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134 Cards in this Set
- Front
- Back
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Which drugs decrease LVEDP?
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Nitrovasodilators, morphine, Ranolazine
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What is the concept of "coronary steal?"
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You would expect nitrate drugs to increase blood flow via collateral circulations to ischemic areas of cardiac tissue, however since nitrates are acting on healthy vessels as well, these can "steal" some of the flow away from the collateral circulation that can perfuse the injured area.
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What are the three elements of Virchow's triad and what is the most important prothrombotic factor?
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3 elements are hypercoagulability, abnormal blood flow, and endothelial injury. Endothelial injury is the most important, greatest determinant of thrombotic injury. 2 factors together dramatically increase risk of clot.
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properties of activated (ie dysfunctional) endothelium?
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Increased stickiness (leukocyte adhesion), local procoagulant state, pro-inflammatory cytokines released, altered vascular permeability and tone. Swollen, interferes with laminar flow.
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What can activate endothelium?
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Turbulent flow, high BP, shock, sepsis, electrolyte abnormalities, inflammation, hypersensitivity, toxins.
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What's the difference between red and white thrombus?
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White is composed mostly of platelets and fibrin.
Red is composed of platelets, fibrin, and RBCs. More common with stasis? Alternating layers of these components creates lines of Zahn. The tail of a clot is fragile, can break off and embolize |
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What is coagulative necrosis, what causes it?
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Caused by thrombus causing occlusion and halted perfusion. Downstream cells will die, see evidence of nuclei loss, fibrosis, etc. General structure will stay the same, but the cells may change.
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What is recanalization?
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Process of maintaining some patent lumen of a blood vessel when a thrombotic process is occluding it. Scarring and collagen deposition are evident. Increased risk of infarction and ischemia downstream.
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What is neointimalization?
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Activated endothelium at site of injury will recruit SMCs from the media, disrupting elastic lamina, and depositing ECM in the intima. Loses contractility, takes up space narrowing lumen. Any vascular injury can cause this.
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What is malignant hypertension and its acute and chronic effects on endothelium?
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MH = extremely high HTN. Acutely, damages endothelium, can be sloughed off, releasing tissue factor, initiating clotting cascade (called fibrinoid necrosis).
Chronically the vessel walls undergo successive stages of remodeling and injury, causing hyperplastic arteriolar sclerosis (onion-skin lesions), layers of neo-intima. Total loss of arteriolar compliance, narrowed lumen. |
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What is hyaline arteriolar sclerosis?
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Hyaline means pink or fibrin-staining. caused by plasma components collecting under endothelium, smudgy look. Seen in diabets, HTN.
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What is an atheroma?
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Part of atherosclerosis affecting the large and midsize arteries. Deposition of lipid SMCs, macrophages under intima in a process similar to neointimization. Contains a central necrotic core of lipid crystals and foam cells (macrophages and SMCs that have ingested oxidized LDL). Can promote thrombosis, interrupt laminar flow, exacerbates endothelial injury.
ather- = lipid |
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What is a fatty streak?
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Accumulation of foam cells and lipid seen grossly in large arteries, can be seen in aortas of adolescents.
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Stages of atherosclerotic plaque formation?
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Intimal thickening -> Fatty streak (foam cells) -> atherosclerotic plaque (fibrous cap, lipid crystal core) -> vulnerable, unstable plaque.
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How is blood pressure currently classified?
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Normal: systolic <120 AND diastolic <80
Pre-HTN: systolic 120-139 or diastolic 80-89 Stage 1 HTN: systolic 140-159 or diastolic 90-99 Stage 2 HTN: systolic >160 or diastolic >100 Diagnosis must be made based on at least 2 separate seated readings. Goal of HTN therapy is <140/90 and >130/80 in DM or renal disease |
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What does HTN put you at risk of?
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Cardiovascular disease (ischemic heart disease, stroke, renal disease, death, atherosclerosis?
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How do many diuretic drugs access the nephron lumen? What can reduce diuretic access to tubules?
