Heart failure

Frank – Starling law(an increase in diastolic filling increases the force of heartbeat) the more stretch placed on a cardiac muscle the stronger the contraction (the more blood a heart is presented with the harder/stronger the heart pumps)

Tricuspid valve – the valve between the right atrium and the right ventricle

Bicuspid/mitral valve – the valve between the left atrium and the left ventricle

Aortic valve – the valve between the left ventricle and the aorta

(No picture available)

Pulmonary valve – the valve between the right ventricle and the pulmonary artery

Normal venous return

Inferior vena cava drains the area below the diaphram

Superior vena cava drains the area above the diaphram

Coronary sinus drains the heart itself

The above 3 drain into the right atrium (80 % is delivered passively)

The right atrium is at a –5mm of pressure (this creates a vacuum)

Valve control

The papillary muscles assist the chordea tendineae in closing the valves (they act like umbrella struts) while the ventricles contract to eject the blood within.

Each lung has 2 veins delivering blood to the left atrium (once again 80 % is delivered passively)

Congestive heart failure (CHF)

General signs and symptoms

Failure in the heart in its function as a pump

Acute (CHF) – inability of the heart to

pump against an overwhelming obstacle. (i.e. massive pulmonary embolism, or massive myocardial infarction)

-  Chronic (CHF) – progressive loss of the heart, strength or effectiveness as a pump due to chronic stresses

Chronic (CHF) is the result of factors intrinsic to the heart itself that weaken its effectiveness as a pump and/or exposure to extrinsic stresses, which chronically overwork it. The heart is congested, it is over-filled with blood that the heart cannot get rid of, causing it to back up into the veins.

Left sided ventricular weakness causes blood to back up into the left atrium which in turn backs up into the pulmonary veins, which in turn congests the pulmonary circulatory system which in turn increases the load of the right ventricle, then the left atrium, then the systemic circulatory system.

Intrinsic factors

·  Wall (septum) or chamber defect (leakage into adjacent chamber)

·  Valve dysfunction (backflow into previous chamber)

·  Heart beat regulation problems

o  (neural [av/sa node firing], irritable focus)

Figure 1 neural pathway with Av and Sv and perkinje fibres

·  Heart wall infarction

o  Contractile strength decreases (decreased amount of healthy muscle tissue, causes a decrease in the force of contraction)

o  Chamber elasticity decreases (necrosis of tissue, and subsequent scarring decreases the ability of muscle to elongate and thus contraction strength is decrease ) (F/S law)

·  Decreased heart wall fitness (due to decreased perfusion of tissue)

·  Ischemic states/decreased perfusion of the heart wall

Extrinsic factors

·  Hypertension

·  Chronic respiratory conditions (heart has to work harder to transport O2 to tissues)

·  Malnutrition of body tissues

·  Obesity (increased distance heart has to transport blood, ~1 mile of blood vessel per pound of adipose)

·  Anemia (decreased erythrocytes to carry O2, heart has to work harder to adequately perfuse body tissue)

·  Smoking (elasticity of artery wall, atherosclerosis, aging)

·  Sedentary life style (the heart is a muscle, and muscles that aren’t used weaken)

·  Liver/ kidney disorders (fluid regulation,)

·  Endocrine dysfunction (thyroid)

·  Conditions/diseases which damage the blood vessels (diabetes, rheumatic fever)

·  Emotional stress

·  Excessive physical stress

CHF progression

Under stress the heart will utilize 3 adaptations to improve its output and meet the demands on it.

  1. Increase heart rate
  2. Chamber dilation (increases chamber volume, increases force of contraction by prestretching fibers) see Frank – Starling law
  3. Myocardial hypertrophy

Each of these adaptations is effective to a certain point; each has inherent potential problems when used to excess.

1.  Increased heart rate

·  Less time spent in diastole causes decreased perfusion of the heart wall (the myocardium is perfused during diastole) (an extreme example is ventricular fibrillation)

·  Decreased time for chamber fill / decreased contraction

·  Oxygenation of the blood/ removal of CO2 can be compromised

·  The increased rate will in itself stress the heart

2.  Chamber dilation

·  Decreased elasticity of chamber wall

·  Exceed optimal stretch parameters of the cardiac cells

·  Valvular incompetence (valve flaps can no longer close)

3.  Myocardial hypertrophy

·  Decreased elasticity

·  Decreased chamber size (decreases the amount of blood that can enter the

·  chamber and therefore decreases the amount that can be circulated throughout the body.)

