Diastolic heart failure and diastolic dysfunction refer to the decline in performance of one (usually the left ventricle) or both (left and right) ventricles during diastole. Diastole is the cardiac cycle phase during which the heart is relaxing and filling with incoming blood that is being returned from the body through the inferior (IVC) and superior (SVC) venae cavae to the right atrium and from lungs through pulmonary veins to the left atrium. In diastolic failure, if the patient has symptoms, there is a pathologic cause inducing them. Diastolic dysfunction can be found when doing a Doppler echocardiography in an apparently healthy patient, mainly in an elderly person.

Untreated hearts with RCM often develop the following characteristics:

- M or W configuration in an invasive hemodynamic pressure tracing of the RA

- Square root sign of part of the invasive hemodynamic pressure tracing Of The LV

- Biatrial enlargement

- Thickened LV walls (with normal chamber size)

- Thickened RV free wall (with normal chamber size)

- Elevated right atrial pressure (>12mmHg),

- Moderate pulmonary hypertension,

- Normal systolic function,

- Poor diastolic function, typically Grade III - IV Diastolic heart failure.

Those afflicted with RCM will experience decreased exercise tolerance, fatigue, jugular venous distention, peripheral edema, and ascites. Arrhythmias and conduction blocks are common.

Heart failure with preserved ejection fraction (HFpEF) is a form of congestive heart failure where in the amount of blood pumped from the heart's left ventricle with each beat (ejection fraction) is greater than 50%. Approximately half of people with heart failure have HFpEF, while the remainder display a reduction in ejection fraction, or heart failure with reduced ejection fraction (HFrEF).

HFpEF is characterized by abnormal diastolic function, which manifests as an increase in the stiffness of the heart's left ventricle and a decrease in left ventricular relaxation when filling with blood before the next beat. There is an increased risk for atrial fibrillation and pulmonary hypertension. Risk factors for HFpEF include hypertension, hyperlipidemia, diabetes, smoking, and obstructive sleep apnea. There is a query about the relationship between diastolic heart failure and HFpEF.

Restrictive cardiomyopathy (RCM) is a form of cardiomyopathy in which the walls of the heart are rigid (but not thickened). Thus the heart is restricted from stretching and filling with blood properly. It is the least common of the three original subtypes of cardiomyopathy: hypertrophic, dilated, and restrictive.

It should not be confused with constrictive pericarditis, a disease which presents similarly but is very different in treatment and prognosis.

Symptoms of aortic insufficiency are similar to those of heart failure and include the following:

- Dyspnea on exertion

- Orthopnea

- Paroxysmal nocturnal dyspnea

- Palpitations

- Angina pectoris

- Cyanosis (in acute cases)

Diastolic dysfunction must be differentiated from diastolic heart failure. Diastolic dysfunction can be found in elderly and apparently quite healthy patients. If diastolic dysfunction describes an abnormal mechanical property, diastolic heart failure describes a clinical syndrome. Mathematics describing the relationship between the ratio of Systole to Diastole in accepted terms of End Systolic Volume to End Diastolic Volume implies many mathematical solutions to forward and backward heart failure.

Criteria for diagnosis of diastolic dysfunction or diastolic heart failure remain imprecise. This has made it difficult to conduct valid clinical trials of treatments for diastolic heart failure. The problem is compounded by the fact that systolic and diastolic heart failure commonly coexist when patients present with many ischemic and nonischemic etiologies of heart failure. Narrowly defined, diastolic failure has often been defined as "heart failure with normal systolic function" (i.e. left ventricular ejection fraction of 60% or more). Chagasic heart disease may represent an optimal academic model of diastolic heart failure that spares systolic function.

A patient is said to have diastolic dysfunction if he has signs and symptoms of heart failure but the left ventricular ejection fraction is normal. A second approach is to use an elevated BNP level in the presence of normal ejection fraction to diagnose diastolic heart failure. Concordance of both volumetric and biochemical measurements and markers lends to even stronger terminology regarding scientific/mathematical expression of diastolic heart failure. These are both probably too broad a definition for diastolic heart failure, and this group of patients is more precisely described as having heart failure with normal systolic function. Echocardiography can be used to diagnose diastolic dysfunction but is a limited modality unless it is supplemented by stress imaging. MUGA imaging is an earlier mathematical attempt to distinguish systolic from diastolic heart failure.