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Transported by OATs. Can be diminished by low GFR or by concurrent OA drug therapy, such as penicillin, furosemide, and some endogenous substances.
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What are the 3 determinants of myocardial oxygen demand?
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1. myocardial wall tension/stress, LaPlace's law, wall stress = (P * r)/2(h), P=pressure, r=radius, h=wall thickness
2. Myocardial contractility, stronger contraction requires more O2. 3. Heart Rate |
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What do dilation and hypertrophy do to wall stress and oxygen demand?
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dilation increases radius without increasing wall thickness, so it will increase wall stress and oxygen demand.
hypertrophy increases wall thickness, decreasing wall stress and oxygen demand. |
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When is coronary flow greatest?
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During diastole. In systole the increased pressure squeezes the coronaries shut, limiting flow.
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Contrast unstable and stable angina
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Stable: 3 months of a predictable pattern of intermittent angina. Typically elicited on exertion and relieved by rest.
Unstable: Accelerated, meaning the symptoms and frequency are increasing, indicating further ischemia. New onset is unstable, as is a variable clinical course. |
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Contrast stable vs vulnerable plaques
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Vulnerable plaques contain a thin fibrous cap that separates substantial thrombogenic lipid core from the blood. Vessel lumen can be well preserved.
Stable plaque has a thick fibrous cap protecting thrombogenic lipid from the blood. Lumen typically more narrowed. |
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What is the potential pattern of radiation in angina?
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C3 to T6 typically, from lower pinna to lower sternum. rarely C2-T9, including occiput to epigastrium.
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Common angina symptoms?
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Retrosternal chest pain not localized to one point, radiates elsewhere. Often not described as pain but rather a heaviness, tightness, pressure, burning, or ache. Radiates more often to left than right.
Usually symptoms build over several minutes then lasts 10-15 minutes, the longer it lasts the worse the ischemia, more likely to indicate MI/ACS. Disappears over a few minutes. |
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What are precipitating and relieving factors in angina?
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Brought on by exertion, excitement, large meal, cold.
Relieved by rest, nitroglycerin. |
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What are some signs/symptoms that indicate chest pain may not be cardiac?
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unremitting pain over hours without infarct evidence, frequent long lasting pain, local tenderness, pain on movement/position, pleuritic chest pain/pain with respiratory pattern, strange radiation
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Associated symptoms of angina
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CAN be totally silent, or accompanied by weakness/sudden fatigue, sudden dyspnea, sudden confusion, sudden sweating and malaise, nausea, vomiting
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Tx options for angina or atherosclerosis?
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organic nitrates, beta blockers, anththrombotic therapy, angioplasty, CABG.
Risk factor modification: diet, exercise, smoking cessation, lipid lowering, HTN management, diabetes management, stress reduction, inflammation reduction |
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What are the 2 types of MI?
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NSTEMI - non ST elevation MI, incomplete occlusion of a CA.
STEMI - ST elevation (tombstone) elevation MI, complete occlusion of CA Normal EKG does not necessarily exclude an MI. |
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Typical clinical presentation of MI?
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Crushing chest pain "elephant on chest" lasting longer than typical angina episode. Can be accompanied by hyper sympathetic or parasympathetic response.
20% cases are ASYMPTOMATIC/SILENT! Causes heart failure (left first, can cause right), low CO, pulmonary congestion, systolic (pumping) and diastolic (filling) dysfunction, acute mitral regurgitation due to papillary muscle ischemia or rupture, ventricular septal rupture. Sudden death via arrhythmia or asystole can occur |
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Besides EKG, how else is MI diagnosed?
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Troponins indicate myocardial necrosis, specific and sensitive.
Myoglobin in serum, first indicator to rise. Creatine kinase, CK-MB ratio. SGOT (ALT), LDH |
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How long does it take for necrosis to occur in ventricle of occluded CA?
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Necrosis can start quickly, within first half hour can have irreversible damage. By 24 hrs can have complete irreversible damage to area supplied.
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What are the classes of diuretics and examples of each?