·  Greater difficulty in perfusing the overbulked heart wall

·  Enlarged heart compresses (restricts ventilation/lung capacity which increases stress on the heart)

CHF progression

(Example of left sided heart failure. The diagram is displaying normal blood circulation)

  1. Systemic hypertension
  2. Left ventricle stress- left ventricle hypertrophy and chamber dilation
  3. Mitral (bicuspid) valve incompetence
  4. Regurgitation into the left atrium
  5. Myocardial hypertrophy and chamber dilation more time spent in active pumping (remember normal is 80% passive)
  6. Blood from lungs encounters resistance entering the left atrium
  7. Increased hydrostatic pressure in vasculature of lungs
  8. Pulmonary hypertension
  9. Pulmonary edema
  10. Right ventricle stress
  11. Right ventricle hypertrophy and chamber dilation
  12. Tricuspid valve incompetence
  13. Regurgitation into right atrium
  14. Right atrium stress
  15. Right atrium hypertrophy and chamber dilation
  16. Right atrium loses negative pressure “vacuum effect”

9. Venous return encounters resistance entering the right atrium

10. System hypertension

a. Systemic edema

remember the arrows would be going backwards to display the backwards progression of CCHF

Cor pulmonale

Heart failure originating on right side due to respiratory dysfunction (occasionally known to be caused by living for extended periods at high altitude)

General R.M.T. concerns or issues in treating a Chronic Heart Failure client.

·  Positioning – based on degree, the following may/must be applied:

o  Prone – applies pressure on the aorta and inferior vena cava and can stress the heart. It also creates more restriction on breathing.

o  Supine – usually best tolerated but some degree of trunk elevation is usually necessary. (Fowler’s position?)

o  Sidelying - often good, maybe a limitation on time, but may be too uncomfortable is there is cardiomegaly and/or pulmonary edema.

o  Seated – is usually well tolerated if it’s physically comfortable. Caution with trunk forward (re. Avoiding aorta and/or inferior vena cava compression.

o  a strong suggestion is to ask the client what position they normally sleep in

·  Hydrotherapy

o  Extremes of temperature and contrast increase the hearts workload so adaptations are needed which match the client’s degree of chronic heart failure.

o  Factors affecting hydrotherapy treatment:

§  Emersion of percentage of body

§  Temperature extremes

§  Duration

§  Hydrostatic pressure on body – weight of water on the body (client may have to bath in a shallow amount of bath water)

§  Type of application – amount of body surface covered.

*All must be considered and rejected or modified.

·  Monitor for sympathetic nervous system activation and avoiding elements that will increase it:

o  Surprise

o  Techniques that stimulate – tapotement, brisk strokes, etc.

o  Temperature (room and body)

o  Comfort level generally in the room and with the therapist and treatment plan.

o  Pain

o  Full bladder

·  Time of day, treatment duration etc.

o  Sometimes “less can be more

o  Consider your treatment a mild form of exercise for the chronic heart failure patient and match to the information you have about (ADL’s) affects of daily living, (CHF) chronic heart failure level, etc.

o  * Start moderately conservatively and enhance treatment if well tolerated. Monitor reactions to treatment during and after.

·  Modify self care advice to be appropriate

o  Hydro

o  Exercise

·  Tissue fragility concerns:

o  Modify pressure and traction to avoid tissue injury and bruising

o  Be aware of dry, fragile skin. (Apply oil or substances, which assist skin integrity.

o  Ulceration concerns

o  Massage therapy role is in prevention

o  Open sores should not be massaged or have oil applied, (Major hygiene concern).

o  Early stage decubitis ulcer formation “red spot stage” contraindicated for onsite massage.

o  Be aware of delayed healing

Trophic changes usually caused by decreased tissue nourishment

·  Awareness of treatment plan elements that increase venous return.

o  These may need modification (i.e. long, broad, continuous strokes of effleurage, while covering their whole back with a thermaphore)