in the management of type II diabetes. Functionally, they reduce the reuptake of glucose and sodium in the proximal renal tubule. Based on recent research findings, SGLT2 inhibitors are considered key agents in the management of HFrEF. For instance, dapagliflozin and empagliflozin impacted an estimated 25% relative risk reduction compared to placebo groups in worsening cases of heart failure and cardiovascular death (Rahm et al., 2023). Treatment guidelines such as the current ACC/AHA and NICE guidelines recommend the use of SGLT2 inhibitors in early-stage HFrEF.

Hypertension and Hypertensive Crisis

Hypertension and hypertensive crisis are considered the most diagnosed, modifiable risk factors for CVD globally. In a 2015 estimate, Public Health England reported a 25% incidence rate of high blood pressure in the national population. Compared to developing and third-world countries in Africa and Asia, the disease burden attributed to hypertension and hypertensive crisis is higher (Mosha et al., 2017). The efficiency of primary healthcare and dieting routines seems to affect prevalent rates in these regions significantly. In the West, acute severe elevations in blood pressure are considered less common in the general population. An increase in awareness campaigns, widespread point-of-care examinations, and the development of better diagnosis and management frameworks are considered the primary reasons for this decline. Considering data from clinical studies and observations over the past decade, the use of antihypertensives seems to considerably improve the prognosis of CVDs and reduce the risk of emergencies.

Although the need to lower significantly elevated blood pressure is widely regarded in medical care, management and care models in this regard are still largely based on expert opinion. There seems to be a lack of robust data to back specific blood pressure targets in at-risk populations and patients at risk of cardiovascular emergencies. Recommendations from leading care experts and guidelines express some level of heterogeneity and inconsistencies, particularly when the patient pool is considerably diverse. This course, however, highlights a series of verified guidelines recommended in the diagnosis, evaluation, management, and monitoring of hypertensive crisis with a primary focus on the direct impact on CVD.

Describing Elevated Blood Pressure States

It is commonplace to find literature on hypertensive crisis in CVDs described under separate headings, including hypertensive urgency, acute severe hypertension, hypertensive crisis, and malignant hypertension. In an attempt to consolidate treatment models and monitoring frameworks, these terms help clinicians distinguish clinical presentations and accurately categorize patients.

Acute Severe Hypertension

In the last few decades, the definition of 'acute severe hypertension' has changed consistently. Presently, most literature describes this state as blood pressure elevated beyond 200/120 mmHg (>200/120). At this level, an urgent attempt to reduce blood pressure is appreciated. However, the degree of urgency seems to depend primarily on the presenting condition, particularly the presence of comorbidities. For instance, a blood pressure of 160/100 mmHg in a patient at high risk of acute end-organ damage - such as people with preeclampsia and kidney failure - is considered a hypertensive emergency. However, high pressure of 180/100 mmHg in a chronically hypertensive patient with a history of poor adherence and no comorbidity is managed as acute elevated blood pressure requiring medical attention (Patel et al., 2016). In this context, the term 'acute severe hypertension' accurately describes patients with acutely elevated blood pressure with no degree of end-organ damage.

Hypertensive Emergency

Many literature studies describe a 'hypertensive emergency' as elevated blood pressure likely to trigger life-threatening end-organ damage if sustained over a few hours. Its damaging effects are progressive, worsening any cases of cardiovascular or renal impairment in patients. Life-threatening emergencies usually linked with hypertensive emergencies include intracerebral hemorrhage (ICH), pulmonary edema, hypertensive encephalopathy, acute renal failure, acute coronary syndrome, and severe preeclampsia/eclampsia. A prominent feature usually reported in the evaluation of hypertensive emergencies is the rapid increase in blood pressure over a short period. Also, in some patients, a moderate elevation of blood pressure may demonstrate clear evidence of potential damage to the cardiovascular and renal systems.