No one single echocardiographic parameter can confirm a diagnosis of diastolic heart failure. Multiple echocardiographic parameters have been proposed as sufficiently sensitive and specific, including mitral inflow velocity patterns, pulmonary vein flow patterns, E:A reversal, tissue Doppler measurements, and M-mode echo measurements (i.e. of left atrial size). Algorithms have also been developed which combine multiple echocardiographic parameters to diagnose diastolic heart failure.

There are four basic Echocardiographic patterns of diastolic heart failure, which are graded I to IV:

- The mildest form is called an "abnormal relaxation pattern", or grade I diastolic dysfunction. On the mitral inflow Doppler echocardiogram, there is reversal of the normal E/A ratio. This pattern may develop normally with age in some patients, and many grade I patients will not have any clinical signs or symptoms of heart failure.

- Grade II diastolic dysfunction is called "pseudonormal filling dynamics". This is considered moderate diastolic dysfunction and is associated with elevated left atrial filling pressures. These patients more commonly have symptoms of heart failure, and many have left atrial enlargement due to the elevated pressures in the left heart.

Grade III and IV diastolic dysfunction are called "restrictive filling dynamics". These are both severe forms of diastolic dysfunction, and patients tend to have advanced heart failure symptoms:

- Class III diastolic dysfunction patients will demonstrate reversal of their diastolic abnormalities on echocardiogram when they perform the Valsalva maneuver. This is referred to as "reversible restrictive diastolic dysfunction".

- Class IV diastolic dysfunction patients will not demonstrate reversibility of their echocardiogram abnormalities, and are therefore said to suffer from "fixed restrictive diastolic dysfunction".

The presence of either class III and IV diastolic dysfunction is associated with a significantly worse prognosis. These patients will have left atrial enlargement, and many will have a reduced left ventricular ejection fraction that indicates a combination of systolic and diastolic dysfunction.

Imaged volumetric definition of systolic heart performance is commonly accepted as ejection fraction. Volumetric definition of the heart in systole was first described by Adolph Fick as cardiac output. Fick may be readily and inexpensively inverted to cardiac input and injection fraction to mathematically describe diastole. Decline of injection fraction paired with decline of E/A ratio seems a stronger argument in support of a mathematical definition of diastolic heart failure.

Another parameter to assess diastolic function is the , which is the ratio of mitral peak velocity of early filling (E) to early diastolic mitral annular velocity (E'). Diastolic dysfunction is assumed when the E/E' ratio exceed 15.

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

The symptoms associated with MI are dependent on which phase of the disease process the individual is in. Individuals with acute MI are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea), as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute MI due to papillary muscle rupture, rupture of a chorda tendinea or infective endocarditis of the mitral valve.

Individuals with chronic compensated MI may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. Over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). Symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. Also there may be development of an irregular heart rhythm known as atrial fibrillation.

Findings on clinical examination depend on the severity and duration of MI. The mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. The first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. Its duration is, as the name suggests, the whole of systole. The loudness of the murmur does not correlate well with the severity of regurgitation. It may be followed by a loud, palpable P, heard best when lying on the left side. A third heart sound is commonly heard.

In acute cases, the murmur and tachycardia may be the only distinctive signs.

Patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. Cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences.

Clinical manifestations of HFpEF are similar to those observed in HFrEF and include shortness of breath including exercise induced dyspnea, paroxysmal nocturnal dyspnea and orthopnea, exercise intolerance, fatigue, elevated jugular venous pressure, and edema.

Patients with HFpEF poorly tolerate stress, particularly hemodynamic alterations of ventricular loading or increased diastolic pressures. Often there is a more dramatic elevation in systolic blood pressure in HFpEF than is typical of HFrEF.

