Chapter 1 Cardiology

Raj Ganeshan, Thomas A. Brown, MD, Sonali J. Shah

Insider’s Guide to Cardiology for the USMLE Step 1

Cardiology is a widely tested subject on the USMLE Step 1, so it is important to achieve a good understanding of both the physiology and pathology of the heart. Become well-versed in pressure-volume loops, the Wiggers diagram, murmurs, and heart sounds (you will likely get a few audio questions on the USMLE that will require you to identify valvular defects based on the qualities of the murmurs detected through a movable virtual stethoscope), action potentials of atrial and ventricular myocytes versus pacemaker cells, and common pathologic conditions of the heart (e.g., rheumatic fever, congestive heart failure, cardiomyopathies, endocarditis). Cardiac pharmacology is also a high-yield subject. The majority of cardiology questions on the USMLE will require you to apply concepts rather than facts, so working through the cases in this chapter will be of tremendous value in your preparation for this subject.

Basic concepts—hemodynamics

1 What are the mathematical determinants of the arterial blood pressure?

The mean arterial pressure (MAP) is determined by how much blood the heart pumps into the arterial system in a given time (the cardiac output [CO]) and how much resistance the arteries have to this input (total peripheral resistance [TPR]). Mathematically, this is expressed as MAP = CO × TPR. Consequently, all drugs that lower blood pressure work by affecting either the CO or TPR (or both).

Note: The primary determinant of systolic blood pressure (SBP) is CO, whereas the primary determinant of diastolic blood pressure (DBP) is TPR. Because approximately one third of the cardiac cycle is spent in systole and two thirds in diastole, the MAP can be calculated as MAP = 1/3 SBP + 2/3 DBP.

2 What are the primary determinants of cardiac output?

The CO is the amount of blood pumped by the ventricles per unit time. It is determined by the volume of blood ejected during each ventricular contraction (stroke volume [SV]) and how frequently the heart beats (heart rate [HR]), expressed as CO = HR × SV. The HR can be affected by a variety of factors but is principally under the control of the autonomic nervous system. Beta blockers can reduce CO by decreasing HR and contractility.

Note: In addition to their negative inotropic effect, the more cardioselective (non-dihydropyridine) calcium channel blockers (verapamil, diltiazem) can also reduce HR by slowing impulse transmission through the atrioventricular (AV) node. They achieve part of their antihypertensive effect through this mechanism.

3 What are the three main factors that affect stroke volume?

The determinants of SV are preload, contractility, and afterload.

4 What is preload, and how does it affect stroke volume?

Preload is the degree of tension (load) on the ventricular muscle when it begins to contract. The primary determinant of preload is end-diastolic volume.

The most widely accepted theory explaining the relationship of preload and SV is the Frank-Starling mechanism, which describes how an increased preload results in an increased SV. It states that stretching of ventricular muscle fibers occurs with increasing end-diastolic volumes, causing greater overlap between actin and myosin within sarcomeres. This results in a greater extent and velocity of myocyte shortening during contraction, which allows for a stronger ventricular contraction and larger SV. This mechanism allows the heart to maintain its ejection fraction in the face of increased preload. By decreasing intravascular volume, diuretics reduce preload and can be used to lower blood pressure. Venodilators also reduce preload and can therefore be used for similar purposes.

In addition, a variety of positions or maneuvers can be tried to manipulate venous return (preload) to the heart. For example, both the Valsalva maneuver (expiration against a closed glottis) and standing will decrease preload, and both squatting and passive leg raising will increase preload. Having the patient perform these actions can be useful when distinguishing various murmurs from one another (Fig. 1-1).

Figure 1-1 Increased ventricular output as a function of end-diastolic volume (reflected by atrial pressure).

(From Guyton AC, Hall JE: Textbook of Medical Physiology, 11th ed. Philadelphia, WB Saunders, 2006, p 112.)

Note: Another theory to explain the Frank-Starling relationship proposes that cardiac troponin becomes increasingly sensitive to cytosolic calcium at greater sarcomere lengths, thereby resulting in increased calcium binding and increased force of muscle contraction. Note that beyond a certain point, increasing preloads will result in less efficient ventricular contraction and a smaller SV. This situation occurs in heart failure.

