Cardiology Part 1 v.S. PDF

Cardiovascular Agenda ACS → Angina → Unstable Angina → Myocardial Infarction 2  ACUTE CORONARY SYNDROME (ACS) ACS – the term is used when a patient presents with acute ches...

Cardiovascular Agenda ACS → Angina → Unstable Angina → Myocardial Infarction 2  ACUTE CORONARY SYNDROME (ACS) ACS – the term is used when a patient presents with acute chest pain due to myocardial ischemia, b/c on initial assessment it is impossible to tell if the pt has a myocardial infarction (MI) or unstable angina (UA) 2/2/20XX P R E S E N TAT I O N T I T L E 3 ACS Myocardial ischemia as a result of inadequate perfusion to meet myocardial Pathophysiolog oxygen demand y Myocardial oxygen consumption is determined by heart rate, afterload, contractility, and wall tension Inadequate perfusion usually results from coronary arterial vessel stenosis as a result of atherosclerotic CAD Reduction of coronary blood flow does not cause ischemic symptoms at rest until the vessel stenosis exceeds 95% obstruction to flow 4  Anatomy of Plaque Disruption Shoulder region Lipid core Media Lumen Lumen Lipid core Fibrous cap “Vulnerable” Plaque “Stable” Plaque Thin, friable fibrous cap Thick fibrous cap separating substantial protecting thrombogenic thrombogenic lipid core lipid core from blood from blood More luminal narrowing Lumen could be well preserved 2/2/20XX Ada pte d from Libby P. Circulat ion. 1995;9 1:2844- 2850, w ith permission. P R E S E N TAT I O N T I T L E 5  Plaque Rupture, Stenosis, and Thrombosis Plaque rupture — intraplaque thrombus Mural thrombus Occlusive thrombosis Total chronic Recanalized Healed plaque occlusion lumen — increased stenosis Healed plaque — decreased stenosis Ada pte d from Davies MJ. In: Schla nt RC, Alexander RW, eds. The Heart, Arteries 2/2/20XX and Ve ins. P8th R E Sed. E N T1994:1 A T I O N 009-102 TITLE 0, with permission. 6  Plaque Rupture and Thrombus Progression Complete Lysis and residual Disease occlusion thrombus progression AMI Lipid- Plaque rich disruptio plaque n Reocclusion Unstable angina Thrombus Partial (labile) occlusion Recurrent pain Adapted from Fuster V. N Engl J Med. 1992;326:242-250, with permission. 2/2/20XX P R E S E N TAT I O N T I T L E 7 2/2/20XX P R E S E N TAT I O N T I T L E 8  In addition to reduced Lumen size, there is also a calcified portion (right side of photo) 2/2/20XX P R E S E N TAT I O N T I T L E 9 2/2/20XX P R E S E N TAT I O N T I T L E 10  Coronary Artery Occlusion: The Evolution of Infarction Progression of myocardial necrosis with time since occlusion 30 min 4h 6 - 12 h Normal Normal Normal myocardium myocardium myocardium “At risk” “At risk” myocardium, myocardium, ischemic but viable ischemic but viable Necrosis starting Necrosis extending Completed infarct subendocardially towards involving whole area subepicardium at risk Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission. 2/2/20XX P R E S E N TAT I O N T I T L E 11 ACS Pathophysiology Myocardial injury occurs at the cellular level as inflammatory, thrombotic, and other debris from the occlusive plaque lesion is released and embolizes into the distal vessel. The introduction of: calcium, oxygen, and cellular elements Causes reperfusion injury, prolonged ventricular dysfunction (known as myocardial stunning), or reperfusion dysrhythmias. 12 Stable Angina Stable Angina Stable angina pectoris, not considered a form of ACS, is transient, episodic chest discomfort resulting from myocardial ischemia. Etiology: atherosclerosis; vasospasm; myocardial hypertrophy; tachycardia; severe anemias; resp disease with oxygen deficit Transient chest pain – myocardial metabolic demands out pace coronary blood supply myocardial ischemia (lactic acid / inflammation / abnormal stretching of ischemic myocardium) afferent sympathetic fibers, which enter spinal cord at C3 to T4 varying locations & radiations patterns 2/2/20XX P R E S E N TAT I O N T I T