Malignant Hypertension

Malignant hypertension is characterized by the physiological impairment of the vascular systems, including the blood vessels. Impairments of this nature have been directly linked to the failure of proper autoregulation of blood flow in patients with chronic, uncontrolled hypertension. On the cellular level, the damage is present as fibroid arteriolar necrosis in vascular tissue beds and characteristic onion skinning of resistance vessels (Domek et al., 2020). In diagnosis, the diastolic blood pressure equals or becomes elevated to more than 120 mmHg with a presentation of progressive complications such as bilateral grade III and grade IV retinopathy as described in the Keith-Wagner-Barker classification. Retinopathy classifications are very important in the accurate monitoring of malignant hypertension. In a 1939 classification for retinopathy changes in malignant hypertension, Keith, Wagner, and Barker provided an evidence-backed framework currently used by clinicians in reporting the clinical presentation of retinopathies in CVDs.

In this classification, bilateral grade III - hard exudates, cotton wool spots, and retinal hemorrhage - and grade IV - optic disc swelling - demonstrate progressive and severe retinal vascular permeability linked with poor prognosis in cardiovascular emergencies (Cremer et al., 2015). It is worth noting that correctly identifying and differentiating grades in this classification may suffer observer bias, and features described in each grade may not be completely noticeable in some patients. For instance, eye changes may be absent in acute cases despite evidence of necrosis on vascular tissue beds of the kidney, brain, and blood vessels, suggesting progressive end-organ damage (Shah et al., 2018). Untreated cases of malignant hypertension have been reported to trigger organ-wide vascular damage, primarily leading to acute renal failure, hypertensive encephalopathy, disseminated intravascular coagulation, and microangiopathic hemolytic anemia.

Patient Assessment and Diagnosis

On presenting with elevated blood pressure with or without clinical evidence of end-organ damage, patients are expected to undergo a detailed medical assessment. Clinicians are expected to document and analyze information covering medical, physical, and family history, including a complete review of available medical and family records of diseases. In patients with comorbidities, a complete review of medications and history of adherence may guide the clinician in drug choice and drug use counseling. Special attention should be placed on the patient's use of recreational drugs, including cocaine, morphine, and other stimulants; herbal formulations, including St John's wort and licorice; and over-the-counter medications, including non-steroidal anti-inflammatory drugs (NSAIDs) and oral contraceptives.

A complete review of systems may help clinicians understand the extent of lifestyle choices and medication use on patients' vitals, including the review of ongoing symptoms and patients' accounts of symptom manifestation. Accurate diagnosis should commence with measuring blood pressure in both arms and observing peripheral pulsation. An observation of retinal changes is recommended in patients presenting with a likely diagnosis of malignant hypertension and severely elevated blood pressure. In women of childbearing age, it is important to consider the possibility of pregnancy and specifically exclude this before determining drug choices. The assessment of progressive end-organ damage should be considered in patients with multiple cardiovascular risk factors, including the laboratory assessment of renal function, electrolyte balance, glucose level, full blood count, and clotting factor.

Imaging can also be considered in patients with clinical presentation suggestive of neurological impairments. MRI scans and CT may be helpful for the diagnosis of malignant hypertension by providing clinical evidence for stroke or a lesion within the central nervous system. Renovascular lesions may also be examined with renal imaging, particularly in patients presenting with elevated creatinine levels.

Management of Hypertension and Hypertensive Emergencies

The aim of therapy in the management of hypertension and hypertensive emergencies, as defined by the European Society of Cardiology (ESC)/European Society of Hypertension (ESH) and AHA/ACC guidelines, is to initiate oral antihypertensive medications while monitoring for any clinical presentations as the patient responds to therapy. In modern practice, guidelines in the management of blood pressure are now pathophysiology-based, with therapy options selected based on comorbidities present and the severity of end-organ damage.

In uncomplicated acute severe hypertension, NICE guidelines recommend a same-day assessment for patients presenting with a blood pressure of equal or higher than 180/120 mmHg and clinical features suggesting acute end organ damage. NICE also recommends a repeat blood pressure measurement within a week for patients presenting with severe hypertension without evidence of end-organ damage. While assessing for signs suggestive of end-organ damage, clinicians are advised to identify and address confounding factors such as pain and distress, particularly in patients presenting to the emergency department for the first time on account of elevated blood pressure. Directly observed therapies (DOT) and biochemical testing may be initiated in cases of suspected non-adherence. Blood pressure lowering should be targeted over days to weeks rather than hours, with preference given to oral therapy over IV medication.

