NURSISWATI

DEPATMENT OF MEDICAL SURGICAL NURSING

Anatomy of Coronary Artery
INFLAMMATION AND INFECTION
IN THE HEART
 RHEUMATIC FEVER
 IS AN ACUTE SYSTEMIC INFLAMMATORY
CONDITION THAT APPEARS TO RESULT FROM AN
ABNORMAL IMMUNE REACTION OCCURING A FEW
WEEKS AFTER AN UNTREATED INFECTION,
USUALLY CAUSED BY CERTAIN STRAINS OF GROUP
A BETAHEMOLYTIC STREPTOCOCCUS
 INVOLVES THE HEART AND OTHER PARTS SUCH AS
JOINTS AND SKIN
 USUALLY OCCURS IN CHILDREN 5-15 YEARS
 THE INFECTION COMMONLY APPEARS AS AN
UPPER RESPIRATORY INFECTION, TONSILITIS,
PHARYNGITIS, OR STREP THROAT.
 ANTIBODIES TO THE STREPTOCOCCUS
ORGANISM FORM AS USUAL AND THEN REACT
WITH CONNECTIVE TISSUE (COLLAGEN) IN THE
SKIN, JOINTS, BRAIN, AND HEART CAUSING
INFLAMMATION.
 DURING THE ACUTE STAGE, THE INFLAMMATION
IN THE HEART MAY INVOLVE ONE OR MORE
LAYERS OF THE HEART:
 1. PERICARDITIS..OUTER LAYER…MAY INCLUDE
EFFUSION
 2. MYOCARDITIS…HEART MUSCLE…ASCHOFF
BODIES, MAY INTERFERE WITH CONDUCTION
 3. ENDOCARDITIS..VALVES…BECOME EDEMATOUS
AND VERRUCAE FORM
 PANCARDITIS
 OTHER SITES OF INFLAMMATION IN PATIENTS
WITH RHEUMATIC FEVER INCLUDE:
 THE LARGE JOINTS, PARTICULARLY IN THE LEGS,
WHICH MAY BE INVOLVED WITH SYNOVITIS IN A
MIGRATORY POLYARTHRITIS
 THE SKIN..RED MACULES OR POPULES THAT
ENLARGE AND HAVE WHITE CENTERS
 THE WRISTS, ELBOWS, KNEES, OR ANKLES
 BASAL NUCLEI IN THE BRAIN…CAUSING
INVOLUNTARY JERKY MOVEMENT OF THE FACE,
ARMS, AND LEGS.
SIGNS AND SYMPTOMS RHD
 LOW GRADE FEVER
 LEUKOCYTOSIS
 MALAISE
 ANOREXIA
 FATIGUE
 TACHYCARDIA, EVEN AT REST
 HEART MUJR MURS INDICATE THE SITE OF
INFLAMMATION
CONT..
 EPISTAXIS & ABDOMINAL PAIN MAY BE PRESENT
 ACUTE HEART FAILURE MAY DEVELOP FROM
ARRYTHMIA
PERICARDITIS
 NYERI PRECORDIAL
 NYERI PERIKARDITIS BERKURANG DG DUDUK
TEGAK DAN MEMBUNGKUK KE DEPAN

 FRICTION RUB…gesekan pericard

 EFUSI PERIKARDIUM…suara jtg lbh lemah
 TAMPONADE JANTUNG
 NADI PARADOKSAL
 EKG…Elevasi ST segmen..tanpa perub QRS
Efusi pericardium
 Impuls apeks jantung dpt hilang atau kadang teraba
 Fluoroskopi memperlihatkan denyut ventrikel
berkurang
 Perkusi pekak

TANDA EWART
TAMPONADE JANTUNG
 PENGUMPULAN CAIRAN INTRAPERICARDIUM
 MENYEBABKN OBSTRUKSI SERIUS THD
MASUKNYA DARAH KE KE2 ATRIUM BS
MENIMBLK TAMPONADE
 250 CC-1000 CC
MYOCARDITIS
 PEMBESARAN JANTUNG & TANDA2 DECOMP
 An infectious organism directly invades the
myocardium
 Local and systemic immunological activation quickly
ensues
 Cellular (CD4+) and humoral (B-cell clonal
multiplication) activation occurs, causing worsening
local inflammation, anti-heart antibody production
and further myonecrosis.
 The first phase is characterised by viraemia in the host
organism. During this time, the cardiotropic RNA
virus enters the host myocyte via receptor-mediated
endocytosis. [18] Here, the viral RNA is translated into
viral protein, and the viral genome is incorporated into
the host-cell DNA as double-stranded RNA. This latter
mechanism has been shown to cleave dystrophin,
which is thought to directly cause myocyte
dysfunction.
 During the second and third phases, macrophages,
natural killer cells, and other inflammatory cells
infiltrate the myocardium. Once in the myocardium,
these cells express inflammatory cytokines including
interleukin-1, interleukin-2, interferon-gamma, and
TNF.
 This results in increased cytokine production and
causes endothelial cell activation resulting in further
infiltration of inflammatory cells. TNF alone also acts
as a negative inotrope.
 In addition, auto-antibodies directed against
myocardial contractile and structural proteins are
produced. This is thought to have cytopathic effects on
energy metabolism, calcium homeostasis and signal
transduction, and also to cause complement activation
resulting in the lysis of myocytes
ENDOKARDITIS
 NON INFEKTIF
 INFEKTIF
MANIFESTASI KLINIS
 KELAINAN VASKULER
 RUPTUR KATUP
 THANKS