The clinical course of HCM is variable. Many people with HCM are asymptomatic or mildly symptomatic, and many of those carrying disease genes for HCM do not have clinically detectable disease. The symptoms and signs of HCM include shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (sometimes known as angina) due to reduced blood flow to the coronary arteries, uncomfortable awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting and sudden cardiac death.

Dyspnea is largely due to increased stiffness of the left ventricle (LV), which impairs filling of the ventricles, but also leads to elevated pressure in the left ventricle and left atrium, causing back pressure and interstitial congestion in the lungs. Symptoms are not closely related to the presence or severity of an outflow tract gradient. Often, symptoms mimic those of congestive heart failure (esp. activity intolerance and dyspnea), but treatment of each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).

Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, LV thickness greater than or equal to 30 mm, abnormal exercise blood pressure and nonsustained ventricular tachycardia.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:

- Shortness of breath

- Syncope (fainting)

- Angina, but only in the presence of ischemic heart disease

A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.

The symptoms and signs of hypertensive heart disease will depend on whether or not it is accompanied by heart failure. In the absence of heart failure, hypertension, with or without enlargement of the heart (left ventricular hypertrophy) is usually symptomless.

Symptoms, signs and consequences of Congestive heart failure can include:

- Fatigue

- Irregular pulse or palpitations

- Swelling of feet and ankles

- Weight gain

- Nausea

- Shortness of breath

- Difficulty sleeping flat in bed (orthopnea)

- Bloating and abdominal pain

- Greater need to urinate at night

- An enlarged heart (cardiomegaly)

- Left ventricular hypertrophy and left ventricular remodeling

- Diminished coronary flow reserve and silent myocardial ischemia

- Coronary heart disease and accelerated atherosclerosis

- Heart Failure With Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart failure

- Atrial fibrillation, other cardiac arrhythmias, or sudden cardiac death

Heart failure can develop insidiously over time or patients can present acutely with acute heart failure or acute decompensated heart failure and pulmonary edema due to sudden failure of pump function of the heart. Sudden failure can be precipitated by a variety of causes, including myocardial ischemia, marked increases in blood pressure, or cardiac arrhythmias.

In individuals with eccentric hypertrophy there may be little or no indication that hypertrophy has occurred as it is generally a healthy response to increased demands on the heart. Conversely, concentric hypertrophy can make itself known in a variety of ways. Most commonly, chest pain, either with or without exertion is present, along with shortness of breath with exertion, general fatigue, syncope, and palpitations. Overt signs of heart failure, such as edema, or shortness of breath without exertion are uncommon.

Subjects' symptoms from non-compaction cardiomyopathy range widely. It is possible to be diagnosed with the condition, yet not to have any of the symptoms associated with heart disease. Likewise it possible to have severe heart failure, which even though the condition is present from birth, may only manifest itself later in life. Differences in symptoms between adults and children are also prevalent with adults more likely to have heart failure and children from depression of systolic function.

Common symptoms associated with a reduced pumping performance of the heart include:

- Breathlessness

- Fatigue

- Swelling of the ankles

- Limited physical capacity and exercise intolerance

Two conditions though that are more prevalent in noncompaction cardiomyopathy are: tachyarrhythmia which can lead to sudden cardiac death and clotting of the blood in the heart.

Mitral insufficiency (MI), mitral regurgitation or mitral incompetence is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the left atrium. MI is the most common form of valvular heart disease.

Signs and symptoms of mitral stenosis include the following:

- Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)

- Palpitations

- Chest pain

- Hemoptysis

- Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation.

- Ascites and edema and hepatomegaly (if right-side heart failure develops)

Fatigue and weakness increase with exercise and pregnancy.

Symptoms usually include one or more of the following: orthopnea (difficulty breathing while lying flat), dyspnea (shortness of breath on exertion), pitting edema (swelling), cough, frequent night-time urination, excessive weight gain during the last month of pregnancy (1-2+ kg/week; two to four or more pounds per week), palpitations (sensation of racing heart-rate, skipping beats, long pauses between beats, or fluttering), and chest pain.