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(1) Loop diuretics (eg furosemide)
(2) Thiazide diuretics (HCTZ, chlorthalidone) (3) K+ sparing diuretics (Amiloride, Triamterene, Spironolactone, Eplerenone) |
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What classes of agents are used in the treatment of angina?
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Decrease oxygen demand: Beta blockers (propranolol, metoprolol, etc), Calcium channel blockers (verapamil, diltiazem, etc), nitrates (nitroglycerin), morphine, late Na+ channel blocker (Ranolazine), ACEis (lisinopril, enalapril), ATII blockers (Losartan)
Anticoagulants: aspirin, Clopidogrel HMG Co-A reductase inhibitors (statins) Potentially thrombolytics if ACS: reteplase, alteplase, tenecteplase (tPA like agents) |
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risk factors for MI?
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Modifiable: Smoking, HTN, diabetes, hyperlipidemia
Non-modifiable: Age, genetics, gender |
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Leading cause of death?
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Ischemic heart disease, usually due to CAD. Can present as angina, MI, chronic ischemic HF, sudden cardiac death
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What % CA occlusion is necessary for symptoms of angina with exercise and at rest?
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75% obstruction with exercise, 90% at rest
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What are the immediate effects of ischemia on cardiac myocytes?
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oxidative phosphorylation stops, ATP depletion starts within seconds. This causes the Na/K ATPase to fail, accumulating Na+ in cell and leading to cell swelling. Anaerobic metabolism kicks in, which lowers pH due to lactic acid buildup. Low pH causes enzymatic dysfunction in cell.
Contractility stops at 1 minute, ATP 50% normal at 10 minutes (10% at 40 minutes), Irreversible cell injury at 30 minutes. Failing Ca+ pump damages mitochondria, cell becomes leaky, which enables testing for troponins, myoglobin, etc. Leads to coagulative necrosis. |
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What are some histological signs that coagulative necrosis is occurring?
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Contraction band necrosis is earliest sign (darkened line spanning myocyte). Loss of cross striations, nuclei absent.
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What steps follow coagulative necrosis in ischemic heart disease?
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1. Inflammation - increase blood flow, leakage of plasma, leukocyte recruitment and adhesion.
2. Phagocytosis by macrophages 3. Healing by fibrosis, deposition of collagen |
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What are the stages of gross pathology of MI?
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No gross changes in first 12 hours.
Dark red hyperemic area first few days, indicates hemorrhage, edema, congestion, neutrophil infiltration Yellow-tan (macrophages, granulation tissue, etc?) with red border indicates weeks old Grey-white scar indicates fibrosis and is >2 months old |
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Common complications of MI?
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Ischemia-reperfusion injury, arrythmias, myocardial rupture -> tamponade, pericarditis, ventricular aneurysm, infarct extension, cardiogenic shock
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What is post-MI myocardial rupture and what are the risk factors?
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Free wall rupture, typically free wall of mid-ventricle. 50% occur within 5 days of MI, 90% within 2 weeks. ONLY occurs with transmural MI (STEMI). Can cause tamponade and death. Can also have in septum, leading to VSD, or papillary muscle causing mitral regurgitation.
RFs: Female, 60+, pre-existing HTN, 1st transmural MI, poor coronary collaterals |
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What is Dressler's syndrome?
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Late pericarditis, happens 1-8 weeks after an MI in 1-3% cases. Also called post-MI syndrome.
Distinct from acute pericarditis which is more common (10%), and more acute, 1-4 days after MI. |
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Where does ventricular aneurysm post-MI typically occur and what are its symptoms?
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Typically in patients with apical transmural MI, causing bulging of apical ventricle. Can cause mural thrombi, arrythmias, and HF
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What causes infarct extension and expansion (they are different!).
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Extension is caused by reocclusion of CA, leading to an enlarged necrotic zone than the original MI. Can reoccur several times and is seen on path. Associated with worse outcome.
Expansion refers to regional dilatation and thinning of the infarcted tissue, "stretching." |
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What is responsible for ischemia reperfusion injury?
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Inflammation, free oxygen radicals, activation of complement.
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Effects of BBs?
