Pericardial Diseases

Pericardial diseases may include:

1)Pericarditis (inflammation of pericardium)
2)Pericardial Effusions
3)Constrictive Pericarditis
4)Cardiac Tamponade

ANATOMY
Pericardium normally contains as much as 20-50mlsof an ultrafiltrate of plasma.
Approximately 100ml of additional pericardial fluid can accumulate in the pericardium without any
significant increase in pressure.
The capacity of the atrium and ventricles to fill mechanically affected with further fluid accumulation
which increases pericardial pressure resulting in reduced stroke volume, dec. CO and hypotension (ie
cardiac tamponade)
The rate/ speed of fluid accumulation of fluid in the pericardium influences the hemodynamic
effect--------------
 
 
 
ACUTE PERICARDITIS
inflammation of pericardium that begins suddenly.

Pathophysiology:
IN most cases of acute pericarditis, the pericardium is acutely inflamed and has an infiltration of
neutrophils, increased vascularity and fibrin deposition the pericardium may develop an effusion.

Etiology:
specific cause of pericarditis include the following:
i)idiopathic
ii)infectious conditions (viral, bacterial including TB infections)
iii)inflammatory disorders such as rheumatoid arthritis, lupus and rheumatic fever.
iv)metabolic disorders such as:
—renal failure: uremic pericarditis is thought to result from inflammation of the visceral and parietal
layers of the pericardium by metabolic toxins that accumulate in the body due to kidney failure.
—hypothyroidism
v)cardiovascular disorders (dressler's syndrome)
vi)neoplastic
vii)drugs (hydralazine)
vii)radiation
ix)cardiovascular procedures
x)trauma
//viruses esp coxsackie viruses are the most common cause of acute pericarditis. They are also
probably responsible for idiopathic pericarditis.

Symptoms:
i) the patient presents with chest pain: sharp, and retrosternal and may radiate to the left shoulder
and is worse with inspiration, coughing, and when lying flat. The pain improves while sitting up and
leaning forward.(when lying down chest wall presses on inflamed pericardium; breathing in lungs
inflate and pressure)
ii)SOB: especially if a sizeable pericardial effusion develops.
ii)palpitations due to a tachycardia or arrhythmias.(myocardium underlies the pericardium so
pericarditis may irritate the myocardium too)
iii)difficulty swallowing (dysphagia) if there is a large pericardial effusion due to the compression of
oesophagus by the large pericardial effusion.

Signs:
i)low grade fever (because inflammation)
ii)pericardial friction(rub): high pitched scratching/grating sound similar to leather rubbing to
leather. The pericardial rub arises from friction bw the inflamed visceral and parietal pericardial
surfaces. The rub has two or three components, each associated with rapid movement of a cardiac
chamber.
—the systolic components: which is related to ventricular contraction is the most common.
—during diastole: there are two components
>one in early diastole resulting from rapid filling of the ventricle.
>late diastole, d/t atrial contraction.
the diastolic components often merge so that only two components are most commonly heard.

Investigations:

LABS:
—CVC: leucocytosis (inc in WBC) d/t inflammation or an infective cause of the pericarditis
—Inflammatory markers: C-reactive protein (found in liver) and ESR(erythrocyte sedimentation rate)
—Renal function test: to rule out kidney disease as a cause
—Autoimmune Screen for autoimmune diseases
—thyroid function test for hypothyroidism esp is pericardial effusion is suspected.
—TB testing.
—Markers for myocardial injury d/t associated myocarditis.
 
 
ECG:
—widespread ST elevation (not just in one area of muscle damage//dd for MI) or PR depression
 
Chest X-ray: in those with suspected pericardial effusions which shows enlarged water bottle shaped
hearts.

ECHO: to look for any pericardial effusion

//imp to note that the pericardium may have an normal appearance in pericarditis without evidence
of fluid

---> if not picking up anything then— CT/MRI scan may be required (not everyone because
expensive)
pericardial thickening is suggestive of acute pericarditis. scans will also show any pericardial
effusions.

>>Pericardiocentesis: removal of pericardial fluid maybe required if—

i)purulent pericarditis is suspected and the pericardial fluid is sent for analysis, or
ii)if TB pericarditis is suspected.
 
 
TREATMENT:
 
1)Aspirin or NSAIDs (ibuprofen) and colchicine(anti inflammatory agent)
//consider low dose corticosterioids if the above fail.
 
2)Treat the cause of the pericarditis.
//antibiotics for bacterial pericarditis
//dialysis for uremic pericarditis.
 
 
 
COMPLICATIONS

A]PERICARDIAL EFFUSIONS
—Presence of an abnormal amount of fluid in the pericardial face

CAUSES:
1)Any cause of pericarditis since pericardial effusion may occur as a result of any cause of
pericarditis.
2)RSHF
3)Low Serum Albumin d/t liver failure or nephrotic syndrome.
 
CLINICAL FEATURES:
1)Pericardial Effusions maybe asymptomatic or it can present with clinical features similar to
pericarditis.(see above)
2)The heart sounds maybe muffled or distant with a large pericardial effusion.
3)Clinical features of cardiac tamponade maybe present if a large pericardial effusion restricts
ventricular filling (see below)
 
 
INVESTIGATIONS:
Same as pericarditis, but:
a)ECG in pericardial effusion may show,
i)low voltage QRS complexes can be seen in large pericardial effusions and in cardiac tamponade.
Ii)electrical alternans(consecutive beat to beat variation in the amplitude or size of the QRS complex
as a result of swinging of the heart in the pericardial fluid) may be seen in large pericardial effusions
and in cardiac tamponade.
// when swinging towards the chest wall near normal; when swinging away from chest wall then
smaller as there is more fluid bw myocardium and chest wall and the QRS complex gets dampened.
Thats why large and small large and small consecutively.
 
b)ECHO: imaging of choice for the diagnosis of pericardial effusions
c)Diagnostic pericardiocentesis(pericardial tap/removal of fluid from pericardial space): fluid sent for
lab analysis.
 
 
TREATMENT:
1)Treat any underlying inflammatory disease with aspirin or NSAIDs and colchicine
// low does corticosteroids if above fail.
2)Treat the cause
//anti bacterial for bacterial pericarditis
3)if anti inflammatory treatments don't correct the problem or the patient has/likely to develop
cardiac tamponade, consider removal of fluid from the pericardial space.
4)the surgical removal of all or part of the pericardium(pericardiectomy) is usually reserved for
patients who have recurring pericardial effusions despite drainage.
 
 
B]CONSTRICTIVE PERICARDITIS
—Occurs when a thickened fibrotic pericardium of whatever cause reduces normal diastolic filling.

PATOPHYSIOLOGY:
>>if inflammation of pericardium is recurrent or of long duration(chronic), this can lead to fibrosis
and scarring of the pericardium with calcium deposition---> the thickened fibrotic pericardium can
restrict filling of the ventricles, and at this point the signs of constrictive pericarditis appear.
 
ETIOLOGY:
—same causes as pericarditis.

