How does the cardiac cycle and electrical activity all relate to blood pressure in the heart?

I know how the cardiac cycle works and understand the electrical activity in the heart such as the AV nodes, SA nodes and Bundles, but how do they work together in relation to blood pressure?

Blood pressure is determined by cardiac output and the total peripheral resistance, where, from Ohm's Law (Q= P/R):

Mean Arterial Pressure (MAP)= Blood flow (Q) x Total Peripheral Resistance (R)

The cardiac cycle and heart activity will essentially control the cardiac output through the FORCE and the FREQUENCY of contraction.

Cardiac output is determined by the stroke volume, and the heart rate:

CO= Stroke volume x HR

Changes in HR is linked to changes to the SAN and is controlled by sympathetic and parasympathetic inputs. An increase in HR, will cause cardiac output to increase, causing an increasing in blood pressure (simply put, other physiological changes can also influence blood pressure, such as vasoconstriction and vasodilation).

With regards to the AVN, SAN and bundles of His, this allows electrical conductance which causes the contraction of the heart. The contraction of the heart leads to blood being ejected (i.e. blood flow, which is linked to cardia output). This, together with the peripheral resistance of blood vessels will be linked to blood pressure.

Sudden Cardiac Arrest (Sudden Cardiac Death)

A natural disaster hits, the power goes off and the lights go out. It's a common scene that plays out during hurricane and tornado seasons, and it's very similar in trying to explain sudden cardiac arrest. The heart sustains an insult, the electricity is short circuited, the heart can't pump, and the body dies.

The heart is an electrical pump, where the electricity is generated in special pacemaker cells in the upper chamber, or atrium, of the heart. This electrical spark is carried through pathways in the heart so that all the muscle cells contract at once and produce a heartbeat. This pumps blood through the heart valves and into all the organs of the body so that they can do their work.

This mechanism can break down in a variety of ways, but the final pathway in sudden death is the same: the electrical system is irritated and fails to produce electrical activity that causes the heart to beat. The heart muscle can't supply blood to the body, particularly the brain, and the body dies. Ventricular fibrillation (V Fib) is the most common reason for sudden death in patients. Without a coordinated electrical signal, the bottom chambers of the heart (ventricles) stop beating and instead, jiggle like Jell-O. Ventricular Fibrillation is treated with electrical shock, but for it to be effective, the shock usually needs to happen within less than four to six minutes, not only for it to be effective, but also to minimize brain damage from lack of blood and oxygen supply. Automatic external defibrillators (AEDs) are commonly available in public places to allow almost anybody to treat sudden death. Less commonly, the heart can just stop beating. The absence of a heart beat is known as asystole (asystole: a=no + systole=beat).

What are the causes of sudden cardiac arrest?

Sudden death is most often caused by heart disease. When blood vessels narrow, the heart muscle can become irritated because of lack of blood supply. In heart attack (acute myocardial infarction), a blood vessel becomes completely blocked by a blood clot, and there is enough irritability of the muscle to cause ventricular fibrillation. In fact, the reason many people with chest pain are admitted to the hospital is to monitor their heart rate and rhythm for signs that might lead to ventricular fibrillation. Sudden death may also be the first sign or symptom of heart disease.

Congestive heart failure and heart valve problems, like aortic stenosis (narrowing of the aortic valve) also increase the risk of sudden cardiac arrest.

Cardiomyopathy is a broad category of heart disease where the heart muscle does not contract properly for whatever reason. Often it is ischemic, where part of the heart muscle doesn't get an adequate blood supply for a prolonged period of time and no longer can efficiently pump blood. People whose ejection fractions (the amount of blood pumped out of the heart with each heart beat) is less than 30% are at greater risk for sudden death (a normal ejection fraction is above 50%). In some people, cardiomyopathy may develop in the absence of ischemic heart disease.

Inflammation of the heart muscle, known as myocarditis (myo=muscle + card=heart + itis= inflammation), can also cause rhythm disturbances. Diseases like sarcoidosis, amyloidosis, and infections can cause inflammation of the heart muscle.

Some people are born with electrical conducting systems that are faulty, which place them at higher risk for rhythm disturbances. Some are due to the wiring, or electrical conduction system, like Wolff-Parkinson-White syndrome, while others are due to the structural basic structural problems within the heart, like Marfan syndrome.

Pulmonary embolus or a blood clot to the lung, can also cause sudden death. Clots form in the leg or arm and may break off and flow to the lung where they decrease the lung's ability to get oxygen from the air to the body. Risk factors for blood clots include surgery, prolonged immobilization (for example, hospitalization, long car rides or plane trips), trauma, or certain diseases like cancer.

Blunt chest trauma, such is in a motor vehicle accident, may result in ventricular fibrillation. (please see commotio cordis below)

Cardiac Arrest Symptoms and Causes

Cardiac arrest is the sudden loss of cardiac function, when the heart abruptly stops beating. Unless resuscitative efforts are begun immediately, cardiac arrest leads to death within a few minutes. This is often referred to by doctors as "sudden death" or "sudden cardiac death (SCD)."

Symptoms of sudden cardiac arrest include:

What about sudden cardiac arrest in the young?

In younger people, sudden death is a rare event, but since it often involves people involved in athletics, cases are often reported in the press. The most common cause is hypertrophic cardiomyopathy (hypertrophy=to grow abnormally large + cardio=heart + myopathy = diseased muscle). This disease is often hereditary, and the walls of the ventricle are larger than they should be. This makes the pumping chamber of the heart smaller, and the heart has to work harder to pump blood out of the heart. As well, the thickened muscle narrows the space for the blood to flow through the aortic valve and to the rest of the body. During exercise, this decreased blood flow can irritate the heart muscle itself and cause ventricular fibrillation, collapse, and sudden death.

Anomalous coronary arteries can also cause sudden death in the young. The heart is a muscle itself, and like any muscle, it needs blood supply to provide oxygen for it to work. Normally, the coronary arteries lie on the surface of the heart. Anomalous arteries dive into the heart muscle itself and may be occluded when the heart muscle that surrounds the abnormally placed artery squeezes aggressively, as with exercise, shutting off blood supply to part of the heart. This irritates the electrical system and can cause ventricular fibrillation and sudden death.