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Reduce myocardial O2 demand, reduce BP, wall tension, HR, contractility, CO, attenuate response to catecholamines, reduce renin secretion from JGA
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Common beta adrenergic agonists?
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epinephrine (nonselective, alpha and beta), NE (not very active at beta2), isoproteronol (beta 1-2)
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Typical tx of stage 1 HTN without compelling indications?
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Thaizide diuretic. May consider BB, CCB, ARB, ACEi, or combo
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Typical tx of stage 2 HTN without compelling indications?
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Two drug combination, usually thiazide diuretic + ACEi, or CCB, BB, ARB
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What are "compelling indications"?
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Comorbidities to HTN that may alter treatment plan, examples include diabetes, heart failure, elderly pts, MI
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What drugs are ideal for use in diabetics with HTN?
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ACEi or ARBs. reduce HTN and avoid renal pathology (decreased rate of proteinuria).
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What drugs are ideal for use in pts with HF and HTN?
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ACEi in combo with a diuretic or digoxin. If ACEi not tolerated, can use combo hydralazine/isorbide dinitrate. Dihydropyridines, ARBs, carvedilol, diuretics also safe when combined with ACEi?
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Which beta blockers cause vasodilation in addition to their effects on the heart?
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Labetalol, carvedilol (both have some alpha blocking activity), and nebivolol (NO potentiation?)
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What are the 2 mechanisms of K+ sparing diuretics, examples of each?
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Direct inhibitors of Na+ channels in principal cells, preventing Na+ reabsorption. Eg, Amiloride, Triamterene
Competitive aldosterone antagonists inhibit effects of aldosterone, like increasing number and activity of ENaC channels. Eg, Spironolactone, Eplerenone |
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What classes of drugs are used in treating hypertension?
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Commonly diuretics (HCTZ), ACEi (ie lisinopril), beta blockers (propranolol, etc).
Also ARBs (Losartan), direct renin inhibitors (Aliskiren), CCBs (Amlodipine, Diltiazem, Verapamil), direct vasodilators (hydralazine) |
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what is the definition of shock?
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Inability of blood flow to meet tissue metabolic demands. Hypoperfusion leads to hypoxia in tissue, leading to anaerobic metabolism and organ dysfunction.
Shock does NOT necessarily mean hypotension. Depends on the patient's baseline. Remember the definition is by PERFUSION, not blood pressure. |
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What changes occur during shock from pre-shock to decompensated shock? What is compensated shock?
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Increased sympathetic tone causes increase in HR, blood pressure is steady. LA slightly increased and bicarb slightly decreased.
In decompensated shock the HR has reached extremely high rate and ultimately drops if not corrected. Systolic BP drops dangerously low. Lactic acid accumulation more rapid, as is drop in bicarb. This late stage may not be reversible. stage 4 reversible, 5 not. |
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how does the body attempt to compensate for shock?
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Increased sympathetic output: raises HR and maintains blood pressure.
RAS - maintain BP by vasoconstriction and enhanced Na and water absorption. ADH release: conserve fluid Hyperventilation: reduces acidosis |
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3 determinants of cardiac pump function / stroke volume?
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preload, afterload, contractility
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3 major types of shock?
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Hypovolemic - loss of blood volume via hemmorhage, etc,
Cardiogenic - , Vasodilatory/Distributive - massive vasodilation via anaphylaxis, sepsis, etc |
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What can cause cardiogenic shock?
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Decrease SV
MI is major cause. cardiomyopathy (non-ischemic) valvular disease ventricular arrythmia Cardiac tamponade (obstructive shock) Pulmonary embolism (obstructive) Decrease HR Complete heart block drug overdose |
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What is obstructive shock?
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not a pumping problem but rather a filling, issue not the pump itself, compression of ventricles or poor blood supply from pulmonaries. PE or tamponade can cause it.
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How much blood must be lost to have hypovolemic shock?
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~1500mL of blood, or about 30%
usually due to hemorrhage, but also dehydration, vomiting, diarrhea, burns |
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What is SIRS and how is it defined clinically (what are the criteria)?
