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Myocardial ischemia, shock, MI

mlinnie's version from 2018-11-09 22:36


Question Answer
Ischemia is defined asthe reduction or absence of blood supply to the heart
Myocardial ischemia is the result of an imbalance betweenoxygen supply and oxygen demand…oxygen supply is not sufficient to meet demand
Coronary artery diseasenarrowing of coronary arteries beyond 50% results in a significant reduction of blood flow, diseased arterial endothelium is prothrombotic, cannot dilate efficiently in response to increased myocardial demand, due primary to a reduction in endothelial nitric oxide (vasodilator)
Increased Myocardial O2 Demand causesIncrease myocardial muscle mass (ventricular hypertrophy), Increased heart rate, Increased contractility
Causes of Increase myocardial muscle mass (ventricular hypertrophy)hypertrophic cardiomyopathy (hypertensive, hypertrophic), aortic valve stenosis (outflow restriction); aortic valve regurgitation (volume overload)
Causes of Increased heart rateexercise, stress, hyperthyroidism, anemia, polycythemia, hypovolemia, pharmacology
Causes of Increased contractility any condition that increases the sympathetic response
Angina Pectorischest pain caused by myocardial ischemia, referred pain in left shoulder/elbow, mid-back, jaw (lactic acid affecting afferent nerve fibers entering C3-T4), diaphoresis, pallor, nausea
Stable anginaPredictable, known triggers (eg, exercise, stress)
Variant anginaUnpredictable, occurs at rest
Silent ischemiaNon-specific discomfort ; eg, severe fatigue, unease. May be experienced in those with diabetes (w/ autonomic dysfunction). More often experienced by women-2/3 of women who die from CAD had no symptoms, Higher rate of mortality from CAD due to underdiagnosis
Electrocardiography Using a combination of electrodes placed on the body’s surface, different views of the electrical activity of the heart can obtained (12-lead ECG). The location of myocardial muscle injury can thus be identified.
Laboratory testsTroponin (specific to heart) I, T (creatinine kinase (CK-MB, LDH). In ischemia, a cell has not died and lysed and released these to the circulation; plasma levels of these are not usually elevated in myocardial ischemia
P waveatrial depolarization
QRS waveventricular depolarization
T waveventricular repolarization
Stress test (increase demand, evaluate supply)treadmill- used as screening tool (ECG changes) (50% accurate). treadmill-sestamibi w/ nuclear scan (uniform distribution of blood flow) (95 % accurate). adensosine or persantine w/ nuclear scan (uniform distribution of blood flow) (95 % accurate). treadmill/bike or dobutamine w/ echocardiography (wall motion)
PericarditisAcute inflammation of the pericardium, Can occur w/ MI w/ or w/o effusion and tamponade needing aspiration also due to viral infection trauma, neoplasm. Can auscultate a “rub”


Treatment of Myocardial Ischemia
Question Answer
AIMRestore the balance between supply and demand by- Reducing myocardial oxygen consumption (demand) and Increasing oxygen supply
Decrease extent of atherosclerotic lesionAlter lifestyle with diet, exercise, PCI (percutaneous coronary intervention), CABG (coronary artery bypass graft; minimally invasive bypass graft)
Pharmacologic treatmentNitrates, B-adrenergic blocking agents, calcium channel blockers, ACE inhibitors, ARBs, anti-platlets, statins, control of diabetes
Nitrates an example of restoring the supply and demand balance
DemandDecreases systolic blood pressure. Decreases ventricular volume, Increases heart rate
SupplyIncreases coronary blood flow, Decreases coronary vascular resistance, Decreases coronary spasm, Increases collateral blood flow


Question Answer
Myocardial infarction describesthe prolonged hypoxia that results in irreversible myocardial cell death
The following mechanisms lead to total occlusion of a vessel resulting in an absence of blood supply to the cells distal to the occlusionAtherosclerotic plaque, Rupture of an unstable plaque with subsequent clotting, Prolonged coronary spasm at site of plaque
Pathophys of MIAnaerobic metabolism -ATP, glycogen stores depleted. Cell death after 20 min of no blood flow. Electrolytes lost from cells leading to inefficient contractions (K+, Ca++). Catecholamines are released from cells, leading to dysrhythmias and release of fatty acids from cells , which furhter harms myocardial cell membranes.
Physical examchest, arm, jaw, or back pain near maximal or maximal. duration of pain usually >30 min, not relieved with nitrates, N/V, diaphoresis, pallor
Lab examsElevated cardiac markers (troponin) in plasma from lysed cells, ST elevation on ECG, Angiography


Classification of Myocardial Infarction
Question Answer
Non-STEMINon-ST elevation MI; death of tissue involves only myocardium directly beneath the endocardium (sub-endocardial MI); ST depression/inversion on ECG; at high risk for further thrombus/occlusion
STEMIST elevation MI; transmural myocardial death; severe myocardial dysfunction; ST elevation on ECG


