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Aina Meducci 2012




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Pathology: Circulatory disturbance

Let refresh physiology! kudos to Prof Noordin!


Circulatory disturbances

Any interference with the blood flow to a portion of the body results in a circulatory disturbance. Homeostasis must be corrected in order to keep the body system well.

Homeostasis - Normal fluid homeostasis encompasses maintenance of vessel wall integrity as well as intravascular pressure and osmolarity within certainphysiologic ranges. It is also means maintaining blood as a liquid until injury causing clot formation. Clotting at the inappropriate site (thrombus), or migration of clot (embolism), obstruct blood flow to tissues and leads to cell death (infarction). Conversely inability to clot after injury results in haemorrhage. Extensive haemorrhage can cause shock.

There are 6 types of circulatory disturbances;

1. Hyperraemia
2. Congestion
3. Thrombus
4. Emboli
5. Haemorrhage
6. Infraction


Hyperaemia is the increase in blood flow in an organ or tissue due to dilatation of arteries or arteriole. Hyperaemia is an active process especially in inflammation where redness can be seen under the skin clearly.

Eg Physiology hyperraemia: In skeletal and cardiac muscle in muscular exercise in splanchnic area after eating.

Eg Pathological hyperraemia: In acute inflammation

Usually, hyperaemia results in erythema

Normal vs hyperaemia

The skin will appear red as the results of active blood flow


Congestion is passive hyperaemia due to engorgement of veins and venules by blood. Usually there are 3 examples of congestion. Systemic venous congestion, Pulmonary congestion, and localized venous congestion.

Systemic venous congestion: Blood accumulates in pulmonary veins all over the body of congestive heart failure of sparing the lung in case of right side of heart failure.

Pulmonary congestion: Blood accumulates in pulmonary veins and their tributaries in the case of left side of heart failure or mitral stenosis

Localized VC: Due to obstruction to blood flow in a limited area or an organ

Normal vs congestion

Edema is an classic example of congestion. Edema is the accumulation of access fluid in the interstitial tissue spaces or body cavity. 5 pathophysilogic mechanism that underlie the development of edema are

1. Decrease oncotic pressure-liver cirrhosis, malnutrition, nephrotic syndrome
2. Increase hydrostatic pressure- congestive heart failure, constrictive pericarditis, venous obstruction
3. Lymphatic obstruction- inflammatory, neoplastic, post surgical
4. Increase vascular permeability (e.i inflammation)
5. Sodium retention-renal insufficiency, increase renin-angiotensin-aldesterone secretion

Edema can occur in various organs such as lungs, skin, liver, brain, spleen and kidney

How edema occurs

Edema in lung. Note that the left picture showing the alveolar spaces is filled with red blood cell


Formation of blood clot (thrombus) in uninjured vessels or thrombic occlusion of a vessel after minor injury. The thrombus if formed of blood elements essentially platelets that develop inside the CVS during LIFE!!

how thrombus occur?

1. Endothelial injury


Any alteration of the coagulation pathways that predispose to thrombosis. Eg genetics and sickle cell anemia

3. Abnormal blood flow

Can cause disrupt the laminar flow bringing platelets into contact with endothelium, promote endothelial cell activation, prevent dilution of the activated clotting factors by fresh flowing blood, retard the inflow clotting factors inhibitors--->thrombus formation

Venous thrombus

eg: Deep vein thrombosis (DVT)

Fate of a thrombus

Propagation- Thrombi may accumulate more platelets and fibrin eventually obstructing other critical vessel

Dissolution- Thrombi may be removef by fibriolytic activity

Embolisation-Detach thrombi from vessels may migrate and block small capillaries (emboli)

Organisation and Recanalisation- Thrombi may induce inflammation and fibrosis (organization) and may eventually recanalize

Infection forming mycotic aneurysm and septic embolisation


A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin99% of the emboli are dislodged thrombi, hence, the term THROMBOEMBOLISM. Potential consequence of embolism is INFARCTION of the tissue distal to it.