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Systemic Inflammatory Response Syndrome.
Need 2 of following: body temp <36 or >38 HR > 90bpm RR of >20pm or arterial PP CO2 < 32 WBC <4000 or >12000 + infection = septic SIRS - infection = aseptic SIRS |
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What clinical findings are common to all types of shock?
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Confusion and lethargy, liver failure, renal failure, anuria, diaphoresis. can cause DIC
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difference between warm and cold shock?
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Warm is early vasodilatory shock, perfusion is still somewhat preserved as indicated by warm normal extremeties.
Cold is all other forms and late vasodilatory, extremeties are cold, pale, cyanotic. ischemia of digits. |
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What interventions are critical in shock?
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Arterial line placement for minute to minute BP readings and pH/gas values.
Central lines for rapid fluid therapy, meds, CVP measurement which approximates right heart preload. Sometimes foley catheter to monitor urine output and hemodynamic monitoring to determine pulmonary wedge pressure (=LA pressure). In cardiogenic shock can use a intraaortic balloon pump (IABP), helps preserve diastolic pressure for coronary perfusion by inflating in early diastole and increase suction during late diastole by deflating to decrease afterload |
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What are simple prognostic measures in shock?
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pH and serum lactate, very useful in predicting mortality.
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What drugs are useful in treating shock?
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Drugs that increase SVR and CO, like catecholamines (dobutamine, dopamine, NE, E, PE). Serious side effects are reflex bradycardia, tissue necrosis, arrythmias.
Vasopressin to increase water retention, increase SVR. |
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definition of heart failure? of congestive heart failure?
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HF: inability of heart to pump blood sufficiently to supply metabolic demands of body. Or the ability to only do so in the presence of elevated cardiac filling pressures. Ability to generate adequate SV (and hence CO) is diminished.
CHF: Same as HF, but associated with signs and symptoms of volume overload and congestion. Signs: pulmonary edema, ascites, peripheral edema, hepatomegaly. Symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea |
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What are determinants of tissue perfusion?
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BP, CO, peripheral resistance to flow
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What are compensatory mechanisms in response to reduced CO in heart failure?
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Decreased CO leads to volume overload in ventricle, increasing EDP, which increases contractility via FS mechanism.
1. SNS activation causes increase HR, contractility, vasoconstriction, and activation of RAS system. These increase CO and preserve BP. 2. RAS causes vasoconstriction, activates aldosterone/fluid retention. 3. ADH release increases circulatory volume as well, contributing to increased preload and hence SV. All lead to adverse remodeling over long term. ANP can also be releaased as counter measure to increased atrial pressure. |
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What are the 2 types of compensatory remodeling that take place in HF?
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Response to pressure overload: increased systolic wall stress leads to myocyte addition in parallel, or concentric hypertrophy.
Response to volume overload: increased diastolic wall stress leads to myocyte addition in series, or eccentric hypertrophy. Misnomer, more of a dilatation. Both will lead to fibrosis |
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What can cause a pressure load to a ventricle, promoting concentric hypertrophy?
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Hypertension and aortic stenosis, promote high pressure systole due to high afterload. Increasing wall thickness is an attempt to reduce wall stress.
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What can cause a volume load to a ventricle, promoting eccentric hypertrophy?
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Increased diastolic volume, caused by aortic or mitral regurgitation/insufficiency, or dilated cardiomyopathy. longer myocytes attempt to maintain contractile force.
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Difference between systolic and diastolic HF?
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Systolic HF = heart cannot pump adequately in systole, decreasing the EF (ie, HF with decreased EF).
Diastolic HF = heart cannot fill adequately in diastole, too stiff (HF with preserved EF) |
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causes of systolic HF?
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MI, MR, AR, DCM (familial, viral)
treatments exist |
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causes of diastolic HF?
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HTN, AS, RCM, HCM, MI, pericardial constriction, tamponade
not many treatments, irreversible |
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Are most HF patients warm/cold, wet/dry?
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Most (67%) are warm and wet, meaning perfusion is still adequate but there is congestion.
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evidence for increased afterload?