The pre-participation athletic physical examination is a useful tool to screen children and adolescents for their risk of sudden cardiac arrest.

Commotio cordis is a situation in which the heart stops when the chest is hit by an object. News stories occasionally report of baseball players who are hit in the chest by a ball and collapse because their heart stops beating. The heart sits behind the breastbone, and the electrical system can be short circuited when a direct blow is sustained.


What are the signs and symptoms of sudden cardiac arrest?

Cardiac arrest symptoms and signs are not subtle:

  • The heart stops beating and blood is not supplied to the body.
  • Almost immediate loss of consciousness occurs, and the affected person will not be able to be aroused.
  • The person will fall or slump over.
  • No pulse is felt (palpable).
  • There will be no signs of breathing.

How do medical professionals diagnose sudden cardiac arrest?

Sudden cardiac arrest is an unexpected death in a person who had no known previous diagnosis of a fatal disease or condition. The person may or may not have heart disease.

What is the treatment for sudden cardiac arrest?

The vast majority of people whose heart stops beating unexpectedly have ventricular fibrillation. The definitive treatment for this is defibrillation using electricity to shock the heart back into a regular rhythm. With technological advances, AEDs are now a routine sight wherever people congregate.

Communities which institute public CPR education, use of AEDs, and rapid activation of 911 emergency medical services have dramatically increased survival rates from sudden cardiac arrest. Unfortunately, because the brain is so sensitive to the lack of oxygen and blood flow, unless treatment occurs within four to six minutes, there is a high risk of some permanent brain damage.

Should the patient survive to be transported to the hospital, the reason for collapse and sudden death will need to be diagnosed. Regardless, the ABCs of resuscitation will be re-evaluated. Airway, Breathing, and Circulation (heart beat and blood pressure) will be supported, and admission to an intensive care unit is most likely.

Diagnostic tests may include repeated electrocardiograms (EKGs), echocardiogram (ultrasounds of the heart), and cardiac catheterization and electrophysiologic studies, in which the electrical pathways of the heart are mapped.

Recent research involving the treatment of survivors of cardiac arrest suggests that prompt institution of hypothermia (cooling of the body) may prevent or lessen the degree of brain injury.

Survivors of sudden cardiac arrest are often candidates for implantable cardiac defibrillators.

Research On PEMF Therapy for Heart Conditions

In dogs’ hearts, considered comparable to human hearts, the natural heart EMFs, due to the beating of the heart, are much larger by adding external EMFs. The heart contributes between 5% and 10% of the total field induced in the human body by external electric and magnetic fields.

Cells or tissues can be protected against a lethal stress by first exposing them to a sublethal dose of the same or a different stressor to produce stress proteins in tissues. This concept is known as “preconditioning” and gives protection against oxidative stress, caused by ischemia/reperfusion, UV light exposure, heat, chemicals and electromagnetic field (EMF) exposure. Rodent heart muscle cells preconditioned by low energy EMFs for 30 minutes have more effective induction of stress proteins than heat. As little as 10 seconds of exposure produce a detectable response at 30 minutes, last for more than 3 hours and can be restimulated by a second exposure to fields of different intensity.

However, in egg embryo studies, continuous exposure to ELF EMFs for 4 days, twice daily for 30 minutes or 60 minutes for 4 days reduced the protective effect. 30-minute exposures once daily and 20-minute exposures twice daily did not reduce protection. A protective role is seen against cardiac ischemia in chick embryos. EMFs for 20 minutes induce stress proteins in the laboratory. This raises the strong possibility that using them before, during and after the surgical trauma can use EMFs for minimizing heart damage from heart surgery or transplantation or heart attack in humans.

For other kinds of cardiac actions, short-term exposure to sinusoidal ELF EMFs (5-8 Hz) in adult and old male rabbits for 15-120 minutes causes mild decreases in the ECG heart rate if exposure lasts 60 minutes. Old rabbits developed extra beats. In animals with experimentally induced myocardial infarctions, EMFs are not necessarily beneficial. There is little data comparing different kinds of EMFs. It remains to be determined what the optimal configurations are for different situations.

One study examined the difference between pulsed (PEMF) and alternating/sinusoidal (AMF) field effects on the hearts of dogs, exposed for an hour per day for 10 days. The AMF caused marked changes in heart dynamics: decreased ventricle function and increased peripheral resistance and end diastolic pressure in the right ventricle, as well as, left ventricular work. Systolic blood pressure (BP) and contractility and heart rate still decrease with PEMFs, but are less marked. Thus, use of PEMFs may be less aggressive for cardiac problems than sinusoidal fields.

Basic actions at the cell level account for these actions. A 16 Hz frequency modulation increases mean flow of Ca++ out of frog heart cells at low intensities. This compares with calcium flow in brain tissue, suggesting that neural tissues may generally react at these modulations and intensities and act through changes in Ca++ in and around cells. Chronic exposure to 50 Hz EMFs of rats at 2 hr/day for lower intensities or 0.5 hr/day to higher intensities produced increased blood flow to the heart tissue and enlargement of the coronary vessels. Higher intensity EMFs affect the heart function of rats (25) with 14 days, 4 hours a day of stimulation. EKG changes are temporary, but, at the end of 14 days of stimulation only heart rate remains decreased.

Hypertension, if untreated for a long time, can cause heart damage and ultimately heart failure. Static magnetic fields (SMF) of 2000 G placed on each carotid sinus area (south and north poles, respectively), decrease systolic, diastolic, and mean blood pressures by 10%. Heart rates were not affected. This action is most likely due to Ca++ transport changes across the carotid pressure receptor membranes.

Stress has very strong actions on the heart. When ultrahigh-frequency (UHF) EMFs are given to dogs subjected to emotional stress, several cardiovascular changes resulting from stress are improved. Stress increases blood pressure by 40-50%, heart rate by 20% and makes the left ventricle function hyperdynamically. Even though the UHF EMF does not eliminate the stress reaction of the cardiovascular system, it is less pronounced overall. UHF EMFs seem to accelerate central adaptation mechanisms, rebalancing circulation and decreasing adaptation time for cardiac stress.