Process of embolism

Fat embolism eg after fractures
Air embolism, eg in open carotid injury, angiographic procedures, Caisson’s disease in deep sea divers
Amniotic fluid embolism in abruption placenta of pregnancy

Emboli in brain


Area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.


  • Myocardial Infraction
  • stroke
  • pulmonary infarct following PTE
  • gangrene of limbs due to PVD
  • tortion of testes causing testicular infarction
  • volvulus intussusception causing bowel gangrene

Factors influencing infarction:
  • Nature of blood supply
  • Lungs have dual supply from pulmonary and bronchial arteries
  • Liver has dual supply from hepatic artery and portal vein
  • Kidney, spleen and brain have end arteries with no anastomosis
Rate of occlusion: if slow, can allow for collateral formation, eg in coarctation of aorta

Tissue vulnerability to hypoxia: neural tissue is the most susceptible, dying within 3 to 4 minutes, and myocardium within 30 to 40 min

Oxygen content in the blood: increased risk of infarction in anemic and cyanosed patient

Gross Morphology:
Infarction starts as a poorly defined wedge shaped area, with exudates and hemorrhagic area, which gets more defined by a rim of inflammation after some days.

2 types of infraction (based on their appearance)

Red infarct

Filled with blood. Characterized by coagulation necrosis and erythrocytes from adjacent arteries and veins. Seen with venous occlusions or within loose tissue that allow blood to collect in the infarcted zone of in organs with dual blood supply (lung, liver) or extensive collateral circulation (brain, smallintestine). The latter results because blood flows from the unobstructed vascular
channels into the necrotic area.

Red infact

White infarct

Lacks blood, also called anemic infarct. (Usually has a red zone at periphery because of capillaries at the border of infarct undergo dissolution and blood seeps into the area of necrosis). Occurs with arterial occlusions in solid organs (heart, kidney).

Area of infarct in spleen


Escape of blood from the cardiovascular system (extravasation).Discharge of blood from the vascular compartment to the exterior of the body orenclosed within a tissue. Capillary bleeding can occur under conditions of chroniccongestion.


  • Trauma
  • subcutaneous or intramuscular hemorrhage
  • Septicemia, viremia or toxic conditions
  • widespread petechiae and ecchymoses
  • Coagulation Disorders
  • hemorrhage thrombocytopenia (decreased numbers of platelets)

Origin of hemorrhage

Hemorrhage by rhexis: due to substantial rant or tear present in the blood vessel or heart. Moderate flow of blood out from vascular system

Hemorrhage by diapedisis: due to small defect or rbc passing through the wall in hyperaemia of inflammation

Types of hemorrhage (according to sizes)

1.Petechiae- pin-point foci of haemorrhage up to 1-2 mm in size
2.Purpura- Hemorrhages 3mm. May be associated with diseases which cause petechiae, vascular inflammation or vascular damage. Often scattered on many body surfaces.


3. Echymoses- Larger than petechiae and usually blotchy or irregular areas up to >1-2 cm in size often seen with trauma and other problems. (eg: subcutaneous hematomas / bruises)


4. Hematoma- Mass of fibrin and red cells surrounded by vascular connective tissue (supplies nutrients and support for phagocytes (macrophages)


Sources: MBBS Medicine.blogspot.com, circulatory disturbance; docslide.com, circulatory of disturbance; Lisa Miller, General Pathology VPM 152

Ps: This is incomplete article. More references needed

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Acid base balance

When it comes to chemistry, it is always about confusion. LOL just kidding :)


Acid base balance

Acid-base balance is critical for maintaining the narrow pH range that is required for various enzyme systems to function optimally in the body.4 Normal blood pH ranges from 7.3-7.4.3 Decreased pH is termed acidemia and is caused by an increase in the concentration of hydrogen ions ([H+]). Increased blood pH is termed alkalemia and is caused by a decrease in the [H+].

