Pharmacology (cardiovascular system pt. 1)

What is the leading cause of death in the world?

Cardiovascular diseases

Different diseases of the veins

* varicose veins
* chronic venous insufficiency
* deep venous thrombosis
* Superior vena cava syndrome (SVC)

What are varicose veins?

Pooling of blood in the veins

What causes varicose veins?

incompetent valves, venous obstruction, muscle pump dysfunction, or combination of these

What is Chronic venous insufficiency

persistent ambulatory lower extremity venous hypertension

Treatment of Chronic venous insufficiency

weightloss, decreased time spent standing and sitting, leg elevation, compression stockings, physical exercise, and endovenous ablation

What is a thrombosis?

a clot (blood)

Deep venous thrombosis (DVT)

clot in a large vein

obstruction of a venous flow leading to increased venous pressure

Factors of DVT (Virchow triad)

* venous stasis
* venous intimal damage
* hypercoagulable

DVT - how to prevent

prevention is crucial

mobilization after surgery, illness, injury

prophylactic low-molecular-weight heparin or direct thrombin indicators

DVT Treatment

Low-molecular-wight heparin

direct thrombin inhibitors

aspirin therapy

catheter directed thrombolytic therapy

pharmacomechanical treatment

Heperine

good med for keeping blood thin

for ppl with clotting issues

What is Superior vena cava (SVC) syndrome

when the superior vena cava is occluded which leads to venous distention in upper extremities and head

Leading cause of SVC

nonsmall cell lung cancer, small cell lung cancer, lymphoma

Clinical symptoms of SVC

edema, venous distention of face neck truck and upper extremities, cyanosis, dyspnea, dysphagia, hoarseness, stridor, cough, chest pain, resp.distress, CNS changes

Treatment of SVC

Radiation and chemotherapy

Doppler

An ultrasound to check for clots

Diseases of the arteries

* hypertension
* orthostatic (postural) hypertension
* aneurysm
* thrombus formation
* embolism
* peripheral arterial diseases
* atherosclerosis
* peripheral artery disease
* coronary artery disease
* myocardial ischemia
* acute coronary syndroms

What is Hypertension?

\-Consistent elevation of systemic arterial blood pressure

\-Elevation of 140 mmHg systolic OR 90 mmHg diastolic or higher

What is isolated systolic hypertension?

elevated systolic BP with normal diastolic BP

How are primary (essential) and secondary hypertension caused?

primary: genetic and environmental factors

secondary: altered hemodynamics from an underlying primary disease or drugs

What does hypertension increase the risk of?

myocardial infarction(MI)

kidney disease

stroke

What is the most significant factor in causing target organ damage?

systolic hypertension

Hypertension risk factors

positive family history, advancing age, females over 70, males over 55, race:black, increased sodium intake, increased potassium+magnesium+calcium, cigarettes, obesity, heavy alcohol use, glucose intolerance/insulin

How is hypertension caused?

increases in cardiac output or total peripheral resistance or both

anything that increases heart rate or stroke volume

Primary hypertension

interactions of genetics and environment, overactitivy of sympathetic nervous system

Secondary hypertension

result of drugs or unmodifiable disorders we do to ourselves,

“caused by systemic disease that raises peripheral vascular resistance and/or cardiac”

complicated hypertension

cells become bigger in myocardium

hypertrophy and hyperplasia inflicting the tunica intima

called vascular remodeling

malignant hypertension (hypertension crisis)

when someone has a rapiding progressive episode(hypertension) and is considered an emergency

can lead to encephalopathy

diastolic pressure usually above 140mmHg

clinical manifestations

early hypertension there is no clinical manifestation other than high BP

its called the silent disease

diagnosis of hypertension

BP at least two separate times averaging whats considered hypertension

Hypertension treatment

\-reducing or eliminating risk factors

\-dietary approaches to stop hypertension

\-stop smoking

exercise programs that promote endurance and relaxation

Hypertension - pharmacologic therapies

\-angiotensin-converting enzymes (ACE inhibitors)

\-angiotensin-receptor blockers (ARBs)

\-aldosterone antagonists

(effective for ppl with heart failure, chronic kidney disease, after an MI, or a recurrent stroke)

