CVS/Cardio Flashcards
Most efficient extractor of oxygen from the blood
Heart
Intracellular junctions responsible for the cardiac syncytium
Gap junctions
Substance that dilates upstream blood vessels
Endothelium-derived relaxing factor (EDRF) aka Nitric oxide (NO)
Most potent vasoconstrictor
ADH (can increase levels of Endothelin-1)
An increase in venous return will increase the heart rate
Brainbridge reflex
An increase in venous return will increase the stroke volume.
Basis: stretching if cardiac sarcomeres will increase contraction
Frank-starling mechanism
Hypertension
Irregular respiration
Bradycardia
Due to activation of the CNS ischemic response and baroreceptor reflex in increased ICP
Cushing reflex
Formula for Blood pressure based ob Ohm’s Law
BP= CO x TPR CO= HR x SV
TPR is synonymous with SVR and increases when arterioles vasoconstricted
Normal pressures at various parts of adult circulation
Large arteries: <120/80 mmHg Sytemic capillaries: 17 mmHg Vena cava : 0 mmHg Pulmonary artery : 25/8 mmHg Pulmonary capillaries : 7 mmHg
At least 10 second pressure over the RUQ
+ response: sustained rise of >3 cm in JVP for at least 10-15 sec after release of the hand
Abdominojugular reflux
Pansystolic murmur of tricuspid regurgitation
Louder during inspiration and diminishes during forced expiration
Carvallo’s sign
Apical pulse is reduced and may retract in systole in CONSTRICTIVE PERICARDITIS
Broadbent’s Sign
High pitched, diastolic, decresendo blowing murmur along the left sternal border due to dilation of the pulmonary valve ring
- occurs in Mitral Valve disease and severe Pulmonary Hypertension
Graham Steell Murmur
Condition where the murmur of Aortic Stenosis may be transmitted downward and to the apex and may be confused with the sytolic murmur of Mitral Regurgitation
Gallavardin Effect
Peripheral Signs of AORTIC REGURGITATION
- ) CORRIGAN’S PULSE: rapidly rising “WATER HAMMER” pulse that collapses suddenly as arterial pressure falls rapidly during late systole and diastole
- ) QUINCKE’S PULSE: capillary pulsations , alternate flushing and paling of the skin while pressure is applied to the tip of the nail
- ) TRAUBE’S SIGN: booming “PISTOL SHOT” sound heard over the femoral arteries
- ) DUROZIEZ SIGN: to-and-from murmur audible if the femoral artery is lightly compressed with steth
Most noninavsive marker of increased CV morbidity/mortality risk
LVH (Left Ventricular Hypertrophy)
Cornerstone in the diagnosis of acute and chronic heart disease
ECG
Ideal imaging modality for cardiac emergencies
2D-ECHO
Gold standard for imaging valve morphology and motion,detection of pericardial effusion and cardiac tamponade, and assessment of LV cavity size, systolic function and wall thickness
2D- ECHO
Gold standard for assessing LV mass and volumes
MRI
Imaging modalities of choice for the evaluation of suspected aortic aneurysm or aortic dissection and in distinguishing between restrictive and constrictive pericarditis
CT scan and MRI
Gold standard in assessing the anatomy & physiology of the heart & associated vasculature
Cardiac catheterization and coronary angiography
Triad of RUPTURED ANEURYSM
- ) Left flank pain
- ) Hypotension
- ) Pulsatile mass
Diagnostic triad of Wolff-Parkinson-White (WPW) ECG Pattern
- ) Wide QRS complex
- ) Relatively short PR interval
- ) Slurring of the initial part of QRS complex ( delta wave)
Triad of CHRONIC RENAL FAILURE in ECG
- ) Peaked T waves (HYPERKALEMIA)
- ) Long QT d/t ST segment lengthening (HYPOCALCEMIA)
- ) LVH ( sytemic hypertension)
3 principal features of tamponade (BECK’S TRIAD)
- ) HYPOTENSION
- ) SOFT/ABSENT HEART SOUNDS
- ) JV DISTENTION with prominent x descent, absent y descent
Plaques that have caused fatal thromboses tend to have
- thin fibrous caps
- relatively large lipid cores
- high content of macrophages
Major determinants of myocardial O2 demand (MVO2)
- Heart rate
- Myocardial contractility
- Myocardial wall tension (stress)
Triad of BUERGER’S DISEASE
- claudication of the affected extremity
- Reynaud’s phenomenon
- Migratory superficial vein thrombophlebitis
VIRCHOW’S TRIAD
- stasis
- vascular/endothelial damage
- hypercoagulability
DRESSLER’S TRIAD
Post MI Pericarditis
- fever
- pleuritic pain
- pericardial effusion
Drugs that INCREASES CONTRACTILITY
- Digoxin
- Dobutamine
- Milrinone
Drugs that REDUCES PRELOAD
- Diuretics ( furosemide)
- Vasodilators ( NItrates, Hydralazine)
- ACEI/ARBS
Drugs that REDUCES AFTERLOAD
- Diuretics ( furosemide)
- Vasodilators ( NItrates, Hydralazine)
- ACEI/ARBS
- Beta Blockers ( Metropolol succinate, Bisoprolol, carvedilol)
Drug for HF:
- binds to activated Na channels and blocks flow of Na ions into cardiac myocyte ( prolongs AP)
IA ( Quinidine, Procainamide, Disopyramide)
Clinical use:
- Afib
- Atrial flutter
- V tach
Drug for HF:
- bind to both activated and inactivated Na channels (shortens AP)
IB ( Lidocaine, Tocainide, Mexiletine)
Clinical use:
- Post ischemic arrhythmia
- V fib
- V tach
Drug for HF:
- binds to activated Na channels ( no effect on AP)