How Environmental and Geomagnetic Fields Impact The Heart

Studies from Eastern Europe have found that changes in the geomagnetic field can worsen heart disease and that the major effects occur on the first or second day after a magnetic storm. Geomagnetic activity can be quiet, unsettled, active, or stormy.

While myocardial infarction rates (MIs) from circulation blockages do not seem to change with geomagnetic activity, cardiac electrical activity is probably more sensitive and affected. The admission rates of patients with new episodes of electrical conduction problems causing paroxysmal atrial fibrillation (PAF) were highest during the two lowest levels of geomagnetic activity, more in males and persons over 65 years. Males under age 65 with PAF are at greater risk of stroke from the PAF. Thus, increases in heart electrical instability appear to happen during periods of lowest geomagnetic activity.

Geomagnetic fields (GMF) also interact with ELF EMF therapy. Even a very weak EMF, up to 70 uT applied to the whole body or locally, for 8-12 minutes, 1-2 times per day for 10-20 days has clinical benefit in most patients. Sensitive patients improve after only one or two days, most others take 5-10 days. On days when GMF increases two-three fold, some patients complain of discomfort during the exposure and have increased blood pressure (BP). In most, (47%) the BP shows no changes, 38% decrease BP and 15% are increased.

Environmental exposure of EMFs also affects cardiovascular function. Average 50-60 Hz working environments do not have much effect on human heart rates. In AM radio station workers exposed to high frequency (HF) fields, 83% have heart rhythm disturbances and decreased signals in their ECGs.

There are significant differences between clinical ELF PEMF systems and high frequency (microwave or cell phone levels) sources. Any publicly oriented article or book, unselectively citing references mixed with ELF exposures and those in the HF kHz and over range, clearly does not understand EMFs and is indiscriminately comparing apples and oranges, in terms of their clinical effects. Indeed, there are many clinical therapy systems that use high frequencies, but they are usually used for tissue destruction, for tumors and colon, bladder, skin and heart arrhythmia lesions, etc. General or public use of EMFs for personal use should be restricted to low strength ELFs or high frequency EMFs that do not create heating.

Duration of exposure to environmental fields is probably important as well. Changes in heart rhythm may be affected in the workers professionally exposed to 50-Hz electric and magnetic fields (EMF) over long periods. There can be a global decrease of cardiac rhythm in both high (over the industry norm) and low (at or below industry norms) professionally EMF-exposed groups compared to the non EMF-exposed control group. These changes may increase the risk of cardiovascular diseases. Other environmental or home-based “electromagnetic pollution” has the risk of inducing health problems. Fortunately, measures can be taken in the home and office to decrease background EMF risks.

Human Studies on PEMF Therapy for Heart Conditions

Experimental studies show that EMFs can affect the function of the centers of the autonomic nervous system controlling cardiac rhythm. A temporary increase in BP is seen with clinical exposure to industrial 50-60 Hz EMFs, but extended exposure causes the systemic pressure to decrease. Microcirculation dilatation occurs, with increased blood flow in the capillary bed and precapillary arterioles and an increased permeability of the vascular wall. Even lymphatic vessel flow increases. Circulation changes produced by EMFs are depending on the functional state of the central regulatory apparatus, especially the hypothalamus. Experimental PEMFs are found to act directly on the tissue of a beating heart.

Medium powerline-type field exposure for 3 hours causes a significant slowing of the heart rate. EMF effects are related to changes occurring during the recovery phase of the cardiac cycle. Humans are more responsive to some combinations or levels of field strength than others.

EMF therapy acts beneficially on the functional state of the nervous and endocrine systems as well as on tissue metabolism. The heart rate and BP decrease and the cardiovascular system is less reactive to adrenaline and acetylcholine. The parasympathetic nervous system is activated. Stimulation of the autonomic ganglia along the spine reduces cortisol and aldosterone. MFs typically cause only a momentary change of the microvascular bed with slowing blood flow. This then changes over to a longer period of an increased heart rate, rate of blood flow and filling of the blood vessels.

How PEMF Therapy Benefits The Human Heart

Sinusoidal PEMFs improve microcirculation in people with ischemic heart disease and vascular diseases of extremities. PEMFs act more strongly than permanent magnets. ELF MFs improve both lipoproteins and cholesterol levels. But, a static magnetic field of more than 50 mT (500 Gauss) at the tissue increases risk of atherosclerosis, with irregularly arranged lipid deposits in middle to large size arteries and fibrosis and calcification. In people with low blood pressure, EMFs improve heart contractions and cause more normal bioelectrical function. In most people, EMFs lower BP by lowering vascular resistance, with vasodilatation.

Hypertensive patients are affected positively, depending on the function of the heart before magnetic treatment. People with normal functioning hearts just have their vascular resistance lowered. EMFs normalize heart function and circulation in patients with high BP, and at the same improve circulation. The improvements in systemic vascular tone, as well as lipid metabolism and coronary circulation make MFs very useful treatment for people with the combination of hypertension and ischemic heart disease.

Early in the course of use of MFs in patients, there are changes in ECGs to a lower wave size pattern, sinus rhythm and extra beats, and a decrease in heart rate. With continuing magnetotherapy, these changes disappear and cardiovascular function is improved. This is common with MF therapy. Meanwhile, there may be temporary worsening while repair and rebalancing is happening, with the outcome being more normal function and health.

To get better results with EMF treatments, understanding the underlying cause of the problem and function of the organ system is critical for designing the proper protocol to use for an individualized approach. The best outcomes occur this way. Without an understanding of the physiology and the type of field to use and how, less than optimal results can happen. Awareness of the potential for initial de-stabilization minimizes misunderstanding in managing the course of therapy and should be carried out with the assistance of a knowledgeable professional.