The buffer systems that maintain this pH balance are bicarbonate, phosphates, and proteins. Bicarbonate is the most important extracellular buffer (blood), while phosphates and proteins contribute mostly to intracellular acid-base balance.The bicarbonate system is the only buffer measured for the calculation of acid-base status in patients and is represented by the equilibrium equation:

CO2 + H2O <—> H2CO3 <—> H+ + HCO3-

This equation allows one to visualize what effects the addition of carbon dioxide (CO2) or bicarbonate (HCO3-) will have on the buffer system and the blood pH. Addition of CO2 to the system will cause the equation to shift to the right, increasing the [H+] and, therefore, lowering the pH. Addition of HCO3- to the system will cause the equation to shift to the left, lowering the [H+] and increasing the pH.

Another way to conceptualize this information is to simply think of CO2 as an acid and HCO3- as a base. If CO2 is increased it will tend to cause acidemia. If HCO3- is increased, then alkalemia is the expected result.

In addition to buffers, the lungs and kidneys play a major role in acid-base homeostasis.The lungs function in ventilation and they are responsible for regulating the amount of CO2 present in plasma. The kidneys are responsible for controlling the amount of HCO3- in the blood by resorbing or excreting it in the proximal tubule.Abnormalities in acid-base status are classified as to whether the primary abnormality lies with the CO2 concentration or the HCO3-concentration ([HCO3-]). If CO2 is primarily affected, then a respiratory disturbance is present. If HCO3- is primarily affected, then a metabolic disturbance is present.

Acid base disorder

Simple acid-base disorders are those that are confined to one primary alteration in CO2 or HCO3- with or without a compensatory response. There are four simple acid-base disorders: respiratory acidosis, metabolic acidosis, respiratory alkalosis and metabolic alkalosis.

Acidosis is a physiologic condition that tends to increase the concentration of hydrogen ions, which will decrease the pH.This condition can be respiratory or metabolic in origin. An increase in the concentration of CO2, expressed as pCO2, is known as respiratory acidosis. Alternatively, a decrease in the [HCO3-] is known as metabolic acidosis. Both of these situations cause the buffer equation to shift to the right, causing an increased [H+] and a decreased pH.

Alkalosis is a physiologic condition that tends to decrease the [H+], which will increase the pH. Like acidosis, alkalosis can be respiratory or metabolic in origin. A primary condition that results in decreased pCO2 is termed respiratory alkalosis and a primary condition that results in increased [HCO3-] is termed metabolic alkalosis. Both situations shift the bicarbonate equation to the left, resulting in a decreased [H+] and an increased pH.

Acidemia and alkalemia are alterations in the pH of the blood. Acidosis and alkalosis (respiratory or metabolic) are the disorders that will cause these pH alterations. Most cases of simple acidosis or alkalosis, such as those described above, will result in acidemia or alkalemia, respectively.

However, there are compensatory mechanisms that the body will employ in an attempt to maintain a normal pH. In these situations it is possible to have an acidosis or alkalosis disorder and maintain a normal blood pH. There are also mixed acid-base disorders in which opposing primary disorders can effectively cancel each other out and produce a normal pH balance.

Let's a look at one by one

Repiratory Acidosis

Respiratory acidosis is caused by any condition which increases the pCO2 (hypercapnia).While increased production of CO2 (hyperthermia, cardiopulmonary arrest) is a possible cause of hypercapnia, the vast majority of cases are due to impaired removal of CO2 through the lungs. Hypoventilation, ventilation-perfusion mismatch and impaired alveolar gas exchange can all lead to hypercapnia. Therefore, the broad categories of disease which can lead to respiratory acidosis include:

  • respiratory center depression
  • neuromuscular disease
  • restrictive extrapulmonary disease
  • intrinsic pulmonary
  • small airway disease
  • large airway obstruction,
  • increased CO2 production with impaired alveolar ventilation.

