Term
| What is Starling's Law? What is the relationship btw Starling's Law and PreLoad? |
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Definition
| The force of ventricular contraction is proportional to muscle fiber length. As a result of this direct relationship, the heart matches its output to the volume of venous return. Preload is the amount of stretch resulting from venous return and determines the force of ventricular contraction. |
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Term
| What is the formula for determining Arterial Pressure? |
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Definition
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Term
| What is main outcome of arterial pressure? |
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Definition
| Arterial Pressure is the force that drives blood through the ARTERIAL side of systemic circulation. |
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Term
| What are the 3 main regulators of ARTERIAL PRESSURE? |
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Definition
| Steady state ANS innervation, Baroreceptor Reflexive ANS control, and RAAS control by the kidney. |
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Term
| What arterial pressure conditions can cause Postural Hypotension? What is the body's response? |
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Definition
| Decreases in AP r/t pooling of blood in veins-->decreased venous return-->decreased CO; decreased SBP, increased HR. |
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Term
| What are the determinants of cardiac output? |
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Definition
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Term
| What are the determinants of Stroke Volume (SV)? |
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Definition
| Myocardial contractility, cardiac AFTERLOAD and cardiac PRELOAD. |
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Term
| What factor contributes to PRELOAD? What is the relationship to SV? |
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Definition
| Force of venous return, an increase in preload will increase the SV |
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Term
| What factor contributes to AFTERLOAD? What is the relationship to SV? |
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Definition
| Arterial pressure that the Left Ventricle has to overcome to eject blood. As afterload increases SV decreases. |
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Term
| What is myocardial contractility? What is it determined by? |
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Definition
| The force with which the ventricles contract. The degree of cardiac dilation primarily determined by the amount of venous return. |
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Term
| What is the relationship of EJECTION FRACTION to SV? |
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Definition
| Ejection fraction = SV/EDV (EDV is end diastolic volume) and lower EF's are a poor indication. |
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Term
| What are the implications of peripheral resistance and pulmonary resistance on CO and blood flow through the CV system? |
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Definition
| Increases in peripheral and pulmonary resistance will increase afterload, decrease SV and decrease CO. Decreased CO decreases blood perfusion throughout the CV system. |
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Term
| What is the definition of INOTROPIC? |
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Definition
| Changes the strength of the heart muscle's contractions. |
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Term
| What is the definition of CHRONOTROPIC? |
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Definition
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Term
| What classes of drugs can DECREASE PRELOAD? |
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Definition
| DIURETICS and VENOUS DILATORS: ACE IHI, ARB, Aldosterone Blockers |
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Term
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Definition
| Body products and fluids. |
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Term
| What classes of drugs DECREASE afterload? |
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Definition
| Arterial Dilators (Ca++ blockers, ACE IHI, ARB's, Antihypertensives) |
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Term
| What classes of drugs INCREASE afterload? |
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Definition
| VASOPRESSORS [causing constriction of blood vessels] (eg dopamine, epinephrine, VASOPRESSIN (aka ADH)) |
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Term
| What is the relationship between CARDIAC DEMAND for O2 and Supply of O2 r/t cardiac output? |
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Definition
| Imbalance btw cardiac O2 supply and demand leads to MI, ischemia and angina pain. |
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Term
| RAS- what are the main actions of angiotensin II? |
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Definition
| ANGIOTENSIN II is a powerful Vasocontrictor; it also promotes the release of aldosterone from the kidneys. |
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Term
| RAS--what are the effects of ALDOSTERONE release from the kidneys? |
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Definition
| Increases blood volume and therefore blood pressure. |
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Term
| Where in the Renin-Angiotensin System (RAS) do ACE Ihi's work? |
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Definition
| They block ACE which prevents it from forming Angiotensin II and Inactivating bradykinin |
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Term
| Where in RAS do BETA BLOCKERS work? |
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Definition
| Decrease renal blood flow and consequently RENIN release. |
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Term
| Where in RAS do ARB's work? |
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Definition
| They block Angiotensin II receptors in BV, the adrenals and all other tissues. |
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Term
| Where in RAS do Direct Renin IHI work? |
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Definition
| They act on Renin to prevent the conversion of Angiotension I to Angiotensin II. |
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Term
| Where in RAS do SARA's work? (selective aldosterone receptor antagonists) |
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Definition
| Block receptors for aldosterone to prevent HTN and heart failure (ie in the kidney activation of aldosterone receptors promotes K excretion and Na/water retention) |
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Term
| ACE IHI: MOA, Indications, Side Effects, Implications: |
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Definition
| Reduces lvls of angiotensin II, TX HTN, heart failure, diabetic nephropathy and MI, PREVENT adverse cardio events in at risk pts; SIDE EFFECTS cough, angioedema, hyperkalemia, first dose hypotension, renal failure FETAL INJURY (2/3 trimester) Implications: can cause Li to build to toxic lvls |
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Term
| ARB: MOA, Indications, Side Effects: |
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Definition
| Block ANGIOTENSIN II receptors, Reduce BP/HTN, Heart Failure, Diabetic Nephropathy, Stroke prevention. Side Effects: Angioedema, Fetal Injury, Renal failure. |
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Term
| Aldosterone Blockers (non selective): MOA, Indications, Side Effects: |
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Definition
| Blocks receptors for Aldosterone AND other steroid hormones. HTN/Heart failure. Gynecomastia, Hirsuitism, Impotence, Menstrual irreg., deeper voice, etc. |
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Term
| SARA's: MOA, Indications, Side Effects: |
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Definition
| Selective antagonists JUST for aldosterone receptors. HTN/Heart failure. Generally well tolerated. |
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Term
| Effects of combining ACE IHI and Diuretics/AntiHTN and CCB and Beta Blockers? |
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Definition
| They will have additive effects! (more vasodilation/hypotension)(Both reduce force of contraction in the heart, bradycardia, AV block and heart failure! |
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Term
| What class of drugs are PRODRUGS? Where are they converted into active drugs? |
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Definition
| ACE Ihi are prodrugs, activated in the small intestines and the liver. |
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Term
| What are the effects of stimulating alpha 1 receptors on peripheral vasculature? |
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Definition
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Term
| What are the CV effects of Beta 1 stimulation? |
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Definition
| increase heart rate, conduction, contractility; increases renal perfusion |
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Term
| What are the CV effects of Beta 2 stimulation? |
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Definition
| Vasodilation in skeletal muscle, heart and lungs; Bronchiodilation. |
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