Rx_1.13 (Cardio) Flashcards
Histologic description of Aschoff bodies
- aschoff body = indicates rheumatic heart dz
- aschoff body = non-caseating granuloma w/multi-nucleated giant cells
Anatomical location of jugular vein
- within carotid sheath
- lateral to the carotid artery
- anterior to the vagus nerve
Young girl w/hypertension @ extremities + narrowing of thoracic aorta on aortogram ==> dx?
- coarctation of aorta
- possibly Turner Syndrome (XO), esp. if other features present
Common features of Turner’s Syndrome
- short stature
- webbed neck
- coarctation of aorta
- bicuspid aortic valve
- streak ovaries
- primary amenorrhea
Fick principle (for calculation of CO)
CO = (total O2 body consumption)/(arterial O2 - venous O2)
Intact right hemidiaphram elevated above left on (inspiratory) xray ==> dx?
damaged right phrenic nerve
Possible severe consequence of untreated UTI
- pyelonephritis
- sepsis
- acute kidney failure ==> hyperkalemia
Common dangerous feature of acute kidney failure
- indicators = high BUN, high creatinine
- consequence = hyperkalemia ==> cardiac arrhytmias
ECG finding in hyperkalemia
- peaked T waves
Presentation of Staph Aureus endocarditis
- acute onset
- IV drug user
- tricuspid valve ==> systolic murmur
- septic emboli from right side ==>
- cough
- pleuritic chest pain
- diffuse pulmonary infiltrates
- pyoneumothorax
Characteristics of S. aureus
- gram +, facultative, cluster-forming anaerobe
- catalase +, coagulase +
- beta-hemolytic
- produces golden yellow pigment in culture
Fxn of carotid sinus baroreceptors
- facilitate response to hypotension
- sends afferent signals via glossopharyngeal nerve to medulla to control sympathetic outflow
- hypotension ==> decreased firing ==> increased sympathetic outflow
- transduce pressures from 50-180mmHg
Fxn of aortic arch baroreceptors
- respond to increases in blood pressure
- less sensitive than carotid sinus
- respond to stretch caused by BP @ 110-200 mmHg
- receptors do not fire in hypotensive state
Characteristics of phases 1-4 of ventricular AP
- 0 = rapid upstroke and depolarization
- voltage-gated Na channels open
- 1 = initial repolarization
- inactivation of voltage-gated Na channels
- K channels begin to open
- 2 = plateau
- Ca influx from volt-gate Ca channels balances K efflexu
- Ca influx triggers release of Ca from sarc reticulum and myocyte contraction
- 3 = rapid repolarization
- massive K efflux due to opening of slow K channels and close of Ca channels
- 4 = resting
- high K permeability through K channels
fixed and widely split S2 ==> dx? (+mechanism)
- Atrial Septal defect
- normal cause for splitting:
- inspiration ==> decreased intrathoracic pressure ==> increased venous return @ RA/RV ==> delayed closure of pulmonic valve
- in ASD:
- shunt ==> constant blood flow across from L => R leads to increased flow into RA/RV ==> constant delay of pulmonic valve independent of breath
3rd trimester pregnant woman + light-headedness when supine ==> dx?
- Inferior vena cava compression by large uterus ==> reduced cardiac output
Tx for pregnant woman w/IVC compression
- lie on left side/prop up right hip
Class of antiarrhytmics that prolong repolarization
- Class III antiarrhythmics
- amiodarone
- sotalol
Characteristics of sotalol
- b-blocker
- antiarrhytmic w/class II and class III properties
Acebutolol: MOA, use
- B1- selective antagonist
- class II antiarrhymic agent
- use: suppresses ventricular ectopic beats
Esmolol: MOA, use
- rapid-acting B antagonist
- class II antiarrhytmic
- use = IV control of afib
Metoprolol: MOA, use
- B1 - selective antagonist
- class II antiarrhymic
Propanolol: MOA, use
- nonselective B antagonist
- class II antiarrhytmic
- use:
- slows sinus rhythm
- prolonged PR interval
Dx + possible causes?
- Torsades de pointes
- potentially fatal rapid ventricular rhythm
- causes
- hypokalemia
- can be caused by K channel blockers (e.g. sotalol)
- congenital syndrome
- e.g. long QT syndrome
- quinidine (antiarrhythmic)
- hypokalemia
“5 T’s” of neonatal cyanosis
- Tetrology of Fallot
- Transposistion of the great vessels
- Truncal arteriosus
- Tricuspid atresia
- Total anomalous pulmonary venous return
cyanotic newborn immediately after birth + mother w/DM ==> dx?
- transposition of great vessels
Tx of transposition of great vessels
- create an atrial shunt if none exists
- give prostaglandin E1 to maintain patent ductus arteriosis
- corrective surgery once infant is stabilized
Rates of conduction in cardiac electrical system
- fastest to slowest:
- His-purkinje (1-4 m/s)
- large cells, many gap jxns
- SA node (1 m/s)
- small cells, few gap jxns
- less time to depolarize
- AV node (0.05 m/sec)
- small cells, few gap jxns
- slow-rising/low-amp APs
- His-purkinje (1-4 m/s)
Tx for Viridans strep endocarditis
Penicillin G
Mitral stenosis murmur
- late, rumbling diastolic murmur at apex
Signs of acute rheumatic fever
- FEVERSS:
- Fever
- Erythema marginatum
- nonpruritic, circular, pink eruption on trunk
- Vavular damage
- Erythrocyte sedimentation rate increased
- Red-hto joints
- Subcutaneous nodule
- Saint Vitus’ dance
