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Uworld Cardio > Cardio 9 > Flashcards

Cardio 9 Flashcards

1
Q

What is the common causes of aortic regurgitation⁉️

A

Aortic root dilation, post inflammatory, congenital bicuspid aortic valve

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2
Q

What can cause aortic root dilation?

A

Marfan syndrome, syphilis

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3
Q

What can cause aortic valve to become inflamed

A

Rheumatic heart disease, endocarditis

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4
Q

What other organ can aortic regurg affect? Pathophysiology?

A

Increase left ventricular end diastolic pressure will cause pulmonary congestion

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5
Q

What kind of heart failure well aortic regurgitation result in? Pathophysiology?

A

Excessive left ventricular stretching later leads to decreased stroke volume and decrease forward blood flow

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6
Q

What happens to stroke volume, cardiac output, LVEDV in aortic regurgitation?

A

Increase LVEDV; compensatory myocardio hypertrophy and ventricular enlargement initially maintains stroke volume and cardiac output

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7
Q

What are the clinical features of aortic regurgitation?

A

Heart failure symptoms, early diastolic decrescendo murmur, widen pulse pressure, collapsing/water hammer pulse

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8
Q

How is aortic regurgitation best heard?

A

Left sternal border while patient is sitting up leaning forward and holding a breath and full expiration

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9
Q

How is bicuspid aortic valve developed?

A

Some cases are developed sporadically, others have an autosomal dominant with incomplete penetrance

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10
Q

How can sudden death result from dilation of the aorta?

A

Dilation of the aortic root or ascending aorta can progress to aortic aneurysm and dissection sometimes causing sudden death

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11
Q

What is the most common cause of AR in developing world? Developed countries in young adults?

A

Rheumatic heart disease; bicuspid aortic valve

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12
Q

What is the murmur heard by hypertrophic cardio myopathy? What can increase the intensity of the murmur?

A

Crescendo decrescendo systolic murmur best heard at the apex; Valsalva maneuver or abrupt standing decreases preload and increases the intensity of the murmur; squatting leg elevation isometric handgrip all increase preload and decrease the intensity of murmur

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13
Q

What makes Theophylline a dangerous drug⁉️

A

Narrow therapeutic index

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14
Q

How does toxicity occur in Theophylline⁉️

A

Reduce clearance, decrease metabolism do two saturation of metabolic pathways, inhibition of cytochrome oxidase system enzymes

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15
Q

How is Theophylline predominantly metabolized?

A

Cytochrome oxidase system in the liver

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16
Q

How can cytochrome oxidase system enzymes in the liver be inhibited⁉️

A

Concurrent illnesses ( cirrhosis, cholestasis, respiratory infection with fever); drugs (Cimetidine, ciprofloxacin Erythromycin clarithromycin verapamil)

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17
Q

What are the symptoms of toxicity for Theophylline⁉️

A

Central nervous system stimulation ( headache, insomnia, seizures); G.I. disturbances (nausea vomiting) and cardiac toxicity (arrhythmias)

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18
Q

What is the best step in a patient who is experiencing the Theophylline toxicity resulting from ciprofloxacin drug intake?

A

Measure serum Theophylline levels to assess for toxicity

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19
Q

What are the most common symptoms associated with pulmonary embolus? Examination findings? What are the other symptoms that can be found?

A

Shortness of breath, pleuritic chest pain; tachypnea tachycardia and hypoxemia; hemoptysis, DVT signs, Low-grade fever

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20
Q

Why is untreated PE have a mortality risk up to 30%?

A

Re-current embolisms is common

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21
Q

What is the best initial treatment for PE? What if the patient also has low GFR?

A

Anticoagulation (heparin); can’t use enoxaparin, fondaparinux, rivaroxaban if the patient has severe renal insufficiency, because reduce renal clearance of anti-Xa activity increases levels and increases bleeding risk

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22
Q

What treatment can be used in a PE patient that has severe renal insufficiency? Why?

A

Unfractionated heparin, more convenient to monitor therapeutic level the activated PTT.

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23
Q

What is the full anticoagulation treatment for PE patients?

A

Heparin until produces therapeutic anticoagulation (goal PTT>1.5~2 times normal), wondering is initiated which can take up to 5 to 7 days to reach therapeutic levels. After reaching therapeutic INR, heparin can be stopped and warfarin can be continued long-term

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24
Q

What is the benefit of taking rivaroxaban⁉️

A

Oral anticoagulant with immediate onset of action therefore no bridging with heparin is indicated. However it can’t be used with patients with renal insufficiency

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25
Q

What is considered severe renal insufficiency⁉️

A

Estimated glomerular filtrate rate < 30 Ml/min/ 1.7 3m2

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26
Q

What are the initial drugs given for stabilization of and acute STEMI⁉️

A

Supplemental oxygen, aspirin 325 Clopidigrel, nitrates (sublingual), beta blocker, high dose Statin (atorvastatin 80 mg), anticoagulation depending on revascularization

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27
Q

In what instance would you not give an acute STEMI patient a beta blocker?