Question Answer
Treatment of Myocardial InfarctionThrombolysis- Tissue Plasminogen Activator (TpA), Percutaneous transluminal coronary angioplasty (PTCA)/stent (PCI)- gpIIb/IIIa inhibitor at time of procedure, Stents—metal or drug eluting + anti-platelets Plavix (clopidegrel) or Effient (prasugrel)), Coronary artery bypass graft (CABG)
Other Supportpressors, antiarrhythmics, nitrates, analgesia, oxygen, left ventricular assist devices
Complications of MIReperfusion injury (dysrhythmias), Pericarditis, Rupture of LV, septum, valve structures, Sudden death, Left ventricular heart failure (cardiogenic shock)
Myocardial ReperfusionDescribes the return of blood to the ischemic heart. Although the prompt return of blood to the ischemic heart is desirable, it is associated with additional myocardial injury. This is known as Myocardial Reperfusion Injury.


Pathophysiology of Early Myocardial Reperfusion Injury Mechanism-consequence
Question Answer
Mechanism-Calcium accumulationConsequences- Early ventricular arrhythmias,decrease force of contractions (stunning)
Mechanism- Endothelial activationConsequences- increased Adhesion molecules, radical, enzyme release causing arrhythmias, stunning, vascular damage
Mechanism- Leukocyte accumulationConsequences- increased Adhesion molecules, radicals, enzyme release causing arrhythmias, stunning, vascular damage; block blood flow in smallest vessels


Question Answer
SHOCKWidespread impairment of cellular metabolism due to the inability of the cardiovascular system to perfuse tissues adequately
Cardiogenic Shock hashigh mortalitiy, decreased cardiac output initiates compensatory mechanisms. shock becomes life threatening when compensatory mechanisms increase myocardial oxygen consumption, which further taxes the heart, treatment focuses on heart failure and enhancement of cardiac output
Cardiogenic Shock Etiology cardiomyopathy due to long standing hypertension, ischemia, infarction, virus, congenital disease, dysrhythmias, drug toxicity, early septic shock
Cardiogenic Shock Common pathophysiology inefficient pump and low cardiac output
The final common pathway in all forms of shock isdecreased cardiac output → decreased tissue perfusion → impaired cellular metabolism


Ventricular remodeling
Question Answer
Hypertrophy and apoptosisIncreased load and neurohormones activate myocyte receptors (eg, NE, AII, TNF) that activate intracellular second messengers to produce excessive adult- and fetal-muscle-specific gene products that lead to myocyte hypertrophy and apoptotic cell loss. Hypertrophied cells contract less efficiently; continued load and subsequent ventricular dilation leads to increased wall stress and O2 supply and demand mismatch
Extracellular matrix changesIncreased deposition of fibronectin, laminin, vimentin, (cytoskeleton) and collagen I, III, VI, IV. Results in loss of force transmission and fiber slippage during contraction


Neurohormonal Responses
Question Answer
RAA systemActivation of the renin-angiotensin aldosterone system by SNS. Angiotensin is a potent vasoconstrictor and increases ADH release. Elevated aldosterone contributes to myocardial fibrosis, vascular damage, baroreceptor dysfunction, blunts NE uptake by myocardium
Atrial Natriuretic PeptideProduced in right atrial myocytes; released with myocyte stretch; Initially may act as a “counter-regulatory” hormone due to natriuresis, diuresis, vasodilation, inhibition of aldosterone, renin, NE secretion. However, physiologic effects of ANP are attenuated in chronic HF patients
Sympathetic responsesInitial increase in NE is good- increase in HR, contractility, preload and vasoconstriction perfuse tissues. Continued NE release results in downregulation of Beta adrenergic receptors and uncoupling of the receptor from adenylate cyclase. Decrease in responsiveness leads to further sympathetic activation. Continued NE release converts compensations to maladaptive
Brain Naturetic PeptideBNP is a 32-amino acid polypeptide primarily secreted from the cardiac ventricles . Produced early in HF in response to ventricular wall stress, and in proportion to the severity of ventricular volume expansion and pressure overload. Acts as a counterbalance to the renin-angiotensin-aldosterone system. BNP is an independent predictor of high left ventricular end-diastolic pressure, and correlates well to the NYHA classes of HF (as BNP increases, NYHA class increases). BNP is easily measured in plasma as an indicator of fluid overload in HF. BNP measurements have been used successfully in hospitals, urgent-care facilities, clinical office practice. Short half-life, giving it the potential to monitor dynamic changes following diuretic and/or vasodilator therapy, and can be used to aid in determining appropriate timing for hospital discharge
BNP has been called a true “paradigm shift” in diagnosis of cardiac decompensation


Question Answer
SV the amount ejected from the heart in a single contraction
EDV the amount of blood in the ventricle immediately before a contraction
Normally, the heart can increase SVif EDV increases, by increasing contraction.
Alteration in the Frank-Starling mechanism in heart failure (cardiogenic shock )at any given end diastolic volume (EDV), there is a decrease in stroke volume (SV) compared to the normal heart. This is due to the inability of the failing heart to increase contraction.