CV

Endocardium

inner most layer of the heart

contractility

Degree of myocardial fiber shortening

Effected by:

• Changes in preload - Frank Starling Law

• Altered inotropic stimuli (epi, norepi, meds)

• Myocardial o2 supply (decreased in hypoxemia)

preload

The volume and pressure inside the ventricle at the end of diastole

effected by:

• end-systolic volume

• venous return of blood during diastole

Measured w/ CVP (R) and PAWP (L)

afterload

Resistance to the ejection of blood from the ventricle

effected by:

• systemic vascular resistance

• total peripheral resistance

stroke volume

Volume of blood eject during systole

effected by:

• preload

• afterload

• contractility

RAAS

Increases preload via sodium/water reabsorption and increased afterload via vasoconstriction

atrial fibrillation

definition: atria beat irregularly and rapidly.

mechanisms: multiple wandering reentrant circuits within the atria

functional consequences: decreased ventricular filling (loss of atrial kick), tachycardia, thromboembolic events

determinants of cardiac oxygen supply

-

determinants of cardiac oxygen demand

-

athersclerosis

accumulation of lipid-laden macrophages in the arterial wall

Steps:

• endothelial injury

• inflammation - unable to maintain anti-thrombic and vasodilating cytokines

• macrophages release cytokines (TNF-a, IFNs, ILs, CRP) that further injury

• free radicals are generated during inflammatory process

• LDL is oxidized by free radicals

• Macrophages penetrate intima and engulf LDL (foam cells)

• Foam cells accumulate and form a fatty streak

• Fatty streaks produce more free radicals and cause more inflammation

• autoreactive T cells are recruited and further damage vessel wall

endothelial injury

can be caused by

• HTN

• smoking

• HLD

• Hyperhomocysteinemia

• Hemodynamic factors

• Toxins

• Viruses

• Immune reactions

foam cells

Oxidized LDL that has been engulfed by macrophages

inflammatory response

triggered by endothelial injury, attracts macrophages to the site furthering endothelial damage and contributing to atherosclerosis

NSTEMI

Presents w/ ST segment depression and T wave inversion w/o ST elevation.

• + biomarkers

• Thrombus disintegrates before complete distal tissue necrosis, resulting in injury to the myocardium

STEMI

level of damage and diagnosis??

Presents w/ ST segment elevation

• + biomarkers

• Thrombus lodges in the vessel and causes transmural damage (endo to epicardium)

sequela of damage from MI

• Glycogen stores decrease/anaerobic metabolism begins

• Accumulation of H+ ions and lactic acid → myocardium vulnerable to suppressed impulse conduction → heart failure

• electrolyte disturbances (loss of IC K, Ca, and Mg)

• Catecholamine release → dysrhythmias

• Angiotensin II is released, causing vasoconstriction, coronary spasm, and fluid retention

• Myocyte injury/necrosis releases CPK-MB and troponins

HFrEF

Impaired contractility of the LV, EF is <40%, inability to generate adequate CO

• Sx: Dyspnea, orthopnea, frothy sputum, fatigue, decreased UOP, edema, S3 heart sound

HFpEF

Pulmonary congestion despite normal SV and CO, filling problem of LV, EF >50%

• Sx: DOE, fatigue, crackles, S4 gallop

neurohormonal compensation

Activation of the SNS and RAAS systems to compensate for decreased cardiac output, causes ventricular remodeling

cardiac remodeling

Myocyte hypertrophy d/t the action of angiotensin II

R sided HF

Inability of the RV to provide adequate flow into pulmonary circulation

Causes: L HF, hypoxic pulmonary disease

Sx: Pulm edema, JVD, fatigue, insp. crackles, S3, pink frothy sputum, dependent edema

HFrEF management

Management:

• Increase contractility, reduce pre and afterload

• Nitrates

• ACEi

• Aldosterone blockers

• Diuretics

• BB

• ARNI - angiotensin receptor-neprilysin inhibitor (entresto)

HFpEF mangement

Management:

• Cardiac rehab

• nitrates

• ACEi

• ARBs

• aldosterone blockers

• HTN management

R HF management

Management:

• Diuretics

• BB

• ACEi

• ARBs

• HTN management

• Digoxin

• L HF management

natriuretic peptides

Are elevated in HF d/t stretching of the atria and ventricles, cause diuresis, vasodilation, and increase sodium excretion

aortic stenosis

aortic semilunar valve narrows → diminishing blood flow from the LV into aorta

• Sx: angina, syncope, HF, midsystolic murmur

aortic regurgitation

Leaflets of aortic valve cannot close properly during diastole

Sx: widened PP, decrescendo murmur

mitral stenosis

Impairment of blood flow from the L atrium to the LV

Sx: opening snap, pulm congestion/HTN, DOE, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis

mitral regurgitation

causes backflow of bloof from the LV into the L atrium

Sx: Flash pulmonary edema, dyspnea, paroxysmal nocturnal dyspnea

mitral valve prolapse

Anterior and posterior cusps of mitral valve billow upward into the atrium during systole