What is Renin-Angiotensin-Aldosterone

Regulates BP and influences salt and water retention by kidneys

What does Renin-Angiotensin-Aldosterone (Angiotensin 2 ) cause

vasoconstriction and mediates arteriolar remodeling

What is orthostatic (postural) Hypotension

decreased in systolic and diastolic BP by 20 mmHg

someone moves from laying to sitting to standing and their blood pressure drops

Lack of normal BP compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation

Orthostatic (postural) Hypotension treatment

lots of salt intake

slow movements when switching from sitting to standing

aneurysm

Dilation or outpouching of a vessel wall or cardiac chamber

True aneurysm

circumferential aneurysms

fusiform aneurysm

three layers of arterial wall are involved

False Aneurysm

leak between a vascular graft and a natural artery

saccular aneurysms

Aneurysm clinical manifestation (x4)

Heart: heart failure, dysrhythmias, embolism of clots to the brain or other vital organs

Aorta: asymptomatic until it ruptures, then it becomes painful

Abdomen: flow to extremity is impaired, causing ischemia

Thoracic: dysphagia(difficulty swallowing) and dyspnea are caused y the pressure

Aneurysm treatment

maintenance of low blood volume and low blood pressure to decrease the mechanical forces, stop smoking, B-adrenergic blockage, surgery

Aneurysm complication

aortic dissection (surgical emergency)

it disrupts the flow through the arterial branches

Embolus

plug” of fat or air or clot

Thrombus:

clot plug

Embolus/thromboembolus causes:

obstruction of vessel with either a clot or other plug

What is Arterial thrombus formation?

activation of the coagulation cascade

Arterial thrombus formation cause

roughening of the tunica intima by atherosclerosis

Treatment of ATF

heparin, warfarin derivatives, thrombin inhibitors, thrombolytic agents, balloon tipped catheters(to remove/compress an arterial thrombus), combinations of drugs and catheter therapies

Embolism

bolus of matter that obstructs blood flow

can lead to stroke, ischemia of infarction or necrosis

distal part of

Embolism can lead to…

\-ischemia or infarction or necrosis distal to the obstruction…almost a waxy whiteness of the skin as a result of the distal area being devoid or erythrocytes

\-numbness and pain as a result of neural ischemia

embolism - thromboembolism

vascular obstruction from dislodged thrombus

embolism - air embolism

room air that enters the circulation…i.e. puncture wound, iv

embolism - amniotic fluid embolism

amniotic fluid that is forced into the mother’s bloodstream

embolism - bacterial embolism

infectious endocartitis

embolism - fat embolism

trauma to long bones causes globules of fat to form in the blood

embolism - foreign matter

enters bloodstream during trauma or through IV or arterial line

What is peripheral vascular disease? How is it caused?

inflammatory disease of the peripheral arteries, it obliterates small and medium sized arteries

thromboangitis obliterans (Buergers disease)

smoking causes this

cyanosis is common

PVD treatment

stop smoking

vasodilators, sympathectomy, exercise

PVD Raynaud phenomenon and Raynaud disease

episodic vasospasm (ischemia) in the arteries and arterioles of the fingers, less common in toes

clinical manifestation:changes in the skin colour and sensation caused by ischemia

Raynaud phenomenon: secondary to other systemic diseases or conditions

Raynoud disease:primary vasospastic disorder of unknown origin

Atherosclerosis

thickening and hardening from accumulation of lipid-laden macrophages in the arterial wall

plaque development

Atherosclerosis patho

endothelial is damaged from chronic hypertension or high cholesterol then causes inflammation then cytokines rush to the area and macrophages too evolves to bad plaque formation \*\*\*

Atherosclerosis clinical manifestation

depends on organ inflicted

Atherosclerosis treatment

controlling diabetes and all risk factors, removing initial cause of vessel damage

exercise, stop smoking, controlling hypertension and cholesterol

Peripheral artery disease

Atherosclerotic disease of arteries that perfuse limbs (especially lower extremities)

plaque builds in peripheral system

cause common in diabetics and smokers

causes claudication (pain in legs when walking due to little blood flow)

Peripheral artery disease treatment

vasodilators, antiplatelet/antithrombotic meds…i.e.aspirin, cilostazol, cholesterol-lowering meds, exercise rehab

coronary artery disease

any vascular disorder that narrows/occludes the coronary arteries

results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients

causes heart attacks

most common cause

atherosclerosis

coronary artery disease nonmodifiable risk factors

family history and advanced age and gender

modifiable risk factors of coronary artery disease

hypertension, smoking, diabetes and insulin resistance, obesity, atherogenic diet, dyslipidemia