5 What is contractility and how does it affect stroke volume?

Contractility is a measure of how forcefully the ventricle contracts at a given preload. Naturally, a more forceful contraction will eject a greater fraction of blood from the ventricle, thereby increasing the SV. Contractility is principally influenced by the activities of the sympathetic nervous system (β₁-adrenergic receptors) and parasympathetic nervous system (muscarinic [M₂] cholinergic receptors) on ventricular myocytes. By antagonizing this sympathetic input to the myocardium, beta blockers exert part of their antihypertensive effects by reducing contractility, which reduces SV, CO, and oxygen demand. Contractility is also increased by increased concentrations of intracellular calcium (which is indirectly achieved by digitalis and decreased concentrations of extracellular sodium). This mechanism will be explained in further detail in the discussion regarding digitalis. In addition to beta blockade, contractility is decreased by systolic dysfunction, hypoxia, hypercapnia, calcium channel blockade, and acidosis (K⁺ loss from cells secondary to H⁺/K⁺ exchange results in a more negative transmembrane potential that decreases myocyte excitability).

6 What is afterload and how does it affect stroke volume?

Afterload is the pressure or resistance against which the ventricles must pump blood, the primary determinant of which is systemic arterial pressure. For a given preload and contractility, increasing the afterload will decrease the SV. A simplified way of understanding this is to think of the time available for electrical and mechanical systole as finite. With increased afterload, more time is taken up by isovolumic contraction to build up to a pressure that exceeds the aortic pressure and allow the aortic valve to open. This step leaves less time for blood to enter the aorta from the ventricle (SV) during the rapid and slow ejection phases.

Note: In aortic stenosis, the stenotic aortic valve increases the afterload, which in the absence of compensatory changes such as ventricular hypertrophy tends to reduce SV and CO. Systemic hypertension also increases afterload by increasing the pressure against which the left ventricle must pump.

7 What are the primary determinants of peripheral resistance?

Total peripheral resistance (TPR) to blood flow is principally mediated by arteriolar diameter, which is modified by arteriolar vasoconstriction and dilation, respectively. Recall that resistance to blood flow through a vessel is inversely proportional to the fourth power of the radius. Hence, relatively small changes in arteriolar diameter (and thus radius) can have profound effects on blood flow.

The sympathetic nervous system promotes arteriolar vasoconstriction by stimulating α₁-adrenergic receptors, which increases calcium influx (via calcium channels) into arteriolar smooth muscle and stimulates their contraction. Consequently, α₁-adrenergic receptors and arteriolar calcium channels are two selective targets for antihypertensive drugs.

In all organs except for the lungs, arteriolar vasodilation is promoted by tissue hypoxia and accumulation of metabolic wastes, such as adenosine, that accumulate when oxygen demand increases (e.g., during exercise). This vasodilation allows supply to meet demand.

Note: In general, there is no direct parasympathetic innervation of the vasculature. However, vasodilation of arterioles can be caused by exogenous cholinomimetic administration. These drugs act on uninnervated muscarinic receptors (M₃-receptors) on endothelial cells and stimulate release of nitric oxide. Nitric oxide diffuses to the adjacent smooth muscle, resulting in vasodilation and decreased peripheral resistance.

8 What is the mechanism by which the sympathetic nervous system responds to a reduction in blood pressure?

When blood pressure drops, arterial baroreceptors located within the carotid sinus (afferent limb mediated by the glossopharyngeal nerve) sense decreased vessel stretch and fire less frequently. This response increases efferent sympathetic outflow and inhibits parasympathetic outflow, which helps restore the blood pressure by increasing heart rate and stimulating peripheral vasoconstriction. Conversely, if the blood pressure increases, baroreceptors in the carotid sinus or aortic arch (afferent limb mediated by the vagus nerve; responds only to increases in blood pressure) fire more frequently because they are being “stretched” more, which causes greater inhibition of the sympathetic outflow (Fig. 1-2).

Figure 1-2 Control of blood pressure by the baroreceptor reflex.

(From Brown TA: Rapid Review Physiology. Philadelphia, Mosby, 2007, p 144.)

Note: The aortic arch and carotid sinuses also have chemoreceptors, which should not be confused with the baroreceptors. Chemoreceptors work to maintain PO₂, PCO₂, and pH.

9 How do the α₁-receptor antagonists work?

The α₁-receptor antagonists include the “zosins” (prazosin, terazosin, doxazosin) and antagonize peripheral vasoconstriction stimulated by the sympathetic nervous system (which is mediated by α₁-receptors). α₁-Receptors are located on vascular smooth muscle and coupled to G_q proteins. Antagonists cause decreased release of inositol triphosphate (IP₃) and subsequently prevent the release of calcium from intracellular stores, resulting in smooth muscle relaxation and arteriolar vasodilation.