IC (Flecainide, Encainide, Propafenone)
Clinical use:
- tx of severe refractory Ventricular arrythmia
Drug for HF:
- blocks Beta 2 receptors
II ( Propanolol, Metropolol)
Drug for HF:
- bind and block K channels ( prolongs AP)
III ( Sotalol, Ibutilide, Bretylium, Amiodarone)
Clinical use:
- atrial and ventricular arrythmias
Drug for HF:
- blocks voltage gated Ca channels
IV ( Verapamil, Diltiazem)
Clinical use:
- Supraventricular tachycardia
- rate reduction in patients with atrial fibrillation
Drugs in HPN:
- causes Na excretion and reduction in blood volume
Diuretics
Drugs in HPN:
- CCB, VESSELS> heart
DHT ( Dihydropyridines)
- Nifedipine
- Felodipine
- Amlodipine
Drugs in HPN:
- CCB, HEART> vessels
Non DHT
- Verapamil
- Diltiazem
Drugs in HPN:
- decreases work load of heart
Beta blockers
Drugs in HPN:
- blocks AT1 receptor of Angiotensin II
ARB’s
Drugs in HPN:
- notorious for drug induced cough by increasing bradykinins
ACEI
Drugs in HPN:
- blocks aldosterone action in collecting tubules
Spirinolactone, Eplerenone
Drugs in HPN:
- Hypertension with BPH
Alpha 1 Antagonists ( Prazosin)
Drugs in HPN:
-maintainace for PRE ECLAMPSIA
Methyldopa
Physiologic basis for normal ECG tracing
- P wave : atrial depo
- QRS complex: vent depo
- T wave: vent repo
Master pacemaker of heart
SA node
Causes depolarization of SA node
Ca influx
Only electrical connection between atria and ventricles
AV node
Failure to increase heart rate during exercise
- <100 bpm
Chronotrophic Incompetence
Most common arrythmia mechanism
Reentry
Only reliable therapy for symptomatic bradycardia in the absence of extrinsic and reversible etiologies
Permanent pacemaking
Most rapid conduction in the heart
His bundle and Bundle branches
Most expeditious technique in the management of AV conduction block
Transcuatneous pacing
Most common arrythmia during extended ECG monitoring
Atrial Premature Complexes
Most common sustained arrythmia
Atrial Fibrillation
Prolongation of PR interval before dropped QRS complex
Mobiltz Type I
- I gets taller
No prolongation of PR interval before dropped DRS complex
Mobitz Type II
Duration that distinguishes sustained from nonsustained ventricular tachycardia
> 30 seconds
Most common POST MI arrythmia
Premature Ventricular Contraction (PVC)
Most common lethal POST MI arrythmia
Ventricular Fibrillation
Most common cause of SYSTOLIC dysfunction that leads to Left Sided HF
Coronary Artery Disease (CAD)
Most Common cause of DIASTOLIC that leads to Left Sided HF
Concentric LVH due to HPN
Most common cause of Right sided HF
Left sided HF
Earliest cardinal symptom of Left sided HF
Dyspnea
Earliest cardinal sign of Left sided HF
Left sided S3
Presentation of Left sided HF
- Dyspnea
- left sided S3
- PND
- MV regurgitation
- inc BNP
- siderophages ( Hemosiderin laden macrophages of HF cells)
- Pulmonary edema ( septal edema, peribronchiolar edema)
Presentation of Right sided HF
- Peripheral ankle edema (HM of Right sided HF)
- NVE
- tricuspid regurgitation
- ascites
- chronic passive congestion of liver (nutmeg liver)
- cardiac cirrhosis
Most sensitive index of cardiac function
Ejection fraction
Single most important bedside measurement to estimate volume status
JVP (internal jugular vein preferred)
Cardinal symptoms of HF
- Fatigue
- SOB
Most important mechanism of dyspnea in HF
Pulmonary congestion with accumulation of interstitial or intra alveolar fluid, which activates juxtacapillary J receptors
Only pharmacologic agents that can adequately control fluid retention in advanced HF
Diuretics
Major problem of Aldosterone antagonists
development of life threatening Hyperkalemia
Cornerstones of modern therapy for HF with a depressed EF
ACEI/ARBS and Beta blockers
Most common side effect of all vasodilating agents
Hypotension
Most commonly used inotropic agents for acute HF
Dobutamine
First choice for therapy in which modest inotropy & pressor support are required
Dopamine
Most common reason for rehospitalization in HF
Failure to meet criteria for discharge
Most common symptom of cor pulmonale
Dyspnea
Murmurs that always signify structural heart disease
Diastolic murmurs (Grade I-II systolic murmurs are usually benign)
- Opening snap
- mid-late diastolic murmur
- typical tethering and diastolic doming on 2D echo
- atrial fibrillation
MITRAL STENOSIS
Leading cause of Mitral stenosis (MS)
Rheumatic Heart Disease
Pansystolic murmur, may due to Mitral valve prolapse
Mitral Regurgitation
Papillary muscle involved more frequently in acute MR because of single blood supply
Postmedial papillary muscle
Most prominent complaints in chronic sever MR
- fatigue
- exertional dyspnea
- orthopnea
Most important finding on auscultation in MVP
Mid- or late (non-ejection) systolic click
Most common ECG finding in MVP
Normal
Most common cause of midsystolic murmur in an adult
Aortic stenosis (AS)
Most common congenital heart valve defect
Bicuspid Aortic Valve Disease
3 cardinal symptoms of AS
- Exertional dyspnea
- Angina pectoris
- syncope