SYMPTOMS:
i)dyspnoea
ii)fatigue
ii)ankle and abdominal swelling. (systemic pressures increase and effusion of fluid)
iv)chest pain may also be present as a result of pericardial inflammation.
v)fever maybe present(because of inflammation)
 
 
SIGNS:
1)
a] the JVP is elevated
//systemic venous pressure is elevated because blood flow entering the heart is elevated.
 
b]Kussmaul's sign(increase in JVP with inspiration):
//usually with inspiration the decrease in intrathoracic pressure is transmitted to the heart and filling
to the right side of the heart increases with a fall in systemic venous pressure.
In patients with constrictive pericarditis this normal response is prevented and the patient develops
kusmaul's sign.--- when you inspire the heart is constricted but the blood wont fill in the right heart
so the JVP.

c]A steep 'Y' descent in the JVP wave form due to rapid emptying of the right atrium as a result of
the high atrial pressure.
** JVP wave reflects pressure changes in the right atrium during the cardiac cycle
 
2)Cannot palpate apex beats
In most patients with constrictive pericarditis, the apical impulse retracts during systole, in these
patients the diseased pericardium prevents the normal outward systolic movement of the ventricles.
 
3)Distant/muffles heart sounds.
 
4)Diastole knock in early diastole along the left sternal border.
—on auscultation a high pitched sound is heard in early diastole just after the second heart sound
S2.
—in patients with constrictive pericarditis the non elastic thickened pericardium, results in a sudden
arrest of ventricular filling which creates the diastolic knocking sound.
 
5)Hepatomegaly, ascites and ankle edema.
—elevated systemic venous pressure can cause fluid accumulation in the liver, peritoneal space and
over the ankles.

 
INVESTIGATIONS

Labs:
—Same labs as pericarditis but also do the liver function test since hepatic congestion can occur.
ECG
—in long standing cases atrial fibrillation may occur
Chest X ray:
—May show calcification of the pericardium
ECHO
—May help differentiate constrictive pericarditis from restrictive cardiomyopathy
CT/MRI scan
—can be used to the thickness of the pericardium and also to look for calcification of the
pericardium.

TREATMENT

Definitive treatment is mainly surgical.

Pericardiectomy(surgical removal of part/all of the pericardium):typically leads to rapid

hemodynamic and symptomatic improvement

C]CARDIAC TAMPONADE

—Accumulation fluid/blood/pus within the pericardial space, that creates an increase in intra
pericardial pressure which restricts cardiac filling which decreases CO and results in hypotension.
—Cardiac Tamponade is emergency and can be fatal if it is not diagnosed and treated quickly.

PATHOPHYSIOLOGY
>> the four chambers of the heart occupy relatively fixed volume in the pericardial sac.
>>the pericardium is normally filled with a small amount of fluid (20-50mls) with an intrapericardial
pressure about the same as the intrapleural pressure. With sudden addition of fluid, the pericardial
pressure can increase at times to the level of the right atrial and right ventricular pressure
 
>cardiac chamber collapse is a common finding in cardiac tamponade
>>the RA and the RV are the most likely to collapse when intra pericardial pressure exceeds
intracardiac pressure within any particular chamber
>> right atrial pressure is minimal during diastole however pericardial pressure is maximal in diastole
when the ventricles are filling. d/t this fact, the first signs of collapse could be seen during right atrial
relaxation/ diastole. Chamber collapse prevents appropriate filling of the heart
From the systemic venous return.
>>left ventricle collapse is uncommon d/t the thickness of the ventricular wall

ETIOLOGY

1)
—can occur as a result of any process that causes pericarditis since pericarditis may result in
pericardial effusion(see above for causes of pericarditis)

2)ANTICOAGULANTS
—malignant disease and trauma are common causes of cardiac tamponade

SYMPTOMS

—SOB common symptom of cardiac tamponade the path genesis probably relates to a reduction in
cardiac output.
—chest pain may be present in patients with pericarditis.
—dizziness and syncope

SIGNS

A] The three classical signs of cardiac tamponade are called BECK's TRIAD
i)elevated JVP
//in addition to the elevated JVP there is loss of the Y descent in the JVP in cardiac tamponade, this is
d/t an inc in intra pericardial pressure, preventing diastolic filling of the ventricles.
>>>>Loss of the Y descent in the setting of elevated JVP should always arouse suspicion of pericardial
tamponade.
ii)Hypotension
—hypotension occurs because of the reduced filling of the heart resulting in a reduced CO.
iii)muffled heart sounds
—pericardial fluid can cause the heart sounds to become muffled or distant d/t the expanding layer
of fluid inside the pericardium

B]Pulsus Paradoxes
—a fall in systolic BP of more than 10mmHg during inspiration
>>arterial systolic BP normally drops less that 10mmHg during inspiration
//pulsus paradoxes is an important physical finding in the diagnosis of cardiac tamponade
But can also be seen in severe pulmonary disease and----------------

C]Pericardial rub may be heard in some patients if the underlying cause id d/t an inflammatory
pericarditis

D] inc heart rate and respiratory rate d/t the hypotension

INVESTIGATIONS

LABS
sames tests as in acute pericarditis
but also do coagulation studies CT/INR and a

ECG
1)sinus tachy cardia: low volatage QRS complexes
3)electrical alternance-------

CXR: cardiomegaly with a bottle shaped heart

ECHO: although ECHO provides useful information, cardiac tamponade is a clinical diagnosis, ECHO
shows diastolic compression/ collapse of the right atrium early diastolic collapse of the right
ventricular free wall
iii)swinging of the heart in the pericardial sac

TREATMENTS:

Pericardiocentesis(removal of pericardial fluid) by needle aspiration

ECHO guided pericardiocentesis is best, the procedure is usually done bw the xiphisternum and the
left coastal margin and the needle is directed towards the left shoulder at a 40degree angle to the
skin.
once pericardial fluid is aspirated, leave a 16 gauge catheter in place for continuous drainage.

III]SHOCK
Refers to an abnormality of the circulation in there is inadequate tissue perfusion resulting in cellular
dysfunction. The causes are divided into 4 groups—

1)hypovolemic shock: due to an insufficient volume of blood. To fill the vascular system
2)cardiogenic shock: d/t an inadequate cardiac output as a result of abnormalities of the heart.
3) distributive shock: also called vasogenic or low resistance shock d/t an increase in the size of the
vascular system produced by vasodilation in the presence of a normal blood volume
4)obstructive shock: d/t inadequate CO as a result of obstruction to blood flow in the lungs or heart

1}HYPOVOLEMIC SCHOCK

Background:
Hypovolemic shock is a life threatening condition in which rapid fluid loss results in inadequate
circulating volume resulting in inadequate tissue perfusion. Most often, hypovolemic shock is
secondary to rapid blood loss (ie haemorrhagic shock).

two common causes of haemorrhagic shock:

—Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders.
Two common causes of rapid internal blood loss are:
—solid organ injury
—rupture of an abdominal aortic aneurism.