α₁-Receptors are also responsible for contraction of the pupillary dilator muscle and intestinal/bladder sphincters. Thus, α₁-receptor antagonists can lead to miosis and bladder/bowel movement.

10 How do the α₁-receptor antagonists cause orthostatic hypotension?

Upon standing from a supine or sitting position, transient hypotension and lightheadedness (from cerebral hypoperfusion) might occur as a result of venous pooling in the lower extremities, which decreases venous return and MAP. This response is ordinarily compensated for by the baroreflex, which promotes peripheral venoconstriction and tachycardia. However, if the α₁-receptors are blocked in the peripheral venules, this reflex will be less effective at restoring the blood pressure. Nevertheless, a reflex tachycardia, which is mediated by β-receptors, will be maintained. This increase in pulse rate can be used in diagnosing orthostatic hypotension.

Note: Reflex tachycardia occurs to maintain CO. Recall that CO = HR × SV. Thus, if SV is reduced because of decreased venous return to the heart, HR must increase to maintain CO.

11 What hemodynamic changes occur during exercise?

Exercise requires more oxygen to be delivered to skeletal muscle to meet its increased metabolic demand. This delivery is accomplished mainly by an increase in CO secondary to increases in both SV and HR. Contraction of the lower limb muscles pushes blood toward the right atrium and increases venous return. MAP is only modestly increased during exercise despite the large increase in CO, because skeletal muscle vasodilation is mediated mostly by local cellular metabolites, which significantly decrease the SVR and allow skeletal muscle to receive up to 85% of the increased CO.

12 Which clinical scenarios would shift the CO and venous return curves to the points labeled 1 to 4 on Figure 1-3?

1. Exercise: Lower limb muscles push blood toward the right atrium and increase venous return. Sympathetic activity increases CO by increasing HR, SV, and contractility.

2. Arteriovenous fistulas: Increased venous return from an arteriovenous fistula will shift the venous return curve to the right. CO does increase but only because of the increased preload (Frank-Starling mechanism); this increase is therefore not due to a change in contractility (inotropy). If these arteriovenous anastomoses were much larger, the operating point of the heart would be shifted to (1) because it would cause a large decrease in SVR and stimulate the activity of the sympathetic nervous system, increasing inotropy; these large anastomoses are sometimes referred to as AV shunts.

3. Compensated heart failure: Patients with this condition have elevated right atrial pressures due to an increased volume status caused by the activity of the renin-angiotensin-aldosterone system (RAAS). Their cardiac function is decreased (decreased inotropy), but they can maintain a normal CO at rest with the increased volume (Frank-Starling mechanism).

4. Ventricular fibrillation: Ventricular fibrillation causes equalization of all pressures. Right atrial pressure increases to become equal to the mean systolic filling pressure. CO in ventricular fibrillation simply becomes equal to zero.

Figure 1-3 Cardiac output (CO) and venous return curves. LVEDV, left ventricular end-diastolic volume.

Basic concepts—excitation-contraction coupling

1 What is the source of cytosolic calcium during ventricular systole?

During the plateau phase (phase 2) of the ventricular myocyte action potential, voltage-gated calcium channels allow calcium influx from the extracellular fluid into the cytosol, stimulating calcium release from the sarcoplasmic reticulum, a phenomenon referred to as calcium-induced calcium release. In fact, the majority of the cytosolic calcium comes from the sarcoplasmic reticulum, not the extracellular fluid. This mechanism of calcium release is in contrast to release from skeletal muscle, in which depolarization of the cell membrane triggers sarcoplasmic calcium release without entry of extracellular calcium into the cytosol.

2 What is the function of calcium in cardiac muscle contraction?

Cytosolic calcium binds to troponin C, resulting in a conformational change that removes tropomyosin from myosin-binding sites on actin to allow for the sliding filament mechanism of contraction. The force of contraction is proportional to the intracellular Ca²⁺ level. Note that unlike skeletal muscle, cardiac muscle is dependent on extracellular calcium influx for contraction to occur.

The cardioselective calcium channel blockers (verapamil, diltiazem) reduce contractility by antagonizing extracellular calcium entry and the subsequent calcium-induced calcium release that occurs in heart muscle. In addition to decreasing heart rate, this action is another mechanism by which calcium channel blockers work to lower blood pressure.