Sx: asymptomatic

Treatment: none needed or BB

hypertrophic cardiomyopathy

Common, inherited heart defect of a thick septal wall

Sx: syncope, angina, palpitations, sudden cardiac death

Treatment: BB or verapamil, resection of myocardium, septal ablation, prophylactic ICD placement

pericarditis

Inflammation of pericardial membranes, pericardial effusion may develop

Sx: Severe chest pain that worsens w/ respiratory movement and laying down, pericardial friction rub, anterior chest pain, fever/myalgias/malaise, ST, may have JVD

Treatment: NSAIDs, colchicine, analgesics, pericariocentesis

arterioles

What determines PVR?

BP control

__ control:

• Heart rate - ANS

• Stroke volume - preload, afterload, contractility

• Baroreceptors detect changes

• Hormonal control (ADH, angiotensin II, epi and norepi, ANP, NO, bradykinin)

• Volume regulation (RAAS, ADH, ANP/BNP)

maintenance of smooth muscle tone

Intrinsic - endothelial regulation (constrictor and dilators)

Neural - Norepi leading to vasoconstriction

Local - myogenic regulation and metabolic regulation respond to changes in local tissue needs

baroreflexes

HR accelerated when BP falls

• increases contractility

• constriction of the systemic arterioles

• can cause orthostatic HoTN

stage 1 hypertension

130-139 / 80-89

stage 2 hypertension

>140 / >90

hypertension risk factors

risk factors:

• Family hx

• increasing age

• gender

• race

• dietary na intake

• glucose intolerance

• cigarette smoking (nicotine vasoconstricts)

• obesity

• etoh consumption

• low dietary K, Ca, Mg

• chronic NSAID use (prostaglandins vasodilate)

hypertension causes

Causes:

• Obesity - neurohormonal, metabolic, CV, renal, changes in adipokines

• Endothelial dysfunction

• Hypercoagulability

• Insulin sensitivity

• Genetics

• Intrauterine influences

secondary hypertension

Hypertension caused by an underlying disease process that raised PVR and CO

end organ damage

Target organs

• Kidneys - Na and h2o retention, increased blood volume, glomerular damage

• Brain - TIA, aneurysm, hemorrhage, infarct

• Heart - LV hypertrophy, MI, L HF, aneurysms

• Eyes - retinal vascular sclerosis

• Arterial vessels of lower extremities - intermittent claudication, thrombosis, gangre

hypertension management

Management:

• First line = lifestyle modification

• Meds: diuretics, ACEi, ARBs, aldosterone antagonists, CCB

myocardium

middle muscular layer of the heart

epicardium

outer layer of the heart

endothelial dilators

• prostacyclin/prostaglandins

• NO

• c-type natriuretic hormone

• insulin

• estrogen

• endothelium-derived relaxing factor

endothelial constrictors

• endothelin

• urotensin II

• Angiotensin II

• thromboxane

• prostaglandins in some receptors

angiotensin II

potent vasoconstrictor:

• produced by the RAAS system and locally by the endothelium

• proinflammatory

• increased vascular permeability - recruits infiltrating monocytes

• responsible for hypertrophy of the myocardium

LCA

Coronary artery

• delivers blood to portions of the L and R ventricles and much of the interventricular spetum

• “widowmaker”

circumflex

Coronary artery

• supplies blood to the left atrium and lateral wall of the L ventricle

RCA

Coronary artery

• supplies R atrium and ventricle in posterior aspect of left ventricle (in most people)

• has 3 branches

conus

Branch of the RCA:

• supplies blood to the upper R ventricle

right marginal branch / posterior interventricular

Branch of the RCA:

• supplies smaller branches to both ventricles

• there’s two

collateral arteries

Coronary arteries

• other connections and/or anastomoses between branches

• protect the heart from ischemia

• formed by arteriogenesis and angiogenesis by the endothelium

diastole (?)

When do the coronary arteries perfuse the heart?

coronary veins

• Coronary sinus

• Great cardiac vein

• Posterior vein of the L ventricle

the endothelium (?)

What is HTN essentially a disease of?

no (?)

Is angiotensin II derived from the endothelium?

hypertrophy (?)

What happens to the vessels in HTN?