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HTN, cool extremities (vasoconstriction), Loud P2 (pulmonary HTN)
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evidence for increased preload?
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L sided: orthopnea/PND, rales, dyspnea, S3 gallup, loud P2
R sided: JVD, HJR, edema, ascites, hepatomegaly |
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evidence for low perfusion (ie low CO)?
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hypotension, nausea, pulsus alternans, cool extremities, fatigue, poor urine output, worsening renal function, hyponatremia
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Evidence for remodeling (dilation or hypertrophy)?
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Dilation: Inferolaterally displaced PMI, MR murmur
Hypertrophy: Enlarged PMI, S4 gallup |
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What are the 4 stages of HF?
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New York Heart Association functional classifications:
I - no limitation of physical activity, ordinary physical activity does not cause symptoms. II - Comfortable at rest but slight limitation of physical activity. III - marked limitation of physical activity, less than ordinary activity causes symptoms. IV - Unable to carry out any physical activity without symptoms, and at rest, worsening with exertion. |
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how would increasing or decreasing preload in a patient with compensated HF change their symptoms?
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Decreasing preload leads to hypotension and symptoms of inadequate perfusion.
Increasing preload will increase left sided pressure and cause symptoms of pulmonary congestion. |
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What types of drugs treat Acute Decompensated Heart Failure (ADHF)?
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Drugs that reduce preload: Loop diuretics (furosemide), Nitrates, Neseritide
Drugs that reduce afterload: ACEi, ARBs, nitrates, other vasodilators (hydralazine), Nesiritide (BNP) Drugs that increase contractility: Inotropes (Milrinone, dobutamine), digoxin |
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What strategies can decrease mortality in chronic compensated HF?
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Neurohormonal blockade and prevention of adverse remodeling
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What groups of drugs are used in Acute decompensated HF and in chronic compensated HF?
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ADHF: Diuretics, vasodilators (ACEi, ARB, hydralazine) Inotropes (b-agonists, bipyridines), natriuretic peptides, nitrates
NEVER Beta Blockers CCHF: Diuretics, vasodilators, inotropes (only end stage CCHF), aldosterone receptor antagonists, BBs, nitrates, cardiac glycosides |
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Drug classes that have been shown to improve survival in systolic HF?
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ACEis, ARBs, BBs, aldosterone antagonists, hydralazine-nitrate combo. BAAAHN
NOT diuretics or vasopressin receptor antagonists, although theoretically they make sense. |
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Drug classes that have been shown to improve survival in diastolic HF?
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No drugs have shown to improve survival
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What are the side effects of ACEi and ARBs?
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Hyperkalemia, reduced GFR and renal insufficiency, Cough (mostly ACEi)
ANGIOEDEMA RARE BUT SERIOUS AE contraindicated in pregnancy, ACEis interact with aspirin (remember bradykinin) |
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Why are inotropes used in HF treatment if they don't increase mortality?
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Improve morbidity and relieve symptoms
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What drug class should never be used in acute decompensated HF and which drug class is reserved mostly for ADHF and end stage chronic HF?
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BBs should never be used. Severely limit heart function.
Inotropes are only used to treat severe, end stage HF. |
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Discuss the different effects of these interventions in decompensate heart failure.
Inotropes Diuretics Vasodilators Inotrope+vasodilator inotrope+vasodilator+diuretic |
Inotropes increase cardiac contractility and output but do not lower high ventricular filling pressures themselves, so pt may still have congestion symptoms.
With a diuretic, filling pressures are diminished due to lowered volume load, but cardiac function is still low so pt may have hypotension/low CO. Vasodilators reduce pre and after load so they can improve both cardiac output and lower filling pressures. Combinations tend to be summative and improve the cardiac function and lower filling pressures. |
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Compare intervention strategies in the 4 stages of heart failure
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Stage 1: Risk reduction, no pharmacotherapy.
Stage 2: Treat HTN, diabetes, hyperlipid. Start on ACEi and ARBs in some pts Stage 3: Add beta blockers. , consider surgical/catheter intervention. Late stage 3 aldosterone antagonist. Stage 4: Inotropes, nitrates, nesiritide. D/C BBs? |
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What is responsible for the a,c,and v waves?
