xX Congestive Heart Failure Xx

Heart Failure: The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body. Pulmonary Edema: An abnormal accumulation of fluid in the lungs. CHF with Acute Pulmonary Edema: Pulmonary Edema due to Heart Failure (Cardiogenic Pulmonary Edema) - Those People who are complaining heart failure will develop later on pulmonary edema which is accumulation of fluids in the interstitial spaces either in the lungs or in dependant extremities (lower limbs) .

Heart Failure : Complex syndrome that can result from any structural ( defect in the structure ) or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation. Main Causes of Heart Failure: - Ischemic Heart Disease (35-40%) , massive myocardial infarction may lead to HF. - Cardiomyopathy(dilated) (30-34%) - Hypertension (15-20%) Other Causes: - Valvular Heart Disease - Congenital Heart Disease - Alcohol and Drugs. - Arrhythmias - Ventricular Dilatation. - Myocyte Hypertrophy. - Salt and Water Retention.

- Sympathetic Stimulation. - Peripheral Vasoconstriction. In general the heart deals with the increase in the demand within physiological limit and in pathological situations. If we have heart failure thats mean decrease in the cardiac output, so in order to deal with it, there will be : - Sympathetic stimulation - Increase in heart rate , contractility ,cardiac output . - Release/formation of Angiotensin II which is involved in increase of the volume preload. - Vasoconstriction _decrease in the after load - Increase in the heart size cardiomegaly Symptoms: Exertional Dyspnoea ( feeling of tiredness at rest ) Orthopnia , difficulty in breath while lying down ! Paraxysmal Nocturnal Dyspnoea Signs: Cardiomegaly Elevated Jugular Venous Pressure Tachycardia Hypotension Bi-basal crackles in the lungs Pleural effusion Ankle Edema Ascites accumulation of fluid in peritoneal cavity Tender hepatomegaly.- feeling of pain while you do palpitation Classification of heart failure I. No limitation. Normal physical exercise doesnt cause fatigue, dyspnea or palpitations, But at the same time if he is doing heavy exercise sings and symptoms will appear Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnea or palpitations.

II.

III. IV.

Marked limitation. Comfortable at rest but gentle physical activity produces marked symptoms of HF. Symptoms of HF occur at rest and are exacerbated by any physical activity. Kussmauls sign :

This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also seen in right ventricular infarction, right heart failure, tricuspid stenosis, and restrictive cardiomyopathy. It is not seen in acute cardiac tamponade- although it may be seen if tamponade occurs with a degree of constricive pericardiditis So, it is an increase in jugular venous pressure and it is a sign of Right side heart failure .

PMI The apex beat, also called the point of maximum impulse (PMI), is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt. The heart located between second and fifth intercostals spaces , but in specific situation the heart may enlarge ( cardiomegaly ). So, the normal apex beat can be palpated in the pericardium left 5th intercostals space, at the point of intersection with the left midclavicular line. The apex beat may also be found at abnormal locations; in many cases of dextrocardia, the apex beat may be felt on the right side. Lateral and/or inferior displacement of the apex beat usually indicates enlargement of the heart (at the 6th or 7th intercostals space). P.S Heart sounds : - S1,S2 produced by the closing of the AV valves and semilunar valves respectively physiological heart sounds

- S3 it occurs at the beginning of diastole after S2 it is physiological for those who are below the age of 40 , and who are above 40 it represents HF. - S4 it occurs just after atrial contraction It is a sign of a pathologic state

Edema : It is accumulation of fluid in the interstitial spaces , mainly the site of edema is the lungs and in the dependant or lower extremities, So you will find bilateral lower extremity edema and hypertrophic cardiac myopathy (thickness of the heart muscle ).

* In the picture above you can see enlargement/thickening in the left ventricular muscle. Compensatory mechanism : In case of HF, the body uses compensatory mechanisms to attempt to compensate the increase in the demand as a result of decrease in the cardiac output, and this by : 1. Increased Heart Rate - Sympathetic = Norepinephrine 2. Dilation - Frank Starling = Contractility 3. Neurohormonal - Redistribution of Blood to the Brain

What will happen ? HF means that the heart is tired , it is already exhausted , so if I stimulate it more and more ,in case of Sympathetic stimulation and increase the contractility what will happen ? The heart will deteriorated more and more ( the heart is already exhausted and I asked to increase the force of contraction and increase heart rate and cardiac output ). This is called "vicious cycle" decrease in cardiac output and the body demand for more! CHF Vicious cycle : Low out put

increased
preload

increased after load

norepinephrine

increase salts

vasoconstriction

renal blood flow

Rennin Angiotensin I Angiotensin II Aldesteron

The body is asking for more blood , so we increase the COP by increasing the preload, after load, Norepinephrine and sympathetic stimulation which lead to formation of Angiotensin II , SO we will have : vasoconstriction, increase " salts + H2O", retention those lead to increase the volume! Vasoconstriction lead to increase the afterload and increase in the Total Peripheral Resistance.

