1-cv 4cin.pdf

Cardiovascular Pathophysiology (4/4) Ricardo L. Garcia MD TODAY’S LECTURE } Congestive Herat Failure (CHF) } Cardiomyopathies Heart Functions Integrated Cardiac output (CO) = heart rate (HR) x stroke vol.(SV) Vas - changes of the heart rate - changes of stroke volume • Control of HR: - a...

Cardiovascular Pathophysiology (4/4) Ricardo L. Garcia MD TODAY’S LECTURE } Congestive Herat Failure (CHF) } Cardiomyopathies Heart Functions Integrated Cardiac output (CO) = heart rate (HR) x stroke vol.(SV) Vas - changes of the heart rate - changes of stroke volume • Control of HR: - autonomic nervous system - hormonal(humoral) control • Control of SV: - preload - contractility - afterload ↑ major anesthetic Asyanotic pt ? Asmanotic condition consideration for diagnosed neonate w R-tow · Record persistant a . Avid : 17 Shuut in vascular systemic resistance (SvR) You want H SUR · 2 ? aflutter ↓PUR management > cardio version sychronized observe you v-uave cannon pt cath on your PA This may that mean pt has ? Tricuspid Regurgitation or Defib 340j Congestive Heart Failure Definition } It is the pathophysiological process in which the heart examenas a pump is unable to meet the metabolic - requirements of the tissue for oxygen and substrates despite the venous return to heart is either normal or increased. } >particular Considered a syndrome. characteristics Etiology } Essential feature: inability to fill or empty the ventricles. } May be caused by: } Impaired myocardial contractility } Cardiac Valve Abnormalities } Systemic Hypertension } Diseases of the pericardium } Pulmonary Hypertension Heart Failure } } Several Forms or Characteristics: } Systolic vs Diastolic } Acute vs Chronic } Left vs Right All Forms have some degree of increased end diastolic pressure because altered ventricular function and neurohormonal regulation. Heart Failure } Classification based on activity } Classes I – IV } Prevalence similar among men and women } Acuity defined by change of signs and symptoms requiring emergency management } } } } Worsening Chronic failure New onset failure (MI, valvular rupture) Terminal disease Chronic is present in patients with long standing disease Heart Failure } Cardiac Index } } Normal: 2.2 – 4 L/min/m2 Most common causes of CHF } Low Cardiac Output: } } } } } Coronary artery disease #1 Cardiomyopathy Hypertension Valvular or pericardial disease High Cardiac Output } } } Anemia # 1 I Pregnancy Hyperthyroidism -> co -> to feed baby Hormonal response , sepsis i demand Pathophysiology - } Complex deterioration of clinical and cellular derangements } Mechanisms Involved: } } } } } Pressure overload Volume Overload Ischemia Inflammatory disease Restrictive diastolic filling - myocardium is sick Pathophysiology - } / Adaptive Response to maintain function } Increase in Stroke Volume } } Frank Starling relationship starling Buscar Activation sympathetic nervous system } } Arteriolar and venous constriction Activation Renin-Angiotensin-Aldosterone system (RAAS) 18 Nat is reabsorbed M volume } Alteration in the inotropic state, heart rate and afterload } Humoral mediated response } } } RASS Increased levels vasopressin Inflamatory mediators Pathophysiology } All this mechanisms become maladaptive leading to: } MYOCARDIAL REMODELING } Myocardial hypertrophy represents the compensatory mechanism for chronic pressure overload. The effects of this mechanism are limited because hypertrophied cardiac muscle functions at a lower inotropic state than normal cardiac muscle. } Cardiac dilation occurs in response to volume overload and increases cardiac output by the Frank-Starling relationship. } it +Oz - lead to IHD The increased cardiac wall tension produced by an enlarged ventricular radius is associated with increased myocardial oxygen requirements and decreased pumping efficiency. ¨ } consumption Ischemic injury is the most common cause of myocardial remodeling and encompasses both hypertrophy and dilation of the left ventricle. Angiotensin-converting enzyme (ACE) inhibitors and aldosterone inhibitors (spironolactone and eplerenone) have been proven to promote a "reverse-remodeling" process. Pathophysiology: Overview Heart Failure: Signs and Symptoms } Dyspnea } } An early subjective finding Orthopnea A } in position A Paroxysmal orthopnea in pulsed pressure } Fatigue and weakness at minimal exertion or even at rest } Anorexia } Nausea } Abdominal pain - Peds- mesentenc } gastritis dysfunction If low cardiac output: confusion - cardiomyopathy Heart Failure: Signs and Symptoms } Physical Findings (common) } } } } } Tachypnea Rales Tachycardia Heart gallop Hypotension } } Narrow pulse pressure with high diastolic pressure - } } } } Cold extrmities Reflects low stroke volume Weight loss Edema (peripheral, lower extremity) Venous jugular distention w . poor EF Heart Failure: Diagnostic Evaluation } Laboratory } } } Renal function panel Serum BNP levels Chest Radiograph } } Evidence of cardiomegaly Pulmonary markings } ECG } Echocardiogram } Essential for diagnosis Heart Failure: Classification 97 transplant pt Heart Failure: Classification } Functional Classification: ACC and AHA 2005 most usual Heart Failure: management manage the symptoms } Aimed to reverse pathophysiologic alterations } Interrupt the ventricular remodeling process } Identify Systolic vs Diastolic Heart Failure } Medical Therapy } } Multimodal Inhibitors RAAS: ACE inhibitors, ARB ↳ stop day before Beta blockers what ↳ dont stop ot rebound pathophy. of Diuretics: aldosterone antagonists hypotension ? exam Digoxin Vasodilators Statins - } } } } is Heart Failure: management } Surgical Therapy } Cardiac Resynchronization therapy (CRT) } Biventricular pacing } Implantable cardioverter-defibrillators (ICD) } Ventricular Assist Devices } Heart Transplantation Heart Failure: Management } Summary Chronic Management 1 cause end organt damage to the kidneys Heart Failure: Management Heart Failure: ACUTE } Often encountered in the perioperative and/or operating room } Acute therapy focus in: } Emergency phase } Most important to us } In hospital management phase } Pre-discharge phase Heart Failure: ACUTE } source Emergency phase } } } ex } it When - Exogenous B-type natriuretic peptide Nesiritide Nitric Oxide Synthase Inhibitors in compartment reve bett at rece att pt NeCNSIS Careful with tachycardia: Increases myocardial oxygen consumption Levosimendan Is the that abd Calcium Sensitizers } : : Phosphodiesterase inhibitors Renal metabolism avoid ↳ Milrinone Catecholamine's (dopamine, dobutrex, epinephrine) ¨ } OR sepsis Loop diuretics -> } go to Inotropic Support } } only way Diuretics and Vasodilators } control Heart Failure: ACUTE } Emergency phase } Nitric Oxide Synthase Inhibitors } Under investigation } Mechanical Devices Heart Failure: Prognosis } Despite advances in therapy, the number of heart failure deaths continues to increase steadily in the United States. } Mortality during the first 4 years after the diagnosis of heart failure approaches 40%. } Factors associated to poor prognosis: } } } } } } } Increased UN and Creatinine Kidney falure AK1 dualisis body cart manage Conduction of iPatacta Hyponatremia and hypokalemia EF lower than 25% HIGH serum BNP very limited exercise tolerance presence of multifocal premature ventricular contractions. , . ↳ x 3 xn , at acute prob1em vach tachyarrhytmia In heart failure patients the prognosis depends on the underlying heart disease and on the presence or absence of a specific precipitating factor. If a correctable cause of heart failure can be effectively eliminated, prognosis improves. Heart Failure: anesthesia management } Perioperative Evaluation } Heart failure is one of the most highly associated risk factor for increased morbidity and mortality. } } Determine other Risk factors Medications } } Diuretics may be discontinued 24 hrs before surgery Keep beta blockers ACE inhibitors may be discontinued 24 hrs before surgery ARB have to be discontinued 24 hrs before surgery Digoxin should be continued ⑧ } } } } & Review recent ECG, ECHO result, Renal function panel Heart Failure: anesthesia management } Intraoperative Management } is UBP contractility Either volatile or intravenous anesthetics can be used ↳ etomidate unless sepsis Thort with caution ↓ : } } } } · adrenal Inhibe cortisol catecholamine Positive pressure ventilation will usually be beneficial Monitoring: standard endogenous } } Avoid hypotension insus Consider more invasive monitoring depending on the surgery Regional anesthesia may be used but remember patient most have and adequate preload Heart transplant: preload dependent, unresponsive to give atropine hypotension riquid : . Heart Failure: anesthesia management } Postoperative Management } Those patients with evidence of heart failure should be transferred to ICU afterwards } Pain control should be aggressively treated: avoid increased afterload and myocardial oxygen consumption } Restart patients usual medications.