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Cardiology
Overall by section
| Question | Answer |
|---|---|
| What is the common presentation of Aortic Stenosis? | Decreased tolerance to exercise and dyspnea, syncope, and angina on exertion. |
| Auscultation of Aortic Stenosis | Mid-to-late peaking systemic murmur at the right upper sternal border and an abnormal S2 |
| Which kind of heart failure has a preserved ejection fraction? | Diastolic dysfunction |
| What are common complications of AS? | Diastolic heart failure, a-fib, and pulmonary hypertension |
| What is the normal range pressure of a healthy right atrium? | 1-8 mm Hg |
| What is the normal pressure range of a healthy right ventricle? | 1-30 mm Hg |
| What is the normal pressure range of the pulmonary artery? | 4-30 mm Hg |
| What is the pressure range of PCWP? | 4-12 mm Hg |
| What is ASD? | Fixed and split S2 murmur |
| What is a possible complication of an ASD? | Allowance of a a venous thromboembolism to enter the left side of the heart and then to the systemic circulation |
| Which murmur often permits the passage of a venous thromboembolism to react to the systemic circulation leading to a stroke? | ASD |
| What causes V-fib? | Reentrant circuits within damaged myocardium |
| What is the auscultation description of Pulmonary valve regurgitation? | Diastolic, decrescendo murmur best heard at the left second intercostal space along the sternal border |
| How is diastole defined in terms of S1 and S2? | Time after S2 and before S1 |
| What is the term given to the time after S2 and before S1? | Diastole |
| What does chronic AS lead to? | Prolonged ventricular systole, high pressures, and ventricular hypertrophy |
| A prolonged ventricular systole is often due to: | Chronic Aortic Stenosis |
| Which chamber is most affected by AS? | Left ventricle, as it develops hypertrophy |
| What are the most significant complications of AS? | LV hypertrophy and angina pectoris |
| What is the description of a PVC? | Wide QRS complex with no preceding P wave |
| What is the description given by a patient with PVCs? | "Skipping a beat" sensation |
| Which leads will have ST-elevation with an MI of the Left Circumflex artery? | Leads I, aVL, V5 and V6 |
| Which artery supplies the left lateral portion of the heart? | Left circumflex artery |
| What is the most common cause of a distributive shock? | Sepsis |
| What are the main hemodynamic changes of a distributive shock? | High cardiac output and low SVR |
| What type of shock would be defined by low SVR and high CO? | Distributive shock |
| What is the simplest and main definition of a Hypovolemic shock? | Low circulating volume |
| What type of shock would be seen in a patient with a severe hemorrhage? | Hypovolemic shock |
| What is the main deficit or cause of a Cardiogenic shock? | Poor pump function |
| What are the main causes of the development of a Distributive shock? | Systemic vasodilation and decrease in SVR |
| What shock is due to extracardiac obstruction blood flow? | Obstructive shock |
| Which adrenoreceptor is stimulated by NE to increase myocyte contractility? | β1-adrenergic receptor |
| What is the result of β1-adrenergic receptor stimulation by NE? | Increased calcium influx into the cells |
| Which particularly important artery is derived from the 3rd aortic arch? | Common and Internal carotid arteries |
| ECG: Varying P wave morphologies and R--R intervals, most commonly in patients with COPD. Dx? | Multifocal Atrial Tachycardia |
| What is a common arrhythmia observed in COPD patients? | Multifocal Atrial Tachycardia |
| What are BNP levels often used for? | Rul out non-cardiac cause of dyspnea |
| What is BNP? | Sensitive marker for congestive HF and is released by ventricles in response to high volume or pressure |
| What is the significance of BNP levels in heart failure? | It will be elevated in both systolic and nonsystolic heart failure |
| What is secreted by the ventricles in response to high volume or pressure levels? | BNP |
| What is the role of BNP? | Decrease sodium reabsorption by acting in the renal collecting ducts, leading to an increase in GFR and causing urinary sodium loss |