Magnetic Therapies To Avoid For Heart Conditions

Good results are not always seen. In one small series, patients were treated with sinusoidal EMFs for arrhythmias caused by ischemic heart disease, post myocardial infarction and cardiomyopathy. A sinusoidal EMF used for 10 sessions daily, alternating between placement to the sternum for 15 minutes and “palm – wrist” area for 5-7 minutes. EMFs did not normalize heart rhythm. One woman had an attack of paroxysmal tachycardia occurred. Six patients reported unpleasant sensations (“sickness at heart” and headache) during or after EMF therapy, occurring most often with cardiomyopathy. A sinusoidal EMF may even increase BP in males, whether exposure was for 20-40 minutes or 1 hour.

Other Magnetic Fields and The Heart

Magnetolaser therapy (MLT) has been studied in single placebo control trial in the treatment of ischemic heart disease patients, with exertional angina and moderately to severely impaired function, post-myocardial infarction. Most had significantly decreased circulation. MLT was applied to 3 tender zones on the chest: in the front over the upper part of the heart and middle of the sternum, and in back between the scapulas to the left of the mid line, for 12 min, 4 min for each exposure zone, daily over 15 days. Work capacity increased in 84% of the MLT group but worsened in the placebo group.

The work increased most for patients with functional classes II and III angina. MLT was also useful for patients with conduction disorders, eliminating extra beats in 29% and decreasing them by more than 70% in 32% of cases and stopping paroxysmal atrial fibrillation in 53%. The treatment lasted through the follow-up period of 12 to 16 months. These impressive results show that MLT facilitates adaptation to a physical load, and promotes rearrangement of central hemodynamics and recovery and stabilization of electrical activity of heart cells, safely and simply.

Heart rate variability (HRV) results from the action of neuronal and cardiovascular reflexes, including those involved in the control of temperature, blood pressure and respiration. Changes in HRV are predictive of a number of cardiovascular disease conditions and specific alterations in HRV have been widely reported to be associated with adverse cardiovascular health outcomes. Low strength, 60-Hz continuous or intermittent MFs in healthy males has little or no effect on HRV, indicating they do not induce stress effects. HRV alterations during magnetic field exposure may occur when accompanied by increases in physiologic arousal, stress, or a disturbance in sleep. There appear to be significant differences in heart rate and mean 24-hour personal exposure to MF between occupational and non-occupational group. It is not yet known whether clinical EMF exposure, in those who’s HRVs shows clear departures from normal, improves the HRV.

Patients with so-called Electrical Hypersensitivity (EHS) have a misbalance of autonomic regulation being more hypersympathetic, as measured by heart rate (HR) and electrodermal activity and sympathetic skin responses to visual and audio stimulation. There are frequency-intensity-duration components to these exposure sensitivities.

Much of the biological effect of high frequency fields is due to tissue heating, not just EMF effects. However, biological effects, not due to tissue heating (nonthermal) have been found with millimeter-range (MMR about 300 GHz) MFs. These EMFs probably affect the command centers of organs through reflex systems. It is preferable to select biologically active points for MMR exposure tender zones and areas of large joints, where tissue sensors are numerous and nerve fibers contact collagen directly. Local skin exposure to MMR EMF affects cerebral function.

Clinical benefits are seen with treating heart angina and hypertension, especially essential hypertension. It is noted that patients with symptomatic, renal hypertension don’t respond. Cardiac rehabilitation in rats with MMR EMF added after myocardial infarction promotes tissue repair and functional recovery. Human clinical studies confirm this. Only favorable effects occur: more rapid tissue healing, activation of ATPases, antioxidant properties, and so on.

The QRS Complex

The QRS complex refers to the combination of the Q, R, and S waves, and indicates ventricular depolarization and contraction (ventricular systole). The Q and S waves are downward waves while the R wave, an upward wave, is the most prominent feature of an ECG. The QRS complex represents action potentials moving from the AV node, through the bundle of His and left and right branches and Purkinje fibers into the ventricular muscle tissue. Abnormalities in the QRS complex may indicate cardiac hypertrophy or myocardial infarctions.


While the basic haemodynamics of established hypertension are undisputed, there is less agreement about the haemodynamic pattern in young individuals with (comparatively) elevated blood pressures. Since an individual’s position within the overall blood pressure distribution tends to remain fairly constant (tracking of blood pressures) these subjects are at high risk of developing hypertension in later life.

In young individuals less than 19 years, most evidence suggests that subjects with the highest blood pressure have increased PVR, though small increases in cardiac index have been seen in some studies. w12 w13 There is evidence that young individuals with hypertension have an increased sympathetic activity, though studies in established hypertension are inconclusive. 8 The question is complicated by methodological difficulties in the assessment of sympathetic nerve activity in vivo and the importance of increased sympathetic activity in the development of hypertension is uncertain. Interestingly, an increased left ventricular mass is a fairly consistent finding in young individuals with raised blood pressure 8 and is also seen in offspring of hypertensives, w14 although the functional determinants of this abnormality are not well understood.

In adults (18–40 years) with raised blood pressure (borderline or mild hypertension) PVR is often in the normal range at rest, and the raised blood pressure is attributable to increased cardiac index and heart rate. A prospective study of young males 8 reported that subjects with high cardiac index/normal total peripheral resistance index pattern changed to a low cardiac index/high resistance pattern at 10 and 20 year follow up it is therefore plausible that haemodynamic patterns in young individuals with high blood pressure undergo this type of change as they age, accounting for the appearance of the high PVR pattern in established hypertension.

Structural changes in hypertension

Both heart and arteries adapt their structure in response to altered load. This occurs physiologically (for example, during somatic growth) and pathologically in hypertension. Increased pressure exerts an increased load on a thin walled chamber or tube by increasing wall tension according to Laplace’s law (fig 3).

Wall stress and tension in a thin walled tube or chamber (Laplace’s law).

More complex expressions for wall tension in the heart or blood vessels exist, but this is a reasonable approximation. A rise in tension results in increased wall tensile stress. Normalisation of wall tensile stress can be achieved either by an increase in wall thickness or by a reduction in chamber/lumen diameter, or both.