Respiratory alkalosis

Respiratory alkalosis is caused by conditions that will decrease the pCO2 (hypocapnia). Hyperventilation will lead to hypocapnia, and it can be caused by hypoxemia, pulmonary disease, direct activation of the respiratory center in the brainstem, overzealous mechanical ventilation, or situations causing pain, fear, or anxiety.

Metabolic acidosis

May result from either an excess of acid or reduced buffering capacity due to a low concentration of bicarbonate. Excess acid may occur due increased production of organic acids or, more rarely, ingestion of acidic compounds.

There are two types of metabolic acidosis. Both are characterized by a decrease in the [HCO3-] but they differ in how that decrease occurs. Secretional metabolic acidosis is caused by a direct loss of bicarbonate-rich fluid such as diarrhea or saliva. Titrational metabolic acidosis is caused by the presence of non-CO2 acids that titrate bicarbonate causing a decreased [HCO3-].

Titration-type metabolic acidosis is the result of increased endogenous or exogenous acids in the plasma. Exogenous acids include ethylene glycol metabolites and salicylate. Endogenous acids include lactic acid, uremic acids, and ketones. It follows then that shock, renal failure, and diabetic ketoacidosis, respectively are common causes of titration-type metabolic acidosis. In cases of hypovolemic shock, perfusion is decreased. Anaerobic metabolism is a consequence of decreased perfusion, so lactic acid accumulates.

In cases of renal failure, uremic acids will accumulate since the kidneys can not effectively excrete them. In cases of undiagnosed or uncontrolled diabetes mellitus, cells cannot utilize glucose due to a lack of insulin. Therefore, the body must metabolize its adipose tissue. Ketones are the byproduct of oxidation of free fatty acids by the liver.

Anion gap

Secretional and titrational metabolic acidosis can be differentiated by their effects on the anion gap (AG). The anion gap is a calculated value based on the principle of electroneutrality which states that the total anions in the body must always be equal to the total cations. We regularly measure the most significant ions: Na+, K+, Cl- and HCO3-. The ions we do not regularly measure are referred to as unmeasured ions.

There are unmeasured cations (Ca+2, Mg+2, and gammaglobulins) and unmeasured anions (albumin, phosphates, sulfates, and organic acids). The unmeasured anions outnumber the unmeasured cations and the difference is the anion gap (Figure 1). The anion gap is easily calculated from the ions we do measure: AG = (Na+ + K+) – (Cl- + HCO3-).4 Unmeasured cations do not undergo significant changes in health or disease and so changes in the anion gap are almost always associated with changes in the unmeasured anions.

Figure 1: Normal anion gap

With secretion-type metabolic acidosis, the anion gap is normal. The body compensates for the increased loss of bicarbonate by a retaining Cl-. As such, as the [HCO3-] decreases, the [Cl-] increases and the anion gap remains normal (Figure 2).

Figure 2: Normal anion gap in secretion acidosis

With titrational metabolic acidosis, the anion gap is increased. Remember that titration type metabolic acidosis is associated with increased levels of exogenous or endogenous acids. Since HCO3- is consumed to buffer these organic acids and there is no effect on the [Cl-], the anion gap increases (Figure 3). The anion gap is therefore very useful in determining a possible etiology for metabolic acidosis that can be confirmed based on history and clinical signs.

Figure 3: Increased anion gap in titration acidosis

Metabolic alkalosis

Causes of metabolic alkalosis include loss of acidic chloride-rich fluids from the body and chronic administration of alkali. In small animal practice, most cases of metabolic alkalosis are caused by vomiting of stomach contents. Abomasal reflux of hydrochloric acid (HCl) into the rumen will cause metabolic alkalosis in ruminants.


Compensation is the process whereby the body attempts to restore the normal blood pH during an acid-base disorder. Overcompensation does not occur. As with the primary disorders, compensation can be metabolic or respiratory in origin.