L E 14 Stable Angina Classic presentation – acute onset substernal pain/pressure radiating down the medial aspect of the left arm – clenched fist on sternum / neck / jaw / both arms / back / epigastric – (mistaken for indigestion, dental pain, or shoulder arthritis) Nature – excruciating, constricting, squeezing, vice like, suffocating, tightness, burning, heavy weight “elephant on chest” Associated signs – diaphoresis, nausea, vomiting, pallor ECG changes – T wave inversion &/or ST depression (subendocardial ischemia), ST elevation in contiguous leads (Variant or transmural ischemia), or unremarkable 15 Stable Angina →The Canadian Cardiovascular Society (CCS) classification for angina is defined as follows: → Class I—no angina with ordinary physical activity; → Class II—minimal limitation of normal activity as angina occurs with exertion or emotional stress; → Class III—severe limitation of ordinary physical activity as angina occurs with exertion under normal physical conditions; and → Class IV—inability to perform any physical activity without discomfort as anginal symptoms occur at rest or with minimal physical exertion 16 Stable Angina → Stable – typical & predictable – stenosed arteries dilate poorly in response to   demand - follows exercise, heavy work, strain, stress, overeating, alcohol consumption, exposure to cold, infection with fever; relieved by rest and nitroglycerin (causes coronary and peripheral vasodilation   workload) 17 Stable Angina Typical angina is: → chest pressure or squeezing lasting several minutes, → provoked by exercise or emotional stress, and → relieved by rest or glyceryl trinitrate. →This symptom complex is most consistently associated with coronary disease Stable Angina Atypical angina is defined as chest discomfort with only two characteristics of typical angina. It is less predictive of coronary disease than typical angina, but may be more frequent in women, people with diabetes, or older people. Some guidelines avoid the term 'atypical' and instead suggest ‘cardiac’, ‘possibly cardiac’, and ‘non-cardiac’ pain, although symptoms alone can not determine the cause of chest pain. Non-specific symptoms → Epigastric → Diaphoresis → Bibasilar rales discomfort → Fatigue → Diminished → Jaw pain → Hypoxia peripheral pulses → Arm pain → Tachycardia → Signs of AAA → Dyspnea on exertion → Heart sounds → Xanthomas or → Nausea / vomiting xanthelasma Risk Factors → Age and sex → Inactivity → Chronic kidney → Smoking disease (CKD) → Diet → Hypertension → Inflammatory and → Race, ethnicity, other diseases → Dyslipidemia geography → Obesity → Diabetes → Psychological → Substance misuse factors and social determinants of → Family history health → pollution 2/2/20XX P R E S E N TAT I O N T I T L E 21 Differential Diagnosis → Pneumonia with → Peptic ulcer disease → Sternoclavicular pleurisy → Costochondritis arthritis → Esophagitis → Fibromyalgia → Herpes zoster virus → Esophageal spasm infection → Rib fracture → GORD → Anxiety disorders and panic attacks → Biliary colic 2/2/20XX P R E S E N TAT I O N T I T L E 22  Unstable Angina 2/2/20XX P R E S E N TAT I O N T I T L E 23 Unstable Angina → Unstable – (pre-infarction angina) unpredictable -  frequency, less stress/exercise to initiate, duration > 20 min at rest and incomplete relief with nitroglycerin; symptoms at rest; angina with ST changes, S3, or crackles; 2/2/20XX P R E S E N TAT I O N T I T L E → New onset  precursor to an AMI 24 Unstable Angina Suspect an acute myocardial infarction if the patient is clinically unstable as this is unlikely to be a feature of unstable angina. This includes any patient with: Ongoing or recurrent pain despite treatment Hemodynamic instability (low blood pressure or shock); Dynamic ECG changes Left ventricular failure; A life-threatening arrhythmia (ventricular tachycardia or ventricular fibrillation) or cardiac arrest after presentation; Mechanical complications