Cardiac remodelling in hypertension and its functional consequences

Cardiac structure is influenced by pressure and volume loads. 9 In hypertension changes in left ventricular structure occur in response to the increased pressure load and represent an attempt by the heart to normalise myocardial wall stress. The increased pressure load in hypertension is primarily caused by the increased resistance, although reduced compliance and possibly altered magnitude and timing of reflected pressure waves make a contribution.

Patterns of remodelling: relation to load

Hypertension is associated with a spectrum of structural change in the left ventricle. w15 The pattern of change may reflect differences between individuals in terms of age, haemodynamics, 24 hour blood pressure profile, arterial stiffness, plasma volume, myocardial performance, neurohormonal status or genetic influences. 10 w15 Hypertensive changes can be classified as showing hypertrophy (an increase in left ventricular mass) or remodelling (normal left ventricular mass, abnormal relative wall thickness) (fig 4).

Major patterns of myocardial and vascular remodelling in hypertension. CR, concentric remodelling CHR, concentric hypertrophy ER, eccentric remodelling IER, inward eutrophic remodelling IHR, inward hypertrophic remodelling. 20

Remodelling is seen in normal aging without hypertension w16 and is probably an adaptation to preserve ejection fraction despite reduced midwall fibre function. It has become apparent that myocardial fibre shortening is reduced in human hypertension. Early clinical investigations assessed cardiac function using endocardial measurements. Recently, it has been appreciated that there is a discrepancy between shortening measured at the endocardium and at the midwall. Midwall shortening is commonly reduced in left ventricular hypertrophy and the process of wall hypertrophy allows total wall shortening to remain normal in spite of a depression in fibre shortening—that is, the change in left ventricular geometry allows the chamber function to remain normal. 11

Normal myocardium contains an interstitial fibrous network upon which the myocytes are arranged. Although hypertrophy primarily involves myocytes, the interstitial network also changes. This occurs initially in a perivascular distribution but progressively extends to cause a widespread interstitial fibrosis. In addition, replacement fibrosis may occur to replace necrotic or apoptotic myocytes. Increased interstitial fibrous tissue is probably important in cardiac dysfunction in hypertension, but the amount of fibrosis is not easy to measure clinically and so differential changes in myocyte hypertrophy and fibrosis cannot easily be assessed in patients.

Most hypertensives have normal left ventricular structure, but left ventricular hypertrophy predicts a poor prognosis, the almost threefold increased risk being independent of the blood pressure level. 12 Whether individual remodelling patterns confer additional risk is disputed (Framingham study) and how left ventricular hypertrophy causes increased risk is uncertain. The increase in ventricular arrhythmias 13 and increased QT duration and QT dispersion seen in left ventricular hypertrophy 14 may account for the increased risk of sudden death, but other mechanisms such as impaired coronary perfusion could also be important. The electrical abnormalities are likely to be caused by heterogeneous conduction in the ventricle due to increased interstitial fibrosis. There is now increasing evidence that regression of left ventricular hypertrophy with antihypertensive treatment provides cardiovascular protection over and above the reduction in blood pressure levels, 15 w17 but again the mechanism of the risk reduction is uncertain.

Consequences of hypertrophy and remodelling

Active relaxation is impaired in hypertrophy and remodelling. w18 The explanation for this is uncertain, although changes in intracellular calcium handling, ion exchangers, and ion channels are implicated. w19 Cardiac hypertrophy is also associated with impaired coronary reserve. This may be caused by a number of mechanisms, including endothelial dysfunction, narrowing of small arteries, microvascular rarefaction, perivascular fibrosis, altered wall mechanics, and relative myocyte hypertrophy. w20 A diminished coronary reserve will lead to myocardial ischaemia in the absence of epicardial coronary disease and may further impair relaxation.

Impaired relaxation results in prolongation of isovolumic relaxation time (from aortic valve closure to mitral valve opening) because it takes longer for left ventricular pressure to decrease below atrial pressure. Once the mitral valve is open the slowed relaxation means that left ventricular filling takes longer and there is more blood in the left atrium by the end of the early filling period. This leads to an increased force of atrial contraction. Echo Doppler studies therefore show an early filling wave (E wave), that has a reduced peak velocity and a prolonged duration (fig 5B) and an increase in the A wave, resulting in a reduced E/A ratio. As diastolic dysfunction progresses there is a decrease in left ventricular compliance caused mainly by the increased interstitial fibrosis. This impairs filling notably. As the heart becomes stiffer, pressure in all the chambers increases. The increased left atrial pressure results in a large pressure gradient in early diastole when the mitral valve first opens, so the peak velocity of the early filling wave is very high. But the reduced ventricular compliance means that pressure increases disproportionately for small changes in volume, so once left ventricular filling begins atrial and ventricular pressures equalise very quickly, resulting in a very short duration early filling wave (fig 5C).

Doppler echocardiographic records showing (A) normal diastolic function, (B) impaired relaxation, and (C) restrictive pattern (that is, severe diastolic function with an increase in left atrial pressure).

Mild diastolic dysfunction is often clinically silent however, if the deterioration of diastolic function is sufficient to significantly reduce ventricular filling and left ventricular end diastolic volume, a reduction in stroke volume will occur and patients may develop low output symptoms such as fatigue. As diastolic dysfunction progresses, left ventricular filling pressures become abnormally high and pulmonary congestion may occur. w21 Thus the symptoms of heart failure may develop in the presence of apparently normal systolic function. Early studies have suggested that over a third of patients with a clinical diagnosis of heart failure have normal left ventricular systolic function w22 however, it is now becoming apparent that there is considerable overlap between diastolic and systolic dysfunction. 16 Therefore it is not surprising that diastolic dysfunction associated with symptoms carries an adverse prognosis. 17

Arterial remodelling in hypertension and its functional consequences

Structural changes in hypertensive vasculature show similarities to those in the heart. In both cases the primary goal appears to be the normalisation of wall stress. The elevated pressure causes an increase in wall tension that is largely experienced by vascular myocytes and the extracellular matrix of the blood vessel. The pattern of remodelling of the vasculature seems highly dependent on the size and function of the artery examined. In part this may reflect the major influence of flow on arterial structure. 18 Flow affects arteries via the frictional force experienced by the wall as a result of the flow of blood (shear stress). The wall shear stress is sensed by the endothelial cells. In response to shear stress the endothelium releases a number of vasoactive factors that affect arterial tone and growth.