The x and y descent? |
a wave = Atrial systole
c wave = tricuspid closure, initiation of ventricular systole v wave = atrial filling while AV (tricuspid) valves still closed x descent (between c and v) = right atrial relaxation y descent (between v and a) = RV filling |
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What is physiological splitting?
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Normal splitting of the S2 heart sound. Heard on inspiration. During inhalation the chest expands, causing negative intrathoracic pressure. This transiently increases capacitance of pulmonary vessels, which delays the time to equilibration of pressure between the RV and pulmonary artery, delaying pulmonic closure (P2). Opposite effect in the aorta as the same effect causes reduced venous return to the LA from pulmonary veins. Reduced filling of LV diminishes stroke volume and shortens time for LV emptying, causing earlier A2 on inspiration compared to expiration. P2 occurs after A2 on inspiration, A2 and P2 are about equal (A2 only slightly earlier on expiration). The slight different of timing of A2 and P2 causes 2 sounds in succession, which is called splitting.
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What causes a fixed split S2 heart sound?
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Atrial Septal Defect. Due to high Right side pressure, the pulmonary arterial system becomes more capacitant with less resistance, causing a delayed pulmonic valve closure due to a lower back pressure. Splitting is heard on inspiration and expiration.
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What causes widened splitting?
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Right bundle block, pulmonary stenosis. These are usually due to pathologically delayed pulmonic valve closure.
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What causes paradoxical splitting?
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Left bundle branch block and aortic stenosis can cause it, because of delayed left ventricular contraction (or prolonged ejection time in stenosis), leading to delayed aortic closure such that A2 follows P2 (abnormal). On inspiration, P2 is delayed as normal, and there may no longer be a split, so this is the opposite situation as normal (splitting heard on expiration instead of inspiration).
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What causes ejection click?
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Stenosis of aortic or pulmonic valve. rapid deceleration of stenosed valve, as reach maximum ascent into great vessel.
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What is an opening snap?
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heart sound heard when mitral or tricuspid valve opens (normally not heard), caused typicall by stenosis. Sharp, high pitched sound. MS more common than TS. Heard best at apex and left sternal border. Can be confused with a S2 plit (or S4?), however should not change with respiration.
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What is an S3?
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Early diastolic heart sound, after S2, during rapid filling of the ventricle. It may be caused by rapid deceleration of blood entering a stiffened ventricle, or tensing of chordae tendineae. It is a normal finding in children and younger adults, indicating a supple ventricle capable of rapid expansion. In middle or elderly aged, is indicates volume overload due to CHF, or increased transvalvular flow from mitral or tricuspid regurgitation.
Sometimes called a ventricular gallop. |
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What is an S4?
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Fourth heart sound, occurring in late diastole, coinciding with contraction of atria. Indicates vigorous contraction of atria against a stiffened ventricle. Indicates cardiac disease, decreased ventricular compliance due to hypertrophy or myocardia ischemia. dull and low pitched like an S3.
Sometimes called an atrial gallop. |
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What is a pericardial knock?
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uncommon, high pitched sound in pts with severe constrictive pericarditis. Early in diastole after S2. can be confused with an OS or S3. louder than the S3 and later than OS. Due to abrupt cessation of ventricular filling in early diastole, a hallmark of constrictive pericarditis.
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What might cause a systolic ejection murmur?
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Typical of aortic or pulmonic stenosis. Usually a crescendo-decrescendo pattern.
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What causes a pansystolic murmur?
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Regurgitation of blood across the mitral or tricuspid valve characterized by uniform intensity throughout systole, or by a VSD.
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What causes a late systolic murmur?
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Commonly mitral regurgitation caused by a mitral valve prolapse. Leaflets bow into the atrium during contraction. Usually preceded by a midsystolic click.
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What causes early diastolic murmurs?
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Regurgitant flow through aortic or pulmonic valve. Aortic more common. Usually a decrescendo.
