CARDIAC EMERGENCIES

CARDIAC EMERGENCIES
CLASSIFICATION
• ARRHYTHMIC
• NON-ARRHYTHMIC

• ARRHYTHMIC
– CARDIAC ARREST
– TACHYARRHYTHMIAS
• VT, SVT, AF, Af
– BRADYARRHYTHMIAS
• Sev. S.Brady, Sinus Arrest, High grade AV Block
 CARDIAC EMERGENCIES
CLASSIFICATION
• NON-ARRHYTHMIC
– CARDIOGENIC SHOCK
– PULMONARY EDEMA (CARDIOGENIC)
– ACUTE M.I.
– UNSTABLE ANGINA
– HYPERTENSIVE CRISIS
– CARDIAC TAMPONADE
– PULMONARY EMBOLISM
– HYPOXIC/CYANOTIC SPELLS
– AORTIC DISSECTION
 CARDIAC ARREST
• Abrupt Cessation of cardiac pump function
– Maybe reversible
– Death in the absence of prompt intervention
• Vf: 75%
• Asystole: 25%
• Pulseless Electrical Activity
– Fast VT, Severe Bradyarrhythmia
CPR
 No movement or response
ADULT BLS
HEALTH CARE
Phone 911 or emergency number get AED PROVIDER
OR send second rescuer (if available) to do this ALGORITHM

Open AIRWAY, check BREATHING AHA 2005

if not breathing, give 2 BREATHS
that make chest rise Give 1 breath every 5-6 seconds
Recheck pulse every 2 minutes
DEFINITE PULSE
If no response check pulse:
Do you DEFINITELY feel pulse within 10 seconds
N
O Give 1 shock
Give cycles of 30 COMPRESSIONS and 2 BREATHS,
until AED/Defibrillator arrives ALS provider take over or Resume CPR immediately
victim starts to move
Push hard and fast (100/min) and release completely for 5 cycles
Minimize interruption in compression.

AED/defibrillator ARRIVES Resume CPR immediately for 5 cycles

Check rhythm every 5 cycles:
cotinue untill ALS providers take over
4/9/2019 9:36 AMrhythm
Check NOT SHOCKABLE or victim starts to move 8
Shockable rhythm?
4/9/2019 9
 AF TREATMENT
• CARDIOVERSION
• ANTIARRHYTHMICS
• DIGOXIN
• ANTICOAGULANT
Second degree type 2 block
3 rd degree block
 INTERVENTIONS
• The major interventions in complete heart
block are:
• Atropine, Transcutaneous pacing,
Catecholamine Infusions (dopamine or
epinephrine), and Transvenous pacemaker.
• If Asystole develops, CPR is used until a
pacemaker can be inserted. Isoproterenol is
rarely indicated.
 Treatment
• Pacemaker therapy
MI
 EMERGENCY
MANAGEMENT
• MONA
• THROMBOLYTICS: STK, t-PA
• ANTICOAGULANTS: Heparin
• Anti-platelets
• PCI/PTCA
• MONITORING
• Beta blockers, ACE inhibitors
• Statins
 CARDIOGENIC SHOCK
• Shock is the clinical syndrome that results from
inadequate tissue perfusion.