In uncomplicated malignant hypertension, oral therapies are the first choice of management except in cases of progressive end organ damage or evident emergency comorbidities. Oral therapies have been demonstrated to gradually reduce mean arterial blood pressure without the risk of a sudden decline in pressure or complications of the renal, cerebral, and myocardial framework. Continued blood pressure monitoring over the first few hours of presentation is considered beneficial to ensure strategic lowering of blood pressure. The recommendations on the choice of first-line medications for malignant hypertension are not definitive. However, clinicians may consider calcium channel blockers, such as amlodipine or long-acting nifedipine formulations. Calcium channel blockers like amlodipine take longer to achieve steady-state concentration, leading to a longer time to achieve the desired blood pressure-lowering effect (Kulkarni et al., 2023).

Clinicians are advised to avoid prescribing repeat doses of these medications within a few hours unless there is clinical evidence suggesting ongoing end-of-organ damage. Atenolol and other beta-blockers may also be considered if there is little or no evidence of cardiovascular complications, including pheochromocytoma. These medications may be switched to first-line agents if clinical evidence suggests end-organ damage. Alpha-blockers such as doxazosin may also be considered in some patients.

Cardiac Arrhythmia

Cardiac arrhythmia describes variation from the normal heart rate or rhythm patterns, lacking a physiological explanation. In a broad sense, it captures a broad spectrum of cardiac rhythmic abnormalities largely classified under two broad headings based on heart rate - tachyarrhythmia and bradyarrhythmia. In the general population, the prevalence of arrhythmia is estimated at 1.5% - 5%, with atrial fibrillation considered as the most clinically reported type (Desai & Hajouli., 2023). Globally, atrial fibrillation is one of the leading causes of stroke, cardiac failure, and death, contributing largely to the burden of CVDs. In 2017, the number of atrial fibrillation cases globally was reported as an estimated 37.6 million people - a rapid increase from the 19.1 million cases reported in 1990 (Wang et al., 2020). Over this period, epidemiological surveys linked the incidence trend of atrial fibrillation to the socio-economic level of citizens across the world and the globalization of the economy.

Peer-reviewed scientific literature published over the last decade has further declassified these headings into classes describing arrhythmias based on origin, means of transmission, and associating syndromes. This course explores the limits of both classifications by first considering arrhythmia in terms of beats per minute before discussing the intricacies of the origin and means of transmission of each arrhythmia. In all, arrhythmia in these classes is directly linked with a rapid increase in the risk of morbidity and mortality.

Describing Cardiac Arrhythmias Based on Heart Rate


In tachyarrhythmia, there is an abnormal heart rhythm with a ventricular heart rate of at least 100 beats per minute. Based on the origin of the arrhythmia, tachyarrhythmia is further classified into supraventricular tachycardia and ventricular tachycardia.

Supraventricular Arrhythmia

Supraventricular arrhythmias originate from above the AV node. Based on origin, supraventricular arrhythmias describe atrial fibrillation, atrial flutter, atrial tachycardia, atrial premature complex, AV nodal reentrant tachycardia, and AV junctional extrasystoles. Based on the mechanism of tachycardia, supraventricular arrhythmia is discussed under three large subheadings - AV reciprocating tachycardia, AV nodal reentrant tachycardia, and atrial fibrillation (Hafeez et al., 2023).

Atrioventricular Reciprocating Tachycardia

Commonly described in Wolff-Parkinson-White Syndrome, this form of supraventricular tachycardia is present outside the AV-node bundle of Kent. A close examination of its mechanism reveals conduction down the accessory path and up the AV node with a prominent formation of a delta wave (antidromic) or conduction down the AV node into the accessory pathway with the absence of a delta wave (orthodromic).

Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

This form of supraventricular tachycardia features a reentry primarily caused by slow and fast fibers in the AV node and peri-nodal tissue. Clinical presentation includes syncope, sudden tachycardia, chest tightness, shortness of breath, and palpitation. ECG findings in AVNRT reveal a narrow tachycardia with P waves in T waves with a heart rate of about 160 beats per minute.

Atrial Fibrillation

Atrial fibrillation is characterized by a disorganized atrial electrical activity accompanied by an atrial rate in the range of 350 to 600 beats per minute. Usually, there is a complete absence of atrial mechanical contraction. Based on the duration, the commonly referenced classification of atrial fibrillation includes the following:

  • New onset (first detected).
  • Paroxysmal: Characterized by spontaneous arrhythmia terminated between 24 hours to seven days.
  • Persistent: Spontaneous arrhythmia not terminated within seven days or severe enough to require pharmacological or surgical intervention.
  • Permanent: Arrhythmia not responding to external intervention with ineffective termination attempts (Schmidt et al., 2011).