A

Hypotension, bradycardia, chronic heart failure, heart block

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28
Q

When would you give a STEMI patient O2?

A

Saturation less than 90%, or dyspnea

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29
Q

What occurs when after treatments STEMI patient has persistent pain, hypertension, or heart failure

A

Intravenous nitroglycerin

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30
Q

What are the contraindications of nitroglycerin for STEMI patients⁉️

A

Hypotension, right ventricular infarct, or severe aortic stenosis

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31
Q

What is given for treatment in persistent severe pain in acute STEMI patients⁉️unstable sinus bradycardia?

A

IV morphine; IV atropine

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32
Q

What is giving to a acute patients with pulmonary edema⁉️ what are the contraindications?

A

IV furosemide; hypotension or hypovolemic

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33
Q

What is the physical examination findings for aortic stenosis? History Findings⁉️

A

Narrow pulse pressure, increased intensity of apical impulse, typical Systolic murmur; Exertional syncope

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34
Q

What is the first-line agent for rapid pain relief in angina pectoris?

A

Sub lingual nitroglycerin

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35
Q

How does the lingual nitroglycerin relieve angina rapidly, mechanism⁉️

A

Systemic vasodilation with decrease let ventricular and diastolic volume and while stress resulting in decreased my cardio oxygen demand

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36
Q

What is the most common cause of community acquired pneumonia? What are the manifestations associated?

A

Streptococcus pneumonia; abrupt fever chills productive cough leukocytosis x-ray evidence of lobar infiltrate

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37
Q

What are all the lung problems that chest x-ray can reveal?

A

Pulmonary edema, consolidation, Pleural effusion, pneumothorax, Hypodensity

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38
Q

What is the initial management of acute exacerbation of chronic obstructive pulmonary disease (AECPOD)⁉️

A

Inhaled short acting bronchodilators, glucocorticoids, and antibiotics

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39
Q

What kind of AECOPD patients who would be considered for noninvasive ventilatory support?

A

Patient with continued symptoms despite medical management

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40
Q

How is non-invasive positive pressure ventilation NPPV delivered?

A

Facemask rather than endotracheal tube, can be continuous positive airway pressure or bilevel positive airway pressure.

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41
Q

What is the preferred method of respiratory support and patience with AEE COPD? What does it do?

A

Non-invasive positive pressure ventilation, decreases work of breathing, improves alveolar ventilation

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42
Q

What are the physiological benefits and using NPPV?

A

Decreases respiratory rate, decreases PaCO2, increases tidal volume, minute ventilation, and PaO2

43
Q

What are the indications for NPPV⁉️

A

The indications with strong as evidence are: 1) hypercapnic respiratory failure due to COPD

2) Cardiogenic pulmonary Edema
3) acute respiratory failure
4) facilitate early extubation

44
Q

What kind of Acute respiratory failure has indications for NPPV⁉️

A

Post operative hypoxemic respiratory failure or, immunocompromise patients

45
Q

What are the contraindications for non-invasive positive pressure ventilation?

A

Cardiac or respiratory arrest or pending arrest, severe acidosis pH less than 7.1, acute respiratory distress syndrome, non-respiratory organs failure, inability to protect airway as in uncooperative or agitated patient, inability to clear secretions resulting in higher aspiration risk, recent esophageal anastomosis, facial or neurological surgery/deformity, Upper airway obstruction, pg 260

46
Q

How does metabolic acidosis occur in post-ictal state?

A

lactic acidosis from prolonged enforceable skeletal muscle activity=> metabolic acidosis with a decrease HCO3

47
Q

How can respiratory acidosis occur in post-ictal state patient⁉️

A

Hypoventilation resulting in respiratory acidosis=> normal or elevated serum bicarbonate

48
Q

What acid-base problem results from Renal failure patients? Why?

A

Metabolic acidosis due to inadequate excretion of metabolically produce acids (sulfates, phosphates)=> Low pCO2 and low bicarbonate level

49
Q

What is the most common acid-base disturbance caused by pulmonary embolism⁉️Why?

A

Respiratory alkalosis due to hyperventilation as a patient tries to overcome hypoxia and VQ mismatching=> low pCO2

50
Q

What tachycardiac patient can qualify for synchronized cardioinversions?

A

Persistent tachyarrthythmia causing hemodynamic instability

51
Q

What is the pathophysiology of ARDS⁉️

A

Lung injury=> fluid/cytokine leakage into alveoli.