| To which part of the ECG tracing does ventricular repolarization correlate to? | T-wave |
| T waves on ECG, are representative of which cardiac action potential phase? | Ventricular repolarization |
| How is ventricular repolarization depicted on the ECG? | T-wave |
| Which wave on the ECG represents atrial depolarization? | P-wave |
| Which wave on the ECG represents ventricular depolarization? | QRS complex |
| Which waver on the ECG represents ventricular repolarization? | T-wave |
| How is sepsis defined? | Fever, leukocytosis, tachycardia, and increased respiratory rate |
| When does Septic shock occur? | Failure to recover blood pressure with volume resuscitation |
| Septic shock will eventually lead to ==> | Decreased PCWP and PVR, with overall increased cardiac output |
| Is CO decreased or increased, in Septic Shock? | Increased |
| What are the main mediators of Coronary artery vasodilation? | Nitric oxide and adenosine |
| What is controlled by Nitric Oxide (NO) and adenosine? | Coronary artery vasodilation |
| What is the first line of treatment of Systolic heart failure? | ACE inhibitors |
| MOA of ACE inhibitors: | Disrupt conversion of AT I into AT-II, leading to decrease activation of Gq and decreased activity of phospholipase C in vascular smooth muscle |
| Which G-pathway is interrupted by ACE inhibitors? | Gq pathway |
| What does the decrease activation of the Gq pathway lead to? | Decrease activity of phospholipase C in vascular smooth muscle |
| What condition is associated with Pulsus paradoxus? | Pericarditis |
| What are the hemodynamic changes seen with Pulsus Paradoxus? | Increased RV filling, decreased LV filling, and decreased stroke volume during inspiration |
| Which heart chamber has a decreased filling in Pulsus paradoxus? | Left ventricle |
| Which phase of the cardiac action potential do B-blocker act on? | Phase 4 and Phase 0 |
| B-blockers, lead to: | Decrease cAMP production and PKA activate to reduce phase 4 and phase 0 slopes |
| What is the result of decrease slopes of Phase 4 and 0 by beta blockers? | Slow down heart rate and AV node conducting velocity |
| MR is characterized by an INCREASE in: | Left atrial pressure during systole |
| What causes the elevated LA pressure in MR? | Regurgitation of blood from the left ventricle not the left atrium through an insufficiency mitral valve |
| What is the auscultatory description of Tricuspid valve regurgitation? | Holosystolic, blowing murmur beast hear at the LLSB |
| What is the S3 heart sound? | Diastolic heart sound heard in states of volume overload and/or ventricular enlargement, particularly in systolic heart failure |
| What are maneuvers that increase preload? | Abrupt squatting, passive leg raise, and volume expansion |
| What is the effect on S3 by maneuvers that increase preload? | Accentuate the S2 heart sound |
| What are two ways to calculate SV? | = EDV - ESV = CO / SVR |
| What is a way to calculate CO? | (Rate of oxygen consumption)/ (arterial oxygen - venous oxygen) |
| What is the most common cause of Pulmonary edema? | Congestive heart failure |
| How is Pulmonary edema clinically presented? | Bilateral crackles and dyspnea and usually precipitated by MI |
| Which common events may precipitate the development of a Pulmonary edema? | MI, infections, increased sodium intake, or the discontinuation of CHF medications |
| Which Starling pressure is increased in Cardiogenic Pulmonary edema? | Capillary fluid hydrostatic pressure |
| What causes the increase in capillary hydrostatic pressure in Pulmonary edema? | Left ventricular systolic or diastolic dysfunction, which leads to fluid moving from the capillaries into the alveoli |
| What condition is characterized by the movement of fluid from the capillaries into the alveoli? | Pulmonary edema |
| What are some features caused by mitral stenosis? | Atrial enlargement, high pulmonary capillary pressures, and pulmonary edema |
| Which heart murmur often causes atrial enlargement, high pulmonary capillary pressures, and pulmonary edema? | Mitral stenosis |
| How is Aortic dissection presented clinically? | Sudden-onset pain in the chest and back and a widened mediastinum on CXR |