Coronary artery disease - Dyslipidemia

abnormal concentrations of serum lipoproteins

strong link between lipoproteins and coronary artery disease

dietary fat packaged into chylomicrons for absorption in the sm intestine

indicator of coronary risk

Coronary artery disease - Dyslipidemia ( VLDL, DL, HDL )

Very low-density lipoproteins VLDL

LDL: mainly cholesterol plus a carrier protein

HDL: mainly phospholipids plus a carrier protein

Coronary artery disease - Dyslipidemia - nontraditional risk factors

\-markers of inflammation, ischemia, thromosis

\-chronic kidney disease

\-adipokines

\-medications

\-microbiome

\-air pollution

\-coronary artery calcification, carotid wall thickness

Coronary Artery Disease - Transient myocardial ischemia

develops if the supply of coronary blood can’t meet the demand of the myocardium for oxygen and nutrients

\-stable angina: causes predictable chest pain

\-prinzmetal angina(varient): causes unpredictable chest pain

\-silent ischemia: causes no detectable symptoms

\-Angina pectoris: causes transient substernal chest discomfort

Myocardial ischemia treatment

nitrates, -adrenergic-receptor lockers, calcium channel blockers, statins, antithromotics, sodium ion channel inhibitors, percutaneous coronary intervention, coronary artery bypass graft, minimally invasive direct coronary artery bypass, gene and stem therapy

What is a Myocardial Infarction

plaque build up in the coronary artery that blocks blood flow and oxygen to heart

MI cellular injury

angiotension two causes vasoconstrition

functional impairment altered left ventricular compliance, decreased injection fraction, SA node malfunction

insulin production is decreased

MI repair

it causes severe inflammatory process

ends with wound repair

repair begins within 24h

initial scarring is weak due to reinjury, 10-14 days after MI ppl start to feel better - scar tissue is formed

full scaring by six weeks

MI clinical manfestation

sudden chest pain, radiate to neck, jaw, L. arm is referred pain according to many women

heavy and crushing

nausea and vomiting may occur due to pain

MI complication

dysrthymias, TIA, left ventricular failure, pulmonary congestion, pericarditis, rupture of heart structure, sudden death

MI DX and TX

diagnosis: ECG, enzyme alterations, clinical findings

Treatment; pain relief, bed rest, monitor cardiac rhythms, risk reduction

ECG

SA node sends impulse P QRS

What causes myocyte necrosis - irreversible damage to the heart muscle?

prolonged ischemia

cellular injury, structural and functional changes, repair

cardiac enzymes

blood test, troponin is high

myocardial infarction

prolonged ischemia causes irreversible damage to heart muscle, cellular death and injury , lots of structural changes

angiotension 2 effects:

yocytes, cardiac fibroblastssystemic effects: periphersal vascoconstriction and fluid retention

local effects: growth factor for vascular smooth muscle cells,

Involves myocardial remodeling

two major types of myocardial infarction

subendocardial infarction

transmural infarction -involves all layers of heart walls

MI clinical manifestation

\-infarcted myocardium is surrounded by a zone of hypoxic injury→could progress to necrosis

\-sudden chest pain

\-ECG changes

\-Troponin 1 elevates

\-creatine phosphokinase

\-hyperglycemia

MI - zones with ECG changes

zone of ischemia

zone of hypoxic injury

zone of infarction and necrosis

MI treatment

hospital, oxygen and asprin, morphine sulfate, bed rest, surgery, PCI

MI complications

dysrhythmias, heart failiure, cardiogenic shock, pericarditis

Coronary artery disease (acute coronary syndromes) - definition, examples, complications

sudden coronary obsturction cause of thrombiosos formation over a ruptures atheroscrosis plaque

i.e. unstable angina, MI

complications: dsyrhythmias, congestive heart failure, sudden death

Unstable angina

reversible myocardial ischemia and a harbinger of impending infarction

episodes of vessel occlusion and vasoconstriction

unstable angina treatment

hospitalization, nitrates, antithrombotics, anticoaugulants, eta blockers, emergent PCI

Disorders of the heart wall (pericardium)

Acute pericarditis

Pericardial effusion

constructive (restrictive) pericarditis

Acute pericarditis

inflammation of the sac that holds the heart - pericardium

pericardial effusion

accumulation of fluid in pericardial cavity

contructive (restrictive) pericarditis

fiber scarring tissue forming in pericardium

Disorder of the myocardium - cardiomyopathies

heart wall, affects neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling

types of cardiomyopathies

dont need to memorize