In all its forms, atrial fibrillation is linked to multiple reentrant wavelets primarily resulting from atrial ectopy from muscle fibers located close to the pulmonary vein.

Ventricular Tachycardia

In ventricular tachycardia, the origin of arrhythmia is located below the AV node. It includes ventricular fibrillation, ventricular premature beats, and ventricular tachycardia (sustained or non-sustained). In non-sustained ventricular tachycardia, the rapid ventricular tachycardia self-terminates within 30 seconds. The pathophysiology of this type of ventricular tachycardia is linked to multiple paths, including metabolic imbalance, electrolyte disturbances, side effects of pro-arrhythmic drugs, and impairments caused by structural abnormalities.

In sharp contrast to non-sustained ventricular tachycardia, sustained ventricular tachycardia is prominently characterized by the presence of damaged fibers in ischemic heart disease, leading to the reentry of current. A considerable percentage of sustained ventricular tachycardia are idiopathic. Ventricular fibrillation is closely similar to sustained ventricular tachycardia, with the reentry leading to disorganized high-frequency excitation. Particularly in cases of cardiomyopathies, ventricular fibrillation is linked to wall tension, a surge in end-diastolic pressure, and the presence of abnormal channels in ventricular fibers.


Bradyarrhythmia is characterized by heart rates below 60 beats per minute, with a common clinical presentation of sinus node disorders, AV blocks, and other rhythm disorders.

Atrioventricular Blocks

In AV blocks, atrial impulses - in the form of electrical signals - to non-excitable tissues and tissues in a refractory state are delayed in conduction. AV blocks are widely discussed under three headings - first-degree AV blocks, second-degree AV blocks, and third-degree blocks. In first-degree blocks, patients are generally asymptomatic with a clinical presentation of increased vagal tone or a decline in normal conduction functions. In the second degree, there is either a progressive prolongation of the PR interval accompanied by a skipped beat (Mobitz type I block) or a dropped QRS complex at random intervals on an ECG examination (Mobitz type II block). Third-degree blocks are complete AV blocks characterized by a total absence of conduction functionality for the atrial impulse to the ventricles. Independent contractions are the hallmark of a total AV block.

Sinus Node Disorders

Rhythmic disorders of the sinus node present as ischemic impairments resulting in the generation of slow-paced impulses at the sinoatrial (SA) node. In sinus pause, the SA node has a delayed generation. In sinus arrest, there is a complete failure of impulse generation. In the SA nodal exit block, impulses generated from the node are not effectively transmitted. On ECG examination, cases of sinus node disorders often appear as dysfunctional P-wave patterns that do not originate regularly.

Managing Cardiac Arrhythmias

The most widely regarded submission and guidelines on managing cardiac arrhythmia in modern medicine are based largely on the Vaughan-Williams classification system. This system broadly classifies antiarrhythmic drugs commonly used today based on ionic channel involvement and physiological effects on sinus node function, action potential, and AV conduction.

Vaughan William Classification of Antiarrhythmic Drugs
Class I: Sodium Channel Blockers 
IaDisopyramide, procainamide, quinidine
IbLidocaine, mexiletine
IcFlecainide, propafenone
Class II: Beta-blockersAcebutolol, atenolol, bisoprolol, carvedilol, esmolol, metoprolol, nadolol, propranolol
Class III: Potassium Channel BlockersAmiodarone, bretylium, dofetilide, dronedarone, ibutilide, sotalol, vernakalant
Class IV: Calcium Channel BlockersDilitiazem, verapamil
OthersAdenosine, Digoxin, Atropine

Class I medications are sodium channel blockers. Lidocaine, quinidine, and flecainide trigger a series of ion exchanges, ultimately resulting in the blockade of the sodium channels. They block the rapid inward sodium current, causing cardiac depolarization and conduction and repolarization prolongation. On automaticity, class I drugs reportedly affect action potential and refractory period duration (Larson et al., 2022). Class II medications (beta-blockers) blunt sympathetic activity and reduce the rate of initial depolarization of the action potential. In effect, this action mitigates automaticity and negates conduction velocity. Clinical submissions on the beneficial effects of beta-blockers in arrhythmia have linked these drugs to a significant reduction in the risk of sudden cardiac death (Al-Gobari et al., 2013). Class II medications are also generally considered in hybrid therapy options, combining pharmacotherapy with implantable cardiac defibrillators (Puljević et al., 2014).