3 What is the mechanism by which β-adrenergic stimulation increases cardiac contractility?

β-Adrenergic stimulation results in an increase in cyclic adenosine monophosphate (cAMP), which promotes cAMP-dependent phosphorylation of a number of proteins via protein kinase A (PKA). Phosphorylation of L-type calcium channels results in increased calcium entry into the myocyte. In addition, β-adrenergic stimulation results in phosphorylation and inhibition of a protein called phospholamban, which normally serves as an inhibitor of the sarco/endoplasmic reticulum calcium adenosine triphosphatase, or ATPase (SERCA). Thus, inhibition of phospholamban allows for increased calcium entry into the sarcoplasmic reticulum and subsequent increase in calcium release during the next action potential, which augments myocyte contractility.

4 What is the contribution of the sympathetic nervous system to ventricular relaxation?

In addition to stimulating calcium influx, the β-adrenergic pathway also stimulates calcium uptake by the ventricular sarcoplasmic reticulum due to phosphorylation of SERCA by PKA. This removal of cytosolic calcium into the sarcoplasmic reticulum is required for ventricular relaxation; so the more rapidly it is removed, the more rapidly the ventricles relax. Such rapid ventricular relaxation at elevated HRs is important to ensure adequate ventricular filling during the decreased period of diastole. Recall that HR is increased with sympathetic stimulation via direct binding of cAMP to special channels in the pacemaker cells that conduct the If current (“funny current”; this current is carried by sodium ions and allows the membrane potential to become progressively less negative during the repolarization phase of the pacemaker cell), which increases the probability of their open time, thereby promoting sodium influx and increasing the slope of phase 4 depolarization.

Note: Calcium uptake into the sarcoplasmic reticulum is an energy-requiring process, and in ischemic heart disease the reduced oxygen delivery makes calcium uptake less efficient, thereby impairing ventricular relaxation and causing diastolic dysfunction.

Basic concepts—arrhythmias

1 What is the relationship between the various phases of the ventricular myocyte action potential and the different ion fluxes across the cell membrane?

In phase 0 of the action potential, the sharp rise in membrane voltage is due to sodium influx. Phase 1 involves a brief repolarization that is due to the transient outward flow of potassium that follows sodium channel inactivation. In phase 2, the action potential plateaus are due to a balance between calcium influx and potassium efflux. During phase 3, there is rapid repolarization due to unopposed potassium efflux. Phase 4 is the resting potential, which is maintained predominantly through the opening of potassium channels. Intracellular concentrations of K+ are maintained at high levels in cardiac myocytes because of the action of membrane-bound Na+K+-ATPase. Opening of potassium channels during phase 4 leads to potassium efflux (down its concentration gradient). Since the cell is permeable only to potassium at this time, negatively charged counter ions for K+ are unable to diffuse outward with potassium. As potassium leaves the cell, anions left behind cause the cell to become increasingly negative in charge. Therefore the effluxed potassium ions are attracted back toward the interior of the cell to maintain resting potential. Because phase 4 is dominated by potassium permeability, it therefore has a value close to the potassium reversal potential (−85 mV) (Fig. 1-4).

Figure 1-4 Phases of the ventricular myocyte action potential.

(From Brown TA, Brown D: USMLE Step 1 Secrets. Philadelphia, Hanley & Belfus, 2004, p 77.)

Note: The antiarrhythmic agents all work by affecting one or more components of the action potential. Class I antiarrhythmics block sodium channels and antagonize phase 0. Class III antiarrhythmics work by blocking potassium channels, which prolongs phase 3 depolarization. Some class IA and all class III antiarrhythmics increase action potential duration as well as the QT interval. Toxicity of these agents can lead to torsades de pointes, which is associated with long QT syndrome.

2 What is responsible for the drifting of the resting membrane potential in nodal cells?

These cells are more permeable to sodium, so sodium influx during the “resting” membrane potential causes the membrane to gradually depolarize. Because nodal cells lack the fast voltage-gated sodium channels (I_Na) found in the rest of the myocardium, this is accomplished by the I_f sodium current, a unique “leaky” sodium channel that promotes the gradual depolarization of these cells through sodium influx. Eventually, when the membrane depolarizes to its “threshold,”; this state will activate slow calcium channels that engender an action potential (Fig. 1-5).

Figure 1-5 Rhythmic discharge of a sinus nodal fiber. The sinus nodal action potential is also compared with that of ventricular muscle fiber.