HYPOPERFUSION

IMBALANCE INFLAMM.
DEL. & REQ. MEDIATORS

CELL. INJURY
CARDIOGENIC SHOCK (contd.)
I. INTRINSIC (FAILURE OF HEART PUMP)
– ACUTE M.I. (> 40%)
– ARRHYTHMIAS
– VALV. HEART DIS. e.g. MS, MR, AS, AR.
– TERM. PHASE OF CHR. FAILURE e.g. DCM, IHD
– RIGHT HEART FAILURE e.g. RV-MI, ARDS, PAH
II. EXTRINSIC/COMPRESSIVE
– CARDIAC TAMPONADE
– INTRATHORACIC PRESSURE
• Tension pneumo, Herniation of abd. viscera,
– ACUTE RIGHT HEART FAILURE (Pulm. Emb.)
CARDIOGENIC SHOCK (contd.)
• PATHOPHYSIOLOGY
– low cardiac output, diminished peripheral
perfusion and elevation of systemic
vascular resistance (FORWARD FAILURE)
– pulmonary congestion, elevation of
pulmonary vascular pressures
(BACKWARD FAILURE)
– systemic venous congestion
(BACKWARD FAILURE)
CARDIOGENIC SHOCK (contd.)
• DIAGNOSIS
– HYPOTENSION (MAP < 60mmHg.) &
ASSOC. ORGAN DAMAGE
– TACHYCARDIA, PALLOR
– TACHYPNEA, ORTHOPNEA,
PULM. RALES
– JVP
• INVESTIGATIONS
ECG, CXR, ENZ., ECHO, PA & PCW Pr.
CARDIOGENIC SHOCK (contd.)
• TREATMENT
1. SUPPORTIVE
• CORRECT HYPOTENSION/HYPOXIA
– O2, INTUBATION, VENTILATION
DOPAMINE (2-5, 5-10, 10-20, 20-50 μg/Kg/min)
NORADRENALINE (2-4μg/min)
• SUPPORT CARDIAC PUMP
– INOTROPES, INODILATORS (DOBUT. 2.5-25 μg/Kg/min)
IABP, CARDIAC ASSIST DEVICES
• RELIEVE VENOUS CONGESTION
– I.V. FUROSEMIDE (40-240mg)
• MONIT. INTRA-ART. Pr., MAINTAIN PCWP 15-20 mmHg
2. SPECIFIC
• PTCA, CABG
• SURGICAL REPAIR – RUPTURE OF PAP. MUSCLE, IVS
• PERICARDIOCENTESIS, CHEST DECOMPRESSION
 PULMONARY EDEMA
• OUTPOURING OF FLUID FROM PULM. CAP.
INTO ALVEOLI
• CARDIOGENIC PULMONARY EDEMA
( PULM. CAP. Pr.)
– LEFT VENTRICULAR FAILURE: ACUTE M.I.
– WITHOUT LVF: M.S.
– SECONDARY TO PA Pr. : POST-MI VSD
(OVERPERFUSION PULM. EDEMA)
PULMONARY EDEMA (contd.)
• PATHOPYHSIOLOGY
– ENGORGEMENT OF PULM. VAS.
– INTERSTITIAL EDEMA - > 18 mmHg
– ALVEOLAR EDEMA - >24 mmHg
– FULL-BLOWN PULM. EDEMA
– UNTREATED – HYPERCAPNEA,
ACIDOSIS, RESP. ARREST
PULMONARY EDEMA (contd.)
• DIAGNOSIS
– ANXIOUS, PERSPIRING
– TACHYPNEA, ORTHOPNEA, PINK FROTHY
SPUTUM
– BILATERAL CREPS, RHONCHI
– CXR: PROM. OF UPPER LOBE VEINS,
DIFFUSE HAZINESS.
– ECG, ECHO
PULMONARY EDEMA (contd.)
• TREATMENT
1. NON-SPECIFIC
• 100% O2 PREFERABLY UNDER POSITIVE PRESSURE
• PROPPED UP POSITION, LEGS DANGLING ?
• I.V. MORPHINE 2-5 mg DOSES
• I.V. FUROSEMIDE, OTHER LOOP DIURETICS
• AFTERLOAD: SOD. NITRO. (20-30 μg/min), NTG.
• INOTROPES: DOPAMINE, DOBUTAMINE
DIGOXIN ( 0.75 – 1 mg IV over 15’)
• AMINOPHYLLINE (240-480 mg I.V.)
PULMONARY EDEMA (contd.)
• TREATMENT
2. SPECIFIC
• PTCA/CABG, BMV, AVR
• EMERGENT/ELECTIVE
3. CARDIAC vs. BRONCHIAL ASTHMA
• Aminophylline
 Hypertensive Emergency
• Accelerated HT
– Diastolic usually > 140mmHg
– End organ effects
• Malignant HT
– Above plus Papilledema
• Hypertensive Emergency/Crisis
 CARDIAC TAMPONADE
• Abnormal accumulation of fluid in the
pericardium causing serious obstruction
to the inflow of blood into the ventricles
• Potentially fatal, eminently treatable
• Normally 15-50 ml of fluid
• Qty. causing tamponade: 200 – 2000ml
CARDIAC TAMPONADE (contd.)

• ETIOLOGY
– NEOPLASTIC
– UREMIC
– TUBERCULAR
– IDIOPATHIC/VIRAL
– TRAUMATIC
CARDIAC TAMPONADE (contd.)

• PATHOPHYSIOLOGY
– RAISED INTRACARDIAC PRESSURES
– IMPAIRED VENTRICULAR FILLING
– REDUCED C.O., HYPOTENSION
– PERICARDIAL Pr. = RA Pr.
– DIASTOLIC EQUALIZATION OF
INTRACARDIAC PRESSURES
CARDIAC TAMPONADE (contd.)

• DIAGNOSIS
– HIGH INDEX OF SUSPICION
– TRIAD: HYPOTENSION, RAISED JVP,
FAINT HEART SOUNDS
– SLOW TAMPONADE: DYSPNEA,
ORTHOPNEA, HEPATOMEGALY
– ECHO
CARDIAC TAMPONADE (contd.)