such as new-onset mitral regurgitation. Associated Symptoms Marked Epigastri Back Dyspnea Syncope sweating c pain pain Differentials → Stable angina → Pericarditis → Prinzmetal (variant or → Myocarditis vasospastic) angina → Aortic dissection → Non-ST-elevation myocardial → Pulmonary embolism infarction → Pleuritis → ST-elevation myocardial infarction → Pneumothorax → Congestive heart failure → Perforated abdominal viscus → Chest wall pain Variant or Vasospastic Angina (Prinzmetal’s) Occurs at rest, often nocturnal, cyclic pattern (e.g. same time each day, or can be unpredictable but is not related to stress or physical activity); Peak incidence 2-3 hrs after getting up and early evening ( sympathetic activity); also on a weekly basis Monday morning shows peak occurrence Coronary vasospasm – responds well to calcium channel blockers, which inhibit vascular smooth muscle contraction 28 Myocardial Infarction Myocardial Infarction Myocardial ischemia – insufficient delivery of oxygenated blood to myocardium mismatch between supply & demand (metabolic needs exceed available supply) dysfunction in cardiac pumping & predisposes to dysrhythmias; severe or prolonged ischemia myocardial infarction (irreversible necrosis and death of cardiac cells) Within 10 min of occlusion ATP levels fall to ½ normal and irreversible cell injury begins within 30 - 40 min of complete occlusion; ischemic necrosis begins in subendocardial zone and spreads across ventricular wall toward epicardial tissues (greatest collateral network of arterial vessels) 30  Type 1—spontaneous MI related to ischemia resulting from Acute a primary coronary event Myocardial Infarction - Type 2—MI secondary to ischemia caused by increased oxygen demand or decreased supply classifications Type 3—sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST segment elevation or new left bundle branch block (LBBB) pattern. Type 4—MI associated with coronary instrumentation, such as occurring after percutaneous coronary intervention (PCI). Type 5—MI associated with coronary artery bypass grafting (CABG). Myocardial - supply & demand Oxygen demand factors: tachycardia /  contractility ( preload) / hypertension ( afterload) / ventricular dilation and hypertrophy (CHF - cardiomegaly) Hemodynamic factors Hypotension – blocked sympathetic innervation (bradycardia) and hypovolemic shock   coronary perfusion Cardiac factors  Diastolic filling (SVT’s or VT) /  ejection fraction (valvular incompetence) / coronary vasospasms Hematologic factors  O2 in blood (severe anemias / high altitude / CO poisoning) 32 Pearl CO required for short term physical activity (e.g. lifting) is accommodated by SV with little initial  in HR, however pts with Hx of CHD will not be able to compensate with an  SV and will have to significantly HR; result of  HR is myocardial O2 and  stress on  - all pts with suspected AMI should not be made to walk or do any physical activity Up to 75% of O2 is used by myocardium with little reserve so  demand  coronary blood flow; Coronary dilation (absence of disease)  blood flow 5X resting levels; compromised artery will not be able to dilate 33 Myocardial Infarction →Typical AMI Event – ulcerated/cracked/ruptured fibrotic plaque in coronary artery platelets adhere activation of clotting cascade thrombosis occludes coronary artery localized  myocardial perfusion myocardial ischemia anaerobic metabolism  lactic acid, inflammatory response, and abnormal stretching of myocardium  chest pain anxiety and apprehension epi and norepinephrine release  pale, diaphoretic, tachycardia  myocardial O2 demands additional myocardial ischemia 34 Myocardial Infarction PUMP -  ATP levels  contractility  SV & ejection fraction  coronary blood flow  myocardial perfusion   risk of cardiogenic shock, PVCs, V-tach, V-fib cardiac arrest RHYTHM -  ATP levels  cellular action potential  irritability threshold ischemic ECG changes  risk of