Pulmonary regurgitation usually caused by pulmonary artery htn. |
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What causes a mid-diastolic murmur?
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Turbulent flow across a stenotic mitral or tricuspid valve.
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What is an example of a continuous murmur?
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Murmur of patent ductus arteriosus. Continuous flow from aorta to pulmonary artery.
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what are some reasons for increased automaticity?
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Drugs like digoxin, anticholingergics, adrenergics.
Increased stretch of atria (pulmonary disease, CHF) |
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What are the 2 general causes of arrythmias?
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Abnormal impulse initiation (automaticity) and abnormal impulse conduction (micro or macroscopic reentry), or a combination.
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3 requirements of Reentry
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(1) Obstacle to homogenous conduction (anatomy, scar)
(2) Unidirectional block (normally tissue can conduct bidirectionally) (3) Delayed conduction (conduction time > refractory period) Requires "PERFECT TIMING" |
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What is R on T phenomenon?
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Occurs when a premature ventricular contraction (PVC) occurs exactly when a T-wave would have been, which can set off VT as the conditions for reentry have been met. You have some areas of unidirectional block, repolarization time is heterogenous, PVCs travel slower than normal beat.
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General treatment strategies for bradyarrythmias?
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Make the heart beat faster with drugs.
Use a pacemaker. |
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General treatment strategies for tachyarrythmias?
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Ablation, implantable defibrillator, antiarrythmic agents.
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what are the action potential effects of class I antiarrythmics?
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decrease conduction velocity, change refractory period, disrupt timing of reentry.
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Explain the concepts of use dependency and reverse use dependency
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use dependency - drug binds transient form of channel (in active or inactive state), more useful in tachycardias where channels are frequently being activated and inactivated.
reverse use dependency - drug binds to resting/durable form of channel, works better with slow heart rates |
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What drugs block the AV node in an atrial tachycardia?
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BB, CCB, digoxin, adenosine
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What drugs treat a reentrant or increased automaticity atrial arrythmia?
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procainamide, flecainide, sotalol, amiodarone, defetilide
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Drugs to treat ventricular reentry?
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Lidocaine, procainamide, amiodarone, dronedarone
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Organism often responsible for prosthetic valve endocarditis?
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Coagulase Negative Staph (CoNS)
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what antibiotics are commonly used in infective endocarditis?
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For Staph aureus, beta lactams, esp for MRSA.
Enterococcus: gentamicin + beta lactam |
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what is gentamicin?
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aminoglycoside antibiotic (DONT give with furosemide). Binds 30S ribosome subunit. Active against all gram negatives and gram positives if the cell wall is disrupted by a penicillin.
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What is recommended for dental prophylaxis? what drug and in what population?
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Single amoxicillin dose 30-60 min prior to procedure.
Only high risk group, ie with prosthetic valve or prior endocarditis. AND for any procedure involving manipulation of gingival tissue, perforation or oral mucosa. |
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What is kussmaul's venous sign?
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lack of normal drop in JVD pressure during inspiration, may paradoxically rise. Constrictive pericarditis is a common cause.
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Difference between class I-II (A) and III (B) aortic dissection?
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A involves ascending aorta, tear can flow into heart/pericardium. Can cause tamponade and aortic insufficiency.
B is descending aorta, rupture into surrounding tissue (distal to left subclavian branch) |
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Differential for severe, acute chest pain?
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Acute MI
esophageal spasm aortic dissection spontaneous pneumothorax acute pulmonary embolus |
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what conditions predispose to ventricular arrythmias?
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myocardial ischemia, scarring/fibrosis, antiarrythmics, electrolyte abnormalities, cardiomyopathies.
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Non-cardiac causes of sudden death?
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syncope, aortic dissection, aortic aneurysm rupture, pulmonary embolism, cocaine toxicity, metabolic imbalance, grand mal seizure
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syncope causes
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1. reflex/vasovagal - most common, benign
2. orthostatic - autonomic dysfunction, elderly, medications 3. cardiac arrythmia - most deadly, usually underlying structural heart disease |
