ST ELEVATION on ECG

Posted by e-Medical PPT Thursday, June 26, 2014 0 comments


Recognize ST segment elevation in conditions other than acute MI

Significance
Unwarranted thrombolytic therapy
Unnecessary emergency angiography
Unnecessary anxiety (for intern)

Normal ST elevation
1 - 3mm elevation in one or more precordial leads in relation to the end of the PR segment (male pattern)
ST segment is concave

Early Repolarization
Most commonly the ST-segment elevation is most marked in V4 with a notch at the J point, and the ST segment is concave
T waves are tall and are not inverted

T-wave Inversion
This normal variant differs from the early-repolarization pattern in that the T waves are inverted and the ST segment tends to be coved
Combination of an early-repolarization pattern and a persistent juvenile T-wave pattern. Often, the findings are so suggestive of acute myocardial infarction that an echocardiogram is necessary to differentiate them, especially if one is not aware of this normal variant. In most cases of this normal variant, the QT interval is short, whereas it is not short in acute infarction or pericarditis.

LV Hypertrophy
Deep S wave
QS pattern in leads V1 through V3
Elevated ST segment is concave in a pt with uncomplicated LV hypertrophy as compared with convex in a pt with acute concomitant MI

Left Bundle Branch Block
Making the dx of acute infarction in the presence of LBBB can be problematic, since the ST segment is either elevated or depressed secondarily, simulating or masking an infarction pattern
Sgarbossa’s criteria is controversial and has not been validated

ABG analysis & Acid-Base Disorders

Posted by e-Medical PPT Tuesday, June 24, 2014 0 comments

Discuss simple steps in analyzing ABGs
Calculate the anion gap
Calculate the delta gap
Differentials for specific acid-base disorders

Steps for ABG analysis
What is the pH? Acidemia or Alkalemia?
What is the primary disorder present?
Is there appropriate compensation?
Is the compensation acute or chronic?
Is there an anion gap?
If there is a AG check the delta gap?
What is the differential for the clinical processes?

Respiratory Acidosis
Acute: for every 10 increase in pCO2  -> HCO3 increases by 1  and  there is a decrease of 0.08 in pH MEMORIZE
Chronic: for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decrease of 0.03 in pH
Respiratory Alkalosis
Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2 and there is a increase of 0.08 in PH MEMORIZE
Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5 and there is a increase of 0.03 in PH

Metabolic Acidosis
Winter’s formula: pCO2 = 1.5[HCO3] + 8 ± 2 MEMORIZE
If serum pCO2 > expected pCO2 -> additional respiratory acidosis
Metabolic Alkalosis
For every 10 increase in HCO3 -> pCO2 increases by 6

5 Functions of the Respiratory System
Provides extensive gas exchange surface area between air and circulating blood
Moves air to and from exchange surfaces of lungs
Protects respiratory surfaces from outside environment
Produces sounds
Participates in olfactory sense

Regulation of breathing
Medullary rhythmicity center
  Nerves extend to intercostals and diaphragm
  Signals are sent automatically
  Expiratory center is activated during forced breathing
Pneumotaxic area
  Controls degree of lung inflation; inhibits inspiration
Apneustic area
  Promotes inspiration

Chemoreceptors
Breathing can be controlled voluntarily, up to a point
Too much CO2 and H+ will stimulate inspiratory area, phrenic and intercostal nerves
Central chemoreceptors: medulla oblongata monitors CSF

Peripheral chemoreceptors
Aortic bodies (vagus nerve)
Carotid bodies (glossopharyngeal nerve)
Respond to fluctuations in blood O₂, CO2 and H⁺ levels
Rapid respond
Pulmonary stretch receptors prevent over inflation of lungs (promote expiration

4 Pulmonary Volumes
Resting tidal volume:
 in a normal respiratory cycle
Expiratory reserve volume (ERV):
 after a normal exhalation
Residual volume:
 after maximal exhalation
 minimal volume (in a collapsed lung)
Inspiratory reserve volume (IRV):
 after a normal inspiration..

POSTOPERATIVE CARDIAC ARREST IN CARDIAC SURGERY PATIENTS

Posted by e-Medical PPT Wednesday, January 8, 2014 0 comments

Cardiac arrest following major cardiac surgery: 0.7-2.9%
Usually preceded by physiological deterioration,
    although it can occur suddenly in stable patients
Specific causes of cardiac arrest (all potentially reversible):
    tamponade, hypovolemia, myocardial ischaemia, pacing failure,
    or tension pneumothorax

Cardiac arrest after cardiac surgery:

If treated promptly survival rate is relatively high.
Rate of survival to hospital discharge is 54% to 79% in adults and 41% in children.
Key to the successful resuscitation of cardiac arrest in these patients is to perform emergency resternotomy early, especially in the context of tamponade or haemorrhage, where external chest compressions may be ineffective.