Acid-Base DisturbancePrimary DisturbanceCompensatory ResponseCompensatory Mechanism
Respiratory acidosisIncreased pCO2Increase [HCO3-]Acidic urine
Respiratory alkalosisDecreased pCO2Decreased [HCO3-]Alkaline urine
Metabolic acidosisDecreased [HCO3-]Decrease pCO2Hyperventilation
Metabolic alkalosisIncreased [HCO3-]Increased pCO2Hypoventilation
Compensatory process

Keyword: Respiratory--> compensate at kidney
Metabolic --> compensate at lungs

Diagnosis of acid base disorder

The values that need to be examined to determine if there is an acid-base imbalance are: blood pH, pCO2, [HCO3-], and the anion gap. If any of these values are outside of the reference range, an acid-base abnormality is present. The blood gas analysis reports pH, pCO2, [HCO3-], and pO2. Blood gas analysis is completed on whole blood collected in heparin (green tube), and the sample should be collected anaerobically and processed as soon as possible after collection. The serum chemistry profile reports the anion gap and total CO2 (TCO2). TCO2, not to be confused with pCO2, is another measurement of [HCO3-] and is often used synonomously.

Most simple acid-base disorders are associated with a change in pH. Once acidemia or alkalemia is detected, the next step is to determine if the primary cause is respiratory or metabolic in nature. This requires analysis of the pCO2 and HCO3- (TCO2) values. Changes in the HCO3- value that correspond to the change in pH reflect a primary metabolic disorder while changes in the pCO2 that correspond to the change in pH reflect a primary respiratory disorder. The next step is to determine if there is secondary compensation by the body to try to correct the primary disturbance.

Mixed acid base disorder

A mixed acid-base disorder is one in which two different primary conditions are acting at the same time. Mixed disorders can be a combination of metabolic and respiratory disorders or a combination of different metabolic disorders. The separate processes may have either a neutralizing or additive effect on the pH.

First, there are mixed disorders which have a neutralizing effect on pH. In these cases, the body may appear to be overcompensating because the pH is normal or close to normal. Since the body does not overcompensate, a mixed disorder should be suspected. A classic example of this type of disorder is a vomiting dog who becomes dehydrated. The loss of stomach acid leads to alkalosis while the dehydration and subsequent lactic acid buildup leads to acidosis.

Second, it is possible to have mixed disorders which have an additive effect on pH.2 For example, a respiratory acidosis and metabolic acidosis can occur concurrently in a dog with thoracic trauma that also has lactic acidosis due to shock. In this case the pH would be dangerously low. Mixed disorders that have an additive effective on the pH will always have an abnormal pH.

Effects of acid base disorder

Many of the clinical signs observed in animals with acid-base disturbances are the result of the primary disease process but there are also clinical signs that can develop as a result of the acid-base disturbance itself. Most notably, changes in neural function, cardiac output and concentrations of calcium and potassium may all occur as a direct result of acid-base abnormalities.

Severe acidosis will impair the ability of the brain to regulate its volume, resulting in obtundation and coma. Severe metabolic alkalosis can induce agitation, disorientation, stupor and coma. Cardiac output is also compromised by severe acidosis. Myocardial contractility decreases when the blood pH falls below 7.2 and acidosis may predispose the heart to ventricular arrythmias or ventricular fibrillation.

Serum ionized calcium concentration can be affected by acid-base abnormalities. Acidosis causes displacement of calcium ions from their binding sites on albumin as the binding sites become protonated and an increase in ionized calcium concentration results. Conversely, alkalosis will cause a decrease in ionized calcium concentration and may lead to muscle twitching.

The distribution of potassium ions between the intracellular and the extracellular fluids (and therefore the blood [K+]) may be affected by acid-base disorders as well. As the blood [H+] rises in cases of acidosis, more H+ ions are pumped intracellularly in exchange for K+ ions that are pumped extracellularly (Figure 4). This exchange of ions is necessary to maintain electrical neutrality. The result is a rise in serum [K+]. This situation has only been observed in cases of titration-type metabolic acidosis caused by non-organic (mineral) acids like hydrochloric acid and secretion-type metabolic acidosis.Even though hyperkalemia can develop, it is not likely to occur if renal function and urine output are normal. Clinical signs of hyperkalemia can include muscle weakness and cardiac conduction disturbances.