Blood Pressure = COP *TPR - COP : come from increase in the venues return which is the filling Pressure from the preload. - TPR : due to vasoconstriction which is afterlaod. SO increase in the afterlaod COP and increase in the preload TPR lead to more and more deteriorated of the heart ! Remember : In the respiratory system we see that the alveoli composed of one cell layer and the capillaries is composed of one layer too, thats mean there is no barriers and the gases exchange occurs between them easily . In case of HF there will be fluids in the interstitial spaces (edema) so the exchange of gases her will be extremely difficult for those who have pulmonary edema (thats mean the fluids will separate between alveoli and capillaries) , in addition those people cant breathe in proper way at rest or while eating.

This man is sitting and almost gasping! why ? because he developed acute pulmonary edema and this due to accumulation of large amount of fluids inside the lungs, this is a life threatening those Patients need to be admitted in the intensive care units "ICU" urgently and to be given diuretics, in order to get rid of these excessive fluids and usually they are incubated, which means endotracheal tube not chest tube, because they cant breathe!

In this picture ( x-ray) The normal air filled lungs is black in the chest x-ray pictures Radiolucence, but if you see whitish discoloration reflect the presence of fluid water in the lungs and note here that the heart is enlarge "cardiomegaly"!

What is the treatment ?? Patients who are complaining of accumulation of fluids should be given: 1. Diuretics . 2. Beta blockers . B1 stimulation leads increase the contractility and heart rate so we give beta blockers to decrease the heart rate, contractility and COP. 3. ACE inhibitors `Angiotesion converting enzymes` as to prevent the conversion of Angiotensin I into Angiotensin II Now at the end of the treatment the afterlaod and the preload will decrease . The role of Angiotensin II : It affects the preload, it increases the volume by (Na +H 2O) retention, increase the absorption of Na and H2O from proximal tubules and collecting ducts. In addition it increases the afterlaod by vasoconstriction. - When we block Angiotensin II by given the patient ACE inhibitors both preload and afterload will decrease . Q) In case that we have exhausted heart and we need more oxygenated blood what we have to do ? The patient here should be given digoxin {this drug use to treat the congestive heart failure} this drug work to increase the force of contraction by increase the Ca concentration in the myocytes and decrease the heart rate. That means pump more blood while the HR is decreased !

Example : If you buy 10 things from the supermarket what is the better to take it as once OR to go 10 times for each thing ? Of course to take it as once is more better , and here Digoxin is work like this "strong pump that give bigger amount and less heart contraction ! But we have a problem, Digoxin isnt a safe drug the therapeutic index of it is narrow, which means that the difference between the therapeutic dose and toxic dose is low. The therapeutic dose of Digoxin is( 0.5 -0.8 ) mg/ml if the patient give little pit high dose they will develop what is call "Digoxin toxicity " Digoxin toxicity signs and symptoms : 1. Dizziness. 2. Confusion 3. Discoloration, the patient will have yellowish discoloration 4. Loose of consciousness Treatment: "Digoxin immune fab or antidote for Digoxin" Sinuses : It is the yellowish discoloration of skin and mucus membranes, we can see it in the patient who has heart failure "central sinuses "

in the lungs or the heart: central "cardiopulumonary cause "

sinuses
peripheral: peripheral vasoconstriction

A student ask : Can we treat the acute pulmonary edema by chest tube ? The answer is No, because around the lungs there is pleural cavity which enclose the lungs and there is no air or fluid in the pleural cavity excessive fluid usually are absorbed. Chest tube is used only in case we have hemothorax or pneumothorax. When the air enter the pleural cavity if we use chest tube the negativity of pleural cavity decrease it will be equal to the atmospheric so the expansion of the lungs will be decrease and the lungs will collapse .

P.S : In some situations we might have vasodilatation and increase heart rate, for example : it occurs in men , those who use "Viagra ". Viagra is general vasodilator lead to reflex tachycardia that cause cardiac arrest, In young men it is normal because it can be compensated but in old age it will lead to death .

Done by : Abeer Dirawi Zain alsalameen

Good Luck