Cardiac arrest is defined as the absence of any spontaneous circulation:
    MAP < 30 mmHg
    non-pulsatile waveform

Near cardiac arrest is defined as:
    MAP 30 - 50 mmHg
    pulsatile waveform

Most common causes of cardiac arrest after cardiac surgery:
Ventricular fibrillation
Cardiac tamponade

Initial resuscitation algorithm:

Confirm that hypotension or cardiac arrest is real
Ensure airway / ventilate with manual resuscitator
Avoid prolonged attempts at intubation
Exclude tension pneumothorax
Briefly disconnect pacer to R/O VF
Discontinue hypotensive agents and sedatives
Ensure vasoactive drugs are being delivered
Consider early chest reopening in all patients

MANAGEMENT OF POSTOPERATIVE ATRIAL ARRHYTHMIAS

Posted by e-Medical PPT Wednesday, January 1, 2014 0 comments

POSTOPERATIVE  ARRHYTHMIAS
Proarrhythmic factors:
Autonomic nervous system
Hypokalemia
Hypomagnesemia
Myocardial ischemia
Myocardial Infarction
Proarrhythmic drugs

Narrow-complex tachycardias:
Sinus tachycardia
Atrial fibrillation
Atrial flutter
Accelerated junctional rhythm
Paroxysmal supraventricular tachycardia
Ectopic atrial tachycardia

SINUS  TACHYCARDIA
Causes:
Pain, anxiety
Surgical stress
Low cardiac output
Hypovolemia
Myocardial ischemia
Catecholamine administration

Treatment:
Treatment directed at the underlying cause
Must be distinguished from other narrow-complex tachycardias
Atrial electrogram (AEG) when diagnosis is uncertain
    Connect the left & right arm ECG cables to the atrial pacing wires
    Alternatively, connect the V lead to one atrial pacing wire

Atrial Electrogram (AEG):
AEG are useful for differentiating supraventricular arrhythmias.
Atrial fibrillation with RVR > 150 bpm, the rhythm may be misdiagnosed as paroxysmal SVT.
Atrial flutter: atrial activity may not be obvious on the surface ECG.
In patients with preexisting bundle-branch block, the development of a postoperative SVT may be difficult to distinguish from VT.
An accurate diagnosis can be readily made if an atrial electrogram (AEG) is recorded.

VOLUME THERAPY IN Cardiac Surgery PATIENTS

Posted by e-Medical PPT Tuesday, December 31, 2013 0 comments

The goal of fluid management and inotropic and vasoactive drug therapy in post-operative cardiac surgery patients is to achieve sufficient tissue perfusion and a normalization of oxidative metabolism.

Cardiac output and oxygen supply are dependent on adequate intravascular volume and cardiac function.

The following parameters are recommended as goals for postoperative cardiovascular therapies.

Fluid management:
In cardiac surgery patients it is common to have relative or absolute volume deficiency in the early post operative phase.
First line treatment in cardiac surgery intensive care medicine consists in the use of artificial colloid solutions.
Medium molecular weight HES derivatives (Voluven) are preferred.
Crystalloid solutions are the second choice of volume substitution.
Plasma volume substitution with human albumin is no longer used in 50% of cardiac surgery intensive care units.

High molecular weight HES (Hespan):
High molecular weight HES (>200 kDa) 10% preparations (Hespan) is associated with increased postoperative bleeding.
High molecular weight HES, hyperoncotic colloids and 10% and 20% albumin, are associated with increased risk of hyperoncotic renal failure.
Hespan is contraindicated in patients with severe increases of Na & Cl.

Medium molecular weight HES (Voluven):

Medium molecular weight HES (130 kDa) 6% (Voluven) is not associated with increased postoperative bleeding.
Medium molecular weight HES (130 kDa) 6% (Voluven) is not associated with increased risk of hyperoncotic renal failure.
There is no scientific evidence to support the use of the more expensive albumin over medium molecular weight (130 kDa) 6% HES preparations.