Figure 4: Exchange oh H+ and K+ in acidosis. Result in hyperkalemia

Just as hyperkalemia can accompany acidosis, hypokalemia can accompany alkalosis.Hydrogen ions moves out of the cell to increase the [H+] extracellularly, so potassium ions move inside the cell to maintain electrical neutrality (Figure 5). Clinical signs of hypokalemia can include muscle weakness, polyuria, polydipsia, impaired urinary concentrating ability, and cardiac arrhythmias.

Figure 5: Exchange of H+ and K+ in alkalosis. May cause hypokalemia

Treatment of acid base disorder

Treatment of respiratory acidosis and respiratory alkalosis is aimed at correcting hypercapnia and hypocapnia, respectively. Therefore, causes of hypoventilation and hyperventilation need to be investigated in order to determine the underlying cause of hypercapnia and hypocapnia, respectively.

Treatment of metabolic alkalosis is aimed at replacing the chloride deficit in cases where vomiting of stomach contents or diuretic administration is the underlying cause.However, potassium and sodium deficits are likely to be present also, so these must be addressed simultaneously. Therefore, the treatment of choice for the correction of metabolic alkalosis in dogs and cats is intravenous administration of a sodium chloride (NaCl) solution with added potassium chloride (KCl). If ongoing gastric losses are present, H2-blocking agents can be useful to decrease gastric acid secretion. In cases where a gastric foreign body is causing vomiting, definitive treatment consists of surgical removal of the foreign body.

Treatment of metabolic acidosis is dependent upon the underlying etiology. Fluid therapy to correct dehydration and electrolyte disturbances, if present, is warranted. However, specific treatments will vary for ethylene glycol intoxication, lactic acidosis, renal failure, and diabetic ketoacidosis.

Ps: Hope this won't be confused no more

Sources: Full article of Acid-Base Balance, an overview; Veterinary Clinical Pathology Clerkship Program

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Cardiopulmonary resuscitation (CPR) in animal

Animal CPR (a big LOL)

During anesthetic class, we were taught to perform CPR on emergency anesthesia. This will not happen if the anesthetists are very careful in monitoring the patient throughout surgical period. So, let's dive in!


CPR in dog

CPR is an emergency technique used to help someone whose heart and/or breathing has stopped. Although somewhat modified, the same techniques used for people – rescue breathing and chest compression – can be used to help treat an animal in distress.

The first lesson to know about CPR is that it doesn't restart a stopped heart. The purpose of CPR, in both humans and animals, is to keep them alive until the heart begins beating on its own or a cardiac defibrillator can be used. In animals, CPR is frequently unsuccessful, even if performed by a trained veterinarian. Even so, attempting CPR will give animal fighting chance.

PCR on cat

At first, we must know the ABC rules!

1.Listen and feel to determine if your pet is breathing/has a pulse.
2.Carefully pull the tongue straight out of the animal’s mouth to open the airway
3. Make sure that the neck is reasonably straight; try to bring the head in-line withthe neck.

WARNING: Do not over-straighten the neck in cases where neck/head trauma exists

4. Attempt 2 rescue breaths, by closing the mouth, and performing mouth-to-nose ventilations. If they go in with no problems continue to B-Breathing.

Step 2: Place pet on his right side (legs away from you)...
Opening airway in dog

See above for positioning to give breaths to a cat.

Opening airway in cat

5. If not, reposition the neck and try5. step 3 again.

6.Visibly inspect the airway by looking into the mouth, and down the throat for foreign objects occluding the airway. Unlike human-CPR, rescuers may reach into the airway and remove foreign objects that are visible.