Cardiac and vascular pathology in hypertension: key points

Increased peripheral vascular resistance (PVR) is the hallmark of established hypertension, but altered cardiac function also probably contributes to the raised blood pressure

Large elastic arteries are important in damping the pulsatile flow created by the heart

Pressure wave reflection from downstream affects the pressure waveform in arteries and this is responsible for raised brachial systolic blood pressure compared with central aortic systolic pressure

Deceleration of left ventricular contraction causes an expansion (suction) wave, which is responsible for aortic valve closure

Hypertension causes cardiac and vascular remodelling and hypertrophy. This helps to normalise left ventricular and arterial wall stress and may compensate for a reduction in myocardial fibre function to preserve cardiac output

Hypertensive vessels are not inherently stiffer than normal blood vessels. All vessels become stiffer as they are distended and the increased stiffness in hypertension is a reflection of this

Hypertension is associated with reduced vasodilator reserve and a reduction in microvascular density

Large elastic and muscular arteries

These arteries do not contribute to peripheral vascular resistance, but influence total arterial compliance and wave reflection. The diameter of large elastic arteries such as the aorta or carotid is increased in hypertension. There is also an increase in wall thickness (or at least intima–media thickness (IMT) as measured by ultrasound). 19 The increase in diameter in these vessels is probably passive the rise in pressure distends the vessel, while the increased media thickness normalises media stress. In smaller more muscular large arteries, such as the femoral, brachial, and radial, arterial diameter is not increased, although IMT is increased and wall:lumen ratio is therefore increased.

Numerous studies have reported that arterial stiffness is increased in hypertension. With the possible exception of the carotid artery of young hypertensives, w23 this increase in stiffness is not caused by a change in the inherent wall properties of arteries (despite the increase in wall thickness) but is a result of the increased distending pressure. Blood vessels do not obey Hooke’s law and are non-linearly elastic—that is, they become stiffer when distended. When this is taken into account, the intrinsic elasticity of hypertensive arteries does not usually differ from normotensive arteries. w24 Indeed, radial artery stiffness has been reported to be decreased compared with normal when pressure effects are allowed for. w25 Interestingly, these recent findings conflict with the widely held view that hypertensive changes in arterial compliance are essentially an acceleration of the aging process. Aging results in increased arterial stiffness probably through degenerative changes in elastin in the arterial wall. In contrast hypertension does not affect the elastic nature of the arterial wall, although the pressure induced increase in stiffness will worsen age related decreases in arterial compliance. A consequence of the increased arterial stiffness in hypertension is that speed of pressure wave travel will be increased (this is often used as a measure of arterial stiffness). It is also likely that changes between one artery and another (impedance mismatching) result in increased wave reflection and increased pressure augmentation as discussed above.

Small muscular resistance arteries, arterioles, and the microvasculature

The lumen diameter as a ratio of wall thickness is reduced in small arteries in all forms of hypertension. In essential hypertension this is caused by inward eutrophic remodelling (fig 4), 20 whereas in some secondary forms of hypertension hypertrophic changes are seen. w26 This remodelling has a number of consequences beyond normalising media stress. Maximum vasodilation (minimum resistance) is reduced this results in a reduced vasodilator reserve (most significant in the coronary circulation) and vasomotor responses are enhanced, as a given shortening will induce an exaggerated vasoconstriction. 21 This effect has been termed the vascular amplifier w27 and is suggested as a mechanism by which the circulation can chronically maintain elevated resistance without excessive vasoconstriction.

Relatively little is known about arteriolar changes in human hypertension. On the basis of animal studies it has been suggested that arteriolar tone may be increased, but there is little evidence for structural changes in individual arterioles except in accelerated or malignant hypertension. In contrast there is good evidence that the density of the microvasculature is reduced. This can be visualised in a number sites including the retina, sclera, and skin. There is doubt about whether the reduction in microvascular density is “functional” (non-perfused vessels) or structural (obliterated vessels). In our view this is an academic question and in any case it is likely that persistently non-perfused vessels are ultimately obliterated. w28 The consequence of this pruning of the microvascular tree is that resistance is increased (by up to 40% in some estimates w27 ) and that maximum tissue perfusion (and consequently nutrient supply) is restricted. This could contribute to the association between hypertension and diabetes (or insulin resistance) as capillary rarefaction in hypertension may result in impaired glucose extraction by skeletal muscle. w29

Blood pressure

During exercise, increases in cardiac stroke volume and heart rate raise cardiac output, which coupled with a transient increase in systemic vascular resistance, elevate mean arterial blood pressure (60). However, long-term exercise can promote a net reduction in blood pressure at rest. A meta-analysis of randomized controlled interventional studies found that regular moderate to intense exercise performed 3𠄵 times per week lowers blood pressure by an average of 3.4/2.4 mmHg (61). While this change may appear small, recent work shows that even a 1 mmHg reduction in systolic BP is associated with 20.3 fewer (blacks) or 13.3 fewer (whites) heart failure events per 100,000 person-years (62). Thus, reductions in blood pressure observed when exercise is included as a behavioral intervention along with dietary modification and weight loss (63, 64) could have a significant impact on CVD incidence.