• TREATMENT
– PERICARDIOCENTESIS
• SUBXIPHOID, CATHETER PLACED
• FLUORO/ECHO GUIDANCE

– SURGICAL DRAINAGE
 Hypoxic/Cyanotic Spells
• Age: 2mths to 2yrs
• TOF
• Sudden increase in cyanosis
• Hyperpnea, increased irritability
• Unconsciousness, Seizures, Death
• Onset following physical activity
– Waking up
– Crying
– Feeding
Hypoxic/Cyanotic Spells

Physical Activity
(crying, tachypnea)

Increased Cyanosis Reduced SVR

Increased flow into Aorta

Reduced Pulomary Flow
 Hypoxic/Cyanotic Spells
TREATMENT
• Knee-Chest Position (Squatting)
• Humidified O2
• Morphine I.V./S.C. 0.1-0.2mg/Kg
• Propranolol I.V. 0.1mg/Kg
• Vasopressors
• Correct Acidosis – Sodabicarb 1ml/Kg
• Treat Complications
 PULMONARY EMBOLISM
• PULMONARY THROMBOEMBOLISM
(fat, air, tumor, amniotic fluid)
• THROMBUS – USUALLY LEG/PELVIC Vv.
• HALF OF ABOVE HAVE PTE - USUALLY
ASYMPTOMATIC
• USUALLY NOT A CARDIAC EMERGENCY
• USUAL CAUSE OF DEATH – PROG. RHF
PULMONARY EMBOLISM (contd.)

• PATHOPHYSIOLOGY - Complex
– pulm. vasc. resist. – obstr./serotonin
– Impaired gas exchange – V-P mismatch
– Alveolar hyperventilation – reflex
– airway resistance – bronchoconstrictn.
– pulmonary compliance – edema,
surfactant
PULMONARY EMBOLISM (contd.)

• PATHOPHYSIOLOGY – EFFECTS ON HEART

– EXTENT OF INVOLV. OF PULM. VASC. BED
25-30%: PA Pr.
> 50% : PA mean Pr.
75% : R.V. Dilatation & Failure
– PRE-EXISTING HEART DISEASE
– R.V. DILATATION: IVS bulge, RCA compression
– L.V. underfilling, CORONARY hypoperfusion
– HYPOTENSION, SHOCK
PULMONARY EMBOLISM (contd.)
• DIAGNOSIS – often difficult
– CLINICAL SETTING
• SURGERY, IMMOBILIZATION, PREGNANCY,
CENTRAL CATHETER, CANCER
– MASSIVE PTE: DYSPNEA, TACHYPNEA,
SYNCOPE, HYPOTENSION, CYANOSIS
– SMALL PTE: PLEURITIC PAIN, COUGH,
HEMPOTYSIS
– FEVER, TACHYCARDIA, LOUD P2, RAISED JVP
PULMONARY EMBOLISM (contd.)

• INVESTIGATIONS
– ECG: Sinus tachy., new Af/AF,
inverted T in V1-V4
– CXR: normal/near normal

D-dimer assay: latex agglutinatn./ELISA

ELISA: > 500ng/ml in > 90% patients
PULMONARY EMBOLISM (contd.)
• INVESTIGATIONS
– RADIONUCLIDE LUNG SCAN
• Albumin for perfusion, Xe/Kr for ventilation
• PTE very unlikely in patients with normal and near-normal
scans
• 2 or more segmental perfusion defects with normal ventilation
• PTE about 90% certain in patients with high-probability scans.
• < 50% of patients with angiographically confirmed PTE have a
high-probability scan.
• 40% of patients with high clinical suspicion for PTE and "low-
probability" scans have PTE at angiography.
– CONTRAST CT-CHEST
• Sensitivity: 60% for Pulmonary artery thrombi
PULMONARY EMBOLISM (contd.)
• INVESTIGATIONS
– PULMONARY ANGIOGRAPHY: GOLD STANDARD
• most specific, detects even 1-2 mm emboli
• Intraluminal filling defect, segmental oligemia/avascularity
• Prolonged arterial phase with slow filling
• Tortuous tapering peripheral vessels
– ECHO: R.V. dilatation and dysfunction,
Rarely PA thrombus, R/o other causes
– VENOUS ULTRASOUND for DVT
• Normal in 1/3 with PTE
PULMONARY EMBOLISM (contd.)
INTEGRATED DIAGNOSTIC APPROACH
PULMONARY EMBOLISM (contd.)
• THERAPY
– PRIMARY: CLOT DISSOLUTION
• THROMBOLYSIS (r-tPA 100mg over 2h)
• EMBOLECTOMY

– SECONDARY: PREVENTING RECURRENCE

• ANTICOAGULATION
– HEPARIN 5000-10, 000 bolus,1000-1500/h, WARF. (INR 2.5-3)
• IVC FILTER (Bird’s Nest/ Greenfield)
Thank You
STEMI-ECG