dysrhythmias tachy or brady-arrhythmias  coronary blood flow  myocardial perfusion   risk of cardiogenic shock, PVCs, V- tach, V-fib cardiac arrest 35 Myocardial Infarction →Anaerobic metabolism (> 30 min) changes in cell structure ( glycogen / mitochondrial swelling / lysosomal release of enzymes) necrosis (irreversible cell damage) injury ECG changes (ST segment elevation) and release of serum cardiac enzymes → [myoglobin  1 hr / creatine kinase CK-MB (helps convert ADP to ATP)  4 hrs (peaks 12 – 20 hrs) / troponin complex I & T (proteins that regulate calcium-mediated contractile process in striated  muscle & not found in skeletal muscle) peaks 24 – 48 hrs.] Myocardial Infarction Factors Affecting Extent of Infarction  Location & area of involvement - endocardium / myocardium / epicardium - Transmural infarct - most common and represents a more prolonged and complete thrombosis - (left ventrical & interventricular septum) vs Subendocardial infarct inner 1/3 –1/2 [ mortality rate and complications but  incidence of subsequent ischemia and reinfarction]  Complete or partial occlusion  Duration of occlusion  Metabolic needs of affected tissue (underlying cardiac rhythm and BP) [glycogen depletion and mitochondrial swelling develop within minutes but are reversible if blood flow is restored]  Extent of collateral circulation built up  Time to Tx Myocardial Physiology Coronary arteries R coronary – conus, marginal artery, posterior interventricular artery (R atrium / RV / inferior wall LV / 1/3 septum / SA node 55% of persons / AV node 90% – crux of the heart) LAD – anterior interventricular artery (LV / 2/3 Septum) [LAD anastomoses with posterior branch of R coronary artery] Circumflex (L atrium / posterolateral wall L ventricle / SA node 45% of persons / AV node 10% of persons) [circumflex continues around atrioventricular sulsus where it anastomoses with R coronary artery] R coronary - Potentiates conduction problems – dysrhythmias L coronary – Potentiates mechanical problems – pump failure Coronary Artery Perfusion →Coronary blood flow -  during diastole and  during systole / anastomoses (L & R arteries at apex) / collateral circulation / 3000 + capillaries per square millimeter (1 cap. per muscle fiber) Myocardial Physiology →Ventricular blood flow – Pre-load (end-diastolic volume – pressure generated at end of diastole – filling pressure – vol of blood stretching resting heart muscle – reflective of venous return) →After-load (resistance to ejection – aortic pressure – systemic vascular resistance and wall tension must be over come - force contracting heart must generate to eject blood) Myocardial Physiology Frank-Starling Mechanism (Starling’s law:  Pre-load =  SV)  Diastolic filling  stretch of myocardial fibers  Length of muscle fiber  cross bridging between actin & myosin  Sarcomere length  strength of contraction  Inotropic effect  stroke volume  End diastolic volume  CO Point of no return – beyond the optimal length many of the cross-bridges will disengage weakening contracting (rubber-band effect – stretching works to a point – stretch too much and the band will break) Myocardial Physiology Functioning deterioration through 4 progressively abnormal contraction patterns Dyssynchrony – dissociation in time with adjacent muscle fibers of myocardium Hypokinesis – reduction in extent of muscle fibers shortening with contraction Akinesis – cessation of shortening of muscle fibers with systolic contraction Dyskinesis – paradoxical expansion of infarcted tissue, occurs with systole “Stunned myocardium” refers to area of ischemia (associated with dyssynchrony) & area of injury (associated with hypokinesis) that is in the process of recovering Heart Sounds Myocardial Infarction Classic presentation – acute crushing substernal pain radiating to left arm-neck-jaw; duration > 15 min; unrelieved by rest/nitro  contains visceral pain fibers enter spinal cord at multiple