Lower ambulatory blood pressure, associated with chronic aerobic and resistance exercise, is thought to be driven largely by a chronic reduction in systemic vascular resistance (65). Contributing to this effect, shear forces, as well as released metabolites from active skeletal muscle during exercise, signal the production and release of nitric oxide (NO) and prostacyclin from the vascular endothelium, which promotes enhanced vasodilation via relaxation of vascular smooth muscle cells (66). This effect is especially significant because a reduction in eNOS activity that occurs with aging or due to NOS3 polymorphism, has been reported to contribute to hypertension (67�). Long-term exercise training increases eNOS expression as well as NO production in hypertensive individuals, consistent with the blood pressure lowering effect of physical activity (70). An important role of NO in mediating the vascular effects of exercise is further supported by results showing that rats with hypertension induced by chronic NOS inhibition undergoing a swimming exercise regimen for 6 weeks have significantly elevated eNOS protein expression and improved acetylcholine-induced vasodilation (71). Thus, improvements in NO production and bioavailability appear to represent significant factors that contribute to improved endothelium-dependent vasodilation following exercise training, which can reduce resting vascular resistance and lower blood pressure. However, in addition to NO-mediated reductions in resistance vascular tone, adaptive reductions in sympathetic nerve activity, prevention or reversal of arterial stiffening, and suppression of inflammation are also likely contributors to the blood pressure lowering effects of exercise, although the impact of exercise on these outcomes may be population specific (e.g., at-risk versus healthy adults) (72�). As with changes in blood lipid profile, it remains unclear to what extent the blood pressure lowering effects of exercise can account for the beneficial effects of exercise on CVD risk and mortality.

When shortness of breath signals heart problems

Many different heart problems can lead to shortness of breath. It may happen suddenly or gradually over time. It may also occur only during physical activity or in stressful situations.

You should never ignore unexplained breathlessness, as it may be due to a serious underlying health condition. If you experience shortness of breath, please seek medical care.

Here at Metropolitan Cardiovascular Consultants, we partner with our patients to prevent and treat conditions and diseases that affect the heart while preserving and improving quality of life.

Dr. Djamson offers a wide range of cardiovascular services at our outpatient clinics. Patients can access advanced cardiac technology to diagnose and treat conditions that range from simple to complex.

If you have heart health concerns, a visit with a cardiologist is paramount. Symptoms of heart disease range widely, and a comprehensive evaluation is needed to identify and treat problems.

Unexplained shortness of breath may signal an underlying problem with the structure or function of your heart. Below is a list of potentially serious and frequently diagnosed heart conditions which may present with Shortness of Breath.

Coronary Artery Disease

Two main coronary arteries, the Left main and Right coronary arteries supply blood to the heart. These arteries may develop problems leading to serious and potentially life-threatening conditions

Coronary artery disease (CAD) is the most common type of heart disease in the US, it develops when there is a buildup of plaque in the walls of the coronary arteries leading to narrowing and eventually occlusion of these arteries.

These cholesterol rich fatty deposits (plaques) decrease blood flow to the heart muscle leading to a condition called Angina and raises the risk for a heart attack. Symptoms may not appear until there is a significant reduction of blood flow.

Shortness of breath, especially during exertion, may be an atypical presentation of Angina and may be due to underlying CAD.

Heart attack

A heart attack occurs when the heart muscle does not receive enough oxygenated blood and nutrients to function properly

Unfortunately, you might not have any symptoms of CAD until you suffer a heart attack. This makes it crucial to form a strong, collaborative relationship with your provider and schedule recommended checkups for prevention and early detection of heart disease. This is especially true if you have risk factors for CAD, these include Hypertension, Diabetes, High cholesterol, smoking and a family history of Coronary artery disease.

While chest pain is the most common symptom of a heart attack, patients especially women may present primarily with Shortness of breath and worsening fatigue.

You may notice a decrease in energy or breathlessness after minimal activity which you may attribute to ageing, a lack of physical activity or weight gain but these may represent early subtle signs of heart disease or a heart attack

Heart failure

Heart failure is a condition where the heart is unable to pump enough blood to satisfy the body&rsquos need for blood, oxygen and other nutrients. This is caused by either diseased heart muscle which is too weak to pump enough blood to the body (heart failure with reduced ejection fraction) or a thick, stiff heart muscle which does not relax enough to be filled with blood (heart failure with preserved ejection fraction)

Shortness of breath is the most common symptom of heart failure. It is a distressing feeling that may cause you to feel smothered, Shortness of breath initially occurs with exertion but may get progressively worse and eventually occur at rest in severe cases. It typically is worse on lying flat on your back and patients sometimes wake up from sleep and sit up to catch their breath.

Causes of heart failure include CAD, long standing hypertension and a diseased Heart muscle termed Cardiomyopathy, this may be hereditary or may be secondary to diseases like Hypertension, CAD and sarcoidosis. A weakened heart muscle may also be caused by infections which directly damage the heart (myocarditis) most notably there have been multiple reports of Covid 19 causing myocarditis and eventually leading to cardiomyopathy and heart failure.

It is important that Heart failure is identified early and treated. Tests are available to help determine the cause of Heart Failure and treatments are available that have been shown to improve quality of life, reduce hospitalizations and death from heart failure

Cardiac arrhythmia

Heart rhythm abnormalities, conditions in which your heart either beats irregularly, out of step, too fast or too slow may present with shortness of breath, these conditions are usually easily identified and can be successfully treated and in some cases cured leading to a complete resolution of symptoms,

Your provider may first notice an arrhythmia during a routine physical exam. An arrhythmia may signal a harmless condition or something more serious. Common symptoms such as shortness of breath and dizziness require careful evaluation by a specialist.
Valvular Heart Disease
Heart valves work normally to perform 2 tasks 1. Open wide to let blood flow through 2.Keep blood flowing in one direction and preventing blood from leaking back in the opposite direction.
Conditions in which the heart valves do not open all the way lead to a narrowing of the valvular opening termed Stenosis if this is severe it may cause shortness of breath either due to the valve disease itself or because it leads to a cardiomyopathy and lung disease. When a valve is diseased and does not shut completely it allows blood to leak backwards this is termed regurgitation and when severe enough may also lead to shortness of breath. Valvular heart disease is easily diagnosed with a thorough physical exam and tests such as an Echocardiogram. Treatment of heart valve disease is more successful if instituted early, before patients develop cardiomyopathy and other irreversible effects of valvular heart disease like lung disease


The pericardium has two thin layers of tissue that surround the heart, and inflammation of the tissue is called pericarditis. If you have pericarditis, you may experience chest pain and shortness of breath. Viral infections and autoimmune disorders can cause pericarditis.

Pericarditis typically resolves on its own, but may be severe or become chronic, it is important to identify and treat the underlying cause.