(From Guyton AC, Hall JE: Textbook of Medical Physiology, 11th ed. Philadelphia, WB Saunders, 2006, p 117.)

Note: The calcium channel blockers verapamil and diltiazem affect heart rate by antagonizing these slow calcium channels on the SA node. These drugs are considered class IV antiarrhythmics.

3 Through what mechanism does sympathetic stimulation increase heart rate?

The release of norepinephrine from sympathetic neurons causes activation of β₁-adrenergic receptors in nodal tissue. These receptors stimulate production of cAMP, resulting in an increase in I_f and a positive chronotropic effect on the heart. In essence, sympathetic stimulation increases the cellular influx of sodium ions and decreases the efflux of potassium ions, thus increasing the slope of the resting potential in the nodal cells. Beta blockers reduce heart rate by antagonizing this effect.

Note: The beta blockers are considered class II antiarrhythmics.

1 What are the types of hypertension and which does this patient most likely have?

The two types of hypertension are essential (primary, idiopathic) hypertension and secondary hypertension. Essential hypertension is thought to account for approximately 90% of cases of hypertension and is most likely to be due to an inability of the kidney to properly excrete sodium at a given filtered load; this has been described through the pressure natriuresis theory. When approaching a patient with hypertension, it is important to first rule out secondary hypertension, which indicates additional pathologic changes. Treatment of secondary hypertension is aimed at addressing the underlying cause of the condition. Potential sources of secondary hypertension include renal artery stenosis, primary hyperaldosteronism, pheochromocytoma, coarctation of the aorta, chronic renal disease, excessive alcohol use, pregnancy, increased intracranial pressure, and various medications, such as monoamine oxidase inhibitors, oral decongestants, nonsteroidal anti-inflammatory drugs, and oral contraceptives. If causes of secondary hypertension are ruled out, then essential hypertension is diagnosed by exclusion.

Note: The mechanisms involved in essential hypertension are poorly understood. A second theory proposes that people with essential hypertension have increased vascular resistance. This may be due to increased circulating vasoconstrictors, increased sensitivity to these substances, or a deficiency of the nitric oxide vasodilation pathway.

2 How is hypertension defined and what are the potential complications?

The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure guidelines (JNC 7) for defining hypertension are presented in Table 1-2.

Table 1-2 Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure Guidelines for Defining Hypertension

Category	Blood Pressure Range (mm Hg)
Category	Systolic	Diastolic
Normal	< 120	<80
Prehypertension	120-139	80-89
Hypertension: stage 1	140-159	90-99
Hypertension: stage 2	≥160	≥100

Evidence suggests that the risk for complications in hypertensive disease is a continuum, increasing as blood pressure rises. It is also largely influenced by comorbid conditions. Major complications of hypertension include accelerated atherosclerosis, premature cardiovascular disease, diastolic (and to a lesser extent, systolic) heart failure, stroke, intracerebral hemorrhage, chronic renal insufficiency, end-stage renal disease, retinopathy, and acute hypertensive crisis.

3 What are four classes of drugs that could be useful in treating this man’s hypertension?

Diuretics (e.g., thiazides, loop, potassium-sparing)

Inhibitors of the renin-angiotensin-aldosterone system (e.g., angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor blockers)

Vasodilators (e.g., direct-acting, calcium channel blockers)

Sympatholytics (e.g., clonidine)

Case 1-1 continued:

Because this patient has received three elevated blood pressure readings in the past 2 months and is unresponsive to lifestyle modifications, he is started on metoprolol.

4 What is the mechanism by which metoprolol will reduce blood pressure in this man?

Metoprolol is a relatively selective β₁-adrenergic receptor blocker. Antagonizing these receptors decreases heart rate and contractility, both of which reduce CO, thereby lowering blood pressure (recall that MAP = CO × TPR). Beta blockers also reduce blood pressure by blocking the renal secretion of renin. Both β₁– and β₂-adrenergic blockers appear to inhibit the renin-angiotensin-aldosterone system (RAAS) to some extent. For this reason, beta blockers might be more effective in hypertensive patients with elevated plasma renin levels as opposed to normal or low plasma renin levels.