Class III medications block the delayed rectifier potassium channel, leading to prolonged repolarization. Amiodarone is widely considered the flagship member of this class with its wide usage in the many studies on its pharmacological effects. It inhibits the calcium and sodium channels in the SA and AV nodes and Purkinje's fibers, prolonging the action potential duration and effective refractory period (Baquero et al., 2011). Calcium channel blockers (class IV medications) inhibit calcium reentry in the SA and AV nodes. The range of action these agents have on the cardiovascular systems is still the subject of many clinical studies today. These medications have also been reported to decrease diastolic depolarization, activity potential inclination, and sufficiency by blocking the calcium channels. They are considered drugs of choice in the management of violent supraventricular tachycardia and atrial fibrillation typical sinus rhythm (Wolff-Parkinson-White Disorder).

Other antiarrhythmic drugs in the Vaughan-William classification, such as adenosine and atropine, act by variable mechanisms. Adenosine particularly acts on specialized conduction tissues in the AV and SA nodes, reducing automaticity in a series of actions that culminate in the reduction of repetitive and paroxysmal monomorphic ventricular tachycardia (Lerman et al., 2014). Digoxin acts by inhibiting the sodium–potassium pump (Na+/K+ ATPase) by raising intracellular calcium levels and enhancing contractility by increasing vagal tone at the level of the AV node. Both actions affect physiological and mechanical changes, lowering conduction velocity and increasing the effective refractory period (Larson et al., 2022). In modern medicine, the use of digoxin in active cardiac emergency cases has been limited to advanced heart failure and refractory atrial fibrillation due to the associated risk of arrhythmia-related mortality linked to its use.

Acute Coronary Syndrome

The term 'acute coronary syndrome' (ACS) describes a group of CADs ranging from S-T elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. Clinical studies on the etiology of ACS have described plaque disruption in coronary arteries as the usual trigger, with common risk factors identified as physical inactivity, male sex, family obesity, poor nutritional practices, obesity, hyperlipidemia, hypertension, and diabetes. Other widely studied risk factors include drug abuse, particularly indiscriminate cocaine use, and a family history of early myocardial infarction.

In the United States alone, there was an estimated 15 million cases of ACS in 2017. According to epidemiological stats published by the AHA, a heart attack is recorded every 41 seconds in the United States; this pushes the number of myocardial infarction cases reported annually to about 1.1 million with about 150,000 patients diagnosed annually with unstable angina (Bracey & Meyers., 2023). In the same vein, the percentage of sudden coronary death attributed to thrombosis and disrupted plaques is estimated to vary between 19% and 81%. Clinical studies focusing on the epidemiology of ACS have suggested that a new coronary plaque rupture independent of the old infarct contributed significantly to the global mortality rate of sudden cardiac death.

Patient Evaluation and Symptoms Presentation

Logically, preventing ACS episodes rather than treating them would be beneficial. However, no definite imaging or laboratory modalities exist to accurately monitor potential plaque ruptures or predict the timing of a rupture. Risk factor identification and modification, proper patient evaluation, and the optimal management of CAD are considered the best approaches in evaluating and monitoring patients at risk of ACS. Differentiating between STEMI, NSTEMI, and unstable angina is considered an important aspect of ACS evaluation. The AHA guideline prescribes an ECG within 10 minutes of presentation for patients presenting to the emergency department with complaints suggestive of ACS (Zègre-Hemsey et al., 2019).

If STEMI is eventually confirmed, the cath lab should be immediately activated. The biological role of cardiac enzymes such as troponin makes them important biomarkers in assessing NSTEMI and myocardial infarction cases. Chest X-ray imaging may provide useful clinical information in diagnosing causes other than myocardial infarction in patients with a primary complaint of chest pain suggestive of pneumothorax and pneumonia. Blood work such as complete blood count and liver function tests can also help clinicians accurately evaluate patients presenting with chest pain patterns consistent with intraabdominal pathology. Based on multiple analysis reports of confirmed ACS diagnosis, chest pain is considered the most classic symptom presentation in patients at a high risk of ACS.