Postoperative hypotension:
Hypovolemia (blood loss anemia, polyuria, 3rd spacing)
Low SVR / vasoplegia
LV systolic dysfunction
LV diastolic dysfunction
RV dysfunction
Pericardial compression
Rhythm disturbance
Withdrawal of vasoactive medications

Stepwise approach to diagnosis:

Confirm the presence of hemodynamic instability
Ensure vasoactive drugs are being delivered
Targeted physical exam
Fluid challenge, inotropic support, cardiac pacing
Obtain ABG, CXR, EKG
TEE if cause of hypotension remains unclear

VASOPLEGIC  SYNDROME
Risk factors:

Prior treatment with ACE-inhibitors
Prolonged CPBP
Low ejection fraction
Early on-cardiopulmonary bypass hypotension
Septic endocarditis
Transfusion of RBC, FFP, platelets

Indicators of cardiocirculatory failure:
Cardiac index < 2.0 L/min/m2
SvO2 < 60%
Mean arterial pressure < 60 mmHg
Urine output < 0.5 ml/h, existing for longer than an hour
Plasma lactate > 2.0 mmol/L
Peripheral vasoconstriction with delayed capillary refill and cool extremities

When LAP/PAD/CVP decrease :

Evaluate response to an increase in preload.
Autotransfusion by means of passive leg raising.
Administration of colloid or crystalloid solution
    (maximum of 10 ml/kg body weight).

If a preload increase does not lead to hemodynamic
    stabilization, an echocardiogram is indicated.

In unstable patients, a 12-lead ECG to rule out acute
    ischemia, and lactate level should be obtained.

Goal directed therapy:
Increase preload
Optimize heart rate & rhythm (avoid tachycardia & arrhythmias)
Vasodilating agents (NTG, nicardipine, nesiritide)
Inotropic agents (milrinone or dobutamine)
Mixed vasoactive agents (epinephrine, norepinephrine)
Drug combinations (inotropic + vasopressor agents)

Treatment of LV diastolic dysfunction:

Optimize preload (LAP 14-18 mmHg)
Avoid tachycardia
Optimize heart rate (80/min) & increase AV delay (180 ms)
Aggressive treatment of atrial fib & tachyarrhythmias
Milrinone (0.5 mcg/kg/min) ± Vasopressin (0.04 units/min)
    or phenylephrine (1-2 mcg/kg/min)  [avoid tachycardia]
Levosimendan (if MAP > 60 mmHg)
IABP

Guidelines for INTENSIVE CARE IN Cardiac Surgery PATIENTS

Posted by e-Medical PPT Wednesday, December 25, 2013 0 comments

Basic principles of the postoperative intensive care of patients after cardiothoracic surgery:
Hemodynamic monitoring
Volume-therapy
Treatment with inotropic drugs and vasopressors

Goals for cardio-circulatory therapy
The goal of fluid management and inotropic and vasoactive drug therapy in post-operative cardiac surgery patients
is to achieve sufficient tissue perfusion and a normalization of oxidative metabolism.

Cardiac output and oxygen supply are dependent on adequate intravascular volume and cardiac function.

The following parameters are recommended as goals for postoperative cardiovascular therapies.

Blood Pressure targets during the first 48 hours:

Normal (MAP >65 mm Hg)     Default BP goal
High (MAP >75 mm Hg)         Age >75
                Poorly controlled HTN
                Pre- or postop- renal impairment
                Uncorrected carotid artery stenosis
                Pre- or postop- ischemic stroke
Low (MAP 55-60 mm Hg)         Age <50 (with low preop- BP)
                High bleeding risk
                Surgery for chronic valve regurgitation

INITIAL ASSESSMENT on ADMISSION TO ICU
Cardiovascular system, ECG, arrhythmias
Verify vasoactive & inotropic drugs, pacemaker, IABP
Respiratory system, ventilator settings, ABG, CXR
Chest drains, bleeding, coagulation tests
Renal system, fluid & electrolytes
Pupil size & reactivity, level of sedation
Core temperature, warming device

ADVANCED HEMODYNAMIC MONITORING
Pulmonary artery catheter: is justified in high risk patients for complex cardiac surgery interventions,
in low cardiac output syndrome,pulmonary hypertension,and for the differentiation between right or left ventricular dysfunction.

The use of a PAC in cardiac surgery patients with a low perioperative risk is not considered necessary.

HEART FAILURE IN NEONATE AND INFANT

Posted by e-Medical PPT Sunday, December 15, 2013 0 comments

Congestive heart failure (CHF) refers to a clinical state of systemic and pulmonary congestion resulting from inability of the heart to pump as much blood as required for the adequate metabolism of the body.

