1. Dilation of chamber

2. Excess blood in chamber

3. Decrease flow out of chamber

The ability to increase CO during increased activity.  Can increase CO by about 5-6x. 

If cardiac failure lose this reserve.

Ionotropic

Chronotropic

1. Factors that effect the contracting ability of the heart = low output failure

2. Factors that effect the workload placed on the heart = Secondary

1. Acute MI

2. CAD

3. Toxic Myocarditis

4. Cardiomyopathies

1. Valvular stenosis

2. Valvular regurgitation

1. Cardiac Tamponade

2. Constrictive Pericarditis

3. Pericardial Effusion

1. Pressure overload

2. Volume overload

3. Excessive work demands (hypermetabolic states)

1. Hypertension

2. Structural defects such as Coarctation of aorta, valve stenosis

Renal failure (volume overload)

Structural defects such as Arteriovenous shunt, valve regurgitation

Hyperthyroidism

Septicemia

Severe anemia

1. Increase in Diastolic volume

2. Increase in ventricular dilation

3. Increase in ventricular wall tension

4. Rise in ventricular end-diastolic pressure

Congestive symptoms

Smaller Ventricular chamber (ventricular hypertrophy, decreased compliance)

1. Age

2. Mitral Stenosis

3. Ischemic heart disease

4. Increase in ventricular wall tension

5. Rise in Ventricular end diastolic pressure

1. Decreased pumping ability of heart

2. Activation of sympathetic compensatory mechanisms

3. Decrease in renal blood flow

1. Frank Starling Mechanism

2. Sympathetic Activation

3. RAAS

4. Cardiac remodeling/hypertrophy

Sympathetic tone

Catecholamines

Baroreceptors

Renin

Aldo

ADH

Endothelin

ANP

Ang II

1. Symmetric Hypertrophy

2. Eccentric Hypertrophy

3. Concentric Hypertrophy

Because there is a proportionate increase in both width and length.

Seen in athletes

Pressure overload

Wall thickness

Volume Overload

Length over Width

Hypertension

Dilated Cardiomyopathy

Diastolic volume

Wall tension

1. Increase in volume leads to increase in preload and venous pressure (edema)

2. Increase resistance leads to increase afterload

3. Reduced ionotropic effects

4. Reduced effect of ANP in kidney (high Ang II)

1. Edema

2. SOB

3. Exercise tolerance

4. Cyanosis

5. Weight loss/ malnutrition

6. Distention of jugular veins in R. HF

7. Diaphoresis and tachycardia

1. Aortic Stenosis

2. Mitral valve regurgitation

3. L. Ventricular Infarction

4. Cardiomyopathy

5. Hypertension

1. Dilation of LV

2. CO falls, but bloods remains in chamber

3. Increase LV vol, so increase workload on heart

4. Increase workload on L.atria = hypertrophy

5. Fluid to lungs cus Capillary pressure >oncotic

6. Compromised O2 exchange

7. Compensatory mech aggravate congestion

1. Dyspnea

2. Fatigue

3. Orthpnea

4. Paroxysmal nocturnal Dyspnea

5. Pulmonary edema

Labored breathing.

Hypoxia increases chemoreceptor firing which increases the workload, more stress, etc (+) feedback mech.

Activation of SNS compensatory mechanisms (selective vasoconstriction and baroreceptor stimulations):

1. Increase in HR

2. Oliguria

3. Cyanosis

4. Fatigue

5. Forgetfulness

1. Conditions that restrict blood flow to the lungs

2. Stenosis or regurgitation of the tricuspid or pulmonic valves

3. R. Ventricular infarction

4. Persistent L.HF

5. Acute or chronic pulmonary disease

1. Systemic edema

2. Liver and spleen enlargement

3. Ascites (fluid from GI tract) (can lead to weight loss)

4. Peripheral vein distention in hand and neck

Class I = No limitation of physical activity

Class II = Slight limitation

Class III = Mark limitation

Class IV = Inability to carry out any physical activity w/out discomfort