To learn more about how you can keep your heart healthy, please reach out to us by phone or request an appointment online at one of our three locations in Beltsville, Bowie, and Columbia, Maryland. You can also send a message to Dr. Djamson and his team

Instead of returning to your usual lifestyle, most patients recovering from a heart attack must make changes once they get home. Your cardiac team is your best resource as you return to life after a heart attack.

Balance problems can have a major impact on your personal and professional life. Bouts of dizziness can leave you disoriented and feeling helpless. A specialized treatment called balance therapy can help.

A pounding, fast, or irregular heartbeat can feel frightening. Most of the time, heart palpitations are not life-threatening. Sometimes though, heart palpitations signal a problem with your heart.

Shortness of breath may be a warning sign of heart trouble. To know for sure, it&rsquos a good idea to check with a trusted cardiovascular specialist, one who can help get to the root of your breathing changes.

Recognizing heart attack symptoms early is key to getting immediate medical care. The longer the heart is starved of oxygen, the worse the outcome. Sudden, severe chest pain isn&rsquot the only symptom. Signs like back pain are more subtle.

When your cardiovascular system is unable to supply your heart or body with oxygenated blood, warning signs often show up during or after exertion. A cardiovascular physician can help you get answers and treatment.

The Apple Watch's ECG app isn't your only option

Portable and home-based ECGs are becoming increasingly common and have the potential to transform medical care, according to a 2018 study in the Journal of Arrhythmia. But, as the study authors note, research supporting their accuracy and ease of use is still scant.

If you think you could benefit from an at-home ECG monitor, talk to your doctor about whether that strategy is right for you and what device they'd recommend.

Pearson has been using AliveCor's KardiaMobile single-lead ECG device with dozens of AFib patients since 2013 and Kardia Pro, a cloud-based software platform that allows him to monitor their results, since 2017. He says the combination is "eliminating any need for short- or long-term cardiac monitors."

The Kardia Mobile takes your ECG via small finger pads, which you can attach to the back of your iPhone.

"It's like night and day how much more information I get and how I'm able to manage their atrial fibrillation without bringing them into my office or an emergency room or putting expensive monitors on them," says Pearson, who does not receive any compensation from AliveCor. "It's dramatic how improved my care is with these devices."

Last month, AliveCor also launched KardiaMobile 6L , the first FDA-cleared direct-to-consumer six-lead ECG. It can detect AFib, bradycardia (abnormally low heart rate), tachycardia (abnormally high heart rate) and more.

What can go wrong?


Some people are born with a heart that has not developed properly in the womb before birth - this is called congenital heart disease.

Cardiovascular system

Problems with your heart and circulation system include:

Heart disease can happen when your coronary arteries become narrowed by a gradual build-up of fatty material - called atheroma.

If your coronary arteries are narrowed or blocked, the blood supply to your heart will be impaired. This is the most common form of heart disease, known as coronary heart disease (sometimes called coronary artery disease or ischaemic heart disease).

Eventually, your arteries may become so narrow they can’t deliver enough blood to your heart. This can cause angina - a pain or discomfort in your chest, arm, neck, stomach or jaw.

If the fatty material breaks off or ruptures, a blood clot will form, which can cause heart attack (or stroke, if the artery affected is carrying blood to your brain).

Electrical system

Normally your heart will beat between 60 to 100 times per minute. This regular rhythmic beating is dependent upon electrical signals being conducted throughout your heart.

If the electrical signals within your heart are interrupted, your heart can beat too quickly (tachycardia), too slowly (bradycardia) and/or in an irregular way. This is called an arrhythmia - see Chest Heart & Stroke Scotland.

Conditions affecting the pumping of your heart

There are some conditions which can damage your heart muscle, making it weak and unable to pump as efficiently as before:

There are also conditions - like high blood pressure (hypertension) - which mean your heart has to work harder.

When your heart muscle can’t meet your body’s demands for blood and oxygen, you can develop various symptoms, like breathlessness, extreme tiredness and ankle swelling. This is called heart failure because of the failure of your heart to pump blood around the body and work efficiently.


Your heart can’t function normally if the heart valves aren't working properly, as it can affect the flow of blood through the heart.

There are two main ways that the valves can be affected:

  • valves can leak - this is called valve regurgitation or valve incompetence
  • valves can narrow and stiffen - this is called valve stenosis

Cardiovascular adaptations to exercise and training

The cardiovascular system provides the link between pulmonary ventilation and oxygen usage at the cellular level. During exercise, efficient delivery of oxygen to working skeletal and cardiac muscles is vital for maintenance of ATP production by aerobic mechanisms. The equine cardiovascular response to increased demand for oxygen delivery during exercise contributes largely to the over 35-fold increases in oxygen uptake that occur during submaximal exercise. Cardiac output during exercise increases greatly owing to the relatively high heart rates that are achieved during exercise. Heart rate increases proportionately with workload until heart rates close to maximal are attained. It is remarkable that exercise heart rates six to seven times resting values are not associated with a fall in stroke volume, which is maintained by splenic contraction, increased venous return, and increased myocardial contractibility. Despite the great changes in cardiac output, increases in blood pressure during exercise are maintained within relatively smaller limits, as both pulmonary and systemic vascular resistance to blood flow is reduced. Redistribution of blood flow to the working muscles during exercise also contributes greatly to the efficient delivery of oxygen to sites of greatest need. Higher work rates and oxygen uptake at submaximal heart rates after training imply an adaptation due to training that enables more efficient oxygen delivery to working muscle. Such an adaptation could be in either blood flow or arteriovenous oxygen content difference. Cardiac output during submaximal exercise does not increase after training, but studies using high-speed treadmills and measurement of cardiac output at maximal heart rates may reveal improvements in maximal oxygen uptake due to increased stroke volumes, as occurs in humans. Improvements in hemoglobin concentrations in blood during exercise after training are recognized, but at maximal exercise, hypoxemia may reduce arterial oxygen content. More effective redistribution of cardiac output to muscles by increased capillarization and more efficient oxygen diffusion to cells may also be an important means of increasing oxygen uptake after training.