levels and map to areas on parietal cortex; visceral pain fibers (as opposed to somatic fibers) are difficult to describe and imprecisely localized discomfort, heaviness, aching as terms, as well as referred locations Acute Chest Pain/discomfort:1) recent onset (< 24 hrs); 2) anterior thorax; 3) distressing, noxious sensation forcing pt to seek medical attention Terms – pressure, tightness, squeezing, fullness are more common than qualifiers such as knifelike, stabbing, or sharp (latter seen with somatic pain and conditions such as pericarditis and dissecting aortic aneurysm AAA) Myocardial Infarction → Atypical presentation – vague chest discomfort (♀) / Silent MI” or Anginal equivalent of “Silent MI” is Asymptomatic MI absence of pain/discomfort but with (diabetics with sudden ventricular decompensation autonomic dyspnea, syncope, palpitations neuropathy) / shortness of breath (most often described complaint > 80 y/o) Myocardial Infarction Associated complaints – n/v; epigastric pain; belching-hiccups; pallor, circumoral cyanosis; diaphoresis; tachycardia (bradycardia, dysrhythmia); SoB; base crackles; anxiety and restlessness – sense of impending doom; arm-leg fatigue; syncope (in elderly assume syncope is caused by dysrhythmia); BP – variable ( - SNS stimulation /  - hypertension /  - heart blocks /  - cardiogenic shock) Dyspnea associated with an MI is usually related to pulmonary congestion Differential Diagnosis Cardiovascular origin Pulmonary origin Gastrointestinal origin  Acute myocardial infarction  Pulmonary embolism  Esophageal reflux, rupture,  Stable, unstable or variant  Pneumonia varices angina  Pneumothorax  Diaphragmatic or Hiatal  Mitral valve prolapse  Pleurisy hernia  Thoracic aortic aneurysm  Pulmonary contusion  Gallbladder disease  Pericarditis  Lung tumor  Peptic ulcer  Myocarditis  Pancreatic disease  Endocarditis  Hypertropic cardiomyopathy Musculoskeletal origin  Cardiac contusion  Muscle tear, bruising  Costochondritis  Resuscitation injury Treatment Oxygen considered a medication, one with significant potential to benefit and harm the patient with ACS Respiratory compromise can occur during ACS, usually as a result of acute pulmonary edema or exacerbation of chronic pulmonary disease Oxygen therapy delivered to normoxic ACS patients can increase both myocardial injury and infarct size Hyperoxia, developing as a result of excessive supplemental oxygen therapy, can potentiate coronary vasoconstriction and increase oxidative stress, worsening outcomes in these patients. 48 Treatment Nitroglycerin Nitrates decrease myocardial preload and, to a lesser extent, afterload. Increase venous capacitance and induce venous pooling, which decreases preload and myocardial oxygen demand. Direct vasodilation of coronary arteries may increase collateral blood flow to the ischemic myocardium In patients with significant, symptomatic coronary vasospasm, NTG can be quite beneficial Limit use in the presence of a STEMI 49 Treatment Antiplatelet Aspirin, the prototypical antiplatelet agent, is the most cost-effective treatment in ACS care It irreversibly acetylates platelet cyclooxygenase, thereby removing all activity for the life span of the platelet (8 to 10 days). stops the production of pro-aggregatory thromboxane A2 The P2Y 12 inhibitors include clopidogrel, ticagrelor and prasugrel more potent platelet inhibitors than aspirin inhibit the transformation of the P2Y 12 receptor into its high-affinity ligand - binding state irreversibly inhibiting platelet aggregation Ticagrelor activity is reversible and occurs via a different mechanism 50 Treatment Antiplatelet Glycoprotein IIb/IIIa Receptor Inhibitors Potent antiplatelet agents; abciximab, eptifibatide, and tirofiban. Clinical usefulness in only the subset of ACS patients undergoing PCI as a reperfusion strategy. This class of medications is not usually given in the ED setting, and other antiplatelet agents (P2Y 12 receptor inhibitors) are preferred for administration in the care of ACS. 51 Treatment Anticoagulant As with antiplatelet therapies in ACS patients, significant reductions in the progression to acute, recurrent, or extensive infarction and death are noted in individuals treated with aggressive anticoagulant therapy. There are currently four options in the setting of ACS, unfractionated heparin (UFH), low-molecular-weight heparin (LMWH) (enoxaparin), direct thrombin inhibitors (bivalirudin), and factor Xa inhibitors (fondaparinux). 