Impaired gas exchange, decreased lung compliance, PHTN

52
Q

What is the management of acute respiratory distress syndrome⁉️

A

Mechanical ventilation (Low TV, high PEEP, permissive hypercapnia)

53
Q

ARDS typically Manifests with what?

A

Dyspnea, cyanosis, tachypnea, tachycardia, diaphoresis, diffuse crackles

54
Q

ARDS is characterized by what?

A

Increased permeability of the alveolar capillary membrane leading to flooding of alveolar space with proteinaceous Edema fluid

55
Q

What triggers ARDS?

A

Direct injury to the lung as observed in aspiration pneumonia, smoke inhalation, near drowning, systemic injury, such as trauma sepsis, burns, long bone fractures, pancreatitis, uremia, transfusion therapy, shock, drugs, cardiopulmonary bypass; most common being aspiration and sepsis

56
Q

What causes the decrease in compliance in ARDS patients⁉️

A

Injury to the lung epithelium decreases resorption of water from alveolar space and causes secretion of abnormal or in adequate adequate quantities of surfactant

57
Q

How does ARDS cause noncardiogenic pulmonary Edema? How does it results in increased work of breathing⁉️

A

Increased permeability pulmonary Adema, right to left intrapulmonary shunting of blood results in refractory hypoxemia and decreased lung compliance that increases the work of breathing

58
Q

How is acute respiratory distress syndrome diagnosed?

A

Hypoxemia, bilateral lung opacities (pulmonary Edema not due to congestive heart failure or or fluid overload), New/worsening respiratory distress within one week of insult

59
Q

How does inoculation occur with histoplasma Capsulatum? How does it usually present?

A

Soil contamination by bird or bat droppings; subclinical immunocompetent patients however subacute pulmonary illness can occur if high dose of exposure

60
Q

What are the common causes of Transudate Pleural effusion?

A

Congestive heart failure or, cirrhosis, nephrotic syndrome, peritoneal dialysis

61
Q

What are the most common causes of exudate Pleural effusion?

A

Infections, malignancy, connective tissue diseases, inflammatory disorders, coronary artery bypass surgery, fluid from abdomen to Pleural space, pulmonary embolism (most common)

62
Q

How can a patient with congestive heart failure or meet exudative criteria?

A

If the patient received aggressive diuretics prior to thoracentesis

63
Q

What is the lights criteria to distinguish translate from exudate?

A

Pleural fluid protein/serum protein ratio greater than .5

LDH ratio greater than .6

64
Q

What is normal pleural fluid pH? Transudative will be at pH?

A

pH 7.60

pH 7.4-7.55

65
Q

How does the body compensate for chronic hypercapnia⁉️

A

Increasing Reno bicarbonate retention and creating compensatory metabolic alkalosis

66
Q

What kind of patients have chronic respiratory acidosis?

A

Patient with chronic hypoventilation due to COPD, obesity hypoventilation syndrome, or neuromuscular resulting in gradual increase in PaCO2

67
Q

What is the initial management in patients with narrow QRS complex tachycardia⁉️

A

Intravenous adenosine

68
Q

What can supraventricular arrhythmias show in EKGs⁉️

A

Mostly narrow QRS complex tachycardia

Usually no regular P Wave but retrograde P waves can occur

69
Q

What are retrograde P waves?

A

Seen in the beginning or end of QRS complex. Occurs when atria and ventricles are not simultaneous. Can occur as spikes (pseudo-R waves in lead III, pseudo-S waves in aVL) or inverted P waves

70
Q

What are the uses of intravenous adenosine?

A

Narrow QRS complex tachycardia, useful in identifying P waves to clarify diagnosis of atrial flutter or atrial tachycardia, can you determine a proximal supra ventricular tachycardia is by interrupting the AV nodal reentry circuit

71
Q

What further evaluation must occur in patients with first-degree AV block with normal QRS duration?

A

This AV nodal conduction delay requires no further evaluation

72
Q

What should be done for patients who have first-degree AV block and prolong QRS complex?

A

Conduction delay below the AV node and should have Electrical physiology testing to determine the nature

73
Q

When can burr cells occur?

A

Liver disease and end stage renal disease

74
Q

What is Scleroderma Renal crisis?

A

Typically presents with acute renal failure or without previous kidney disease and malignant hypertension.

75
Q

What is seen in your analysis and peripheral blood smear are in scleroderma Renal crisis?

A

Mild proteinuria.
Microangiopathic hemolytic anemia or DIC with schistocytes.
Thrombocytopenia

76
Q

What is found in x-ray bronchoscopic biopsy and physical exam and patience with histoplasma capsulatum infection?