| What is the most common association of Aortic dissection? | Severe hypertension |
| What are some important risk factors for development Infective endocarditis? | IV drug use, dialysis, and dental procedure |
| What condition is due to reversal of a left-to-right shunt? | Eisenmenger syndrome |
| How is Eisenmenger syndrome presented? | Cyanosis and hypoxemia |
| Is the murmur associated with HCM systolic or diastolic? | Systolic murmur |
| Does standing cause an increase or decrease in preload? | Decrease preload |
| How can a person cause a decrease in preload and intensity a HCM murmur? | Standing |
| What is the definition of "decreased preload"? | Decreased left ventricular blood volume |
| What are common maneuvers that will decrease preload? | Valsalva maneuver Standing Hypovolemia Nitrates Beta agonists |
| What does an increase in preload mean? | Increased left ventricular blood volume |
| An increase in preload will cause a decrease or increase HCM murmur intensity? | Decrease murmur |
| What some common maneuvers lead to an increase in preload? | Leg elevation Squatting Volume expansion Hand grip Alpha agonistes |
| Decrease or Increases Preload: Valsalva? | Decrease preload |
| Decrease or Increase Preload: Standing? | Decrease preload |
| Decrease or Increase Preload: Hypovolemia? | Decrease preload |
| Decrease or Increase Preload: Nitrates and B-agonists? | Decrease preload |
| Decrease or Increase Preload: Leg elevation? | Increase preload |
| Decrease or Increase Preload: Squatting? | Increase preload |
| Decrease or Increase Preload: Hand grip? | Increase preload |
| Decrease or Increase Preload: Volume expansion and alpha agonists? | Increase preload |
| What conditions are two causes that develop LV hypertrophy? | HCM and severe and chronic Aortic stenosis |
| What chamber is increased (hypertrophied) in a patient with chronic, severe Aortic stenosis? | Left ventricle hypertrophy |
| What causes chest pain in HCM? | Increased oxygen demand due to LV hypertrophy |
| What is the main maneuver to cause an increase in Venous return /Preload? | Leg raise and Squat |
| What are the main maneuvers to cause a decrease in Venous return/preload? | Valsalva and Standing |
| Which maneuver is known to mainly cause in increase in afterload? | Handgrip |
| Which drug is used to specifically decrease the afterload? | Amyl nitrate |
| Which murmurs increase intensity by an increase in Preload? | MS, AS, MR, AR, and VSD |
| Which are common ways to increase the intensity of MS/MR/AS/AR/VSD? | Leg raise and Squat, as these increase the preload |
| What is the MCC of mesenteric ischemia? | Arterial embolism for a cardiac source |
| How does sepsis cause ARDS? | Neutrophil release of cytokines and proteases, increase capillary permeability and movement of fluid into the alveoli |
| What are the most relevant hemodynamic changes seen with Septic shock? | Decrease PCWP and PVR, with increase CO |
| What is the MCC of systolic HF? | Ischemic heart disease, with or without Hx of MI |
| What does ARVC stand for? | Arrhythmogenic right ventricular cardiomyopathy |
| What is the pathological mechanism of ARVC? | Myocardial cell apoptosis of the RV, which leads to fibrofatty replacement and thinning, dilating, and predisposition to fatal arrhymias |
| What cardiac condition is due to RV tissue replacement with fibrofatty tissue? | Arrhythmogenic right ventricular cardiomyopathy |
| What happens physiologically in bilateral RAS? | Hypoperfusion of the kidneys inducing activation of the RAAS and impairs Na+ excretion, which cause an increase in blood pressure. |
| What type of cardio-related drugs are contraindicated in patients with bilateral RAS? | ACE inhibitors and ARBs |
| Why are ACE-inhibitors and ARBs contraindicated in bilateral RAS? | Kidneys of bilateral RAS patients are dependent on ELEVATED levels of AT II to maintain renal perfusion and support GFR |
| What are the most common clinical features or Pericarditis? | Chest pain that is relieved by leaning forward, a pericardial friction rub, and diffuse ST-segment elevation on ECG |
| What are the ECG findings of pericarditis? | Diffuse ST-segment elevations |
| What is the viral pathogen commonly causative of Pericarditis? | Coxsackie B virus |