52 Treatment Fibrinolytics Rapidly reestablishing perfusion in the infarct-related coronary artery using fibrinolytic therapy or PCI increases the opportunity for myocardial salvage, with resultant reductions in mortality and improvements in quality of life post-MI 90-minute patency predicts improved survival rates and preserves left ventricular function Options for fibrinolytic therapy include streptokinase (the original fibrinolytic agent) tissue-type plasminogen activator (t-PA) r-PA (reteplase) and tenecteplase (TNK). 53 Reperfusion Timing AMI Complications Sudden Death 30% - 50% from ventricular fibrillation secondary to PVC’s (within first 4 hrs of onset, often within 1st hr) Dysrhythmias 90% have an arrhythmia (ischemia / necrosis / inflammation in conduction tissue) – types – sinus tachycardia / PSVT/SVT / VT / heart blocks / PVCs (6+ in a row = run-salvo VT) Congestive Heart Failure  LV ejection fraction; rupture of papillary muscles (usually 3-5 days post MI) valvular insufficiency AMI Complications Spontaneous coronary artery dissection (SCAD) An unusual, but important cause of ACS. SCAD is defined as a separation of the layers of an epicardial coronary artery wall by intramural hemorrhage, with or without an intimal tear, and usually presents with chest pain that often radiates to the arms, shoulders or back. Approximately 90% of patients with SCAD are women aged 47 to 53 years. AMI Complications Ventricular Aneurysm → Transmural infarction – 2nd – 3rd day post-infarction tissue degradation (removal of necrotic fibers) begins a process that leaves a thinned out ventricular wall or interventricular septum, which balloons out on systole risking rupture & sudden death ( risk at 1–2 wks) – after a couple of weeks fibrous connective (scar) tissue replaces muscle tissue AMI Complications Cardiogenic Shock –  risk with 40% or more of LV involvement & mortality with AMI & cardiogenic shock  80% Tx. – 1st Rate, 2nd Volume, 3rd Pump – vasopressor Dopamine (5-10 g/kg/min - titrated) – significant hypotension (systolic < 90 mmHg)   CO with only small  in vascular resistance; Dobutamine – pts in  CO with pulmonary congestion AMI Complications Law of Laplace as applied to blood vessels during extreme hypotension: falling pressure in a blood vessel occurs when wall tension forces exceed distending forces allowing radius to  and resistance to   blood flow; distending pressure may fall to a point (< 20 mmHg  “critical closing pressure”) at which it is no longer possible to hold the blood vessel open  cardiovascular collapse AMI Complications Pericarditis – 2-3 days post-infarction – inflamed epicardium effusion of a small amount of fluid into pericardial sac sharp/stabbing chest pain aggravated with deep inspiration & positional changes; large amount of fluid accumulation PEA; Dressler’s syndrome - pericarditis that develops a few weeks post-infarction and often associated with pneumonia & pleurisy Occurs in 10–20% of pts; more common in transmural MI; Pericardial friction rubs are detected more often with inferior and R ventricular infarction b/c the R ventricle lies immediately beneath the chest wall AMI Complications Thromboembolism  acute PE or stroke (mural wall thrombus) Electrolyte & Metabolic Imbalances -  K+ risks VF (Sodium bicarbonate used for hyperkalemia) & metabolic acidosis; (CHF pts on diuretics may be in hypokalemia)