A

Bilateral Opacities, hilar lymphadenapathy, bronchoscopic biopsy revealing granulomas in Yeast forms

77
Q

What is the most dangerous complication of Marfan syndrome? How does it present? What is and aortic problem propagation of aortic dissection

A

Aortic dissection, present is tearing chest pain radiating to the back or neck, aortic regurgitation

78
Q

What is a common cause of orthostatic hypotension and orthostatic syncope in elderly patients especially?

A

Hypovolemia

79
Q

What electrolyte urine imbalance is present in patients with hypovolemia? Why⁉️

A

Decreased urine sodium due to decreased renal perfusion and activation of RAAS

80
Q

Why are elderly patients more susceptible to orthostatic hypotension and orthostatic syncope in the setting of hypokalemia?

A

Impaired baroreceptor sensitivity (automatic failure)

81
Q

What are the instances in which hypovolemic patient do not have decreased urine sodium?

A

If they are taking diuretics or experiencing significant Renal impairment

82
Q

What is the clinical presentation of Pancoast tumor⁉️

A

Classic description involves pain radiating down the arm due to tumor erosion into brachioplexus. Erosion into cervical sympathetic chain causing Horners syndrome, C8-T2 neurological involvement, supraclavicular lymph node enlargement and weight loss, SVC syndrome can occur

83
Q

What is Horner’s syndrome⁉️

A

Ipsilateral ptosis, meiosis, anhidrosis over the face and fore head

84
Q

What should be obtained in all patients with syncope? Why?

A

Transthoracic echo cardio gram, due to suspected structural heart disease( aortic stenosis, hypertrophic cardiomyopathy he, Leventry give her dysfunction, cardiac Tamponde)

85
Q

What are the clinical symptoms of aortic stenosis⁉️

A

Exertional symptoms such as chest pain dyspnea dizziness and syncope, delayed and diminished carotid pulse, single and soft S2 audible S4, crescendo decrescendo systolic murmur radiation to carotid

86
Q

What signs on the x-ray may add to the diagnosis pulmonary embolism?

A

Hampton hump and Westermark sign

87
Q

What is associated with poor prognosis of PE?

A

Atrial fibrillation and low oxygen saturation

88
Q

How does reactivated latent tuberculosis present itself?

A

Apical cavitary lesion seen on x-ray, chronic low-grade fever, night sweats, weight loss, hemoptosis

89
Q

What is pulseless electrical (PEA) activity⁉️

A

The presence of organize rhythm on cardiac monitoring without measurable blood pressure or palpable pulse in cardiac arrest patient

90
Q

How should PEA be managed?

A

CPR and vasopressor therapy (epinephrine)=> in order to achieve cerebral and coronary perfusion

91
Q

What are the reversible causes of asystole/pulseless electrical activity?

A

5Hs and 5Ts; Hypovolemia hypoxia hydrogen ions acidosis hypo or hyperkalemia hypothermia; tension pneumothorax Tamponade toxins (narcotics, benzodiazepines) and Thrombosis (pulmonary or coronary), trauma

92
Q

What is seen on the EKG for atrial fibrillation?

A

Irregular RR intervals, absent P waves, narrow QRS complexes

93
Q

What are their prominent findings on ECG for PE patients

A

Prominent S in lead I, Q in lead III, inverted T in lead III

94
Q

What is a serious side effects of long term amiodarone use⁉️ what should be done before the initial use of amiodarone?

A

Pulmonary Toxicity, Thyroid test; pulmonary function test and chest radiograph

95
Q

What are the signs of amiodarone that can be the result of pulmonary toxicity

A

Cough fever and dyspnea

96
Q

Pulmonary toxicity in amiodarone use usually presents with what lung aliments⁉️

A

Acute respiratory distress syndrome and chronic interstitial pneumonitis most common)

97
Q

What myocardial infarction complication can result in rapid decompensation or unresponsiveness at the fifth day?

A

Ventricular free wall rupture

98
Q

For the management of ST EMI what are the dangers of given to patient nitrates?

A

Hypotension, Right Ventricular infarction, Aortic Stenosis

99
Q

What are the options of anticoagulation agent for S TEM I?

A

Unfractionated heparin low molecular weight heparin and bivalirudin

100
Q

What are the risk or contraindications of beta blockers in the management of STEMI⁉️

A

Risk of cardiogenic shock, bradycardia, contraindicated in overt heart failure

101
Q

What is the management for ST segment elevation myocardial infarction⁉️

A

Oxygen, nitrates, Anti-platelet therapy, anticoagulation, beta blockers, PCI, Statin therapy as soon as possible

102
Q

What is required in pulmonary Edema secondary to STEMI⁉️

A

Intravenous Furosemide=> not if patient is hypertensive or hypovolemic

103
Q

What’s the paddle emetic agent causes people a dilation?

A

Cocaine

Uworld Cardio (5 decks)

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