Often described as 'crushing or pressure-like,' ACS-related chest pain, as described in multiple clinical studies, radiates to the jaw and left arm. In many cases, chest complaints are often complicated with other symptoms, such as breathing difficulties, epigastric pain, nausea, dizziness, diaphoresis, and general body weakness. Females, patients with multiple comorbidities, and aging adults may present with other vague symptoms that might complicate the accurate evaluation of ACS. Physical examination may reveal general distress and suboptimal heart sounds (galop and murmurs), although heart sounds may be perfectly normal in many cases. Lung examination may be normal, or crackles suggestive of congestive heart failure (CHF) may be heard. In cases of CHF complications, bilateral leg edema may be present.

Pathophysiology of Acute Coronary Syndrome

In all its presentations, the underlying pathophysiology of ACS is the reduction in flow rate to parts of the heart musculature secondary to plaque rupture and formation of thrombus. Vasospasms with or without atherosclerosis may also be implicated in ACS. In atherosclerosis, the multiplication of smooth muscles within fatty streaks creates complicated plaques. With the progression of coronary plaques, arteries narrow until blood flow is significantly impeded, and ACS results. New reports from ACS studies in animal models have described the auto-immune-mediated inflammatory stage of atherosclerosis as another trigger of plaque formation. In these models, cells of the medium-sized and large arteries, including leukocytes, smooth muscle cells, and endothelial cells, are impaired by systemic immune-mediated inflammation. The occurrence plays an important role in mediating all stages of atherosclerosis, from initiation to plaque formation and rupture stages, as described in ACS.

The exposure of the endothelium to thrombogenic substances, including platelets and clotting factors, has also been linked to the formation of thrombus preceding the impedance of blood flow in large and medium-sized vessels (Anderson & Morrow, 2017). Platelet binding on the exposed endothelial surface occurs via glycoprotein (GP) IIb/IIIa receptors on the platelet membrane, linking other platelets to other activated platelets with fibrinogen. In the same vein, activated monocytes release metalloproteinases and tissue factors interacting with the vulnerable plaque. These series of activation and cross-linkages activate the clotting cascade that eventually leads to thrombus formation. In partially occluded vessels, unstable angina or NSTEMI may occur. STEMI is mostly linked with complete occlusion of the vessels. In animal models of ACS and clinical studies, it appears the degree of occlusion and timing of presentation directly dictates the severity of myocardial damage (Anderson & Morrow, 2017).

Management of Acute Coronary Syndrome

In August 2023, the ESC released the current reference treatment guideline for managing ACS. Developed by the task force on the management of ACS of the ESC, this guideline exhaustively described recommendations for pre-clinical care and emergency care for patients with complaints consistent with an ongoing myocardial infarction and unstable angina.

Antithrombotic Therapy in ACS

In the 2023 ESC guideline, antithrombotic management is considered an important component of the management of ACS regardless of patient categorization. Clinicians are guided to understand how treatment decisions, including choice of combination therapy, time of therapy initiation, and treatment duration, should depend solely on various patient and procedural factors. Treatment decisions should also consider the benefits of antithrombotic therapy against the risk of bleeding and other complications.

A complete recommendation of treatment regimen under this guideline is summarized below.