| How is ST-segment elevation MI presented? | Sustained chest pain |
| What medication mimics Tissue Plasminogen? | Alteplase |
| What is the role of Alteplase? | Catalyzes the conversion of plasminogen to its active form (plasmin) as part of the fibrinolytic process. |
| What is a commonly "tested" adverse effect of Hydralazine? | Reflex tachycardia and SLE-like syndrome |
| Which enzyme is inhibited by Milrinone? | PDE-3 |
| MOA of Milrinone? | Inhibition of PDE-3 --> increase intracellular cAMP levels in cardiac muscle and vascular smooth muscle |
| What is the effect of increased levels of cAMP n myocardial cells? | Increase cardiac contractility |
| What is the effect of elevated cAMP levels in smooth muscle cells? | Decreased peripheral vascular resistance |
| What is pulsus paradoxus? | Fall in systolic blood pressure of > 10 mm Hg during inspiration |
| What condition is strongly associated with pulsus paradoxus? | Pericardial effusion |
| What is the result of pulsus paradoxus in respect to heart volume? | Increase RV filling, decreased LV filling, and decreased stoke volume during inspiration |
| How is Diastolic HF defined? | Congestive HF with a normal (>50%) LV ejection fraction |
| Nonsystolic HF results in: | 1. Impaired LV filling and, 2. High ventricular pressures --> high LA and PCWP --> dyspnea |
| What are "contraction bands" in a MI? | Histologic structures caused by a massive calcium influx and result in hypercontraction of the sarcomeres |
| What is the term given to the hypercontraction of sarcomeres following a MI? | Contraction bands |
| What are common complications of Aortic Stenosis? | HF with preserved EF, AFIB, and pulmonary HTN |
| What type of heart failure is associated with chronic AS? | Diastolic HF |
| What form of hypertension is seen as a complication of AS? | Pulmonary hypertension |
| AFIB is a common complication of which heart murmur? | Aortic stenosis |
| What is a complication of Left-sided Infectve Endocarditis? | Septic emboli that lodges in the brain, spleen, kidney, and gut. |
| How does a Tension pneumothorax occur? | One-way valve and no capability to escape for air trapped in the pleural space |
| What are features associated with tension pneumothorax? | Hypotension, tachycardia, and mediastinal shift away from the affected side |
| What condition is suspected in a patient with low BP, HR>120, and mediastinal shift to the right, with evidence of severe trauma to the left chest? | Tension pneumothorax |
| Hypertension can be a common cause for: | LV hypertrophy and nonsystolic HF |
| What is a common condition that leads to chronic high afterload and myocyte hypertrophy? | Hypertension |
| Which drugs are known to cause Rhabdomyolysis? | Statins |
| How is Statin-induced rhabdomyolysis clinically diagnosed? | Elevated Cr, heme-positive urine, and no RBC in UA |
| Which antihyperlipidemic medication promotes gallstone formation? | Fibrates |
| How do fibrates promote gallstone formation? | Reducing cholesterol solubility and bile acid synthesis via inhibition of 7-α-hydroxylase |
| Which enzyme is inhibited by Fibrates? | 7-α-hydroxylase |
| How do nonselective B-blockers help in cardiac pathologies? | Decrease heart rate, contractility, and renin release |
| Which pump is directly inhibited by Digoxin? | Na+/K+ pump |
| Which pump is INDIRETCTLY inhibited by Digoxin? | Na+/Ca2+ exchanger |
| Does the use of Digoxin increase or decrease Ca2+ intracellularly? | Increase intracellular Ca2+ |
| Does digoxin have a positive or negative inotropic effect on the heart rate? | Positive inotropic effect |
| Which very common drug produces an indirect increase intracellular Ca2+ and a positive inotropic effect on HR? | Digoxin |
| MOA of Fibrates: | Stimulate lipoprotein lipase by active the PPAR-α protein |
| Which enzyme is ultimately stimulated by fibrate activation of the PPAR-a-protein? | Lipoprotein lipase |
| What are the most common adverse effects of Adenosine? | Flushing, hypotension, chest pain, bronchospasm, and a sense of impeding doom |
| What are common adverse effects of Niacin? | Flushing and increasing risk of gout |
Created by:
rakomi
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