Hypovolemic shock can result from significant fluid loss, other than blood loss.
Two examples secondary to fluid loss include:
—severe gastroenteritis
—extensive burns

The prognosis of hypovolemic shock is depended on the amount of volume loss.

Pathophysiology

The body responds to acute hypovolemia s/t (secondary to) by activating the following systems.
i)hematologic system:
—responds to an acute sever blood loss by activating the coagulation cascade and contracting the
bleeding vessels (by means of local thromboxane release)
ii)CVS:
—the cardiovascular system initially responds to hypovolemic shock by increasing the heart rate,
increasing myocardial contractility, and constricting peripheral blood vessels.
>> This response occurs secondary to and increased release of catecholamines and a decrease in
vagal tone (regulated by the baroreceptors in the aortic and carotid vessels)
— the cardio vascular system also responds by redistributing blood to the brain heart and kidneys
and away from the skin muscle and GI tract
ii)renal system:
—responds by stimulating an increase in renin secretion from the juxtaglomerular apparatus renin
converts angiotensinogen to AGI which is then converted to AGII by the lungs(?). AGII has two main
effects both of which help to reverse vasoconstriction of the smooth muscle of the arterioles, and
stimulation of aldosterone secretion by the adrenal cortex.
Aldosterone is the responsible for active Na+ reabsorption and the conservation of water.
iv)neuroendocrine system:
responds to the haemorrhagic shock by causing an increase in circulating antidiuretic
hormone(ADH). ADH is released from the posterior pituitary gland in response to a decrease in blood
pressure(as detected by the baroreceptors). ADH leads to increased reabsorption of water by the
distal tubule and the collecting duct.

**The mechanisms listed above, are effective in maintaining vital organ perfusion in severe blood
loss. However without fluid and or blood resuscitation and correction of the underlying pathology
causing the haemorrhage or fluid loss, cardiac perfusion eventually diminishes, and multiple organ
failure soon follows.

Causes:
The main causes of haemorrhagic shock are trauma, vascular, GI, or pregnancy related.

i)Vascular disorders than can result in significant blood loss:

—aneurisms and dissections
ii)GI disorders that can result in haemorrhagic shock:
—bleeding oesophageal varices
—bleeding peptic ulcers
—mallory-weiss tear: a tear in the mucosa of the lower oesophagus and it is most often caused by
repeated forceful vomiting.
iii)pregnancy related disorders: ruptured ectopic pregnancy—hypovolemic shock s/t an ectopic
pregnancy is common.

 
 
History:
In a pt with possible shock s/t hypovolemia, the history is vital, in determining the causes and in
directing the investigation.
—Hypovolemic shock s/t external blood loss is usually obvious and easily diagnosed.
—Internal bleeding may not be as obvious as pts. may complain only of weakness, lethargy, or have
a change in mental status.

Symptoms:
— of shock such as weakness, light headedness and confusion should be assessed in all patients.
>> in the pt with trauma, the pt if conscious may be able to indicate the location of pain.
>>chest abdominal/ back pain may indicate a vascular disorder.
Classical symptom of
>thoracic aneurism is a tearing chest pain radiating to the back
>abdominal aortic aneurism usually result and or back pain
 
 
**in pt. with GI bleeding, ask the pt. about hematemesis melena, alcohol history, excessive NSAID
use and coagulation disorders.
—The sequence of vomiting and hematemesis should be determined. The pt who presents with
hematemesis after many episodes of forceful vomiting is more likely to have Boerhaave's
syndrome(spontaneous rupture of oesophagus) or a Mallory-weiss tear, whereas a pt. with a
history of hematemesis from the start is more likely to have peptic ulcer disease or oesophageal
varices.
—if an obstetric cause is being considered, ask about the following:
last menstrual period, risk factors for ectopic pregnancy(eg history of fallopian tube history, vaginal
bleeding including the amount and duration), vaginal passage of products of conception
(foetal, placental tissue), and pain. All females of child bearing age should undergo a pregnancy test
regardless of whether they believe that they are pregnant.

PHYSICAL EXAMINATION:
—Should always begin with an assessment of the airways, breathing and circulation.(ABC). Once
these have been evaluated and stabilized, the pt should be evaluated for clinical feature of shock.
***Do not rely on the systolic BP as the main indicator of shock as this may result in a delayed
diagnosis.
Compensatory mechanisms prevent a significant decrease in systolic a BP until the pt has lost 30% of
the blood volume. More attention should be payed to the pulse, respiratory rate, and skin perfusion.
Also, pt taking beta blockers may not present with tachycardia regardless of the severity of shock.

Initial signs of shock may include, tachycardia HR>100bpm, inc RR, a dec in pulse pressure, cool
sweaty pale skin, and delayed capillary refill.
**The decrease in pulse pressure is a result of increased catecholamine levels which causes an
increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.
Later signs may include a decrease in systolic BP, decreased urine output(less that 400mLs in an
adult), and significant changes in mental status such a confusion agitation or even loss of
consciousness.

The patients entire body should be checked for external bleeding. The abdomen should be examined
for tenderness/distension, which may indicate intra abdominal injury.
**In the pts. without trauma the majority of the haemorrhage is in the abdomen therefore the
abdomen should be examined for tenderness, distension and bruits. Look for evidence of an aortic
aneurism such as a pulsatile abdominal mass whose diameter expands laterally by more than 3cms.
—In the pregnant women check for abdominal tenderness.

Hypovolemic shock must be distinguished from other causes of shock. These include:
i)Cardiac Tamponade(muffled heart sounds, distended neck veins)
ii)tension pneumothorax(deviated traches, dec breathing sounds)
iii)spinal cord injury (warm skin with vasodilation), lack of expected tachycardia and neurological
defects
 
INVESTIGATIONS
A]LABS
i)CBC:
— dec in Hb d/t haemorrhage or may show dec in platelets as a cause of haemorrhage
ii)Renal Function Test:
—since shock may result in acute kidney injury and renal function will go up.
iii)Blood glucose:
— may rise in hypovolemic shock d/t inc in cortisol.
iv)coagulative studies:
—PT/INR and activated partial thromboplastin time(APT) since coagulation disorders may be cause
of haemorrhage.
v)Lactate levels:
—in hypovolemic and other forms of shock inadequate tissue perfusion leads to increase anaerobic
glycolysis with the production of large amounts of lactic acid.
—In severe cases, the blood lactate levels rises from a normal value of about 1milimole/litre to 9
milimole/litre or more.
—The resulting Lactic acidosis represses the myocardium, decreases peripheral vascular
responsiveness to catecholamine, and maybe severe enough to cause coma.
vi) arterial blood gases (ABG) per PH and bicarbonate
vii)urine analysis for haematuria in urogenital injury in pts. With trauma
viii)urine pregnancy test for ectopic pregnancy
ix) blood should be typed and cross matched in haemorrhagic shock

B] IMAGING STUDIES: in pts with trauma and clinical features of hypovolemia is directed toward
finding the source of blood loss. Abdominal ultrasound is done in the pt, if a traumatic abdominal
inury is suspected.

A CT scan can also be done in a stable pt..

If thoracic(aortic) dissection is suspected, do ECHO, aortogram or CT scan of the chest.
The pt. with no history of trauma requires abdominal ultrasound in the emergency dept. If an
abdominal aortic aneurism is suspected.
If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage can be done
(involves placing a tube through the mouth, orogastric or through the nose(nasogastric) into the
stomach.
Flush saline solution into the stomach, followed by suction of the gastric content.
Nasogastric lavage may comfirm, upper GI bleeding. Endoscopy can be done,usually after the pt. Has
been admitted to find the source of GL bleed.
An upright chest x-ray, should be done if a perforated ulcer or Boerhaave syndrome is suspected.
Upright chest Xray will show air under the diaphragm in these situations.
If the pt is pregnant and in shock, bedside pelvic ultrasound should be done in the emergency dept.

TREATMENT

A]Prehospital care.
—the treatment of pts. with hypovolemic shock d/t haemorrhage often begins at the scene of an
accident or at home.
—the prehospital care team should work to prevent further blood loss, prevent further injury; start
appropriate treatment and transport the pt. to the hospital ASAP
—direct pressure should be applied to external bleeding vessels to prevent further blood loss.
—prevention of further injury, applies mostly to the pt. With trauma and may involve, immobilizing
the cervical spine.
—STARTING appropriate treatment, includes:
A:securing an adequate airway
>eg placing an oropharyngeal(OP) airway to prevent of relieve upper airway obstruction.
B:assess breathing
>pts who are not properly ventilating for any reason may require endotracheal intubation
C:maximize circulation
> by placing IV lines and starting IV fluid resuscitation.

B]Emergency dept care.

—the goals in the emergency dept. Wrt the treatment of the pt. With hypovolemic shock is as
follows.
i)maximize oxygen delivery
ii)high flow supplemental oxygen should be given to all pts and ventilatory support should be given if
needed.
—while oxygen and ventilation are necessary, excessive positive pressure ventilation can be
detrimental for a pt. With hypovolemic shock and should be avoided.
—in a pt. With hypovolemic shock, excessive positive pressure ventilation may decrease venous
return, decrease CO and worsen the shock state
iii)fluid resuscitation
—two large bore IV lines should be inserted, once IV access is obtained, initial fluid resuscitation is
done with a crystalloid such as normal saline
—an initial bolus of 1-2 L is given in an adult (20mls/kg in a paediatric pt.), and the pts response is
assessed.
—most pts require blood transfusions and the decisions to give blood should be based on the initial
response to fluids.
a)if vital signs return to normal: the pt is monitored to ensure stability and blood should be sent for
type and cross match
b)if vital signs transiently improve crystalloid infusion should continue and type specific blood
obtained and given
c)if little or no improvement is seen crystalloid infusion should continue and type O blood should be
given
Type O Rh- blood does not have any antigens and so is the universal donor type because it is
compatible with any blood type
—The position of the pt. Can be used to improve circulation. One eg, is raising the hypotensive pts
legs while fluid is being given.
—another eg. is rolling a hypotensive pregnant pt. Onto her left side which displaces the foetus from
the inferior vena cava

iii)control further blood loss, determine the cause of bleeding and provide definitive care as quickly
as possible
—control of further blood loss depends on source of bleeding and often requires surgical
intervention
— in the pt with trauma, external bleeding should be controlled with direct pressure, and internal
bleeding requires surgical intervention.
—somatostatin and octreotide infusions have been shown to reduce GI bleeding from varices and
peptic ulcer disease, these drugs decrease blood flow to the portal system by vasoconstriction, they
have similar effects as vasopressin, but DO NOT cause coronary vasoconstriction.
—Almost all causes of obstetric bleeding that cause hypovolemia, (eg ectopic pregnancy) require
surgical intervention.

CARDIOGENIC SHOCK
—a state in which inadequate tissue perfusion results from cardiac dysfunction--- most often
systolic.
—it is a major and and frequently fatal complication, occurring most commonly after MI

PATHOPHYSIOLOGY
A] Myocardial effect
—tissue hypoperfusion with resultant cellular hypoxia causes
i) anaerobic glycolysis with the accumulation of lactic acid and intracellular acidosis.
ii)myocyte membrane transport pumps fail, which decreases transmembrane potential and causes
intracellular accumulation of Na+ and Ca2+ resulting in myocyte swelling.
—if ischemia is severe and prolonged, myocardial cellular injury becomes irreversible and leads to
necrosis.

B]Systemic effects
I) Decreased cardiac output results in tissue hypoperfusion resulting in anaerobic glycolysis, lactic
acid formation and lactic acidosis.
—the lactic acidosis also worsens the systolic function of the myocardium

C] Shock State
—all forms of shock are characterised by inadequate perfusion to meet the metabolic demands of
the tissues.
—this results in cellular hypoxia and vital end organ dysfunction resulting in multisystem organ
dysfuntion syndrome.
*multi system organ dysfuntion syndrome is considered a continuum where the extent of dysfuntion
can vary greatly from mild impairments to irreversible failure.
The organs of vital importance are the brain, heart, and kidneys diminished perfusion of the brain,
results in a decline in higher cortical function which leads an altered mental status ranging from
confusion and agitation to coma.
—Depressed coronary perfusion leads to worsening cardiac dysfunction and a cycle of progressive
widespread hypoperfusion of tissues
—Reduced renal perfusion results in decreased glomerular filtration, causing decreased urine output
and subsequent renal failure.

ETIOLOGY

Cardiogenic shock can result from the following types of cardiac dysfuntion:
A]Systolic dysfuntion
—the causes of systolic dysfuntion that can lead to cardiogenic shock are
>ischemia or MI
>valve disease
>severe myocarditis
>end stage cardiomyopathy
>myocardial depressant drugs such as--------------

-----------MISSED--------
3)RESTICTIVE CARDIOMYOPATHY
4)external compression by cardiac tamponade

C]Greatly increased afterload.

—the causes of increased afterload, that can lead to cardiogenic shock are
i)aortic stenosis
ii)severe hypertension
iii)hypertrophic cardiomyopathy
iv)coarctation of the aorta

D]valvular and other structural abnormalities.

—the causes of valvular and other structural abnormalities that can lead to cardiogenic shock are
i)infective endocarditis
ii)mitral stenosis
iii)mitral regurgitation/aortic regurgitation.
iv)capillary muscle dysfuntion/rupture.
v)ruptured interventricular septum or free wall rupture

E] Arrhythmias
—ventricular tachyarrhythmias are often associated with cardiogenic shock
 
 
CLINICAL FEATURES
i)Hmx of MI may be present in some pts.
ii)Hypotension (systolic BP below 90 mmHg)
iii)clinical signs of poor tissue perfusion: cool extremities, cyanosis, altered mental status (confusion),
and decreased urine output.
iv)peripheral pulse is tachycardic and weak
v)pulse pressure may be reduced (difference bw systolic and diastolic pressure)
vi)peripheral pulse may be irregular if an arrhythmia is present
vii) a S3 or S4 maybe present.
viii)a systolic murmur, is heard in pts with acute mitral regurge or ventricular septal rupture.
ix) crepitations in the lungs is usually present.
x) jugular venous distension (inc jvp) <<<DD from hypovolemic shock>>>
xi) peripheral edema may be present

INVESTIGATION

LABS
i) CBC (three things: Hb, Pt WBC count.)
ii)Renal function test (to asses for renal dysfuntion).
ii)Electrolytes (is electrolytes are out of order can get a very serious arrhythmia)
>Abnormalities of K,Ca, Mg
iv)Liver function test ( to assess for liver dysfunction)
v)Cardiac Enzymes (troponin, and CKMB--Creatinine Kinase Myocardial Bound)
>to check for MI
vi)arterial blood gases- acidosis can have a detrimental effect on myocardial function
vii)lactate: an elevated serum lactate is an indicator of shock
viii)BNP: a low BNP level may rule out cardiogenic shock

ECG
to exclude other causes of shock.
>Tension pneumothorax
>Lung collapse

ECHO should be done early to establish the cause of cardiogenic shock

Coronary angiogram is urgently indicated in pts. with myocardial ischemia who develop cardiogenic
shock----------------------

Invasive hemodynamic monitoring

>SWAN-GANZ catheterization: also known as pulmonary artery or right heart catheterization is very
useful to exclude other type of shock (eg hypovolemic shock)
//SG catheterization is the insertion of a catheter into the pulmonary artery. The PA catheter allows
direct measurement of pressures in the RA, RV, pulmonary artery and the filling pressure('wedge') of
the left atrium.
>in hypovolemic shock the wedge pressure of LA is low.

TREATMENT

1) Correct any hypovolemia if present.

2) Early restoration of coronary blood flow.
>for pts. With cardiogenic shock d/t myocardial ischemia or MI.
------PCI is treatment of choice but if PCI is not available; use a thrombolytic drug such as TPA.
3)Correct any electrolyte or acid base abnormalities.(Low K, Mg, acidosis)

4)Drug Therapy
a)Pts. With MI or ACS, are given Aspirin and Heparin
b)Inotropic with or without the addition of vasopressor drug therapy.
>>this maybe necessary in pts with inadequate tissue perfusion and adequate intravascular volume
so as to maintain mean arterial pressure of 60 mm Hg.
----Dopamine infusion is the DOC to improve cardiac contractility in pts with hypotension.
//Moderate dose dopamine stimulates both beta 1 receptors and dopamine receptors producing
cardiac stimulation and renal vasodilation respectively.
//The infusion rate of dopamine is adjusted according to the BP
>>>if the pt. Remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor
such as noradrenaline infusion is started and titrated(adjusted) to maintain a mean arterial pressure
of 60mmHg.
>>>Noradrenaline is a potent alpha agonist.
**why is norAD only if moderate dopamine doesn't work?
because you dont want to further decrease cardiac output.

—Dobutamine may be preferable to dopamine if the systolic BP is higher than 80 mmHg

>>>dobutamine is a strong beta 1 agonist.

c)phosphodiesterase inhibitors (Milrinone)

—are inotropic agents with vasodilating properties and long half lives that are beneficial in pts. With
cardiac pump failure, but they may require adding a vasopressor.
—the mechanism of action is that they prevent the breakdown of cyclic AMP, thereby increasing
intracellular cAMP levels---- resulting in a positive ionotropic effect on the myocardium and
peripheral vasodilation (dec. Afterload)
 
 
 
SINUS BRADYCARDIA

—is defined as a sinus rhythm with a resting heart rate of 60 bpm or less.
Few pts, actually become symptomatic until their heart rate drop to less than 50 bpm.

ETIOLOGY

Physiological causes:
a]Athletes—
—training results in high vagal tone
b]Healthy young adults
c]a sleeping pt.

Pathological Causes:

1)Sick Sinus syndrome—

—involves a dysfuntion in the ability of the sinus node to generate or transmit an action potential to
the atrium
—most commonly occurs in the elderly pt. with CVS diseases;

2)although most cases are idiopathic some studies have shown a functional decrease in the number
of nodal cells. While other studies have shown the presence of antibodies to the nodal cells.

3)Electrolyte disorders (K, Ca, Mg)

4)Hypothyroidism.
5)Raised intracranial pressure
//bad reflex in late stage raised intra cranial pressure: cushings triad
triad: HTN, Bradycardia and irregular respiration
//These signs are related to brain stem compression and or ischemia
6)Worsening Hypoxia
7)Sleep apnea
8)Hypoglycemia
9)Hypothermia (When body temp falls below 35 deg C)

10) Inferior wall MI:

—this may result in bradycardia d/t either
i)inferior wall supplied by right coronary artery (also supplies the SA nodes as such ischemia of the
SA nodes)
ii)increased vagal tone(inferior wall ischemia results in simulation of C-fiber afferent in the inferior
wall of the heart resulting in the inc in vagal tone this is known as the Bezold Jarisdh effect

11) Medications such as beta blockers, calcium channel blockers (s/a verapamil and diltiazem, and
digoxin(inc vagal tone)

12)Sinus node maybe affected as a result of rheumatic fever or viral myocarditis.

SYMPTOMS

Sinus bradycardia is most often asymptomatic. However symptoms may include the following when
sinus bradycardia is severe:
i)dizziness
ii)syncope
iii)fatigue
iv)chest pain
v)SOB
vi)exercise intolerance

SIGNS
i)palpation of peripheral pulses reveal a slow, regular heart rate
ii)the physical examination may also include—
a)poor perfusion--- prolonged capillary refill time
b)dec. level of consciousness
c)cyanosis
d)pulmonary edema (d/t low HR)
e)SOB
f)peripheral edema

INVESTIGATIONS

LABS:
1)CBC: WBC, PT and HB
—WBC inc in myocarditis.
2)Electrolyte levels(renal function)
—K, Ca, and Mg.

3)Thyroid function test. to exclude hypothyroidism

4)Glucose to exclude Hypoglycaemia

5)Cardiac Enzymes s/a troponin.

IMAGING STUDIES
>routine imagine studies are rarely of value in the absence of a specific indication.

ECG
to confirm the diagnosis of sinus bradycardia and to rule out MI.

TREATMENT

Prehospital Care
A) supplemental O2, IV access, and cardiac monitoring should be started
>in symptomatic pts. IV atropine maybe used (atropine blocks cholinergic receptors in the heart)

B)Emergency Dept Care.

i) Care in the emergency dept should first rapidly ensure stability of pts condition
>Pt. should have continuous cardiac monitoring and IV access
ii)Pt in unstable condition may require intubation and non invasive transcutaneous (external) pacing
>Transcutaneous external pacing is a temporary means of pacing a pts. Heart during an emergency
by electrically stimulating the heart externally through a set of electrode pads.
>>low BP is a major risk for arrhythmias--- arrest.

iii)this is followed by an investigation into the underlying cause of the bradycardia and treatment of
the cause for eg correction of electrolytes.

iv)transcutaneous external pacing is also recommended in symptomatic pts. Who are unresponsive
to atropine or who responds to atropine only for a short time.

v)in sick sinus syndrome, drug treatment have been disappointing

>atropine may help on a short term basis however most pt. eventually require placement of a
pacemaker

vi) if sinus bradycardia is asymptomatic or produced by a reversible cause, pacing is not indicated.

vii) in pt. With sinus bradycardia secondary to digoxin beta blockers or Ca+ ch blockers,
discontinuation of the drug is often all that is necessary.
>Occasionally IV atropine and temporary pacing are required.

Viii) Treatments of post infectious bradycardia usually requires permanent pacing.

ix)in pts. With hypothermia who have confirmed sinus bradycardia with a pulse, atropine and pacing
are usually not recommended.
>Re warm the pt and supportive measures are the main treatment.

C)Long Term follow-up

>regular follow up is necessary for pts in whom a permanent pacemaker is placed.
>permanent pace makers: contain a pulse generator and one or more pacing leads. Permanents
pacing involves trans venous placement of one or more pacing electrodes within a chamber or
chambers of the heart while the pacemaker (pulse generator) is implanted inside the skin under the
clavicle.

ATRIOVENTICULAR BLOCK
>aka heart block . AV block.

—AV block is partial or complete interruption of impulse transmission from the Atria to the ventricle.
>the most common cause is idiopathic fibrosis of conducting system.
>Diagnosis is by ECG.
>Symptoms and treatment depend on the degree of block. But treatment when necessary, usually
involves pacing.

> The most common causes of AV block are

i)idiopathic fibrosis of the conduction system about 50% pts.
ii)ischemic heart disease (40%)
iii)the remaining causes of AV block are caused by:
—drugs beta blockers, Ca ch blockers (verapamil) and digoxin
—increased vagal tone (athletes)
—valve disease (eg infective endocarditis can result in an abscess within the heart which can affect
the conducting system.
—congenital heart disease

>>AV block may be partial or complete

—1st deg and 2nd deg blocks are partial
—3rd deg blocks are complete

1ST DEGREE AV BLOCK

*transmitting but trans mitting slowly (AV node working in a sluggish way)
—for 1st degree AV block conduction is slow with skipped QRS beats(complexes). All normal P waves
are followed by QRS complexes, but the PR interval is longer than normal (greater than 0.2
secs.)*one small sq is 0.04 secs and normal PR interval is 3-5 squares
—1st deg AV block maybe physiological in younger pts. With high vagal tone and in well trained
athletes.
—1st deg AV blocks are rarely symptomatic and treatment is required.
—further investigation maybe indicated when 1st deg AV block accompanies another heart disorder,
or appears to be caused by drugs

2ND DEGREE AV BLOCK

*some are transmitting
—some normal P waves are not followed by QRS complexes
—there are two types of 2nd degree AV BLOCK
i)MOBITZ type I (aka WENCKEBACH type)
Ii)MOBITZ type II
>in Mobitz type the PR interval progressively lengthens with each beat until the atrial impulse is not
conducted and the QRS complex is dropped. AV nodal conduction the restarts with the next beat,
and the sequence is repeated

Mobitz type 1 AV block

>maybe physiological in younger and more athletic patients. The block occurs at the AV node in
about 75% of cases with a narrow QRS complex and at intranodal sites (Hiss bundle and bundle
branches) in the rest.
> If the block becomes complete, a reliable junctional escape rhythm typically develops. (the bundle
fibres cause it)
//but note higher in conducting system the more reliable the tissue system is.
// also lower down means the escape rhythm is slower.

---Treatment is therefore unnecessary unless the block causes symptomatic bradycardia

Mobitz Type 2 AV block.

>the PR interval remains constant. Beats are intermittently not conducted and QRS complexes
dropped, usually in a repeating cycle of every 3rd or 4th P wave.
—it is always pathological.
—The block occurs. At the His bundle in 20% of pts. And in the bundle branches in the rest. (overall
lower down in the conducting system).
—Pts. maybe asymptomatic or experience dizziness or syncope depending on the ratio of conducted
to blocked beats.
—pts are at risk of developing symptomatic complete AV block in which the escape rhythm is likely to
be ventricular and therefore too slow and unreliable to maintain systemic perfusion. Therefore a
pacemaker is indicated.

//escape rhythm (?)

3rd degree AV Block or complete block.

*nothing is transmitting
—Heart block is complete.
—There is no electrical communication bw the atria and ventricles, and no relationship bw the P
waves and QRS complexes on the ECG. (AV dissociation)
—Cardiac function is maintained by an escaped junctional or ventricular pacemaker.
—Escape rhythms originating above the His bundle produce a narrow QRS complex which is
relatively rapid (> 40bpm) and reliable heart rates, and mild symptoms (for eg. Fatigue)
Escape Rhythms occurring below the His bundle produce wider QRS complexes, slower and
unreliable heart rates, and more severe symptoms.(eg. Dizziness, syncope, Heart Failure.)

//Risk of sudden death is greater if low escape rhythms are present. Most pts require a pacemaker.
Wolff Parkinsons White Syndrome WPW Syndrome

>In addition to the AV node, pts with WPW syndrome have an accessory pathway (AP), that
connects the atria and the ventricles. This accessory pathway(tract) is known as the BUNDLE OF
KENT.
—The AP is made up of cardiac muscle cells and so can transmits impulses directly from atria to
ventricles.
>>WPWS involves pre-excitation(ie: early activation of some of the ventricles, which occurs because
of conduction of an atrial impulse through the accessory pathway(AP).

To make diagnosis:
classic ECG findings that are associated with WPW syndrome include the following.
i)presence of a short PR interval(beginning of P wave to beginning of QRS complex--- less than 3
small squares; less than 0.12secs )
---The PR interval is shortened because of the early activation of some of the ventricle by the the AP
ii)a widened QRS complex (more than 3 small squares; more than 0.12 secs)
---the QRS complex is widened because some of the ventricle is initially activated through the AP
(which lies outside the normal conducting system) producing a relatively slow initial conduction of
depolarization through the ventricle
iii) a slurring(slow rise) of the beginning of the upstroke of the QRS complex called a delta wave.

>> consequences of the AP

a)this abnormal cardiac tissue connecting the atria to the ventricles provide a pathway or a re-entry
circuit, and this may result in a re-entrant supraventricular tachycardia(SVT), which can be
symptomatic
b)A.fib in pts with WPW syndrome is very common----impulses get directly conducted into the
ventricle without being discerned by the AV node and might even cause V.fib.
c)pts with WPW are at in risk for dangerous ventricular arrhythmias if they develop atrial fibrillation;
because the conduction of impulses from the atrial fibrillation across the accessory bypass tract will
result in very rapid and irregular depolarisation of the ventricles with the possibility of developing
ventricular fibrillation.
—in the normal heart a person with a fib is protected from extremely high ventricular rates by the
relatively long refractory period of the AV node. In pts with WPW syndrome, however the accessory
pathway may have a shorter refractory period than the AV node, allowing much faster transmission
of impulses to the ventricles resulting in extremely high ventricular rates. (may exceed 300bpm)
d)as a result a small % of WPW syndrome pts are at risk for sudden cardiac death.

**there is presence of CIRCUS movement in WPW syndrome.(THE CICULAR PATHWAY CAUSES THE
ARRHYTHMIA)
//this is called re-entry tachycardia (as the impulse re-enters the atrium)
---the arrhythmias are episodic.
SA node depolarising can go two ways; as even through the bundle of kent. But bundle of kent only
connected to some part of ventricle. And once it reached that part, it transfers to other parts of
ventricle which is slower(as it is cell to cell). And by that time normal conduction takes place.

>purkinje fibres are present so that your ventricles can depolarize at the same time.
>bundle of kent has a longer refractive period. So if the SA node sends an early transmission, the kent
might be in RP but not the AV node so the transmission will go down the AV node. And normal
conduction.
**note that if there is no early beat there is normal circulation. Only is there is early beat will there
be circular circulation and arrhythmia.

>>arrhythmias in MI has similar mechanism. Because of the circular circulation around dead tissue.
Doesn't need bundle of kent.
--- might event cause ventricular fibrillation

PATHOPHYSIOLOGY

>>>AP or connections, bw the atrium and ventricle are the result of abnormal development of
myocardial tissue which bridges the fibrous tissue that separates the two chambers
—this allows electrical conduction bw the atria and ventricles, at sites other than the AV node
***passage through the AP
—bypass the usual conduction delay bw the atria and ventricles, which normally occurs at the AV
node
—predisposes the pt to develop re-entry tachyarrhythmias

>>the assessory pathway can conduct impulses in either anterograde ie from atrium to ventricles; or
a retrograde ventricle to atrium manner
>>the presence of an accessory pathway sets up the electrical circuit for a re-entrant tachycardia to
be established; or for pre-excited( early activation of the ventricle) tachycardia in the setting of atrial
fibrillation.
>>the re-entrant mechanism: is the main cause of supra ventricular tachycardia (SVT) which pts with
pre-excitation(early activation) are at risk..
>> the formation of the re-entrant SVT in WPW syndrome involves the presence of two conducting
pathways bw the atria and the ventricles
i)the normal AV node-his-purkinje system
ii)the atrio-ventricular accessory tract ie that is the bundle of kent fibres.

These two pathways usually have different conduction properties and refractory period that
encourage re-entry.
>>the effective refractory period: the time necessary for electrical recovery needed to conduct the
next impulse of the accessory tract is often longer than that of the normal AV node-his-purkinje tract
and requires time for conduction to recover before allowing re-entry.
>>the amount of pre-excitation (early activation) on a surface ECG in a person with WPW syndrome
can be estimated by the width of the QRS and the length of the PR interval.
>>a wider (more pre-excited) QRS with a short PR interval reveals that most of the depolarisation of
the ventricle occurs through the accessory pathway insertion rather than through the AV node- his-
purkinje system.
>>the types of SVT in WPW syndrome include
—autodromic tachycardia: the impulse travels down the AV node-his-purkinje system and
retrograde backward conduction up the AP.
—antidromic tachycardia: impulse travels down the AP and retrograde conduction is up the his-
purkinje system and AV node.
—in pts with WPW syndrome 95% of the SVT id d/t autodromic tachycardia and 5% is d/t antidromic
tachycardia

AUTODROMIC TACHYCARDIA:
>when a premature ectopic atrial impulse occurs, it has the tendency to block at the AP (since the
effective refractory period of the accessory tract is often longer than the AV node) but conduct down
the normal AV node-his purkinje pathway.
>The impulse then re-enters the AP from ventricle to atrium in a retrograde or backward fashion to
continue a CIRCUS(circle)movement of the impulse such re-entrant tachycardia is described as
autodromic.

>>a critically timed premature atrial beat that occurs during the refractory period of the assessory
pathway starts the autodromic tachycardia.
>The premature atrial impulse therefore only travels down the AV node but returns in a retrograde
manner through the accessory pathway resulting in a continuing CIRCUS re-entry tachcardia.

MISSED*****

On the ECG during autodromic tachycardia the delta wave is absent, the QRS complex is normal and
the Pwaves are typically inverted, in the inferior and the lateral leads.
//how does atrium get depolarised(SA node) in autodromic tachycardia, it gets depolarised from
below ir from the AP(from the ventricles) and thus it is inverted.

ANTIDROMIC TACHYCARDIA
>>less commonly, some pts with WPW syndrome have a shorter refractory period in the AP than in
the AV node and this will result in blockade of a premature (early) ectopic atrial impulse in the
normal AV node pathway with antegrade(forward) conduction down the AP, and then retrograde re-
entry of the impulse in the AV node pathway.
//ventricle being depol. By the AP and thus conduction not by purkinje fibres and so cell to cell
conduction thus longer to depolarize; so the QRS is wider.
---on the ECG in antidromic tachycardia, the QRS is wide, ie that is a wide QRS tachycardia. Reflecting
the slow conduction (depolarization) through the ventricular tissue.
>>>will a delta wave be present in the ECG?
----there is slow depolarization and whole ventricle is getting depolarized.
>>but its hard to pick up because the whole ventricle gets depolarized and slurred upstroke.
---such tachycardias are difficult to differentiate from ventricular tachycardias since these are also
wide QRS tachycardias.

ETIOLOGY
i)WPW syndrome is congenital
ii)WPW syndrome may have a genetic component some pts. with WPW syndrome have 1st degree
relatives with pre-excitation(early activation) or the ventricles.
iii)WPW syndrome may be associated with hypertrophic cardiomyopathy
.

SYMPTOMS
>>pts are not symptomatic bw episodes of tachycardia.
>>in pts with WPW syndrome the tachcardia that produce symptoms maybe a supraventricular
tachycardia or an atrial fibrillation.
>>episodes of tachycardia have their onset from anytime from childhood to middle age and
symptoms can vary in severeity from mild chest discomfort or palpitations with or without syncope
to severe hypotension and cardiac arrest.
>>during episodes of tachycardia, pts may have:
—palpitations
—dizziness
—syncope: because of insufficient cerebral circulation d/t rapid ventricular rate during hypotension.
—chest pain: d/t inc demand for blood(tachycardia) and dec blood supply to the myocardium. d/t
less time in diastole and d/t hypotension.
—SOB: d/t dec time to fill the ventricle resulting in pulmonary edema; and also in dec in cardia
output.
—reduction in the tolerance for activity d/t the dec time to fill the ventricle with blood; resulting in
pulmonary edema and a dec in cardiac output.

SIGNS
i)if the pt is seen in bw the episodes of tachyarrhythmia(ie not currently having it) cardiac
examination is normal in most cases.
ii)if the pt is seen during episodes of tachyarrhythmia signs may include
a)hypotension
b)tachycardia:
—rhythm is regular if the tachyarrhythmia is d/t re-entry supraventricular tachycardia(SVT) such as a
autodromic tachycardia.
—rhythm is irregular is the tachyarrhythmia is d/t a.fib.
c)cold peripheries d/t hypotension and dec in perfusion of the peripheries.
d)sweating d/t activation of the autonomic nervous system.
e)crepitations in the lung bases from pulmonary edema during or following an SVT episode d/t the
rapid heart rate dec the filling time of the ventricle.
f)during the SVT the jugular venous pressure can be elevated d/t dec time for filling of the ventricles.
g)clinical features of any associated cardiac conditions:
eg—hypertrophic cardiomyopathy.

INVESTIGTIONS

LABS:
—to rule out non cardiac conditions which can trigger a tachycardia

1)CBC:
>look for anemia
>or a WBC inc in myocarditis.

2)Renal function test and electrolytes

>including K, Mg and Ca which may all potentially contribute to arrhythmias

3)Thyroid function test.

B[ECG
----diagnosis of WPW syndrome is typically made with a 12 lead ECG, the classic ECG features are as
follows,
i)a short PR interval(<1.12 seconds)
ii) a slurring(slow rise) of the beginning of the upstroke of the QRS complex (delta wave)
iii)a widened QRS complex more than 3 small squares ie >.12 secs.
C] SVT is best diagnosed by documenting an ECG during the tachycardia for eg by using a Holter
monitor(ie a 24 hr ECG//wrap around chest and can take home it will record)

D] ECHO is needed to exclude associated congenital heart defects for eg hypertrophic

cardiomyopathy.

E] Electrophysiologic studies(commonly known as EP studies) can be used in pts with WPW

syndrome do determine:
i)the location of the AP(necessary for catheter ablation
ii) to determine the electrical properties of the accessory pathway (for eg refractory period of the AP
or the conduction ability of the AP)
—evaluation for the presence of very short refractory periods of the AP is important bc these pts
carry a higher chance of developing serious complications.

TREATMENT.

in arrhythmias you only need to break the cycle and put back into sinus rhythm.

A]treatment of WPW syndrome associated arrhythmias comprise the following.

i)termination of the acute episode of re-entry SVT in stable(bp normal) is as follows:
—in a stable pt with narrow complex re-entrant tachycardia vagal manoeuvres can be tried first.
//For eg: carotid sinus massage.(inc in vagal activity will temp block AV node and may help stop the
circus conduction)---here you're not treating the AP but treating the tachycardia.
—when these measures fail, IV adenosine is the first line agent and is effective in approximately 90%
re-entrant narrow complex tachycardias
---adenosine causes significant changes in AV node conduction leading to transient AV node block
resulting in termination of the tachycardia.
—adenosine does not affect the AP conduction; if adenosine fails then try IV Verapamil a CCB to
block AV node conduction and terminate the tachycardia.

****these treatment can also be used in other tachycardias****

ii)termination of a.fib or wide complex tachcardia in stable pts.is as follows

—give IV amiodarone if a.fib or a wide RQS complex tachycardia is present and ventricular
tachycardia cannot be excluded.
a)Amiodarone prolongs the refractory period in myocardial tissue (and so can terminate a.fib) and
the AV-accessory pathway or tract
b)class 1A drug (quinidine) and class 1C drugs (flekanind) are Na+ channel blockers and can so
terminate a.fib. And also slow conduction velocity in the AP.[1A not used mostly 1C used though]
--- property (advantage) of 1A especially is that it is also a K+ blocking property.
///class 1A drugs which also was K+ ch blocking properties can also prolong the refractory period in
the assessory pathway.

//how? Does amiodarone do that.

it is class III; K channel blocker thus inc. Refractory period. Gonna take longer in downstroke,
(repolarization);;;thereby stopping the arrhythmia because no more conduction since still in
refractory period.
///a.fib/ischemia or inc atrial pressures affecting electrical function. Say there's a spot(normally
there's many many) not conducting the current then sinus beat as current can just go around.
But if there is early beat is present(ectopic) then one part of is in refractory period and other is not,
thus re-entry and circus movement in a.fib.
***explanation how to break the pathway in a.fib (he needs to continue explaining.)
i)since this fibrillation is in the atrium in the myocardium---- you need Na channel blockers to
temporarily break the cycle by stopping the depolarisation---the conduction.
ii)another way is to inc. the refractory period of the cells ie using K ch blockers.
---after temporarily stopping, the SA node will retake its position as pacemaker; but all it needs is a
ectopic beat for the a. fib to start again because the myocardium is damaged structurally already
with the 'spots'

B]The initial treatment of choice for hemodynamically unstable tachycardia is direct current
electrical cardioversion.
***in pt with any tachyarrhythmia with bp going down--- DC shock.(not the same for a
bradyarrhythmia with bp going down; because problem here is that there is no current production)
***how to treat brady arrhythmia then>>>simple pacemaker.
you need to check if it is stable; check what is causing.

B] in pts with WPW who don't have arrhythmias currently

—radio frequency catheter ablation:
flexible catheters are threaded through blood vessels to the heart. Electrodes at the catheter tips are
heated to destroy ablate the assessory pathway which causes WPW syndrome.
—radio frequency ablation is indicated in the following pts.
i)pts with symptomatic atrioventricular re-entry tachycardias
Ii)pts with atrial fibrillation that have rapid ventricular response via the assessory pathway (they are
likely to get
iii)pts with WPW syndrome and a fmx of sudden cardiac death.

----------------------------------------------------------------------------------------------------------------------------------

ATRIAL FIBRILLATION (MOST COMMON SUSTAINED ARRHYTHMIAS)

—most common sustained irregular heart rhythm a normal heart beat
— begins with an electrical impulse from the sinus node, a single point in the hearts right atrium.
—during atrial fibrillation, electrical impulses fire rapidly from multiple sites in both atria resulting in
a very fast irregular rhythm in the atria.
—the rate of impulses in the atria can range from 300 to 600 bpm.
—many impulses spread through the atria, competing for a chance to travel through the AV node.
—the AV node reduces the number of impulses since the conduction velocity is slow in the AV node
that travel to the ventricles but many impulses still get through in a fast and irregular manner.
—As a result, the ventricles contract fast and irregular leading to a rapid and irregular pulse.
—because the electrical impulses in the atria are fast and not coordinated, the atria cannot contract
as a whole and squeeze blood into the ventricle.

>>>Atrial fibrillation has strong associations with other CVS diseases such as heart failure
CAD, valvular heart diseases, DM and hypertension.
—the exact mechanisms by which CVS disease predispose the a.fib are not fully understood.
However inc atrial pressure; ischemia, catecholamine excess and atrial inflammation may play a part.
Classification of A.fib is into the following patterns:
1)Paroxysmal a.fib.
—episodes of a.fib the terminate spontaneously within 7 days. Most episodes last <24 hours.
2)Persistent a.fib, these are episodes of a.fib, that last 7 days to 1 year.
3)Long standing persistent a.fib.
—this referred to a.fib that has lasted more than 1 year.
4)Permanent a.fib.
—in this type the normal heart rhythm cannot be restored and the pt remains permanently in a.fib.
(usually people with very dilated atrium/structurally bad)