6. If you still can’t breath into the animal,proceed to the Heimlich maneuver.

Heimlich maneuver

Use to remove choking material that cause inability in breathing

1. Turn the animal upside down, with its back against your chest 2. Hug the animal with your fist in your hand, just below the rib-cage ( for cats, just squeeze 1 hand in the same place)

2. With both arms, give 5 sharp thrusts (bear hugs) to the abdomen. Perform each thrust as if it is the one that will expel the object

3. Stop, check to see if the object is visible in the airway, if so, remove it and give 2 mouth-nose rescue breaths. If the breaths do not go in, go back to step 1

Heimlich maneuver


After achieving a patent airway, one must determine whether the animal is breathing, and whether this breathing is effective:

1. Carefully pull the tongue straight out of the animal’s mouth to open the airway


3. Breathe at 12 breaths per minute (1 every 5 seconds)With each breath just make the chest rise (do not overinflate, expecially on a small animal)

IMPORTANT: If the breaths do not go in, stop and return to A-Airway!

Proceed to C-Circulation, while continuing breathing support as necessary.

Check the femoral pulse!

Step 3 (Dog): Check pulse at femoral artery (where hind leg meets torso), If no pulse…


Step 3 (Cat): Check pulse at femoral artery (where hind leg meets torso), if no pulse…


C- Circulation

This is the final step of CPR and should only be started after the A-airway and B-breathing steps have been completed:

1. Make sure that there are no major (pooling/spurting blood) points of bleeding. Control as necessary by applying pressure with your hand

2. Check for a pulse in the groin (check carefully on a conscious dog or cat!)

3. Lay the animal on its right side

Step 4 Gently take animal’s left front leg and bend it at the elbow, rotating it at the shoulder.  Where his elbow touches his body is where you place your left hand for compressions.

4. Locate your hands where its left elbow touches the chest, approximately the middle of the rib-cage (for cats use 1 hand in asqueezing motion).

Compressions for medium to large dogs: With you left hand, push on the chest 10-15 times (approximately 3 compressions every 2 seconds) and then deliver 2 more breaths. Repeat.  Every 4 cycles, check for a pulse.

Location of heart

Compress the chest 15 times followed by 2 rescue breaths (3 compression every 2 seconds). Deliver 2 more breath. Repeat. Every 4 cycle for a pulse.

Compressions for small cats and dogs:  Use fingertips to compress heart in place of your left hand or place 4 fingers of your left hand under the animal’s chest and compress on the top with left thumb: 5 compressions/1 breath and check for a pulse every 8-10 cycles.

Compression for small cats and dogs: Use fingertips to compress heart in place of your left hand or place 4 fingers of your left hand under the animal’s chest and compress on the top with left thumb: 5 compression/1 breath and check for a pulse every 8-10 cycles.

If there are two people, one breathes and the others compresses at the rate of one breath for every 2-3 compression

After the CPR is successfully performed, quickly send the animal to the nearest vet!

Precaution in CPR

1. Take care not to over inflate the lungs, observe that you ventilate with a normal rise and fall to the chest.

2. Never breathe or compress on an animal that is breathing or has a pulse.

3. When doing compression, realize you must compress 1/4 to 1/3 the width of the chest. You must flex the ribs, press the lungs in order to squeeze the blood out of the heart and release so that it can flow around and back into the other chamber.

4. For barrel-chested breeds, you may position dog on his back and compress chest human-style (hand on top of hand over chest): 15 compressions/2 breaths checking for a pulse every 4 cycles.

For barrel-chested breeds (like Fala and Winnie above) you may position dog on his back and compress chest human-style (hand on top of hand over chest):  15 compressions/2 breaths checking for a pulse every 4 cycles.

Barrel-chested dog

**Perform CPR until you have reached a veterinary hospital. After 20 minutes, however, the chances of reviving an animal are extremely unlikely.

Maybe you can learn something here..

Sources: Sheraton luxuries; CPR guide, CPR in dogs;petplace.com, dailywag; Martha steward.com; Pet first aid

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