Antiplatelet Drugs

Antiplatelet Drugs
AspirinLoading dose (LD) of 150–300 mg orally or 75–250 mg IV if oral ingestion is not possible, followed by oral maintenance dose (MD) of 75–100 mg once daily; no specific dose adjustment in CKD patients.
P2Y12 receptor inhibitors (oral or IV)
ClopidogrelLD of 300–600 mg orally, followed by an MD of 75 mg; no specific dose adjustment in CKD patients.
Fibrinolysis: At the time of fibrinolysis, the initial dose is 300 mg (75 mg for patients older than 75 years of age).
PrasugrelLD of 60 mg orally, followed by an MD of 10 mg daily. In patients with body weight < 60 kg, an MD of 5 mg daily is recommended. In patients aged ≥75 years, prasugrel should be used with caution, but an MD of 5 mg daily should be used if treatment is deemed necessary. No specific dose adjustment in CKD patients. Prior stroke is a contraindication for prasugrel.
TicagrelorLD of 180 mg orally, followed by an MD of 90 mg twice daily. No specific dose adjustment in CKD patients.
CangrelorBolus of 30 micrograms (mcg)/kilogram (kg) IV followed by 4 mcg/kg/minute infusion for at least 2 hours or the duration of the procedure (whichever is longer).
In the transition from cangrelor to thienopyridine, the thienopyridine should be administered immediately after discontinuation of cangrelor.
GP IIb/IIIa receptor inhibitors
EptifibatideDouble bolus of 180 mcg/kg IV (given at a 10-minute interval) followed by an infusion of 2.0 mcg/kg/minute for up to 18 hours.

For Creatinine Clearance (CrCl) 30–50 milliliters (mL)/minute: First LD, 180 mcg/kg IV bolus (max 22.6 mg); maintenance infusion, 1 mcg/kg/min (max 7.5 milligrams (mg)/hour). Second LD (if percutaneous coronary intervention [PCI]), 180 mcg/kg IV bolus (max 22.6 mg) should be administered 10 minutes after the first bolus.
Contraindicated in patients with end-stage renal disease and with prior intracerebral hemorrhage (ICH), ischemic stroke within 30 days, fibrinolysis, or platelet count <100,000/mm3

TirofibanBolus of 25 mcg/kg IV over 3 minutes, followed by an infusion of 0.15 mcg/kg/minute for up to 18 hours.
For CrCl ≤ 60 mL/minute: LD, 25 mcg/kg IV over 5 min followed by a maintenance infusion of 0.075 mcg/kg/min continued for up to 18 hours. Contraindicated in patients with prior ICH, ischemic stroke within 30 days, fibrinolysis, or platelet count <100,000/mm3
(ESC, 2023; Galli et al., 2023)

Anticoagulant Drugs

Anticoagulant Drugs
Unfractionated heparin (UFH)Initial treatment: IV bolus 70–100 units (U)/kg followed by IV infusion titrated to achieve an activated partial thromboplastin (aPTT) of 60–80 seconds.
During PCI: 70–100 U/kg IV bolus or, according to activated clotting time (ACT), in case of UFH pre-treatment.
EnoxaparinInitial treatment: for treatment of ACS 1 mg/kg twice daily subcutaneously for a minimum of 2 days and continued until clinical stabilization. In patients whose CrCl is below 30 mL per minute (by Cockcroft–Gault equation), the enoxaparin dosage should be reduced to 1 mg per kg once daily.
During PCI: for patients managed with PCI, if the last dose of enoxaparin was given less than 8 hours before balloon inflation, no additional dosing is needed. If the last subcutaneous administration was given more than 8 hours before balloon inflation, an IV bolus of 0.3 mg/kg enoxaparin sodium should be administered.
BivalirudinDuring PPCI: 0.75 mg/kg IV bolus, followed by IV infusion of 1.75 mg/kg/hour for 4 hours after the procedure.
In patients whose CrCl is below 30 mL/min (by Cockcroft–Gault equation), maintenance infusion should be reduced to 1 mg/kg/hour.
FondaparinuxInitial treatment: 2.5 mg/day subcutaneously.
During PCI: A single bolus of UFH is recommended.
Avoid if CrCl < 20 mL/min.
(ESC, 2023; Galli et al., 2023)

Post-revascularization Antithrombotic Maintenance

Post-interventional antiplatelet treatment is recommended under the ESC guideline. A default dual antiplatelet therapy (DAPT) regimen consisting of a potent P2Y12 receptor inhibitor and aspirin should be given for 12 months; this can be reconsidered in patients with contraindications. DAPT therapies for revascularization maintenance can be shortened, extended, or modified. The P2Y12 inhibitors often used include ticagrelor, prasugrel, and clopidogrel; however, the older P2Y12 inhibitor (clopidogrel) is used less frequently. The medication(s) used and the dosage depends on if surgical methods are used and the patient's bleeding risks (Towashiraporn & Krittayaphong, 2022).

