Pumps blood throught the lungs

Right ventricle ---> pulmonary artery (no oxygen) ---> lungs ---> pulmonary vein (oxygen) ---> left ventricle

Pumps blood to organs and tissues

Left ventricle --> aorto to organs/tissues --> right atrium (via superior or inferior vena cava)

Time where the heart refills with blood after systole

Tricuspid valve and Mitral valve are open and the Pulmonary valve and Aortic Valve are closed

Contraction of the heart

Tricuspid and mitral valves are closed and the pulmonary and aortic valves are open

T-P Factor

Cathepsin P

Tonin

Chymase

CAGE

Cathepsin P

Consequences of Angiotensin II on AT I Receptor

Vascular Smooth Muscle Growth

(Generally negative consequence)

Increase arteriolar constriction

Consequences of Angiotensin II on AT I Receptor

CNS

(Generally Negative Consequences)

Stimulate to increase cardiac output

Consequences of Angiotensin II on AT I Receptor

Adrenal Cortex

(Generally negative consequences)

Aldosterone stimulation

Increase renal sodium reabsorption

Consequences of Angiotensin II on AT I Receptor

Kidney

Generally negative consequences

Increase filtration fraction

Increase GFR

(Over a chronic fashion, it can damage the kidneys)

Consequences of Angiotensin II on AT I Receptor

Brain

Generally negative consequences

Increase ADH (antidiuretic hormone) and thirst

Increase free water intake

Generally positive consequences

Vasodilation

Anti-proliferation

Cell differentiation

Tissue repair

Consequences of Aldosterone

Heart

Myocardial fibrosis

Ventricular arrhythmias

Left ventricular hypertrophy (LVH) (enlargening of the heart to decrease the burden on the heart)

Consequences of Aldosterone

Kidney

Sodium retention

Magnesium and potassium loss (hyperkalemia)-Specifically with aldosterone blockers

Consequences of Aldosterone

Vasculature

Hypertension

Endothelial dysfunction

Inhibits nitric oxide synthesis

Prothrombotic

Consequences of Aldosterone

CNS

Sympathetic activation

Parasympathetic inhibition

May lead to cardiac remodelling, it can lead to blood backing up into lungs, etc. if preload is high

Pressure stretching the ventricle of the heart after atrial contraction and subsequent filling of the ventricle

End diastolic volume (clinically)

Tension or pressure used by the chamber of the heart in order to contract and eject blood out of the chamber

End systolic volume (clinically)

Stroke Volume

(SV)

SV = End diastolic volume - End systolic volume

What actually got pumped out of the heart

Cardiac Output

(CO)

Amount of blood pumped per unit of time

L/min

CO = Heart rate x SV

Cardiac Index

(CI)

CO adjusted for BSA

L/min/m²

CI = CO / BSA

Ejection Fraction

(EF)

Fraction of blood ejected by the left ventricle (LV) during contraction or ejection phase of cardiac cycle

EF = SV/EDV (End-Diastolic Volume) x 100%

55-75% is normal

Mean Arterial Pressure

(MAP)

Average blood pressure in an individual

MAP = (CO x Systemic vascular resistance [SVR])+Central venous pressure (CVP))

MAP=[(2 x Diastolic pressure)+systolic pressure]/3

Pulmonary Capillary Wedge Pressure

(PCWP)

Under most circumstances provides an accurate estimate of the diastolic filling (preload) of the left heart

During diastole when mitral valve is open, the PCWP reflects LVEDP. LVEDP is an index of left ventricular end-diastolic volume (preload)

Clinical Assessment of Hemodynamic Parameters

Preload

Hepatomegaly (enlarge liver, measure LFTs, palpatate their liver)

Jugular venous distention (JVD)

Peripheral edema

Pulmonary crackles

S3 heart sound (seen w/ extreme heart failure and increased preload)

Mucous membrane and skin turgor

Daily weight

Clinical Assessment of Hemodynamic Parameters

Afterload

Vascular diastolic pressure (decrease) systolic pressure may increase or stay the same

Pulse pressure

Pulses

Clinical Assessment of Hemodynamic Parameters

Role of the Swan Ganz Catheter

Used to measure pulmonary artery pressure, especially in the acute decompensated heart failure patient

Diagrams showing placement of catheter

(Measures pressure)

Subset of arteriosclerosis

Formation of atheroma (fibrous fatty intimal plaques) in arterial walls

Ischemic Heart Disease

(IHD)

aka

Coronary Heart Disease (CHD), Coronary Artery Disease (CAD), Atherosclerotic Vascular Disease (AVD)

Ischemia is a lack of oxygen tension at the cellular level and results in loss of high enery phosphates due to disruption of aerobic metabolism

Cardiovascular dysfunction occurs at the cellular level due to imbalance between myocardial oxygen supply and myocardial demand, may be transient or permanent (cell death), cellular dysfunction translates into organ dysfunction

Etiology: Atherosclerosis

1. Endothelial dysfunction

2. Fatty streak formation

3. Fibrous plaque

4. Thrombus formation

1. Maintenance of permeability barrier

2. Maintain nonthrombogenic blood-tissue interface (regulate thrombosis, thrombolysis, and platelet adherence)

3. Modulate vascular tone and blood flow

4. Regulate immune and inflammatory reactions (control leukocyte interactions within the vessel wall)

5. Modify lipoproteins in the artery wall

6. Regulate the growth of other cell types, particularly smooth muscle cells

Age (Not modifiable)

Sex (Male>Female)

Smoking

Family history of CHD (Not modifiable)

Dyslipidemia (Increase total cholesterol or LDL, decrease HDL-C)

Obesity

Diabetes

Hypertension

Increase homocysteine

Vasoconstriction, pro-thrombotic, and pro-inflammatory

Angiotensin II and endothelin produced as a result of the dysfunctional endothelium resulting in vasoconstriction

Inside the artery wall monocytes differentiate into macrophages

Macrophages engulf lipoproteins (LDL) and then form foam cells

Both macrophages and foam cells secrete growth factors and cytokindes resulting in cell proliferation, inflammation, matrix degradation

Foam cells accumulate and expand in the lining of the artery wall

Smooth muscle cells from the middle layer of the artery (media) move into the layer of endothelial cells (intima)

Plaque grows and protrudes into the lumen of the blood vessel

Fibrous cap of connective tissue overlays the fibrous plaque (prevents vessel from bursting)