5 What pharmacologic property makes certain beta blockers more “cardioselective” than others?

Some beta blockers (atenolol, esmolol, nebivolol, and metoprolol) are more selective for the β₁-receptors on the heart, with less effect on the β₂-receptors that lead to smooth muscle relaxation in the bronchioles and skeletal muscle arterioles. Thus, specific β₁-antagonists have less affinity to inhibit catecholamine-mediated bronchodilation and peripheral muscle vasodilation.

6 Caution should be used in prescribing beta blockers for patients with which comorbid conditions and why?

Asthma: Risk of worsening bronchospasm by preventing β₂-mediated bronchodilation. (Even β₁– “selective” antagonists have some effect, especially at high doses.) For the purpose of the USMLE, remember that β₁-selective blockers should be used in patients with pulmonary disease.

COPD (chronic obstructive pulmonary disease) patients for similar reasons.

Peripheral arterial disease: Exacerbation of claudication. (Vasodilation in skeletal muscle arterioles is mediated by β₂-adrenergic receptors present on vascular smooth muscle cells.)

First-degree atrioventricular (AV) block: Beta blockers decrease AV conduction and thus further lengthen the already prolonged PR interval on the electrocardiogram (ECG). This can result in excessive cardiac depression. (Beta blockers should not be given at all to patients with second- or third-degree AV block because they could delay AV conduction even further. Certain calcium channel blockers, such as verapamil and diltiazem, might also reduce AV conduction and, when used in combination with beta blockers, can produce a serious AV block.)

Diabetes: Beta blockers reduce the normal symptoms of hypoglycemia (e.g., headache, confusion, slurred speech, anxiety, tremors, palpitations) that provide warning to diabetic patients prior to reaching dangerously low blood sugar levels.

Because of their ability to reduce myocardial oxygen demand, beta blocker use has been shown to have a survival benefit in patients with congestive heart failure. However, caution should be used when placing patients on beta blockers, as they may initially exacerbate CHF symptoms (decompensated heart failure).

Erectile dysfunction: beta blockers may inhibit b2 adrenergic receptor-mediated vasodilation.

Depression: Mechanism of action is unclear, but presumably involves alterations in monoamine neurotransmitter signaling.

Case 1-1 continued:

After a number of months, the patient returns to the office complaining of an impaired ability to keep up with his wife on their daily hikes. He feels that he gets tired more quickly, attributes this to the metoprolol, and plans to quit taking his medication.

7 What might be occurring in this patient and how would you recommend he discontinue his medication?

Beta blockers are likely impairing his exercise tolerance by preventing the necessary increase in HR to meet his oxygen demand. Trying him on another class of antihypertensives would be reasonable, but his metoprolol should first be tapered because chronic beta blocker use substantially increases the sensitivity of the heart to catecholamines by upregulating beta receptors on cardiomyocytes. Consequently, sudden withdrawal of these drugs can lead to tachycardia, arrhythmias, and acute myocardial infarction. For this reason, patients should always be gradually weaned off beta blockers.

Summary Box: Hypertension

Essential hypertension is the most common type of hypertension.

The most common causes of secondary hypertension are renal artery stenosis and primary hyperaldosteronism.

Beta blockers lower blood pressure in part by reducing renin secretion from the kidneys (primarily a β₁-receptor–mediated effect).

Beta blockers decrease atrioventricular (AV) conduction and therefore should be used cautiously in patients with first-degree heart block.

Case 1-2

A 48-year-old man is newly diagnosed with both type 2 diabetes mellitus and hypertension. To help control his blood sugar, he is started on metformin.

1 How would the fact that this patient also has diabetes influence treatment for his hypertension? Consider drug choice and aggressiveness of treatment

Angiotensin-converting enzyme (ACE) inhibitors are the preferred first-line antihypertensives in diabetics. ACE inhibitors have been shown to reduce the progression of proteinuria (and the subsequent nephropathy) in diabetic patients. Although the mechanism behind the nephroprotective actions of ACE inhibitors remains unclear, it could be related to their ability to preferentially dilate the efferent arteriole and thereby reduce glomerular filtration pressures.

Diabetes is a cardiovascular risk factor and predisposes patients to both microvascular and macrovascular damage. Tight blood pressure control is critical in diabetics to reduce the mortality risk from macrovascular disease (CAD, CVA, PVD). Additionally, it reduces the risk of microvascular complications such as retinopathy, nephropathy, and neuropathy.

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Apr 7, 2017 | Posted by admin in NURSING | Comments Off

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12 Which clinical scenarios would shift the CO and venous return curves to the points labeled 1 to 4 on Figure 1-3?

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