Alternative Therapy Options

Alternative non-pharmacologic therapy options in the management of cardiac emergencies are largely discussed under two headings: implantable devices and bioactive herbal preparations. Unlike pharmacological management with medications, patient monitoring and therapy assessment are not exactly definitive. There are no guideline recommendations for alternative therapies as most options are experimental with no review evidence on patient improvement.

Electronic pacemakers were introduced as early as the 1930s as an experimental option for managing cardiac arrhythmia. Pacemaker devices deliver an electrical pulse to depolarize the myocardium. At the stimulation threshold, electronic pacemakers are considered a standard therapy option for symptomatic bradycardia-related symptoms caused by AV node block or sinus node dysfunction. Pacemakers have also been used in the symptomatic management of severe left ventricular dysfunctions. Although pacemaker-like devices have been developed as non-pharmacological therapy options for cardiac emergencies, these options still have major shortcomings (Kingma et al., 2023). Cost of therapy, lead failure, cardiopulmonary collapse, and risk of infections are notable shortcomings in the wide use of these devices in modern medicine.

Reports of a new level of implantable devices leveraging gene-therapy-based manipulation of ionic currents, modifying cardiomyocytes to provide automaticity and stem cell treatments that add pacemaker syncytia to the heart have recently surfaced in multiple science literature (Farraha et al., 2018). These innovations are reportedly designed to solve the conventional problems associated with conventional devices. Similarly, the use of natural-sourced herbal extracts to manage cardiac emergencies has been widely reported in Central Asia and Sub-Saharan African countries. Under different therapy systems, locals have reportedly used different plant extracts based on their chemical components to relieve the acute symptoms of cardiac emergencies in different patient demographics (Dhinakaran et al., 2019).

Plants belonging to the different botanical families, including Mangifera indica (Anacardiaceae family), Terminalia arjuna (Combretaceae family), Ficus racemosa (Moraceae family), and Momordica charantia (Cucurbitaceae family), have been reported to have been used for their cardioprotective and anti-ischemic properties in cardiovascular-related diseases. The table below summarizes medicinal plants used as adjunctive treatments under different healthcare systems globally.

Medicinal Plants in Cardiac Emergencies
Plant NameBotanical FamilyChemical ConstituentsProperties (reported)
Pithecellobium dulceFabaceaeTannin, fixed oil, olein, glycosides, steroids, saponins, lipids, phospholipids, glycolipids, polysaccharides.Cardioprotective, anti-hyperlipidemic, antioxidant, antiseptic, antibacterial, anti-inflammatory.
Ficus racemosaMoraceaeLupeol, lupeol acetate, amyrin, sitosterol, stigmasterol, coumarin, psoralen, friedelin, kaempferol, gallic acid, bergenin, bergapten, rutin, ellagic acid, arabinose, racemosic acid.Cardioprotective, anti-hyperglycemic, antioxidant, analgesic, anti-inflammatory.
Terminalia arjunaCombretaceaeTriterpenoids, arjunic acid, arjunolic acid, tannins, flavonoids, gallic acid, ellagic acid, arjuna glycosides, and phytosterols.Cardioprotective, inotropic, anti-ischemic, antioxidant, antihypertensive, anti-atherogenic, anti-hypertrophic, hypolipidemic, antiplatelet.
Mangifera indicaAnacardiaceaeXanthone glycoside, urushiols, kaempferol, quercetin, tannins, flavonoids, polyphenolic compounds.Cardioprotective, anti-viral, antioxidant, anti-inflammatory.
Nelumbo nuciferaNymphaeaceaeNuciferine, alkaloids, glycosides, myricetin, quercetin, flavonoids, adenine, sitosterols.Cardioprotective, diuretic.
(Bachheti et al., 2022; Shaito et al., 2020)


Cardiac emergencies cast a huge burden on the global healthcare systems. A general call for awareness strategies developed by many countries seems to have resulted in a decreasing trend of regional prevalence and incidence. Although patients' presentation may vary even for the same diagnosis, newly developed guidelines standardizing the diagnosis and evaluation process may help clinicians deliver personalized healthcare strategies. Reorienting clinicians with updated information about diagnosis, patient evaluation, and management is expected to reduce the global mortality of cardiac emergencies. Developing healthcare systems encouraging interdisciplinary team collaborations can also greatly enhance care outcomes in managing cardiac emergencies.

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Implicit Bias Statement

CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.


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