Clinical picture of CHF results from a combination of “relatively low output” and compensatory responses to increase it

CLINICAL MANIFESTATIONS IN INFANTS WITH HEART FAILURE
  Feeding difficulties
  Rapid respirations
  Tachycardia
  Cardiac enlargement
  Gallop rhythm (S3)
  Hepatomegaly
  Pulmonary rales
  Peripheral edema
  Easy fatigability
  Sweating
  Irritability
  failure to thrive

CLASSIFICATION
NYHA Heart Failure Classification is not applicable
Ross Heart Failure  Classification was developed for global assessment of heart failure severity in infants
Modified to apply to all pediatric ages
Modified Ross Classification incorporates
    Feeding difficulties
    Growth problems
    Symptoms of exercise intolerance

MODIFIED ROSS HEART FAILURE CLASSIFICATION FOR CHILDREN
Class I
Asymptomatic
Class II
Mild tachypnea or diaphoresis with feeding in infants
Dyspnea on exertion in older children
Class III
Marked tachypnea or diaphoresis with feeding in infants
Marked dyspnea on exertion
Prolonged feeding times with growth failure
Class IV
 Symptoms such as tachypnea, retractions, grunting, or diaphoresis at rest

Tetralogy of fallot

Posted by e-Medical PPT Saturday, December 14, 2013 0 comments

Tetralogy of fallot
First anatomic description…Danish anatomist Niels Stensen, in 1672...
Described in detail by fallot in 1888…’la maladie bleue’

Tetralogy of fallot with pulmonary atresia…10%
Rarer variants include tetralogy of fallot with absent (or dysplastic) pulmonary valve and tetralogy of fallot with common atrioventricular canal[<5%]
Prevalence … 0.26 to 0.48 per 1,000 live births

In about 70% of tetralogy of Fallot patients, a putative genetic etiology remains to be determined.

Genes identified : NKX2.5, [4%];  JAG1 in Alagille syndrome.; TBX5 in Holt-Oram syndrome.

Sibling recurrence rate …2.5% to 3% if only one sibling is affected…likely to increase substantially if more than one sibling is affected.
Environmental factors
maternal diabetes [threefold increased risk], retinoic acids, maternal phenylketonuria (PKU), and trimethadione

Genetic cause : heterogeneous
Syndromes and associations…..
DiGeorge/Velocardiofacial syndrome, Down syndrome, Alagille syndrome, cat's-eye syndrome, recombinant chromosome (or San Luis Valley) and Kabuki syndromes, and CHARGE and VATER/VACTERL associations

Pathophysiology and Hemodynamics
Severe cyanosis in profound RL shunting,
Some pts have a net LRshunt.

Hemodynamic features…RV hypertension because of the large VSD, with normal or low PAP.The low distal PAP is maintained as a result of the various levels of pulmonic obstruction. The PVR in the distal pulmonary arterial bed is usually normal.

The extent and direction of shunting ….determined by the cumulative amount of obstruction to PBF(Subpulmonic obstruction in all; obstruction @ valvular, supravalvular, and branch arteries are also common).

HYPERCYANOTIC SPELLS OR TETRALOGY SPELLS :
best described in TOF;can occur with other forms of structural heart disease…. mediated, in part, by dynamic changes (acute increase)in subpulmonic obstruction….. changes in contractility  due to ‘endogenous catecholamines or exacerbated by hypovolemia’
other mechanisms[pulmonary atresia and VSD] …. decrease in systemic vascular resistance.
Child may assume squatting posture (instinctive) during spells …
Pathogenetic mechanisms : Vulnerable respiratory control centres ;Increase in HR ; Increase in CO & VR ;Increase in R L shunt; Infundibular contraction may reinforce,but does not initiate

Systolic Murmurs

Posted by e-Medical PPT Thursday, December 12, 2013 0 comments

Systolic Murmurs

Definition of murmur
Relatively prolonged series of audible vibrations , Characterized by the timing in  cardiac cycle, intensity (loudness), frequency (pitch), quality, configuration, duration and direction of radiation
Due to disturbance in blood flow which manifest as turbulence

FREEMAN & LEVINE GRADING
GRADE 1-faintest murmur which can be heard only with special effort.
GRADE 2-soft but readily audible
GRADE 3-loud without thrill
GRADE 4-loud with thrill
GRADE 5-heard with steth partially off the chest
GRADE 6-heard with steth held off the chest wall.

Ejection systolic murmur
Most common murmur heard in everyday practice.
“Murmur starting after some time interval from first heart sound and reaching peak by mid-systole or later and ending before the second heart sound of its origin”.
It could be  PATHOLOGICAL or INNOCENT/PHYSIOLOGICAL
    Ventricular outflow obstruction
    Dilation of aorta and pulmonary trunk
    Accelerated systolic flow into aorta or pulmonary trunk
    Innocent midsystolic murmur( including those due to morphological changes of valve with no obstruction)

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