The shortness of breath is often described by PPCM patients as the inability to take a deep or full breath or to get enough air into the lungs. Also, patients often describe the need to prop themselves up overnight by using two or more pillows in order to breathe better. These symptoms, swelling, and/or cough may be indications of pulmonary edema (fluid in the lungs) resulting from acute heart failure and PPCM.

Unfortunately, patients and clinicians sometimes dismiss early symptoms because they appear to be typical of normal pregnancy. Yet, early detection and treatment are critically important to the patient with PPCM. Delays in diagnosis and treatment of PPCM are associated with increased morbidity and mortality.

It is important to note that occasionally patients present with other signs or symptoms. This is demonstrated by one report of a woman with liver failure five weeks postpartum who was being considered for liver transplant. An echocardiogram was performed and revealed PPCM and heart failure as the cause of her severe liver failure. Conventional heart failure medications were administered. She survived and completely recovered from both the liver failure and PPCM.

It is also quite common for women to present with evidence of having an embolus (clot) passing from the heart to a vital organ, causing such complications as stroke, loss of circulation to a limb, even coronary artery occlusion (blockage) with typical myocardial infarction (heart attack).

For these reasons, it is paramount that clinicians hold a high suspicion of PPCM in any peri- or postpartum patient where unusual or unexplained symptoms or presentations occur.

In cardiology, ventricular remodeling (or cardiac remodeling) refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling). The injury is typically due to acute myocardial infarction (usually transmural or ST segment elevation infarction), but may be from a number of causes that result in increased pressure or volume, causing pressure overload or volume overload (forms of strain) on the heart. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that lead to progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.

Physiological remodeling is reversible while pathological remodeling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand make mismatches inevitable. Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.

Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an aspect of cardiomyopathy, of which there are many types. Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload.

Although there are many signs and symptoms associated with PVCs, PVCs may have no symptoms at all. An isolated PVC is hard to catch without the use of a Holter monitor. PVCs may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a potentially fatal abnormal heart rhythm. Overall it has been seen that the symptom felt most by patients experiencing a PVC is the mere perception of a skipped heartbeat. The more frequently these contractions occur, the more likely there are to be symptoms, despite the fact that these beats have little effect of the pumping action of the heart and therefore cause minimal if any symptoms.

Some other possible signs and symptoms of PVCs:

- Abnormal ECG

- Irregular heart beat

- Dyspnea

- Dizziness

- Feeling your heart beat (palpitations)

- Feeling of occasional, forceful beats

- Increased awareness of your heart beat

- Perception of a skipped heartbeat

Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively "backward failure" (in the part of the circulation which drains to the ventricle).

There are several other exceptions to a simple left-right division of heart failure symptoms. Additionally, the most common cause of right-sided heart failure is left-sided heart failure. The result is that patients commonly present with both sets of signs and symptoms.

High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal due to increased peripheral demand. There is a circulatory overload which may lead to pulmonary edema secondary to an elevated diastolic pressure in the left ventricle. These individuals usually have a normal systolic function but symptoms are those of heart failure. With time, this overload causes systolic failure. Ultimately cardiac output can be reduced to very low levels.

It may occur in situations with an increased blood volume, from excess of water and salt (kidney pathology, excess of fluid or blood administration, treatment with retaining water steroids), chronic and severe anemia, large arteriovenous fistula or multiple small arteriovenous shunts as in HHT or Paget's disease of bone, some forms of severe liver or kidney disorders, hyperthyroidism, and wet beriberi, and acutely in septic shock, especially caused by Gram-negative bacteria.

Athletic heart syndrome (AHS), also known as athlete's heart, athletic bradycardia, or exercise-induced cardiomegaly is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting heart rate is lower than normal.

The athlete's heart is associated with physiological remodeling as a consequence of repetitive cardiac loading. Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one.

Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete's heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in higher cardiac output, which also allows it to beat more slowly, as more blood is pumped out with each beat.

Another sign of athlete's heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as the diastolic pressure of the irregularly shaped heart creates a disordered blood flow. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition.

The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic circulation (the rest of the body except for the pulmonary circulation). Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased "work" of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema.

Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

"Backward" failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise.

"Cardiac asthma" or wheezing may occur.

Compromise of left ventricular "forward" function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest.