PATHOLOGY OF CARDIOVASCULAR TRACT

Definition:

I.C.C.

Clinical syndrome in which the heart is incapable to ensure adequate blood flow, usefull for the metabolic necessities of the body the heart can not excessively limit the venous

return, even if the ventricles filling is satisfactory

The definition excludes the cardiac syncope, the colapse and hypodiastolic failure

Practically, the heart failure = myocardic failure

Physiopathology.: myocardic failure=> CO (cardiac output) consequences: downstream of heart - A.P oxygenation failure of the tissues upstream of the heart The heart can not get blood flow (output) - pulmonary - venous systemic venous congestion (stasis) visceral (pulm., liver, kidney, so on) peripheral (edema)

the CO decrease attracts: cardiac modifications elongation hypertrophy sweating dilatation of myocardic fibers tachicardy discharge of catecholamines T.A. min. activation of the renin-angiotensin-aldosterone Retention of Na+ and H2O oliguria edemas

Etiology finishing stage in affections: C.C.M. especially with a large shunt L-D Infectious miocarditis, endocarditis , Rheumatic fever

Rhythm disturbances (AF, AFl, complete block, paroxistic atrial tachycardia) iatrogenic: liquid overloading, Adriamycin, ventriculotomy

extracardiac
severe anemia, septicemy, pulmonary diseases thyrotoxicosis, colagenoses storage and neuromuscular disease

Clinical manifestations signs and symtomes

Signs of pulmonary venous congestion: tachipnea (> 60/min, in infant- sign almost sure) wheezing ales on auscultation crackles nutritional difficulties irritability Dyspnea at effort coughing cyanosis

Mechanism
increased filling pressure Interstitial edema Bronchiolar edema alveolar edema respiratory effort transport of O2

2. Signs of systemic venous congestion:

hepatomegaly turgid jugular Peripheral edemas - facial

Mechanism RV pressure of filling Hepatic venous congestion transudate aldosteron

3. Affect the cardiac output:

precordial activities peripheral pulse capillary refilling

Mechanism inotropic status inotropic function systemic perfusion

4. Volume overloading:
precordial activity noises Mechanism Chamber dilatation Keep the inotropic status ventricular filling

5. Pressure overloading:
noises breathes Mechanism postload compliance poststenotic turbulence

6. Adaptative modifications:
tachicardy paleness Mechanism neuronal response 1 - adrenergic activity 1 and angiotensin response vasoconstriction

7. Other modifications:
Decreased urinary debit urinar Deficient body weight curve sweating

Mechanism renal perfusion metabolic needs sympathetic and cholinergic stimulation

Left C.C.F Right C.C.F Global C.C.F manifestations - pulmonary manifestations - cardiac - periferic - visceral - cardiac

In infant and small child triad: tachipnea ( pulmonary stasis) hepatomegaly ( hepatic stasis) tachicardy (cardiomegaly)

Treatment Eliminate the precipitant causes - correct the malformations - control of tachidisritmia - correct anemia
Objectives of C.C.F. treatment: contractile performance effort of the heart overloading of volume

I.
-

general measurements
repause in bed physical activities => metabolic needs in big child, adolescent O2 in those hypoxic Fenobarbital consume of O2 peripheral 3-5 mg/kg/day in 1-2 doses PO or IM

II. Preload reduction aim improvement of dyspnea,

phenomena of cardiac right failure and congestive edema from CCF Diuretics excessive volume load of the heart Divided into: loop diuretics thiazides antagonists of aldosteron

Loop diuretics

- Action at the level of distal segment of -

Furosemid - 1 mg/kg/dose I.V./I.M. at 8-12h - After a few days follows the therapy P.O. 25 mg/kg/day, in 2-3 doses

Henle loop Inhibates the active reabsorption of cations of Cl and passive reabsorption of Na ions and water

Thiazides

- Action at the level of distal convoluted tube Inhibates reabsorption of Na

Clorotiazid
20-40 mg/kg/day

Hidroclorotiazid
2-5 mg/kg/day PO

Antagonists of aldosteron

Spironolacton
Weak diuretic effect It is used in association with other pp 1-2 mg/kg/day PO, in 2 doses The action starts after 2-3 days Limits the losses of K

III. Improve heart contractility inotropic agents Digital - Fundamental agent used in treatment of -

CCF in children force of ventricular contraction Used for fast digitization 0,03 mg/kg in infants, up to 0,05 mg/kg/24-48 hours (0,04 pt. Lanatozid) as dose of attack (fast saturation) 1phial of 2 ml = 0,5 mg is dissolved in 24 ml sol. glucose 10-20-33%

If it is administered. I.M., it will not be diluted and the dose calculated is administered I.V., then at 8 h interval/at 12 h interval When signs of efficiency appear ( tachipnea, hepatomegaly) we change with D for maintenance: - 1/3 from Datac (in new born = 1/6) If we pass to administration of PO of digoxin, the dose will increase with 30% (absorbtion 70%) For children there are preparations of digoxin: Phial of 20 ml ( 1 ml = 0,5 mg = 50 pic.) compr. of 0,25 mg.

Rules: Infants and small children are more sensitive at toxic effects of the digitalicelor Will be correctly monitored - temperature - vomiting - Na+, K+ hypopotasemia enhances the digital toxicity Do NOT administrate calcium in the same time

III. Improve heart contractility inotropic agents simpatomimetic - Use din acute states Izoproterenol - inotrop, cronotrop - pulmonary and peripheral vasodilatator - D: 0,001-0,1 g/kg/min - Side effects.: tachicardia, aritmia Dopamin natural cathecolamin - precursor of NE

Dopamin
In small doses - 2-5 g/kg/min produces renal vascular vasodilation Medium doses - 10-20 g/kg/min - effect -adrenergic, increase the inotropic stimulation of the heart Big doses- effect -adrenergic, which determine vasoconstriction and limit the increase of cardiac debit

Dobutamin
simpatomimetic agent stimulates 1-2 and -receptor adrenergic Primary effect of of cardiac debit and myocardic contractility (positive inotrop ) It starts with a dos eof 5 g/kg/min Up to 20 g/kg/min

Milrinone
Inhibits the action of fosfodiesterasis upon adenozid monosphate ciclic, AMPc Increases intracellular AMPc and contractility Administered in bolus 50 g/kg, hen it is continued with 0,25-0,75 g/kg/min

IV. Postload reduction (peripheral

resistance) Peripheral vasodilatators In consequence cardiac debit vene capacity a patului vascular sistemic and volume of filling => venous congestion reduction Nitroprusiat de sodiu (acute treatment) It is started with small doses, of 0,5-1 g/kg/min Increased up to 3-4-10 g/kg/min

postload reduction

Prazosin 0,01-0,05 mg/kg/dose, p.o. Captopril 0,1-0,5 mg/kg/dose, p.o. at 8-12 h in infant/new born 6,25-12,5 mg/dose, p.o. at 8-12 h in adolescents maximum 50-75 mg/day

Postload reduction

Prolonged treatment Hidralazin, which dilutes the arteriolar

bed increasing the C.O. Start with 1 mg/kg/day PO in 3-4 doses, then gradually increased we get the desired effect

Nutrition in ICC

As these infants have enough intake and

increased metabolic requests, they need more than 100 200 kcal/kg/day with minimum necessities of salt and liquids Na 2 3 mEq/kg/day intake of 7 12 mEq/l sol First, start with 130 140 kcal/kg/day. Intolerance to liquids manifests through body weight growth, more than 30 g/day with hepatomegaly and dispnea Treatment of iron anemia max 15 mg/day to prevent anemia, because any decrease of hemoglobin leads to a peripheral decrease of O2 intake

COLLAPSE (SHOCK)
Collapse static notion
- semiologic - shows a circulation insufficiency shock dynamic notion - physiopathological in practice is mistaken with Definition: clinical state with systemic perfusion inadequate for the body metabolic necessities

The shock - Unspecific acute syndrome: Deficient tissue perfusion - common factor to all types of shock sympatic tonus endocrin and metabolic modifications - unspecific Reaction of response to: traumatism arsuri hemorrhages (syndrome and a symptom, disease, separated entity)

 Tissue perfusion stagnant hypoxia metabolic acidosis It is not equal with hypoTA or hypovolemia It is not always with D.C. (in infections it can be n./, and tissue needs) the arterial pH is not always Variable peripheral resistance (although not always means vasodilatation) Organic lesions - general, difuse: - Shocking lung, shocking kidney and so on self-maintenance intervention (feed-back +)

Essential factors in treatment: time (precoceus treatment) ensure the right volemia

physiopathology:

Imbalance between content (blood mass) contentor (patul vascular)

Physiopathology classification

colapse of relaxation - vagal excitation colapse of centralization circulant mass - infant, small child- centralization, adrenergic tonus (decreasedvolemia according with Scorp) colapse paralitic vasomotor paralysis: severe infectious diseases, sfinishing stage in the other 2 forms

1) hipovolemic
mass

clinico-etiologic classification
shock- through circular

2) cardiogen shock 3) neurogen shock- traumatisma 4)

- anesthetic anafilactic shock alergens medicines vaccins poison insects stinging

5) septic

6) Shock of different causes

shock- toxico-septic - infectious - endotoxinic - septicemic - bacteriemic - with gram-negative germs

EPA, massive pulmonary embolia endocrin, metabolic disease anevrism disecant by aorta exogen intoxications

Hipovolemic shock

circulant mass
a. haemorragic (different haemorages) b. anhidremic (dehydration, burns)

 LEC loss(interstitial) - trece intravascular (p. col-

osm , pe seama glicemiei > after haemorrage) - the report of compart. plasmatic/interstitial-1:3 - adm. of 3-4 x > liquids than the lost blood Crystalloid solutions admin. Go in the intracellular space, after filling , filtration and diuresis appear Appreciate the balance restoration - after 24 h of perfusion (Ht, Hb, and so on) The same with the plasma substituents (Dextranii -hyperosmolar besides crystalloid solutions (thus, the intracellular space and kidney suffer)

cardiogen shock pericarditis miocarditis rhythm disorders hyperpotasemia Obstructive MCC After surgeries on cord deschis

D.C. depends of: Hemodinamic modifications *preload, preload = blood supply to the heart *afterload, postload =peripheral resistance

 VD debit determined by peripheral

all

resistance VS debit determined by peripheral resistance Myocardium contractility (inotropia) Cardiac frequency (! Pay attention to disritmii) Blood viscosity => - D.C. -tissue hypoperfusion - stagnant hypoxia

The aim of hemodynamic therapeutic modifications: Increase of DC Combat tissue hypoperfusion Increase the intake of O2 (prevent hypoxia)

key keep adequate volemia

Pathogenic aspects
Phases of hipovolemic shock Peripheral vasoconstriction

The whole capillary unit - arteriola - venula - pre and postcapillar sphincter

lactacidemia
relaxes the precapillar sphincter (not the
postcapillar)

Stase in the whole capillary system, venous st. Increases the capillary permeability plasma vessel leaves TA , blood viscousity - - -> disseminated intravascular coagulation (DIC)

The phases of the shock toxico-septic vasodilatation kinin ( tissue peptides) Under the action of endotoxins ( warm shock) peripheral resistance DC is n or cellular insufficiency of O2 caption arterial

vasoconstriction

Simpaticomimetic action of endotoxins

Symptomatology
cardinal symptoms (major) pulse alteration of big vessels(carotid, femural) TAs < 60 mmHg Cold, pale, cyanotic extremities, recolor time > 3 sec. Intrarectal temperature 10C than skin (centralization) Stop the diuresis Consciousness disorders
agitation, sleepiness, tiredness, coma

Other symptomes: - Weak tissue perfusion (deficiency of O2; glucose) Signs of toxicity: tachicardy tachipnea sweating Sensation of cold Cold, sticky skin Increased sensitivity
hypotension - tardive sign

Lab diagnosis

Blood analyze (Hgb haemorragic shock,

L, FL septic shock, Tr. Disorders of coagulation haemorragy Creatinic, Uree, GOT, GPT, ionogram Ech acido-basic ( metabolic acidosis) PVC, pO2, IC Thorax Rx

Treatment - emergency
15 minutes severe forms 60 minutes the mild forms about 30 minutes anaphylaxis shock administration of adrenalin therapeutic order in any other form : V = ABC - ventilation P = perfusion C = heart (suport the function of pumping) M = medicines

ABC
A airway airway assessment open,

patent B breath breath assessment + oxigen (100%), intubation and ventilation when needed C circulation improvement

General measurements:

Position with decliv head covering with a blanket (heat) Release the respiratory ways Administration of oxigen (aerotherapy) ventilation (when needed)

perfusion- pathogenetic treatment, the base of the treatment 1. blood -10-20 ml/body kg , repetable - only in hemorrhagic shock -hardly accessible - transmits viral hepatitis, HIV 2. Plasm -10-20 ml/body kg , repetable - inaccessibility disadvantage - risk of infections transmission idem 3. coloidal substituent of plasma - 10-20 ml/body kg corp repetable

Groups of substituents Dextran- plasmaexpander Dextran 70, 40 Macrodex Rheo-macrodex gelatin Products Marisang, Plasmagel, Haemacel 4. Human Albumin (sol. 5-10%) - 10-20 ml/body kg - There is no risk to transmit the infection - It expands SEC very well (1g retains 18 g liquid)

5. Crystaloid solutions ~ izotonic ~ Composition more similar to blood - SF - sol. Ringer - sol. Starter, and so on ~ 20-30 ml/ body kg, repeated 1-2 times ~ Associations between crystaloids, plasma, substituents, even artificial blood

Practical rules: In phial/syringe any other medicine is forbidden The liquid chosen has < import. Than quantity As fast as possible - in bolus 10 ml/kg plasma, albumin, substituents of plasma or 20 ml/kg sol. crystaloids, repeteated as long is necessary successful perfusion = PVC with 5 cmc H2O (n = 4-8, PVC max. in child: 12 cmc H2O) agressive therapy, liquid, with atb and which support the heart, prevent the irreversible phase of the shock essential factors: - time , volemia

C support the heart - inotrope

Effects Dopamin Splahnic Vasodilat 1 agonist ( contract, DC, conductibilit sinoatr) 2 agonist vasodilat peripheral i agonist 1 i 2 Dose (mcg/kg/min) 25 Type of shock septic Secondary effects Arrhythmia

5 10
10 20 0,1 - 2 5 - 20 0,1 septic cardiogenic Shock resistant to liquid resuscitation cardiogenic Arrhythmia Ventricular arrythmia ischemic extremities

Adrenalin Dobutamin Noradrenalin

agonist
1 redus

cAMP, Ca, I, Inihibitors of fosfodiesteraa peripheral e - amrinon vasodilatator

0,75 mg/kg n 2 3 min

adjuvante medicines ( + specific)

In new born, infant, have risk of hglic glc. 0,5 - 1
g/kg i.v. in a continuous PEV Ca (mediate coupling excitation contraction) CaCl2 10% 10 - 20 mg/kg i.v. NaHCO3 controversies acidosis decreases contraction and interferes with the functioning of catecholamines. NaHCO3 can accentuate the intracellular acidosis, correcting the extracellular. -acidosis secondary to the shock is corrected through perfusion. HCO3 = DB x G (kg) x 0,3 without Astrup 0,5 1 mEq/kg in 1 2 min i.v. Corticosteroids controversated only in purpura fulminans and severe septic shock (HHS 50 100 mg/m2/zi i.v.) etiologic treatment Other methods: dialysis, ECMO, and so on

 Sever cases: syndrome of multiple organic

dysfunction => graduated deterioration syndrome of respiratory detresis type adult (the liver of shock) The same with the infantile (BMH) alveolo-capilary terminal unit endangered by water accumulation, electrolytes and proteins in the gap Modification of ventilation/perfusion report => hypoxia (mortality ~ 60%)

Particularities in child (etiologic)

CRS insufficiency
supraglotic obstruction (epiglotitis, dyphteric croup) glotic obstruction (strange body, Congenital malformation, acute lesions) subglotic obstruction (LTB, bacterial tracheita ) CRI insufficiency Crysis of asthma or bronchilitis pCO2 > 55 mmHg = respiratory failure

 Metabolic collapse
intoxication
alcohol aspirin CO ethilen glicol

Diabetic Cetoacidosis Hepatic and renal insufficiency Inborn errors of metabolism Alteration signs of vital functions Corect acidosis (HCO3 1-2 mEq/kg)

Intoxicated child treatment of support adjuvante up to causal treatment